WILDERNESS MEDICINE
WILDERNESS MEDICINE Sixth Edition Paul S. Auerbach, MD, MS, FACEP, FAWM Redlich Family Professor of Surgery Division of Emergency Medicine Department of Surgery Stanford University School of Medicine Stanford, California
1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899
WILDERNESS MEDICINE
ISBN: 978-1-4377-1678-8
Copyright © 2012, 2007, 2001, 1995, 1989, 1983 by Mosby, an imprint of Elsevier Inc. Chapter 83 © 2012 by Michael E. Jacobs and Charles G. Hawley Chapter 3 all figures, tables, and photographs © Dr. Mary Ann Cooper Chapter 29 photographs © Dr. Grant S. Lipman, Elsevier granted non-exclusive license to publish Chapter 20 © Swaminatha Mahadevan No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).
Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of product liability, negligence, or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Wilderness medicine / [edited by] Paul S. Auerbach.—6th ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4377-1678-8 (hardcover : alk. paper) I. Auerbach, Paul S. [DNLM: 1. Wilderness Medicine. 2. Emergency Treatment—methods. 3. Environmental Exposure. 4. Recreation. 5. Rescue Work. 6. Survival. WB 107] LC classification not assigned 616.9′8—dc23 2011032078 Acquisitions Editors: Dolores Meloni and Stefanie Jewell-Thomas Developmental Editor: Lucia Gunzel Publishing Services Manager: Anne Altepeter Associate Project Manager: Jessica Becher Design Direction: Steve Stave Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1
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Contributors Javier A. Adachi, MD, FIDSA, FACP
Associate Professor, Department of Infectious Diseases, Infection Control, and Employee Health, The University of Texas MD Anderson Cancer Center; Adjunct Professor, The University of Texas Health Science Center at Houston, Medical School and School of Public Health; Adjunct Professor, Baylor College of Medicine, Houston, Texas; Visiting Professor, Universidad Peruana Cayetano Heredia, Lima, Peru
Martin E. Alexander, BScF, MSc, PhD, RPF
Adjunct Professor, Wildland Fire Science and Management, Department of Renewable Resources, Alberta School of Forest Science and Management, University of Alberta; Honorary Research Associate, Faculty of Forestry and Environmental Management, University of New Brunswick, Fredericton, New Brunswick, Canada; Senior Fire Behavior Research Officer (Retired), Canadian Forest Service, Northern Forestry Centre, Edmonton, Alberta, Canada
Robert C. Allen, DO, FACEP
Colonel, United States Air Force MC CFS (Retired), Contingency Operations Division, United States Air Force School of Aerospace Medicine, Brooks City, Texas
Susan Anderson, MD, MS
Clinical Associate Professor, Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, California; Travel, Tropical, and Wilderness Medicine Consultant, Travel Medicine and Emergency/Urgent Care, Palo Alto Medical Foundation, Palo Alto, California
Aaron L. Baggish
Associate Director, Cardiovascular Performance Program, Division of Cardiology, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts
Jennifer G. Baine, MD
Clinical Instructor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California
Buddha Basnyat, MD, MSc, FACP, FRCP(E)
Medical Director, Nepal International Clinic, Himalayan Rescue Association; Principal Investigator, Oxford University Clinical Research Unit, Patan Academy of Health Sciences, Kathmandu, Nepal
Ryan P. Bayley, MD
Resident Physician, Emergency Medicine, New York-Presbyterian Weill Cornell Medical Center and Columbia University Medical Center, New York, New York
Greta J. Binford, PhD
Associate Professor of Biology, Lewis and Clark College, Portland, Oregon
Nicholas H. Bird, BA, MD, DABFM, DABPM
CEO and Chief Medical Officer, Divers Alert Network, Durham, North Carolina
Christopher J. Andrews, BE, MBBS, MEngSc, PhD, JD, EDIC, DipCSc, GDLP
Ryan Blumenthal, MBChB (Pret), MMed (Med Forens) Pret, FC for Path (SA), Dip For Med (SA)
E. Wayne Askew, PhD
Jolie Bookspan, MEd, PhD, FAWM
Mt Ommaney Family Clinic, Australia
Colonel, United States Army MSC (Retired), Professor and Chair, Division of Nutrition, University of Utah, Salt Lake City, Utah
Dale Atkins, BA
Forensic Pathologist, Department of Forensic Medicine, University of Pretoria, Pretoria, Gauteng, South Africa
Medical Director, Neck and Back Pain Sports Medicine, Academy of Functional Exercise Medicine, Temple University, Philadelphia, Pennsylvania
President, American Avalanche Association; Vice President, Avalanche Rescue Commission; International Commission for Alpine Rescue, North America Training and Education Manager, RECCO, AB, Boulder, Colorado
Ralph S. Bovard, MD, MPH, FACSM
Paul S. Auerbach, MD, MS, FACEP, FAWM
Warren D. Bowman, MD, FACP
Redlich Family Professor of Surgery, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California
Kira Bacal, MD, PhD, MPH, FACEP
Phase 2 Director, Medical Programme Directorate, University of Auckland, Auckland, New Zealand
Howard D. Backer, MD, MPH
Director, California Emergency Medical Services Authority
Department of Occupational and Environmental Medicine, HealthPartners, St. Paul, Minnesota
Clinical Associate Professor Emeritus, Department of Internal Medicine, University of Washington School of Medicine, Seattle, Washington; Staff Physician (Retired), Department of Internal Medicine, Division of Hematology-Oncology, The Billings Clinic, Billings, Montana
Leslie V. Boyer, MD
Director, Venom Immunochemistry, Pharmacology, and Emergency Response Institute; Associate Professor of Pathology, University of Arizona, Tucson, Arizona
v
CONTRIBUTORS
John E. Bradford, RN, MPAS, PA-C
Charles Clarke, MA, MBBCh, FRCP
Mark A. Brandenburg, MD
Kenneth S. Cohen, MA, MSTh
Peace Corps Medical Officer, United States Peace Corps, Malawi, Lilongwe, Malawi, Africa; Clinical Adjunct Professor, University of Utah Physician Assistant Program, Salt Lake City, Utah
Medical Director, Emergency Department, Bristow Medical Center, Bristow, Oklahoma; Medical Director, Emergency Medical Services, Tulsa Technology Center, Tulsa, Oklahoma
Beau Briese, MD
Resident Physician, Division of Emergency Medicine, Stanford/ Kaiser Emergency Medicine Residency Program, Stanford University, Stanford, California
Colin M. Bucks, MD
Clinical Instructor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California
George H. Burgess
Florida Program for Shark Research, Florida Museum of Natural History, University of Florida, Gainesville, Florida
Sean P. Bush, MD, FACEP
Honorary Consultant Neurologist, National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom
Independent Scholar, Traditional Healer, Nederland, Colorado
Stephen D. Coleman, MD
Clinical Assistant Professor, Department of Anesthesia, Pain Management Division, Stanford University School of Medicine, Stanford, California
Bryan R. Collier, DO, FACS, CNSP
Assistant Professor of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee
Shon Compton, MPAS, PA-C
Major, Specialty Corps (Retired), Chief Instructor, Center for Predeployment Medicine, United States Army Medical Department Center and School, Fort Sam Houston, Texas
Benjamin B. Constance, MD
Professor of Emergency Medicine, Loma Linda University School of Medicine, Loma Linda, California
Chief Resident Physician, Division of Emergency Medicine, Stanford/Kaiser Emergency Medicine Residency Program, Stanford University, Stanford, California
Frank K. Butler Jr., BS, MD
Donald C. Cooper, PhD, MBA, EMT-P
Dale J. Butterwick, ATC(C), BA, MSc
Jimmy L. Cooper, MD, FACEP
Chairman, Committee on Tactical Combat Casualty Care, Defense Health Board, Pensacola, Florida
Associate Professor, Faculty of Kinesiology, University of Calgary; Former President, Canadian Pro Rodeo Sport Medicine Team, Calgary, Alberta, Canada
Steven C. Carleton, MD, PhD
Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio
Betty Carlisle, MD
Adjunct Assistant Professor, Department of Public Health and Preventive Medicine, State University of New York Upstate Medical University; Staff Physician, Emergency Department, St. Joseph’s Hospital, Syracuse, New York
Scott P. Carroll, PhD
Department of Entomology, University of California, Davis, California
John W. Castellani, PhD
Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts
Samuel N. Cheuvront, PhD
Research Physiologist, Division of Thermal and Mountain Medicine, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts
Richard F. Clark, MD
Professor of Clinical Medicine, Director, Division of Medical Toxicology, University of California, San Diego, San Diego, California
vi
State Fire Marshal, Department of Commerce, State of Ohio, Columbus, Ohio
Staff Physician, Department of Emergency Medicine, Director, Center for Predeployment Medicine, San Antonio, Texas
Mary Ann Cooper, MD, FAMS, FAAEM
Emerita Professor, Department of Emergency Medicine, University of Illinois College of Medicine, Chicago, Illinois
Kevin Coppock, BSc, MSc
Head of Mission, Northern Sudan, Médecins Sans Frontières, Khartoum, Sudan
Larry I. Crawshaw, PhD
Professor Emeritus, Department of Biology, Portland State University, Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, Oregon
Joy E. Crook, MD, MPH
Instructor, Department of Emergency Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland
Gregory A. Cummins, DO, MS
Assistant Clinical Instructor, Department of Internal Medicine, Kansas University of Medicine and Biosciences; Hospitalist, Department of Medicine, North Kansas City Hospital, Kansas City, Missouri
Tracy A. Cushing, MD, MPH, FACEP, FAWM
Assistant Professor, Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, Colorado; Attending Physician, Fellowship Director, Denver Health Wilderness Medicine Fellowship, Department of Emergency Medicine, Denver Health Medical Center, Denver, Colorado
Specialty Doctor, Emergency Department, Bristol Royal Infirmary, Bristol, United Kingdom
Daniel F. Danzl, MD
Professor and Chair, Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky
Ian Davis, MBBCH, BSc (Hons)
Herbert L. DuPont, MD
Professor and Director, Center for Infectious Diseases, University of Texas School of Public Health and Medical School; Chief of Internal Medicine, St. Luke’s Episcopal Hospital; Vice Chairman, Department of Medicine, Baylor College of Medicine, Houston, Texas
Blair Dillard Erb, BS, MD, FACP, FACC
Past President, Wilderness Medical Society, The Study Center, Townsend, Tennessee
Resident Medical Officer, Department of Accident and Emergency, Cirencester Hospital, Gloucestershire; Polar Medicine, Medical Cell, Royal Geographical Society, London; Chief Medical Officer, Polar Challenge, Venture Group, Cirencester, England, United Kingdom
Timothy B. Erickson, MD
Kathleen Mary Davis, BScF, MSc
Charles D. Ericsson, MD
Kevin Davison, ND, Lac
Peter J. Fagenholz, MD
Superintendent, Montezuma Castle and Tuzigoot National Monument, National Park Service, Camp Verde, Arizona
Director, Maui Prolotherapy Clinic, Hamakuapoko, Peahi, Haiku, Maui, Hawaii
Chad P. Dawson, BS, MPS, PhD
Professor, Forest and Natural Resources Management, State University of New York College of Environmental Science and Forestry, Syracuse, New York
Janice A. Degan, RN, MS
Senior Research Nurse, Venom Immunochemistry, Pharmacology, and Emergency Response Institute, Arizona Health Sciences Center, University of Arizona, Tucson, Arizona
Thomas G. DeLoughery, MD, FACP
Professor, Department of Emergency Medicine, Division of Medical Toxicology; Director, Center for Global Health, University of Illinois College of Medicine, Chicago, Illinois
Professor of Medicine, Head, Clinical Infectious Disease, Division of Infectious Disease, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, Texas
Department of Surgery, Division of Trauma, Emergency Surgery, and Critical Care, Massachusetts General Hospital; Instructor in Surgery, Harvard Medical School, Boston, Massachusetts
Joanne N. Feldman, MD, MS
Clinical Faculty, Division of Emergency Medicine, University of California, Los Angeles, Los Angeles, California
D. Nelun Fernando, BA, MA, PhD
Department of Geography, Rutgers University, New Brunswick, New Jersey
Murray E. Fowler, BS, DVM
Professor of Medicine, Pathology, and Pediatrics, Head, Benign Hematology Section, Oregon Health and Science University, Portland, Oregon
Professor Emeritus, Veterinary Medicine and Epidemiology, University of California, Davis, California
Arlene E. Dent, MD, PhD
Assistant Professor, Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio
Clinical Associate Professor, Department of Dermatology, University of North Carolina School of Medicine, Chapel Hill, North Carolina
Thomas F. Ditzler, PhD, MA, FRSPH, FRAI
Michael E. Franco, Major, MSM, MPAS, PA-C
Director of Research, Department of Psychiatry, Tripler Army Medical Center, Honolulu, Hawaii
Mark Donnelly, MD
Salem Emergency Department, Salem, Oregon
Howard J. Donner, MD
Wilderness Medicine Instructor, Mountain Medical Seminars, Bozeman, Montana; Adventure Training Coordinator, The Finer Points of Flying, San Francisco, California
Mark S. Fradin, MD
Chief, Plans and Operations, United States Army Environmental Management Systems Programs Office, United States Army Medical Department Center and School, Fort Sam Houston, Texas
Luanne Freer, MD, FACEP, FAWM
Medical Director, Medcor, Yellowstone National Park, Wyoming; Founder and Director, Everest Base Camp Medical Clinic, Himalayan Rescue Association, Kathmandu, Nepal
Eric Douglas, BA, EMT, DMT
Steven P. French, MD, BS, MS, IUCN, ASNE, SFW
Jennifer Dow, MD, FACEP, FAWM
Nathan K. Friedline, MD
Director, Education, Divers Alert Network, Durham, North Carolina
Medical Director, Denali National Park and Preserve; Medical Director, National Park Service, Alaska Region, Department of Emergency Medicine, Alaska Regional Hospital, Anchorage, Alaska
Co-founder and Research Director, Yellowstone Grizzly Foundation, Jackson Hole, Wyoming
Resident, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah; Captain, United States Army, 32nd Medical Brigade, Fort Sam Houston, Texas
vii
CONTRIBUTORS
Jon Dallimore, MB, BS, MSc, MRCGP, MCEM, FFTM RCPS (Glasg), DCH, DRCOG
CONTRIBUTORS
Raymond R. Gaeta, MD
Charles G. Hawley, BS
Tom Garrison, BS, MA, PhD
David M. Heimbach, MD
Associate Professor, Department of Anesthesiology, Medical Director, Pain Management Service, Stanford University School of Medicine, Stanford, California
Professor, Department of Oceanography, Orange Coast College, Costa Mesa, California; Adjunct Professor, Higher Education, University of Southern California, Los Angeles, California
Daniel Garza, MD
Assistant Professor, Department of Orthopaedic Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California
Alan Gianotti, MS, MD
Clinical Assistant Professor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California
Gordon G. Giesbrecht, BPE, BTh, MPE, PhD
Professor of Thermophysiology, Health Leisure and Human Performance Research Institute, University of Manitoba; Professor, Department of Anesthesia, University of Manitoba, Winnipeg, Manitoba, Canada
Kimberlie A. Graeme, BS, MD
Division of Emergency Medicine, Naval Medical Center San Diego, San Diego, California
Colin K. Grissom, MD
Associate Professor of Medicine, University of Utah School of Medicine; Associate Medical Director, Shock Trauma Intensive Care Unit, Intermountain Medical Center, Murray, Utah
Kirby R. Gross, MD, FACS
Trauma Services, United States Army Medical Department, Walter Reed Army Medical Center, Washington, DC
Peter H. Hackett, MD
Clinical Professor of Surgery, Department of Emergency Medicine, Altitude Research Center, University of Colorado Denver School of Medicine, Denver, Colorado; Director, Institute for Altitude Medicine, Telluride, Colorado
N. Stuart Harris, MD
Chief, Division of Wilderness Medicine, Director, Wilderness Medicine Fellowship, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery, Harvard Medical School, Boston, Massachusetts
Patricia R. Hastings, DO, MPH, FACEP, RN, NREMT
Colonel, Medical Corps, United States Army; MEDCOM Liaison, Department of Homeland Security, Washington, DC, Department of Emergency Medicine, Brooke Army Medical Center, San Antonio, Texas
Seth C. Hawkins, MD, FACEP, FAWM
Director, Mountain Emergency Physicians; Medical Director, Burke Emergency Medical Services Special Operations Team; Executive Director, Appalachian Center for Wilderness Medicine, Morganton, North Carolina; Assistant Professor, Emergency Medical Care Program, Western Carolina University, Cullowhee, North Carolina
viii
Vice President, West Marine, Safety at Sea Moderator, United States Sailing Technical Board Member, American Boat and Yacht Council, Santa Cruz, California
Professor of Surgery, University of Washington School of Medicine, Seattle, Washington
Carlton E. Heine, MD, PhD, FACEP, FAWM
Clinical Instructor, University of Washington School of Medicine, Seattle, Washington; Attending Physician, Emergency Department, Bartlett Regional Hospital, Juneau, Alaska
Lawrence E. Heiskell, MD, FACEP, FAAFP
International School of Tactical Medicine, Palm Springs, California
John C. Hendee, PhD
Emeritus Professor and Dean (Retired), University of Idaho, College of Natural Resources, Moscow, Idaho
Henry J. Herrmann, DMD, FAGD Dentist, Falls Church, Virginia
Ronald L. Holle, BS, MS
Meteorologist, Holle Meteorology and Photography, Oro Valley, Arizona
Renee Y. Hsia, MD, MSc
Assistant Professor, Department of Emergency Medicine, University of California, San Francisco; Attending Physician, Department of Emergency Services, San Francisco General Hospital, San Francisco, California
Franklin R. Hubbell, DO
Physician and Director, Urgent Care and Spine Center, Saco River Medical Group; Physician, Director of Education, Stonehearth Open Learning Opportunities Schools; Author, Wilderness Medicine Newsletter, TMC Books, Conway, New Hampshire
Stephen E. Hudson, CEO, NTC
National Training Coordinator, National Cave Rescue Commission, National Speleological Society, Huntsville, Alabama; President, Pigeon Mountain Industries, Lafayette, Georgia
Cynthia L. Idzik-Starr, DDS
Assistant Professor, Director of Urgent Care, Department of Oral and Maxillofacial Surgery, University of Maryland Dental School, Baltimore, Maryland
Christopher H.E. Imray, PhD, MB, BS, DiMM, Clin Med Sci, FRCS, FRCP
Professor of Surgery, Warwick Medical School, Department of Vascular Surgery, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, United Kingdom
Kenneth V. Iserson, MD, MBA, FACEP, FAAEM, FIFEM
Professor Emeritus, Department of Emergency Medicine, The University of Arizona, Tucson, Arizona
United States Coast Guard Licensed Captain; Founder and Program Director, MedSail (Medicine for Mariners and Safety at Sea); Medical Director, Vineyard Medical Services, Martha’s Vineyard, Massachusetts
Ramin Jamshidi, MD
Fellow, Department of Pediatric Surgery, Children’s Hospital of Wisconsin; Clinical Instructor, Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin; Adjunct Professor, Physics Department, University of California, San Francisco, San Francisco, California
James M. Jeffers, BA, LLB, LLM, MPhil
PhD Candidate, Department of Geography, Rutgers University, New Brunswick, New Jersey
Jamie G. Jenkins, MD
Brian J. Krabak, MD, MBA
Clinical Associate Professor, Department of Rehabilitation, Orthopedics, and Sports Medicine; Team Physician, Seattle Children’s Sports Medicine, Seattle University Athletics, University of Washington; Team Physician, USA Swimming; Medical Director, RacingThePlanet: 4 Deserts Ultra Marathon Series, Seattle, Washington
Andrew C. Krakowski, MD
Pediatrician and Dermatologist, Rady Children’s Hospital of San Diego, University of California, San Diego, San Diego, California; Founder and Director, boonDOCS Wilderness and Travel Medicine, La Jolla, California
Peter Kummerfeldt, AD
President, OutdoorSafe, Former Survival Training Director, United States Air Force Academy, Colorado Springs, Colorado
Ultrasound Fellow, Department of Emergency Medicine, Washington Hospital Center, Georgetown University Hospital, Union Memorial Hospital, Washington, DC
Ashley R. Laird, MD
Kirsten Johnson, MD, MPH, CCFP-EM
Carolyn S. Langer, MD, JD, MPH
Assistant Professor, Department of Family Medicine; Director, University Humanitarian Studies Initiative; Affiliated Faculty, Institute for Health and Social Policy, McGill University, Montreal, Canada; Affiliated Faculty, Harvard Humanitarian Initiative, Harvard University, Cambridge, Massachusetts
Hemal K. Kanzaria, MD
Resident Physician, Department of Emergency Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, California
Emergency Physician, Sonora Regional Medical Center, Sonora, California
Instructor, Harvard Massachusetts
School
of
Public
Health,
Boston,
Patrick H. LaValla
CEO, ERI International; Operations Chief, All Hands Consulting; Former President, National Association for Search and Rescue, Olympia, Washington
Jay Lemery, MD, FACEP, FAWM
Lee A. Kaplan, MD
Clinical Professor, Department of Dermatology, University of California, San Diego Health System, La Jolla, California
Assistant Professor, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital; President-Elect, Wilderness Medical Society; Visiting Scientist, François-Xavier Bagnoud Center for Health and Human Rights, Harvard School of Public Health, Boston, Massachusetts
Misha R. Kassel, MD
Lisa R. Leon, PhD
Stephanie Kayden, MD, MPH
Benjamin D. Levine, MD, FACC, FACSM
Clinical Instructor, Departments of Emergency Medicine and Orthopaedic Surgery, Stanford University School of Medicine, Stanford, California
Director, Harvard International Emergency Medicine Fellowship; Attending Physician, Brigham and Women’s Hospital; Instructor, Harvard Medical School; Faculty, Harvard Humanitarian Initiative, Boston, Massachusetts
James W. Kazura, MD
Professor of International Health and Medicine, Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio
Robert W. Kenefick, PhD
Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts
Alexa B. Kimball, MD, MPH
Vice Chair, Department of Dermatology, Massachusetts General Hospital; Associate Professor, Harvard Medical School, Boston, Massachusetts
Judith R. Klein, MD, FACEP
Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts
Director, Institute for Exercise and Environmental Medicine; S. Finley Ewing Jr., Chair for Wellness, Texas Health Presbyterian Dallas; Harry S. Moss Heart Chair for Cardiovascular Research; Professor of Medicine and Cardiology, Distinguished Professorship in Exercise Science, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas
Matthew R. Lewin, MD, PhD, FACEP
Director, Center for Exploration and Travel Heath, California Academy of Sciences, San Francisco, California
James R. Liffrig, MD, MPH, FAAFP
Chair, Department of Family Medicine, Womack Army Medical Center, Fort Bragg, North Carolina; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland
Grant S. Lipman, MD, FACEP
Clinical Assistant Professor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California
Assistant Professor, Department of Emergency Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, California ix
CONTRIBUTORS
Michael Jacobs, MD, FAWM
CONTRIBUTORS
Joanne Liu, MDCM, FRCPC
Board of Directors, Médecins Sans Frontières-Switzerland, Assistant Professor, Sainte-Justine Hospital, Montreal, Canada
Vicki Mazzorana, MD, FACEP, FAAEM, FAWM
Andrew M. Luks, MD
Assistant Professor, Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington
Associate Clinical Professor, Department of Emergency Medicine, University of Nevada School of Medicine; Codirector, Wilderness Medicine Clerkship; Co-medical Director, Death Valley, Joshua Tree National Park, Mojave National Reserve; Ringside Physician, Nevada Athletic Commission, Las Vegas, Nevada
Binh T. Ly, MD, FACMT
Loui H. McCurley, RAT, TRS
Professor, Director, Medical Toxicology Fellowship, Division of Medical Toxicology; Director, Emergency Medicine Residency, Department of Emergency Medicine, University of California San Diego, California Poison Control System, San Diego, California
Edgar Maeyens Jr., MD
Board of Visitors, Nicholas School of the Environment, Duke University, Durham, North Carolina; Private Practice Dermatology, Dermatopathology and Mohs Surgery, Coos Bay, Oregon
Swaminatha V. Mahadevan, MD, FACEP, FAAEM
Associate Professor of Surgery and Associate Chief, Division of Emergency Medicine, Stanford University School of Medicine; Emergency Department Medical Director, Stanford University Medical Center, Stanford, California
Rick Marinelli, ND, MAcOM
Clinical Professor, National College of Natural Medicine, Doctoral Faculty, Division of Biomedicine, Oregon College of Oriental Medicine, Portland, Oregon
David S. Markenson, MD, FAAP, FACEP
Medical Director, Disaster Medicine and Regional Emergency Services, Westchester Medical Center, Maria Fareri Children’s Hospital; Professor of Pediatrics, New York Medical College; Director, Center for Disaster Medicine and Professor of Clinical Public Health, New York Medical College School of Health Sciences and Practice, Valhalla, New York
Millicent Marmer, BA, MS
Graduate Student, Alden March Bioethics Institute, Albany Medical College, Albany, New York
Armando Márquez Jr., MD, FACEP
Assistant Clinical Professor, Director, Emergency Medical Services, Department of Emergency Medicine, University of Illinois College of Medicine, Chicago, Illinois
Denise Martinez, MS, RD
Adjunct Faculty, Division of Nutrition, University of Utah, Salt Lake City, Utah
Nicholas P. Mason, MB, ChB, FRCA
Consultant in Intensive Care Medicine, Royal Gwent Hospital, Newport, United Kingdom
Michael J. Matteucci, MD, FAAEM
Assistant Professor, Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Director, Emergency Medicine Residency Program, Emergency Medicine Department, Naval Medical Center San Diego, San Diego, California
x
Technical Rescue Specialist, Alpine Rescue Team, Evergreen, Colorado; Technical Director, Vertical Rescue Solutions; Vice President, Pigeon Mountain Industries, Denver, Colorado
Marion C. McDevitt, DO, MPH
Associate Director, Wilderness Medicine Emergency Medical Services Fellowship; Associate Director, Global Health Fellowship; Assistant Professor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah
Marilyn McHarg, MSc (A), LLD (Hon)
Executive Director, Médecins Sans Frontières-Canada, Toronto, Ontario, Canada
Scott E. McIntosh, MD, MPH
Assistant Professor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah
Christopher M. McStay, MD, FACEP, FAWM
Assistant Professor of Emergency Medicine, Chief of Service, Bellevue Hospital Center Emergency Department, Department of Emergency Medicine, New York University School of Medicine, New York, New York
Timothy P. Mier, BA, EMT-P
Deputy Fire Marshal, Cuyahoga Falls Fire Department, Cuyahoga Falls, Ohio
Alicia B. Minns, MD
Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Division of Medical Toxicology, University of California, San Diego, San Diego, California
John Mioduszewski, BA, MA
Department of Geography, Rutgers University, New Brunswick, New Jersey
James K. Mitchell, PhD
Professor of Geography, Rutgers University, New Brunswick, New Jersey
James Moore, RN, BSc (Hons), Dip TravMed, MFTM, RCPS (Glasg), FRGS
Director, Travel Health Consultancy, Exeter, Devon, United Kingdom
Larry A. Moore, MD
Department of Emergency Medicine, Penrose-St. Francis Hospital, Wilderness Medicine Instructor, WildernessWise, Colorado Springs, Colorado
Barry Morenz, MD
Associate Professor of Psychiatry, Department of Psychiatry, College of Medicine, University of Arizona, Tucson, Arizona
Professor of Surgery and Biomedical Informatics, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee
Roger B. Mortimer, MD
Health Sciences Associate Clinical Professor, Department of Family and Community Medicine, University of California, San Francisco; Fresno Medical Education Program, Western Region Coordinator, National Cave Rescue Commission, Fresno, California
Michael J. Mosier, MD
Assistant Professor of Surgery, Loyola University Medical Center, Maywood, Illinois
Parveen K. Parmar, MD, MPH
Associate Director, International Emergency Medicine Fellowship, Brigham and Women’s Hospital; Associate Faculty, Harvard Humanitarian Initiative, Harvard Medical School, Boston, Massachusetts
Naresh J. Patel, DO
Private Practice, Fort Wayne Allergy and Asthma Consultants, Fort Wayne, Indiana
Sheral S. Patel, MD, FAAP
Consultant, Pediatrics and Pediatric Infectious Diseases, Hartford, Connecticut
Martin I. Radwin, MD
Robert W. Mutch, BA, MScF, DF (Honorary) Consultant, Fire Management Applications, Darby, Montana
Department of Medicine, Granger Medical Clinic, Chief of Gastrointestinal Endoscopy, Department of Medicine, Pioneer Valley Hospital, Salt Lake City, Utah
Kei Nagashima, MBSS, DMSci
Sheila B. Reed, MS
Professor, Laboratory of Integrative Physiology (Body Temperature and Fluid Laboratory), School of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan
Mayumi Nakamura, PhD
Consultant, Disaster Risk Reduction and Development, Middleton, Wisconsin
William P. Riordan Jr., MD, MS†
Visiting Researcher, Faculty of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan
Assistant Professor of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee
Eric K. Noji, MD, MPH
Robert C. Roach, PhD
Chairman and CEO, Noji Global Health and Security LLC, Director (Retired), International Emergency and Refugee Health Program, Centers for Disease Control and Prevention, Washington, DC
Robert L. Norris Jr., MD
Professor of Surgery, Stanford University School of Medicine; Chief, Division of Emergency Medicine, Stanford University Medical Center, Stanford, California
Director, Altitude Research Center; Co-Chair, International Hypoxia Symposia, Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, Colorado
David A. Robinson, PhD
Professor and New Jersey State Climatologist, Department of Geography, Rutgers University, New Brunswick, New Jersey
Eloy Rodriguez, PhD
Command Surgeon, United States Army Training and Doctrine Command, Fort Monroe, Virginia
James A. Perkins Endowed Professor of Environmental and Toxicology Studies, Institute of Comparative Environmental Toxicology, Department of Plant Biology, Cornell University, Ithaca, New York
Lesley J. Ogden, MD, MBA, FACEP
Nancy V. Rodway, MD, MPH, MS
Karen K. O’Brien, MD
Staff Physician and Assistant Emergency Room Director, Department of Emergency Medicine, Samaritan North Lincoln Hos pital, Lincoln City, Oregon; Clinical Faculty, Department of Emergency Medicine, Western University of Health Sciences, Pomona, California; Affiliate Assistant Professor, School of Medicine, Oregon Health and Science University, Portland, Oregon
Bohdan T. Olesnicky, MD
Medical Director of Occupational Medicine and Ambulatory Care, Lake Health Hospital System, Painesville, Ohio; Adjunct Faculty, Department of Occupational Medicine, Ohio State University College of Medicine, Columbus, Ohio
Richard S. Salkowe, DPM, FACFAS, FAWM
PhD Candidate, Department of Geography, Environmental Science, and Policy, University of South Florida, Tampa, Florida
SWAT Team Physician, Palm Springs Police Department, Palm Springs, California; Partner, Global Protection Medical Group, Indian Wells, California; Director of EMS, Eisenhower Medical Center, Rancho Mirage, California
Sandra M. Schneider, MD
Sheryl Olson, BSN, RN, FAWM, CCRN
Robert B. Schoene, MD, FACP
Outdoor Survival and Navigation Instructor, Flight Nurse, Wilderness Safety Instructor, Colorado Springs, Colorado
Edward J. Otten, MD
Professor of Emergency Medicine and Pediatrics, Director, Division of Toxicology, University of Cincinnati, Cincinnati, Ohio
Professor and Chair Emeritus, Department of Emergency Medicine, University of Rochester, Rochester, New York
Clinical Professor of Medicine, Division of Pulmonary and Critical Care Medicine, University of Washington School of Medicine, Seattle, Washington, Bozeman Deaconess Hospital, Bozeman, Montana
Justin Sempsrott, MD, EMT
Emergency Medicine Resident, University of Nevada School of Medicine, Las Vegas, Nevada †
Deceased.
xi
CONTRIBUTORS
John A. Morris Jr., MD, FACS
CONTRIBUTORS
Jamie R. Shandro, MD, MPH
Assistant Professor, Division of Emergency Medicine, University of Washington School of Medicine, Seattle, Washington
Charley Shimanski
Education Director and Past President, Mountain Rescue Association; Senior Vice President, Disaster Services, American Red Cross, Washington, DC
Uta S. Shimizu, MD
Clinical Instructor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California
David R. Shlim, MD
Jackson Hole Travel and Tropical Medicine, Jackson, Wyoming
Joshua D. Shofner, MD
Resident, Department of Dermatology, Massachusetts General Hospital, Boston, Massachusetts
Julie A. Switzer, MD
Assistant Professor, Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, Minnesota; Director, Geriatric Orthopaedic Trauma Program, Regions Hospital, St. Paul, Minnesota
Robert I. Tilling, BA, MS, PhD
Senior Research Volcanologist, Volcano Science Center, U.S. Geological Survey, Menlo Park, California
Ken Tokizawa, PhD
Assistant Professor, Faculty of Sport Sciences, Waseda University, Tokorozawa, Saitama, Japan
Joseph E. Tonna, MD
Division of Emergency Medicine, Stanford/Kaiser Emergency Medicine Residency Program, Stanford University School of Medicine, Stanford, California
David A. Townes, MD, MPH, DTM&H
Eunice Singletary, MD, FACEP
Clinical Associate Professor, Department of Emergency Medicine, University of Virginia, Charlottesville, Virginia
Associate Professor of Medicine, Division of Emergency Medicine; Adjunct Associate Professor of Global Health, Department of Global Health, University of Washington School of Medicine, Seattle, Washington
Kieran Smart, MBChB, MSc, MPH, MRCGP
Stephen J. Traub, MD
Physician, Florida FL-3 Disaster Medical Assistance Team, Florida State Medical Response Team Region 4; Advisor, Space Medicine Associates; Adjunct Clinical Assistant Professor, Department of Community Health and Family Medicine, University of Florida College of Medicine, Gainesville, Florida
Jennifer Cohen Smith, MD
Medical Toxicologist, Banner Good Samaritan Medical Center, Phoenix, Arizona
Will Smith, MD, EMT-P
Clinical Faculty, Division of Emergency Medicine, WWAMI, University of Washington School of Medicine, Seattle, Washington; Medical Director, Teton County Search and Rescue, Jackson Hole Fire/EMS, Grand Teton National Park; President and Medical Director, Wilderness and Emergency Medicine Consulting, LLC; Faculty, Student/Resident Rotation Coordinator, Department of Emergency Medicine, St. John’s Medical Center, Jackson, Wyoming
Matthew C. Spitzer, MD, DTMH
Chairman, Department of Emergency Medicine, Mayo Clinic Arizona, Phoenix, Arizona; Assistant Professor of Emergency Medicine, Mayo Medical School, Rochester, Minnesota
Yuki Uchida, MS
PhD Student, Laboratory of Integrative Physiology (Body Temperature and Fluid Lab), Graduate School of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan
Sydney J. Vail, MD, FACS
Director of Trauma Surgery, Medical Director, Tactical Medicine Program, Trauma Center, Maricopa Medical Center, Phoenix, Arizona
Karen B. Van Hoesen, MD
Clinical Professor, Department of Emergency Medicine, University of California, San Diego; Director, University of California San Diego Diving Medicine Center; Director, Undersea and Hyperbaric Medicine Fellowship, University of California San Diego, San Diego, California
President, Doctors Without Borders/Médecins Sans Frontières, Member, International Council and International Council Board, Médecins Sans Frontières; Assistant Clinical Professor of Medicine, Director, Predoctoral Education, Center for Family and Community Medicine, College of Physicians and Surgeons of Columbia University, New York, New York
Michael VanRooyen, MD, MPH, FACEP
Alan M. Steinman, MD, MPH, FACPM
Raghu Venugopal, MD, MPH, FRCPC
Rear Admiral (Retired), United States Public Health Service, Director of Health and Safety, United States Coast Guard, Olympia, Washington
Robert C. Stoffel
CEO, Emergency Response International; Prime Survival Training Contractor, Department of Homeland Security; Customs and Border Protection, United States Coast Guard Aviation Survival Technician Program, Cashmere, Washington
Jeffrey Suchard, MD
Professor of Clinical Emergency Medicine, Director of Medical Toxicology, Department of Emergency Medicine, University of California, Irvine Medical Center, Orange, California xii
Chief, International Division, Department of Emergency Medicine, Brigham and Women’s Hospital; Director, Harvard Humanitarian Initiative, Harvard University; Associate Professor, Department of Emergency Medicine, Harvard Medical School, Boston, Massachusetts
Assistant Professor of Medicine, University of Toronto; Attending Physician, Department of Emergency Medicine, University Health Network, Toronto, Ontario, Canada
Brandee L. Waite, MD
Medical Director, Racing The Planet: 100, Ultra Marathon Series; Assistant Professor, Physical Medicine and Rehabilitation, Sports Medicine, University of California, Davis Medical Center, Sacramento, California
John Walden, MD, DTM&H
Professor and Chairman, Department of Family and Community Health, Marshall University Joan C. Edwards School of Medicine, Huntington, West Virginia
Emeritus Professor of Tropical Medicine, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom
Eric A. Weiss, MD, FACEP
Associate Professor of Surgery, Director, Wilderness Medicine Fellowship, Division of Emergency Medicine, Stanford University School of Medicine; Medical Director, Office of Emergency Management, Stanford University Medical Center, Lucile Packard Children’s Hospital, Stanford, California
Jan West, PhD
Visiting Professor of Biology, Soka University of America, Aliso Viejo, California
James A. Wilkerson III, MD
Merced Pathology Medical Group (Retired), Merced, California
Tamae Yoda, PhD
Associate Professor, Department of Interdisciplinary Studies, Faculty of International Liberal Arts, Dokkyo University, Soka, Saitama, Japan
Lynn E. Yonge, MD, FAAFP, FAWM
Chairman, Environmental Council, Wilderness Medical Society, Director, Wilderness Medicine Training, Outward Bound, Assistant Clinical Professor, The University of South Alabama College of Medicine, Mobile, Alabama
Ken Zafren, MD, FAAEM, FACEP, FAWM
Clinical Associate Professor of Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California; Staff Emergency Physician, Alaska Native Medical Center, Alaska Mountain Rescue Group, Anchorage, Alaska; Vice President, International Commission for Mountain Emergency Medicine; Associate Medical Director, Himalayan Rescue Association, Kathmandu, Nepal.
xiii
CONTRIBUTORS
David A. Warrell, MA, DM, DSc, FRCP, FRCPE, FMedSci, HonFZS, FRGS
Foreword Two hours into my first trans-Pacific flight to Hong Kong (on my way to Nepal), a flight attendant put out a call to see if there was a physician on board. I raised my hand and was taken to see a 22-year-old American soldier who was suffering a moderately severe allergic reaction to peanuts. The young man was flushed, had a diffuse urticarial rash, and felt some swelling in his throat. He was so itchy he could not sit still. The reaction had been going on for 45 minutes. As I looked him over, the captain of the plane came down the aisle to talk to me. “We’re as close as we’re going to be to Anchorage,” he said. “We can dump the entire trans-Pacific load of fuel and land there, if you say so.” I greeted this with disbelief. A few hours into my first trip to Asia, and suddenly I was in charge of the plane. I did not want to land in Anchorage if we did not have to (apart from not wanting to dump 40,000 gallons of fuel into the ocean). I asked the flight attendants to bring me the first-aid kit from the plane. I would give the soldier a shot of epinephrine and an antihistamine tablet, and we could keep going. “We don’t carry a first-aid kit,” came the reply. “We have a few bandages, that’s it.” I looked at the soldier. I did not think he was in danger of dying, but it would be a long flight for him with itchy skin and a swollen face. On the other hand, hundreds of people would be delayed a day or more, at a cost of hundreds of thousands of dollars, if we diverted to Anchorage. It occurred to me that someone on a Boeing 747 with 400 passengers might be carrying a bee sting kit. I asked the flight attendant to make an announcement, and three people raised their hands. I accepted one of the kits, injected the soldier, gave him some diphenhydramine, and watched him quickly improve. I told the captain that we could continue flying to Hong Kong. Solving problems with what you have at hand is one of the main themes of wilderness medicine, a discipline that had yet to evolve in 1979 when I was on that flight. Ten days later, I was trekking on my way to the Himalayan Rescue Association Aid Post at Pheriche, a yak-herding village at 14,000 feet, near the base of Mt Everest. Eating dinner at a teahouse next to the Thyangboche monastery, I was asked if I could help an 84-yearold Sherpa man just up the valley in Pangboche. He had fallen down his stairs and sustained a scalp laceration the day before. I was not carrying suture supplies, but I had just visited the Kunde Hospital and was familiar with the staff, so I wrote a note to request instruments and suture material. A Sherpa runner carried the note and would return with the supplies the next morning. In the morning, I walked a couple of hours to Pangboche, where I was led to the house of the man who had fallen down. He lay inside, moaning, and his hair was densely matted with blood. We carried him outside into the sun, where it was warm enough to work and there was good light. I put the instruments in a pot of water and boiled them on the hearth inside. I had no gloves and no sterile field. I poured povidone-iodine into the bowl that held the instruments and used the bowl as my sterile field, reaching into the disinfectant each time I needed to use an instrument. This kept both my hands and the instruments relatively sterile as I worked. The laceration was truly major. It split the old man’s right eyebrow and extended across his forehead and over the crown of his head to the back of his neck. A huge skin flap had been created, so I lifted it up and irrigated underneath it with copious quantities of water I had boiled earlier. I began to sew. The man moaned and muttered as I worked. I asked one of the Sherpas what he was saying. “He’s saying, ‘Leave me alone. I just want to die.’ ”
I finished the repair and placed a padded dressing on his head. I gave instructions to his son and continued my journey to the Pheriche aid post. Three days later in Pheriche, the defining case in my wilderness medicine education arrived on the back of a yak. The patient being carried down the valley was a young New Zealand nurse named Barbara. She had not been feeling well for 2 days at 16,000 feet and was no longer able to descend under her own power. Barbara was alert and oriented, although she appeared very tired. She denied having a headache, nausea, or shortness of breath over the past 2 days, and she had just descended 2000 feet. I gave her a cup of tea. She drank half the cup and then lay down and fell asleep. I sat in a chair across the room and watched her. I half-convinced myself that she looked a little blue, then talked myself out of it. She had just descended a considerable distance, with only mild symptoms of possible altitude illness. She could not have high-altitude cerebral edema (HACE). I continued this internal debate for about an hour, until I felt like I needed to know if she was okay. I touched her shoulder and spoke her name. She did not respond. I shook her gently, and she shifted slightly and made unintelligible sounds. I shook her more vigorously, but she was unable to wake up. She was no longer just sleeping—she was unconscious. There was no radio at the aid post. I sent a written note to the park ranger in Namche, requesting a helicopter rescue for early the next morning. I gave her intravenous dexamethasone and put an oxygen mask over her mouth and nose running at 2 liters per minute, trying to conserve the only two small bottles of oxygen that we had on hand. A little while later, she suddenly stirred and vomited all over her sleeping bag. Over the course of the night, she deteriorated steadily. I observed the effects of every additional drop of fluid that leaked into her brain. She became decerebrate, then flaccid, then unresponsive to deep pain. She was clearly dying. It was now just a matter of whether the helicopter would arrive in time. I felt very alone, wondering if there was anything more that I could do. The night had been completely clear when I had stepped outside before taking a short nap. When I awoke at 6:00 A.M., it was snowing. I did not think a helicopter could fly through the mountains in a snowstorm. I had kept up my hope for rescue all night long, but at that moment I began to feel that she might not make it. When that thought hit me, I found myself emotionally unprepared to watch her die. Alone in a remote aid post, with one Sherpa helper and the patient’s best friend, the circumstances were too intimate, the patient too like myself. I realized what it meant to do medicine in a wilderness setting. You are on your own. There is no one to call, no one to help. You just have to do the best you can with whatever limited resources you have. At 10:00 A.M., a Sherpa arrived carrying a portable radio. This enabled me to tell the park ranger how desperate the situation had become. His response was not encouraging. He informed me that he had been unable to reach Kathmandu by radio to request a helicopter. Later in the day, he was finally able to contact Kathmandu, but the trekking company refused to guarantee payment for a helicopter evacuation. The park ranger offered to guarantee the money himself. It got worse from there. A helicopter was ready at the airport, but the pilot had gone home for the day. When they tried to telephone him, they found that the phone lines had just gone dead. By this point, Barbara was completely unresponsive to deep pain and barely breathing at a rate of 4 times per minute. She had even lost her corneal reflexes. xv
FOREWORD
At least it had stopped snowing. I sat near the radio, waiting. The park ranger called again. “Maybe we should just try to organize the helicopter for tomorrow,” he told me. “She’s going to die this afternoon if we don’t rescue her,” I replied. “If you can’t get a helicopter this afternoon, there won’t be any point in sending one tomorrow.” “Got that,” said the ranger. Another hour went by. Finally, I heard the ranger’s voice. “Pheriche, Pheriche, Pheriche. This is Namche. The pilot has landed here and set off fuel. He’s on his way up the valley, but the weather is bad and he wants the patient ready to go.” I pulled out the intravenous line, and we secured Barbara in her sleeping bag. Her friend would fly out with her. I stepped outside the clinic and looked down the valley. Clouds whipped past the peaks. I spotted the Alouette III helicopter emerging from the clouds. I had never before been involved in a helicopter rescue, and the miraculous appearance of the aircraft seemed like an angel descending from heaven. The helicopter flew past the clinic, made an abrupt turn, and landed. The pilot shut down the rotors, but left the engine running. He waved impatiently for us to bring the patient. We carried her outside with the help of some trekkers and slid her onto the floor in the back of the helicopter, which immediately took off. We turned our faces away from the dust as the chopper disappeared down the valley, back into the clouds. It was 3 days before we got word about Barbara. She had arrived in the emergency room at Patan Hospital in Kathmandu an hour and a half after leaving us, having descended 10,000 feet. On arrival at the hospital, she was breathing 18 times per minute and was already responding to pain. Twenty-four hours later, she was sitting up in bed and eating. Thirty years later, I recognize that the key things I have learned about wilderness medicine were introduced during my experience of caring for Barbara. I was on my own, with no expert to whom I could turn for advice. I had to care for a patient in ways that I had never done in a hospital setting. I had to clean her up, turn her, catheterize her—all by candlelight, in addition to trying to figure out how to medically treat and evacuate her. Although her presentation of HACE remains the most atypical I have ever encountered, I still had to make a diagnosis and act on it, with no further tests or opinions to rely on. As I reflect back on these events, I still recall the depth of my fear that she would die despite my efforts. I have since witnessed on a number of occasions that this is a not-uncommon feeling among rescuers, who often feel devastated when the person they have tried to rescue ends up dying. Barbara’s illness taught me the value of personal experience. After this episode, the lectures I gave every day that season at the aid post on the prevention of altitude illness carried a sense of personal authority that I could not otherwise have evoked. Symptoms can be subtle. Altitude illness really can be fatal. Descent really is lifesaving. My career in medicine ran parallel to the development of the field of wilderness medicine. In the mid-1970s, physicians and mountain guides began to meet to discuss what was then called “mountain medicine.” The topics included altitude illness, first aid, frostbite, hypothermia, and evacuation. Lectures and handson workshops were included. Gradually the gatherings expanded to include topics of hiking and rafting and the skills that supported those activities, such as water disinfection, treatment of traveler’s diarrhea, and heat and cold injury. Because we were no longer talking only about the mountains, this new field was dubbed wilderness medicine. Lecturers shared their anecdotal experiences and opinions, but soon they mined the research literature and carried out investigations of their own. In 1983, the first edition of Wilderness Medicine was published. It was also in 1983 that I moved to Kathmandu to begin a 15-year stint working at the CIWEC Clinic Travel Medicine Center and started carrying out my own research into the diseases and injuries that affect travelers in Nepal. Wilderness Medicine now appears in its sixth edition. Rather than wilderness medicine defining what should be in the textbook, the textbook has helped define what is in the field of wilderness medicine. Instead of focusing solely on traditional xvi
areas, the editor has opted for inclusiveness, covering topics that include such stalwarts as lightning and frostbite, but also volcanic eruptions, combat casualty care, alligator and crocodile attacks, global humanitarian medicine, and space travel. Despite this wide range of knowledge, the specialty of wilderness medicine still has a common denominator: when something bad happens in the field, immediacy and bonding lead to an increased emotional requirement from the rescuers. In addition to diagnosis and treatment of the patient, one is confronted with limited resources and the compounding factors of weather, terrain, and isolation. Not infrequently, rescuers have to place themselves in harm’s way. At the very least, they may have to endure their own discomfort and exhaustion. Although these factors create a different dynamic of medical care, ultimately the goal is the same—to ease or prevent suffering in the patient. The quest for adventure may take travelers to countries with little or no available medical care. Many adventurers think only of their personal medical situation or of the risks that they are taking in a remote environment. They may give little or no thought to the thousands of people along their routes who can live entire lives without access to even basic medical care. The plight of the world’s poorest people may only briefly come to light at those times when a major disaster strikes. Wilderness medicine aficionados have frequently been rescuers in these extreme situations. Their experiences have sometimes taught the physicians what it really means to try to practice medicine on behalf of people who have no resources. They often return with a newly discovered desire to share medical knowledge and skills around the planet on an ongoing basis. They have come to recognize that all human beings are the same in wanting to be happy and free from suffering. Seen in this light, there is no difference between a mountaineer with altitude illness, the traveler with diarrhea, a Tibetan refugee with frostbite, the woman in an African village in the midst of a difficult birth, or a child shivering with the fever of malaria. My initial attraction to high-altitude medicine had far-reaching consequences in my personal life that I could never have foreseen. After three trekking seasons in the mountains, I moved to Kathmandu, and within a year I had volunteered to be the doctor for a Tibetan Buddhist monastery. The head of the monastery, Chokyi Nyima Rinpoche, became my teacher and close personal friend. By applying his teachings on Buddhist philosophy to my medical practice, I became more the physician I wanted to be— calmer, kinder, clear thinking, and willing to help. Our friendship led to collaboration on a book about how to train in compassion. I strongly believe that there is a way to connect wilderness medicine to conventional medicine, and even further, to our personal lives. This advice can be condensed into three key principles. First, there is competence. We should be advocates of learning and apprenticeship in the backcountry and not be satisfied with merely attaining just enough fitness to be guided on an adventure. Although one can take pleasure from achieving a distinct goal, one’s satisfaction is greatly enhanced by the cultivation of skills gained through lectures, practice in the field, and extensive personal experience. When one starts to plan a journey or an adventure, one needs to do research and fully understand the limitations imposed by that activity. Are there hazards of weather and terrain that could result in being stranded for long periods? Is there the possibility of rescue? Where is the closest medical care? To what degree are we prepared to accept the situation? Commitment means accepting the risks and limitations of a given adventure before facing the challenge, so that one can deal with it realistically. Ideally one would like to avoid having to say, “If I had known it was going to be like this, I would never have gone.” Finally, no matter what happens, one should always make decisions with full consideration of compassion. This could involve abandoning one’s own goals to help someone else or modifying the trip so that everyone can succeed. There is a famous Tibetan Buddhist saying that is true in all aspects of our lives, including our wilderness adventures:
Adventures in the wilderness, by occasionally taking us close to our limits, can teach us a great deal about our true nature. A well-known mountaineer, after living through a major rescue drama on Mt Everest, once said, “The person I wanted to be met the person I actually was.” In such defining moments, I have observed that those who abandoned their own ambitions in order to help others have always ended up happier than those who pursued only their own goals.
The wilderness is a proving ground that draws us in with its physical splendor, then tests us with hardship. We are often changed by these encounters. Whether we perceive these changes as positive or not may depend less on whether we have succeeded in our adventurous goals and more on how we learned to conduct ourselves in pursuit of those goals. The elderly Sherpa with the head laceration healed without infection and lived for 3 more years, before dying of old age. David R. Shlim, MD Author, Medicine and Compassion: A Tibetan Lama’s Guidance for Caregivers Jackson Hole, Wyoming
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FOREWORD
All the joy the world contains Has come through wishing happiness for others. All the misery the world contains Has come through wanting pleasure for oneself.
Preface The sixth edition of Wilderness Medicine arrives at an exciting juncture for the field and its practitioners. Except at the time of the origin of the practice of medicine, when one might argue that perhaps all of medicine was “wilderness medicine,” there has never been greater need for people to heal in austere settings. With each natural disaster, adventure into uncharted territory, and global humanitarian relief effort, medical professionals and amateurs alike must make diagnoses with their eyes, ears, fingertips, and noses; better understand the unique physiology and pathophysiology of extreme environments; and recognize the limitations of technology in the deepest jungles and on the most remote mountaintops. More than any other specialty of medicine, wilderness medicine engages humans with Planet Earth, as it constantly calls the question, “What can we do to help?” We should help our fellow humans, while we always seek to preserve the planet. On the eve of the sixth edition, it is fair for an editor to reminisce. I suspect that many readers of this book were not born when the first edition of Wilderness Medicine (then titled Management of Wilderness and Environmental Emergencies) was published. I owe so much to the contributors to each and every edition, who in the beginning ranged from savvy clinicians and hardy explorers to youthful (and upstart) innovators. Without the collaboration of my best friend, Edward Geehr, and inspiration from the legendary professors Charlie Houston and Dave Sabiston, this book would have never exited my typewriter. In the beginning, it was no more complicated than the fact that Ed and I loved the outdoors. We had been medical students together at Duke, where we camped and hit the beach, and then enjoyed what little free time we had as interns at Dartmouth hiking and cross-country skiing. During medical school, I had been an extern on the prairie for the Indian Health Service at Fort Belknap in Montana and Ed an instructor in the mountains of New Hampshire for Outward Bound. When we were emergency medicine residents at the University of California, Los Angeles, we attended one particular mountain medicine symposium at the Yosemite Institute and listened to Charlie Houston, Herb Hultgren, John Dill, and other experts spin tales of intertwined adventure and medicine. There was no book for physicians that covered what we had heard and what more we wished to learn, so we proposed the first edition of what became Wilderness Medicine. After more than a few turndowns, the book was published as a title in the Nursing Division at Macmillan, because even though we were young and unknown, an acquisitions editor believed in us. We endured a tempestuous relationship with our senior editor, so we eagerly moved to Mosby for the second edition. The book has remained here through a series of mergers with Saunders and Elsevier. It has been a blessing to have a publisher with a vision for the vitality and relevance of wilderness medicine, and the imagination to understand that this field crosses into uncharted territory. In this edition, Dolores Meloni, Lucia Gunzel, and Jessica Becher have put forth their wonderful Elsevier spirit. My lifelong wilderness medicine buddies are too numerous to count, sustaining me for more than three decades. Each generation has raised the bar. With every edition, we used the book to push the envelope. As the content of Wilderness Medicine expanded, so did the training, practice, research, and education. It was not my intention to define the specialty, but it happened. Somewhere around the third edition, numerous aspects of a thriving specialty emerged, eminently capable leaders arose, and I could put the cart behind the horse. Now, we run to catch up, and I suspect that it will be that way forever. As change abounds, we daily appreciate novel interrelationships that are integral to a complete understanding of wilderness
medicine. High altitude is not just about hypoxia. It is about exercise physiology, genetics, ventilatory response during sleep, and much more. Understanding frostbite requires superb knowledge of anatomy, cell membrane function, reperfusion injury, and much more. To comprehend the field management of trauma, one must integrate all of the complexities related to hemorrhage, shock, hypoxia, and pain. The entire field of wilderness medicine does much more than overlap with military medicine, disaster medicine, sports medicine, environmental medicine, and travel medicine—it defines many of their most important features. Wilderness medicine is much more holistic than I would ever have imagined. Yet as robust as it has become, it will continue to expand, because we have only scratched the surface and our need is so great to know more. In recognition of venues in which wilderness medicine has been applied, to support a continuing effort to deliver credible information about the wilderness environment, and based upon requests from readers, much has been added to this sixth edition. Some of the chapters, such as Expedition Medicine, Global Humanitarian Medicine and Disaster Relief, and Ultrasound and Telemedicine in the Wilderness, are completely new, whereas others are refinements derived from wanting to leave no stone unturned. Because wilderness medicine volunteers are so capable under difficult circumstances, such as while providing disaster or global humanitarian relief, I have invited experts to broaden the coverage and better meet the information needs of the readers. Wilderness Medicine is affected by an accelerating sea change in the publishing world. Electronic publishing—words, images, and multimedia presentations—will one day render paper pages obsolete, except for collectors. Information is available instantly and disseminates at light speed, so the obligations of authors and editors have multiplied and deepened. This edition of Wilderness Medicine occurs at a watershed, when the contributors have provided much more material than can be economically offered in printed volumes. As a result, the traditional book contains the information one must be able to retrieve even when the power fails (… and if you are willing to carry 20 pounds of textbook with you); the entire electronic offering with its additional features will be there when your Internet connection is good or the power for your tablet or e-reader is plentiful. For authors, all of this takes a bit of acclimation. For readers, I suspect the transition will be welcome. There is much discussion these days about the future of medicine and in particular, if it is headed in a good direction. The camaraderie of the wilderness medicine community negates any doubts about whether or not medicine is still a desirable career path. In the days immediately after the January 2010 earthquake in Haiti, I stood side by side in Port-au-Prince with wilderness medicine colleagues from around the globe—pediatric surgeons from Switzerland, logistics experts from Norway, mountaineers from the United States, ocean divers from Spain— to put our collective skills to the most difficult challenge of our careers. Time and time again, military medical personnel make essential use of research and practice advances generated by wilderness medicine specialists that decrease morbidity and improve survival in extreme environmental settings. During global humanitarian relief efforts, when there are scarce resources, physicians, nurses, and other health care professionals who have learned how to make do with what is at hand through wilderness medicine education programs are vital to their adopted communities. The doctor who accompanies climbers to the base camp at Mt Everest also builds clinics in rural Nepal, and a nurse who leads adventure treks is moved to staff a refugee camp in the Sudan. Wilderness medicine resides at the core of what it means to be a healer. xix
PREFACE
Wilderness is at the center of wilderness medicine. To a certain degree and appropriately so, wilderness will always remain enigmatic and mysterious. Its verdant landscapes and abundant wildlife should be approached with the explicit understanding that human intrusion on its current scale is a recent phenomenon. The best that our collective environmental efforts have been able to do for wilderness is limit its destruction. We speak and write of managing wilderness, but that activity really means that we are trying to protect it from humansponsored consumption and devastation. Humans are a force of nature, so if wilderness is to cease shrinking and unimpeded fulfill its destiny, without wholesale alteration of patterns and disruption of natural cycles, then our behaviors must change. Today wilderness is considered austere because it is remote and not defined by modern technology. Our appreciation for it grows greater because breathtaking scenery is becoming more elusive. If we are not proactive, then tomorrow’s wilderness will be desolate because it has become used up and bleak. For heaven’s sake, we cannot let that happen. For the rest of my career, I am going to try to give something back. My wife, Sherry, and I began doing that with three wonderful children—Brian, Lauren, and Danny. By helping to establish a specialty, a research tradition, the Wilderness Medical Society, a peer-reviewed journal, education programs, affinity groups, clubs, and an ethos of service and multiple goals to which wilderness medicine enthusiasts can aspire, this book has accomplished its mission. Wilderness medicine in the modern
xx
age has passed its infancy and is now into childhood. There is still so much to be done. Let us together go forward with integrity and optimism.
Paul S. Auerbach, MD, MS, FACEP, FAWM
Photo credits for cover images and part openers Cover: Photographs on the cover are provided courtesy of fine art landscape photographer Elizabeth Carmel from Truckee, California. Her wonderful images may be viewed at www.ElizabethCarmel.com and www.TheCarmelGallery.com. (All images copyright ElizabethCarmel.com.) Back Cover: For cover photos and other outdoor images, visit www.TheCarmelGallery.com. Part 1: Upper: Courtesy Paul S. Auerbach, MD; Middle and Lower: Courtesy Mathias Schar, MD Part 2: Upper: Courtesy Mathias Schar, MD; Lower: Courtesy Paul S. Auerbach, MD Part 3: Upper: Courtesy R.W. Halsey, California Chaparral Field Institute; Middle: Courtesy NASA; Lower: Courtesy Michael Poland, U.S. Geological Survey Part 4: Upper: Courtesy Paul S. Auerbach, MD; Middle: Courtesy Sheri Trbovich and Weber County Sheriff’s Department; Lower: Courtesy Jack Putnam, Maridocs Part 5: Upper: Courtesy Will Smith; Middle: Courtesy Kris H. Green; Lower: Courtesy Mathias Schar, MD Part 6: Upper: Courtesy Timothy Floyd; Middle: Courtesy Jan Ove Rein; Lower: Courtesy Michael Cardwell Part 7: Upper: Provided by K. Davison and R. Marinelli; Middle: Courtesy asimulator via flickr.com; Lower: Courtesy Daniel Ryan Part 8: Upper: Courtesy Brenda Tiernan, RN; Middle and Lower: Courtesy Paul S. Auerbach, MD Part 9: Upper and Lower: Courtesy Carl Roessler; Middle: Courtesy Marty Snyderman Part 10: Upper: Courtesy Paul S. Auerbach, MD; Middle: Courtesy Francesco Zizola, Médecins Sans Frontiéres; Lower: Courtesy N. Stuart Harris, MD Part 11: Upper: Courtesy N. Stuart Harris, MD; Middle: Courtesy Mathias Schar, MD; Lower: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal Part 12: Upper: Courtesy Corbis; Middle: Courtesy Craig Gray; Lower: Courtesy Paul S. Auerbach, MD Part 13: Upper: Courtesy Arius Hopman; Middle: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal; Lower: Courtesy Paul S. Auerbach, MD Index: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal Preface: Courtesy Chuck Liddy, The News & Observer, 2010
xxv
CHAPTER 1
High-Altitude Medicine and Physiology PETER H. HACKETT AND ROBERT C. ROACH
The Population More than 40 million tourists visit recreation areas above 2400 m (7874 feet) in the American West each year. Hundreds of thousands visit central and south Asia, Africa, and South America, many traveling to altitudes above 4000 m (13,123 feet). In addition, millions live in large cities above 3000 m (9843 feet) in South America and Asia. The population in the Rocky Mountains of North America has doubled in the past decade; 700,000 live above 2500 m (8202 feet) in Colorado alone. Increasingly, physicians and other health care providers are confronted with questions of prevention and treatment of high-altitude medical problems (Box 1-1), as well as the effects of altitude on preexisting medical conditions. Despite advances in high-altitude medicine, significant morbidity and mortality persist (Table 1-1). Clearly, better education of the population at risk and those advising them is essential. Altitude illness should be considered a public health problem. In this chapter, we emphasize clinical issues likely to be encountered in lowlanders visiting high-altitude locations by reviewing basic physiology of ascent and the pathophysiology, recognition, and management of medical problems for both visitors and residents of high altitudes (see Box 1-1).
Definitions HIGH ALTITUDE (1500 to 3500 M [4921 to 11,483 FEET]) The onset of physiologic effects of diminished partial pressure of inspired oxygen (PIO2) includes decreased exercise performance and increased ventilation (lower PaCO2) (Box 1-2). Minor impairment exists in arterial oxygen transport (arterial oxygen saturation [SaO2] at least 90%), but PaO2 is significantly diminished. Because of the large number of people who ascend rapidly to 2500 to 3500 m (8202 to 11,483 feet), high-altitude illness is common in this range (Table 1-2; see Table 1-1).
VERY HIGH ALTITUDE (3500 to 5500 M [11,483 to 18,045 FEET]) Maximum arterial oxygen saturation falls below 90% as PaO2 falls below 50 mm Hg (Figure 1-1; see Table 1-2). Extreme hypoxemia may occur during exercise, sleep, and high-altitude pulmonary edema or other acute lung conditions. Severe altitude illness occurs most commonly in this range.
EXTREME ALTITUDE (HIGHER THAN 5500 M [18,045 FEET]) Marked hypoxemia, hypocapnia, and alkalosis characterize extreme altitude. Progressive deterioration of physiologic function eventually outstrips acclimatization. As a result, no permanent human habitation is above 5500 m (18,045 feet). A period of acclimatization is necessary when ascending to extreme altitude; abrupt ascent without supplemental oxygen for other than brief exposures invites severe altitude illness.
The Environment of High Altitude Barometric pressure falls with increasing altitude in a logarithmic fashion (Table 1-3). Therefore the partial pressure of oxygen 2
(21% of barometric pressure) also decreases, resulting in the primary insult of high altitude: hypoxia. At approximately 5800 m (19,029 feet), barometric pressure is one-half that at sea level, and on the summit of Mt Everest (8848 m [29,029 feet]) the inspired pressure of oxygen is approximately 28% that at sea level (see Figure 1-1 and Table 1-3). The relationship of barometric pressure to altitude changes with distance from the equator. Thus, polar regions afford greater hypoxia at high altitude in addition to extreme cold. West565 has calculated that barometric pressure on the summit of Mt Everest (27 degrees N latitude) would be about 222 mm Hg instead of 253 mm Hg if Mt Everest were located at the latitude of Mt McKinley (62 degrees N). Such a difference, he claims, would be sufficient to render impossible an ascent without supplemental oxygen. In addition to the role of latitude, fluctuations related to season, weather, and temperature affect the pressure-altitude relationship. Pressure is lower in winter than in summer. A lowpressure trough can reduce pressure 10 mm Hg in one night on Mt McKinley, making climbers awaken “physiologically higher” by 200 m (656 feet). The degree of hypoxia is thus directly related to barometric pressure, not solely to geographic altitude.565 Temperature decreases with altitude (average of 6.5° C [11.7° F] per 1000 m [3281 feet]), and the effects of cold and hypoxia are generally additive in provoking both cold injuries and highaltitude pulmonary edema.419,559 Ultraviolet light penetration increases approximately 4% per 300-m (984-foot) gain in altitude, increasing the risks for sunburn, skin cancer, and snowblindness. Reflection of sunlight in glacial cirques and on flat glaciers can cause intense radiation of heat in the absence of wind. We have observed temperatures of 40° to 42° C (104° to 107.6° F) in tents on both Mt Everest and Mt McKinley. Heat problems, primarily heat exhaustion, are often unrecognized in this usually cold environment. Physiologists have not yet examined the consequences of heat stress or rapid, extreme changes in environmental temperature combined with the hypoxia of high altitude. Above the snow line is the “high-altitude desert,” where water can be obtained only by melting snow or ice. This factor, combined with increased water loss through the lungs from increased respiration and through the skin, commonly results in dehydration that may be debilitating. Thus, the high-altitude environment imposes multiple stresses, some of which may contribute to or be confused with the effects of hypoxia.
Acclimatization to High Altitude Although rapid exposure from sea level to the altitude at the summit of Mt Everest (8848 m [29,029 feet]) causes loss of consciousness in a few minutes and death shortly thereafter, climbers can ascend Mt Everest over a period of weeks, without supplemental oxygen, because of a process termed acclimatization. A complex series of physiologic adjustments increases oxygen delivery to cells and also improves their hypoxic tolerance. The severity of hypoxic stress, rate of onset, and individual physiology determine whether the body successfully acclimatizes or is overwhelmed. Recently, a revolution has taken place in our understanding of the molecular mechanisms of human responses to hypoxia. At the center of this rapidly changing field is hypoxia-inducible factor (HIF), a transcription factor that modulates the expression
BOX 1-2 Glossary of Physiologic Terms
Lowlanders on Ascent to Altitude • Acute hypoxia • High-altitude headache • Acute mountain sickness • High-altitude cerebral edema • Cerebrovascular syndromes • High-altitude pulmonary edema • Symptomatic pulmonary hypertension • High-altitude deterioration • Organic brain syndrome (extreme altitude) • Peripheral edema • Retinopathy • Disordered sleep • Sleep periodic breathing • High-altitude pharyngitis, bronchitis, and cough • Ultraviolet keratitis (snowblindness) • Exacerbation of preexisting conditions
PB P O2 PIO2 PAO2 PACO2 PaO2 PaCO2 SaO2 RQ Alveolar gas equation
Barometric pressure* Partial pressure of oxygen Inspired PO2 (0.21 × [PB − 47 mm Hg] (47 mm Hg = vapor pressure of H2O at 37° C [98.6° F]) PO2 in alveolus PCO2 in alveolus PO2 in arterial blood PCO2 in arterial blood Arterial oxygen saturation (HbO2 ÷ total Hb × 100) Respiratory quotient (CO2 produced ÷ O2 consumed) PAO2 = PIO2 − (PACO2/RQ)
*Pressures are expressed as mm Hg (1 mm Hg = 1 Torr).
on repeated exposure if rate of ascent and altitude gained are similar, supporting the notion of important genetic factors. Successful initial acclimatization protects against altitude illness and improves sleep. Longer-term acclimatization (weeks) primarily improves aerobic exercise ability. These adjustments disappear at a similar rate on descent to low altitude. A few days at low altitude may be sufficient to render a person susceptible to altitude illness, especially high-altitude pulmonary edema (HAPE), on reascent. The improved ability to do physical work at high altitude, however, persists for weeks.317 Persons who live at high altitude during growth and development appear to realize the maximum benefit of acclimatization changes; for example, their exercise performance matches that of persons at sea level.365
Life or Long-Term Residents of Altitude • Chronic mountain sickness (chronic mountain polycythemia) • Symptomatic high-altitude pulmonary hypertension with or without right heart failure • Problems of pregnancy: preeclampsia, hypertension, and low-birth-weight infants • Exacerbation of lung disease and congenital heart disease
of hundreds of genes, including those involved in apoptosis, angiogenesis, metabolism, cell proliferation, and permeability processes.90,423,484-487,503,504 In chronic hypoxia, HIF activation by hypoxia has the positive effect of elevating oxygen delivery by boosting hemoglobin mass. But HIF also plays a role in carotid body sensitivity to hypoxia, which in turn largely determines the ventilatory response to hypoxia. As a master regulator of the hypoxia response in humans, HIF has some beneficial and harmful effects at different stages in the time course of human exposure to hypoxia, and in different cells in the body. See Figure 1-2 for an overview of some of the hundreds of processes in which the response to hypoxia is modulated by HIF. Individuals vary in their ability to acclimatize, no doubt reflecting certain genetic polymorphisms, including HIF. Some adjust quickly, without discomfort, whereas acute mountain sickness (AMS) develops in others, who go on to recover. A small percentage fails to acclimatize even with gradual exposure over weeks. The tendency to acclimatize well or to become ill is consistent
VENTILATION By reducing alveolar carbon dioxide, increased ventilation raises alveolar oxygen, improving oxygen delivery (Figure 1-3; see Figure 1-1). This response starts as low as 1500 m (4921 feet) (PIO2 = 124.3 mm Hg; see Table 1-3) and within the first few minutes to hours of high-altitude exposure. The carotid body, sensing a decrease in PaO2, through a HIF-mediated process, signals the central respiratory center in the medulla to increase ventilation.153,281 This carotid body function (hypoxic ventilatory response [HVR]) is genetically determined562 but influenced by a number of extrinsic factors. Respiratory depressants such as alcohol and soporifics, as well as fragmented sleep, depress HVR. Agents that increase general metabolism, such as caffeine and coca, as well as specific respiratory stimulants, such as progesterone277 and almitrine,192 increase HVR. (Acetazolamide, a respiratory stimulant, acts on the central respiratory center rather than
TABLE 1-1 Incidence of Altitude Illness in Various Groups
Study Group
Number at Risk per Year
Western state visitors
30 million
Mt Everest trekkers
12,000
Mt McKinley climbers Mt Rainier climbers Mt Rosa, Swiss Alps
1200 10,000 †
Indian soldiers Aconcagua climbers Kilimanjaro hikers
Unknown 4200 2500
Maximum Altitude Reached (m [ft])
Average Rate of Ascent*
~2000 (6562) ~2500 (8202) ~≥3000 (9843) 3000-5200 (9843-17,060)
3500 (11,483)
1-2
5500(18,045)
3000-5300 (9843-17,388) 3000 (9843) 2850 (9350) 4559 (14,957) 3000-5500 (9843-18,045) 3300-5800 (10,827-19,029) 2700-4700 (8858-15,420)
6194 4392 2850 4559 5500 6962 5895
1-2 (fly in) 10-13 (walk in) 3-7 1-2 1-2 2-3 1-2 2-8 2-6
Sleeping Altitude (m [ft])
(20,322) (14,409) (9350) (14,957) (18,045) (22,841) (19,341)
Percent With AMS 18-20 22 27-42 47 23 30-50 30 67 7 27 † 39 (LLS >4) 50-83
Percent With HAPE and/or HACE
Reference
0.01
214
1.6 0.05 2-3 — — 5 2.3-15.5 2.2 †
376 181 286 323 99, 323, 475 499, 500 405 106, 242
AMS, Acute mountain sickness; HAPE, high-altitude pulmonary edema; HACE, high-altitude cerebral edema; LLS, Lake Louise score. *Days to sleeping altitude from low altitude. †Reliable estimate unavailable.
3
CHAPTER 1 High-Altitude Medicine and Physiology
BOX 1-1 Medical Problems of High Altitude
PART 1 MOUNTAIN MEDICINE
TABLE 1-2 Arterial Blood Gases and Altitude* Population
Altitude Meters †
Altitude residents Acute exposure
Subacute exposure
1646 2810‡ 3660‡ 4700‡ 5340‡ 6140‡ 6500§ 7000§ 8000§ 8400|| 8848§ 8848¶
Feet
PB (mm Hg)
5400 9219 12,008 15,420 17,520 20,144 21,325 22,966 26,247 27,559 29,029 29,029
630 543 489 429 401 356 346 324 284 272 253 253
PaO2 (mm Hg)
SaO2 (%)
PaCO2 (mm Hg)
73.0 60.0 47.6 44.6 43.1 35.0 41.1
(65.0-83.0) (47.4-73.6) (42.2-53.0) (36.4-47.5) (37.6-50.4) (26.9-40.1) ± 3.3
95.1 91.0 84.5 78.0 76.2 65.6 75.2
35.6 (30.7-41.8) 33.9 (31.3-36.5) 29.5 (23.5-34.3) 27.1 (22.9-34.0) 25.7 (21.7-29.7) 22.0 (19.2-24.8) 20 ± 2.8
36.6 24.6 30.3 30.6
± ± ± ±
67.8 ± 5 54 58 ± 4.5
2.2 5.3 2.1 1.4
(93.0-97.0) (86.6-95.2) (80.5-89.0) (70.8-85.0) (65.4-81.6) (55.5-73.0) ±6
12.5 ± 1.1 13.3 11.2 ± 1.7 11.9 ± 1.4
PB, Barometric pressure; PaCO2, arterial partial pressure of carbon dioxide; PaO2, arterial partial pressure of oxygen; SaO2, arterial oxygen saturation. *Data are mean values and (range) or ± SD, where available. All values are for subjects age 20 to 40 years who were acclimatizing well. † Data from reference 302. ‡ Data from reference 343. § Data for chronic exposure during Operation Everest II from reference 526. || Data from near the summit of Mt Everest from reference 172. ¶ Data from the simulated summit of Mt Everest from reference 430.
SaO2
160
100
140
90
PIO2
120
80
100 80
70
PaO2
60
SaO2 (%)
Partial pressure oxygen (mm Hg)
on the carotid body.) Physical conditioning apparently has no effect on HVR. Numerous studies have shown that a good ventilatory response enhances acclimatization and performance and that a very low HVR may contribute to illness433 (see Acute Mountain Sickness and High-Altitude Pulmonary Edema, later). However, over a normal range of values, HVR is not a reliable predictor of susceptibility to altitude illness. Other factors influence ventilation on ascent to high altitude. As ventilation increases, hypocapnia produces alkalosis, which acts as a braking mechanism on the central respiratory center and limits a further increase in ventilation. To compensate for the alkalosis, within 24 to 48 hours of ascent the kidneys excrete bicarbonate, decreasing the pH toward normal; ventilation increases as the braking effect of the alkalosis is removed. Ventilation continues to increase slowly, reaching a maximum only after 4 to 7 days at the same altitude (see Figure 1-3). The plasma bicarbonate concentration continues to drop and ventilation to increase with each successive increase in altitude. Persons with
60
40 20 0
2000
4000
6000
50 8000 10,000
Altitude (m) FIGURE 1-1 Increasing altitude results in decreasing inspired PO2 (PIO2), arterial PO2 (PaO2), and arterial oxygen saturation (SaO2). Note that the difference between PIO2 and PaO2 narrows at high altitude because of increased ventilation and that SaO2 is well maintained while awake until over 3000 m (9843 feet). (Data from Morris A: Clinical pulmonary function tests: A manual of uniform lab procedures, Salt Lake City, 1984, Intermountain Thoracic Society; and Sutton JR, Reeves JT, Wagner PD, et al: Operation Everest II: Oxygen transport during exercise at extreme simulated altitude, J Appl Physiol 64:1309, 1988.)
4
lower oxygen saturation at altitude have higher serum bicarbonate values; whether the kidneys might be limiting acclimatization or whether this reflects poor respiratory drive is not clear.102 This process is greatly facilitated by acetazolamide (see Acetazolamide Prophylaxis, later). The paramount importance of hyperventilation is readily apparent from the following calculation: the alveolar PO2 on the summit of Mt Everest (about 33 mm Hg) would be reached at only 5000 m (16,404 feet) if alveolar PCO2 stayed at 40 mm Hg, limiting an ascent without supplemental oxygen to near this altitude. Table 1-2 gives the measured arterial blood gas levels resulting from acclimatization to various altitudes.
CIRCULATION The circulatory pump is the next step in the transfer of oxygen, moving oxygenated blood from the lungs to the tissues. Systemic Circulation Increased sympathetic activity on ascent causes an initial mild increase in blood pressure, moderate increases in heart rate and cardiac output, and increase in venous tone. Stroke volume is low because of decreased plasma volume, which drops as much as 12% over the first 24 hours577 as a result of the bicarbonate diuresis, a fluid shift from the intravascular space, and suppression of aldosterone.35 Resting heart rate returns to near sea level values with acclimatization, except at extremely high altitude. Maximum heart rate follows the decline in maximal oxygen uptake with increasing altitude. As the limits of hypoxic acclimatization are approached, maximum and resting heart rates converge. During Operation Everest II (OEII), cardiac function was appropriate for the level of work performed and cardiac output was not a limiting factor for performance.417,518 Interestingly, myocardial ischemia at high altitude has not been reported in healthy persons, despite extreme hypoxemia. This is partly because of reduction in myocardial oxygen demand from reduced maximal heart rate and cardiac output. Pulmonary capillary wedge pressure is low, and catheter studies have shown no evidence of left ventricular dysfunction or abnormal filling pressures in humans at rest.174,236 On echocardiography, the left ventricle is smaller than normal because of decreased stroke volume, whereas the right ventricle may become enlarged.518 The abrupt increase in pulmonary artery pressure can cause a change in left ventricular diastolic function, but because of compensatory increased atrial contraction, no overt diastolic dysfunction results.7 In trained athletes doing an ultramarathon, the strenuous exercise at high altitude did not result in left ventricular damage; however, wheezing, reversible pulmonary hypertension, and right ventricular dysfunction occurred in one-third of those completing the race and resolved within 24 hours.107
Pressure, Estimated Partial Pressure of Inspired Oxygen, and the Equivalent Oxygen Fraction at Sea Level*
m
ft
PB
PIO2
FIO2 at SL
Sea level 1000 1219 1500 1524 1829 2000 2134 2438 2500 2743 3000 3048 3353 3500 3658 3962 4000 4267 4500 4572 4877 5000 5182 5486 5500 5791 6000 6096 6401 6500 6706 7000 7010 7315 7500 7620 7925 8000 8230 8500 8534 8839 8848 9000 9144 9500 10,000
Sea level 3281 4000 4921 5000 6000 6562 7000 8000 8202 9000 9843 10,000 11,000 11,483 12,000 13,000 13,123 14,000 14,764 15,000 16,000 16,404 17,000 18,000 18,045 19,000 19,685 20,000 21,000 21,325 22,000 22,966 23,000 24,000 24,606 25,000 26,000 26,247 27,000 27,887 28,000 29,000 29,029 29,528 30,000 31,168 32,808
759.6 678.7 661.8 640.8 639.0 616.7 604.5 595.1 574.1 569.9 553.7 536.9 533.8 514.5 505.4 495.8 477.6 475.4 460.0 446.9 442.9 426.3 419.7 410.2 394.6 393.9 379.5 369.4 364.9 350.7 346.2 337.0 324.2 323.8 310.9 303.4 298.6 286.6 283.7 275.0 265.1 263.8 253.0 252.7 247.5 242.6 230.9 215.2
149.1 132.2 128.7 124.3 123.9 119.2 116.7 114.7 110.3 109.4 106.0 102.5 101.9 97.9 95.9 93.9 90.1 89.7 86.4 83.7 82.9 79.4 78.0 76.0 72.8 72.6 69.6 67.5 66.5 63.6 62.6 60.7 58.0 57.9 55.2 53.7 52.6 50.1 49.5 47.7 45.6 45.4 43.1 43.1 42.0 40.9 38.5 35.2
0.209 0.185 0.180 0.174 0.174 0.167 0.164 0.161 0.155 0.154 0.149 0.144 0.143 0.137 0.135 0.132 0.126 0.126 0.121 0.117 0.116 0.111 0.109 0.107 0.102 0.102 0.098 0.095 0.093 0.089 0.088 0.085 0.081 0.081 0.077 0.075 0.074 0.070 0.069 0.067 0.064 0.064 0.060 0.060 0.059 0.057 0.054 0.049
Exp, Exponent; FIO2, fraction of inspired oxygen; PB, barometric pressure; PIO2, partial pressure of inspired oxygen; SL, sea level. *Barometric pressure is approximated by the equation PB = Exp (6.6328 − {0.1112 × altitude − [0.00149 × (altitude2)]}), where altitude = terrestrial altitude in meters/1000 or km. PIO2 is calculated as the PB − 47 (where 47 = water vapor pressure at body temperature) × fraction of O2 in inspired air. The equivalent FIO2 at sea level for a given altitude is calculated as PIO2 ÷ (760 − 47). Substituting ambient PB for 760 in the equation allows similar calculations for FIO2 at different altitudes.
Pulmonary Circulation On ascent to high altitude, a prompt but variable increase in pulmonary vascular resistance from hypoxic pulmonary vasoconstriction increases pulmonary artery pressure. Mild pulmonary hypertension is greatly augmented by exercise, with pulmonary pressure reaching near-systemic values,174 especially in persons with a previous history of high-altitude pulmonary edema.32,110 During OEII, Groves and colleagues174 demonstrated that even with a mean pulmonary artery pressure of 60 mm Hg, cardiac output remained appropriate and right atrial pressure did not rise above sea level values. Thus, right ventricular function was intact
in spite of extreme hypoxemia and pulmonary hypertension in these well-acclimatized subjects. Administration of oxygen does not completely restore pulmonary artery pressure to sea level values,324 likely because of vascular remodeling with medial hypertrophy. See Stenmark and associates509 for an excellent review of molecular and cellular mechanisms of the pulmonary vascular response to hypoxia, including remodeling. Pulmonary vascular resistance returns to normal within a few weeks after descent to low altitude. Cerebral Circulation Cerebral oxygen delivery, the product of arterial oxygen content and cerebral blood flow (CBF), depends on the net balance between hypoxic vasodilation and hypocapnia-induced vasoconstriction. CBF increases, despite hypocapnia, when PaO2 is less than 60 mm Hg (altitude greater than 2800 m [9186 feet]). In a classic study, CBF increased 24% on abrupt ascent to 3810 m (12,500 feet) and returned to normal over 3 to 5 days.491 These findings have been confirmed by positron emission tomography and brain magnetic resonance imaging (MRI) studies showing both elevations in CBF in hypoxia in humans and striking heterogeneity of the CBF, with CBF rising up to 33% in the hypothalamus and 20% in the thalamus, with other areas without significant changes.66,396 Cerebral autoregulation, the process by which cerebral perfusion is maintained as blood pressure varies, is impaired in hypoxia. Interestingly, this occurs both in newcomers, with acute246,296,521,547 and prolonged hypoxia,522 and in natives to high altitude.246 This observation raises questions about the importance of this process in AMS and acclimatization, because it appears to be a uniform response in all humans made hypoxemic. Overall, global cerebral metabolism seems well maintained with moderate hypoxia.103,356
BLOOD Hematopoietic Responses to Altitude Ever since the observation in 1890 by Viault550 that hemoglobin concentration was higher than normal in animals living in the Andes, scientists have regarded the hematopoietic response to increasing altitude as an important component of the acclimatization process. On the other hand, hemoglobin values apparently have no relationship to susceptibility to high-altitude illness. In response to hypoxemia, erythropoietin is secreted by the kidneys and stimulates bone marrow production of red blood cells.483 The hormone is detectable within 2 hours of ascent, nucleated immature red blood cells can be found on a peripheral blood smear within days, and new red blood cells are in circulation within 4 to 5 days. Over a period of weeks to months, red blood cell mass increases in proportion to the degree of hypoxemia. Iron supplementation can be important; women who take supplemental iron at high altitude approach the hematocrit values of men at altitude202 (Figure 1-4). The increase in hemoglobin seen 1 to 2 days after ascent is due to hemoconcentration secondary to decreased plasma volume, rather than a true increase in red blood cell mass. This results in a higher hemoglobin concentration at the cost of decreased blood volume, a trade-off that might impair exercise performance. Longer-term acclimatization leads to an increase in plasma volume as well as in red blood cell mass, thereby increasing total blood volume. Overshoot of the hematopoietic response causes excessive polycythemia, which may impair oxygen transport because of increased blood viscosity. Although the “ideal” hematocrit at high altitude is not established, phlebotomy is often recommended when hematocrit values exceed 60% to 65%. During the American Medical Research Expedition to Mt Everest (AMREE), hematocrit was reduced by hemodilution from 58% ± 1.3% to 50.5% ± 1.5% at 5400 m (17,717 feet) with no decrement in maximum oxygen uptake and increased cerebral functioning.465 Oxyhemoglobin Dissociation Curve The oxygen dissociation curve (ODC) plays a crucial role in oxygen transport. The sigmoidal shape of the curve allows wellmaintained SaO2 up to 3000 m (9843 feet), despite significant 5
CHAPTER 1 High-Altitude Medicine and Physiology
TABLE 1-3 Altitude Conversion: Barometric
PART 1 MOUNTAIN MEDICINE
Ub Ub
A Normoxia
PHD2
HIF-1α
Fe2+ 2-OG Ascorbate
PHD1 O2
Ub
PHD3
HIF-1α
HIF-1α
OH OH OAc
OH OH OAc
VHL
VHL
B Hypoxia HIF-1α HIF-1α
Ub Ub
Ub
26s Proteasome
Proteolytic degradation
HIF-1α HIF-1α p300/CBP HIF-1α
Nucleus
HIF-1β
HIF-1β HRE
Angiogenesis Erythropoiesis Apoptosis
Cell proliferation and survival
HIF-1 target genes
Proteolysis pH regulation Glucose metabolism
FIGURE 1-2 Regulation of oxygen sensing by hypoxia-inducible factor (HIF). The HIF is produced constitutively, but in normoxia the α subunit is degraded by the proteasome in an oxygen-dependent manner. Hypoxic conditions prevent hydroxylation of the α subunit, enabling the active HIF transcription complex to form at the hypoxia-response element (HRE) associated with HIF-regulated genes. A range of cell functions are regulated by the target genes, as indicated. CBP, CREB binding protein; OAc, acetylation of HIF-1α; 2-OG, 2-oxoglutarate; PHD, prolyl hydroxylase; Ub, ubiquitin; VHL, von Hippel–Lindau tumor suppressor. (Reprinted from Carroll VA, Ashcroft M: Targeting the molecular basis for tumour hypoxia, Expert Rev Mol Med 7:1, 2005.)
decreases in PaO2 (see Figure 1-1). Above 3000 m (9843 feet), small changes in PaO2 cause large changes in SaO2 (Figure 1-5). Because PaO2 determines diffusion of oxygen from capillary to cell, small changes in PaO2 can have clinically significant effects. This is often confusing for clinicians because SaO2 appears relatively well preserved. At high altitude, small changes in PaO2 lead to lower O2 uptake that can have a large effect on systemic hypoxemia, and thus on clinical status, while the SaO2 may appear relatively unchanged. In 1936, Ansel Keys and colleagues266 demonstrated an in vitro right shift in position of the ODC at high altitude, favoring release of oxygen from blood to tissues. This change, due to increased 2,3-diphosphoglycerate, is proportional to the severity of hypoxemia. In vivo, however, the alkalosis at moderate altitude offsets this, and no net change occurs. In contrast, the marked alkalosis of extreme hyperventilation, as measured on the summit and simulated summit of Mt Everest (PaCO2 8 to 10 mm Hg, pH greater than 7.5), shifts the ODC to the left, facilitating oxygen-hemoglobin binding in the lung that raises SaO2 and is advantageous.462 Persons with a very left-shifted ODC, caused by an abnormal hemoglobin (Andrew-Minneapolis), when taken to moderate (3100 m [10,171 feet]) altitude, had less tachycardia and dyspnea and remarkably had no decrease in exercise performance.208 Highaltitude adapted animals also have a left-shifted ODC.
TISSUE CHANGES The next link in the oxygen transport chain is tissue oxygen transfer, which depends on capillary perfusion, diffusion distance, and driving pressure of oxygen from the capillary to the cell. Banchero20 has shown that capillary density in dog skeletal muscle doubled in 3 weeks at a barometric pressure of 435 mm Hg. A recent study in humans noted no change in 6
capillary density or in gene expression thought to enhance muscle vascularity.316 Ou and Tenney395 revealed a 40% increase in mitochondrial number but no change in mitochondrial size, whereas the study of Oelz and colleagues392 showed that highaltitude climbers had normal mitochondrial density. A significant drop in muscle size is often noted after high-altitude expeditions because of net energy deficit,316,319 resulting in increased capillary density and ratio of mitochondrial volume to contractile protein fraction as a result of the atrophy. Although there is no de novo synthesis of capillaries or mitochondria, the net result is a shortening of diffusion distance for oxygen.316,319
SLEEP AT HIGH ALTITUDE Disturbed sleep is common at high altitude. There are multiple causes. Reflecting the great interest in sleep, more than 160 papers in the last 10 years have addressed sleep at altitude. The interested reader is referred to recent reviews.67,308,551,561,569 Nearly all subjects complain of disturbed sleep at high altitude, with severity increasing with the altitude. At moderate altitude, sleep architecture is changed, with a reduction in stages 3 and 4 sleep, stage 1 time increased, and little change in stage 2. Overall, there is a shift from deeper sleep to lighter sleep. In addition, more time is spent awake, with significantly increased arousals. Clinicians have reported either slightly less rapid eye movement (REM) time or no change in REM compared with what occurs at low altitude. REM sleep may improve over time at altitude.268 The subjective complaints of poor sleep are out of proportion to the small reduction (if any) in total sleep time and appear to be due to sleep fragmentation. With more extreme hypoxia, sleep time was dramatically shortened and arousals increased, without a change in ratio of sleep stages but with a reduction in REM sleep.10 The mechanisms of this change in sleep architecture and
~10% decrease
80 10 8 40
PACO2 (mm Hg)
~ No change
12
SaO2 (%)
· VE (L/min, BTPS)
100
CHAPTER 1 High-Altitude Medicine and Physiology
14
60
40
35
B
20
30 25
A
0 0
100
20
40
60
80
100
120
SaO2 (%)
PaO2 (mm Hg) FIGURE 1-5 Oxygen-hemoglobin dissociation curve showing effect of 10-mm Hg decrement in arterial partial pressure of oxygen (PaO2) on arterial oxygen saturation (SaO2) at sea level (A) and near 4400 m (14,436 feet) (B). Note the much larger drop in SaO2 at high altitude. (Modified from Severinghaus JW, Chiodi H, Eger EI, et al: Cerebral blood flow in man at high altitude: Role of cerebrospinal fluid pH in normalization of flow in chronic hypoxia, Circ Res 19:274, 1966.)
90
80 0 1 Denver
2
3
4
5 Placebo
Days at 4300 m FIGURE 1-3 Change in minute ventilation ( V E ), end-tidal carbon dioxide (PACO2), and arterial oxygen saturation (SaO2) during 5 days’ acclimatization to 4300 m (14,108 feet). BTPS, Body temperature pressure saturated. (Modified from Huang SY, Alexander JK, Grover RF, et al: Hypocapnia and sustained hypoxia blunt ventilation on arrival at high altitude, J Appl Physiol 56:602, 1984.)
50
Hematocrit (%)
100 80 SaO2 (%) 60 40
Acetazolamide
Men Women (+Fe)
48 46
Women (−Fe) 44 42 40
Respiratory pattern
Sea level 1
20
40
60
Days at 4300 m
FIGURE 1-4 Hematocrit changes on ascent to altitude in men and in women with and without supplemental iron. (Modified from Hannon JP, Chinn KS, Shields JL: Effects of acute high altitude exposure on body fluids, Fed Proc 28:1178, 1969.)
fragmentation are poorly understood. Periodic breathing appears to play only a minor role in altering sleep architecture at high altitude.461 The arousals have been linked to periodic breathing in some studies but not in others. Other factors might include change in circadian rhythm and perhaps body temperature.98 Obesity may explain susceptibility to both deranged sleep and sleep-disordered breathing in some individuals.155 Recent studies
Respiratory pattern 100 80 60 40
SaO2 (%)
FIGURE 1-6 Respiratory patterns and arterial oxygen saturation (SaO2) with placebo and acetazolamide in two sleep studies of a subject at 4200 m (13,780 feet). Note pattern of hyperpnea followed by apnea during placebo treatment, which is changed with acetazolamide. (Modified from Hackett PH, Roach RC, Harrison GL, et al: Respiratory stimulants and sleep periodic breathing at high altitude: Almitrine versus acetazolamide, Am Rev Respir Dis 135:896, 1987.)
of infants and children590 and athletes in simulated altitude devices used for training also revealed deranged sleep quality in these groups.269,270,401 Although deranged sleep is a frequent complaint in high-altitude visitors, it seems to have little relation to susceptibility to altitude illness or other serious problems. Symptomatic treatment that avoids respiratory depression is safe (see Treatment under Acute Mountain Sickness, later). Periodic Breathing Periodic breathing is most common in early and light sleep, may occur during wakefulness when drowsy, and does not occur in REM sleep. The pattern is characterized by hyperpnea followed by apnea (Figure 1-6) and is caused by a battle for control of 7
100
SaO2 (%)
80 60 40 Arrival Acclimatized
20
0
50
100 150 200 250 300 350 400 450 500 Time asleep (min)
FIGURE 1-7 Sleep oxygenation improves with acclimatization to same altitude. Top line is maximum, and bottom line is minimum arterial oxygen saturation (SaO2) in an acclimatized person. Shaded area is maximum and minimum SaO2 values for new arrival at 5360 m (17,585 feet). (Modified from Sutton JR, Gray GW, Houston CS, et al: Effects of acclimatization on sleep hypoxemia at altitude. In West JB, Lahiri S, editors: High altitude man, Bethesda, Md, 1984, American Physiological Society, pp 141-146.)
breathing between peripheral chemoreceptors (carotid body) and the central respiratory center. Respiratory alkalosis during hyperpnea acts on the central respiratory center, causing apnea. During apnea, SaO2 decreases, carbon dioxide increases, and the carotid body is stimulated, causing a recurrent hyperpnea and apnea cycle. The apnea is central, not associated with snoring, and occurs with absence of rib cage movement. Persons with high hypoxic ventilatory response have more periodic breathing,55 with mild oscillations in SaO2,282 whereas persons with low hypoxic ventilatory response have more regular breathing overall but may suffer periods of apnea with extreme hypoxemia distinct from periodic breathing.192 As acclimatization progresses, periodic breathing lessens but does not disappear, especially over 5000 m (16,404 feet), and sleep SaO2 increases (Figure 1-7; see Figure 1-6).10,55,524 Periodic breathing has not been implicated in the etiology of highaltitude illness, but nocturnal oxygen desaturation has been implicated.55,133,150 Eichenberger and colleagues130 have also reported greater periodic breathing in persons with HAPE, secondary to lower SaO2. As with fragmented sleep, intensity of periodic breathing is quite variable. Total sleep time with periodic breathing can vary from 1% to over 90%.598 Most studies report no association between periodic breathing and AMS.55 This may relate to the fact that persons with periodic breathing tend to have higher HVR and greater average ventilation and oxygenation.561 Pharmaceutical Aids Acetazolamide, 125 mg at bedtime, diminishes periodic breathing and awakenings, improves oxygenation and sleep quality, and is a safe and superior agent to use as a sleeping aid (see Figure 1-6). It has the added benefit of diminishing symptoms of AMS. Other agents include diphenhydramine (Benadryl, 50 to 75 mg) or the short-acting benzodiazepines such as triazolam (Halcion, 0.125 to 0.25 mg) and temazepam (Restoril, 15 mg).308 Although caution is warranted for any agent that might reduce ventilation at high altitude, some studies have suggested that benzodiazepines in low doses are generally safe in this situation.124,164,384 Another option is to use both acetazolamide and a benzodiazepine. Bradwell and colleagues63 showed that acetazolamide (500 mg slow-release orally) given with temazepam (10 mg orally) improved sleep and maintained SaO2, counteracting a 20% decrease in SaO2 when temazepam was given alone. The nonbenzodiazepine hypnotic zolpidem (Ambien, 10 mg) was shown to improve sleep at 4000 m (13,123 feet) without adversely affecting ventilation.45
EXERCISE Maximal oxygen consumption drops dramatically on ascent to 2 max ) falls from high altitude.151,434 Maximal oxygen uptake ( VO 8
sea level by approximately 10% for each 1000 m (3281 feet) of altitude gained above 1500 m (4921 feet). Persons with the 2 max values have the largest decrement in highest sea level VO 2 max at high altitude, but overall performance at high altitude VO 2 max .392,428,566 In fact, is not consistently related to sea level VO many of the world’s elite mountaineers have quite average 2 max values, in contrast with other endurance athletes.392 VO Acclimatization at moderate altitudes enhances submaximal 2 max (Figure 1-8).151 endurance time but does not enhance VO Oxygen transport during exercise at high altitude becomes increasingly dependent on the ventilatory pump. The marked rise in ventilation produces a sensation of breathlessness, even at low work levels. The following quotation is from a high-altitude mountaineer: After every few steps, we huddle over our ice axes, mouths agape, struggling for sufficient breath to keep our muscles going. I have the feeling I am about to burst apart. As we get higher, it becomes necessary to lie down to recover our breath.347 In contrast to the increase in ventilation with exercise, at increasing altitudes in OEII, cardiac function and cardiac output were maintained at or near sea level values for a given oxygen consumption (workload).417 Recent work has attributed the 2 max to the lower PIO2, impairment altitude-induced drop in VO of pulmonary gas exchange, and reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third 2 max .76 However, mechanisms to explain the of the loss in VO impairment of gas exchange and the lower blood flow remain elusive. Wagner556 proposes that the pressure gradient for diffusion of oxygen from capillaries to the working muscle cells may be inadequate. Another concept is that increased cerebral hypoxia from exercise-induced desaturation is the limiting factor.91,241,356,519,520 Mountaineers, for example, become lightheaded and their vision dims when they move too quickly at extreme altitude (Figure 1-9).564 Training at High Altitude Optimal training for increased performance at high altitude depends on the altitude of residence and the athletic event. For aerobic activities (events lasting more than 3 or 4 minutes) at altitudes above 2000 m (6562 feet), acclimatization for 10 to 20 days is necessary to maximize performance.104 For events
180 Endurance time · VO2max
160 Sea level performance (%)
PART 1 MOUNTAIN MEDICINE
SLEEP SATURATION AT 5360 m
140 120 100 80 60 40 0
2
4
6
8
10
12
Days at altitude FIGURE 1-8 On ascent to altitude, maximum oxygen consumption 2max ) decreases and remains suppressed. In contrast, endurance ( VO 2max ) time (minutes to exhaustion at 75% of altitude-specific VO increases with acclimatization. (Modified from Maher JT, Jones LG, Hartley LH: Effects of high altitude exposure on submaximal endurance capacity of men, J Appl Physiol 37:895, 1974.)
Alveolar
Arterial
PO2 (torr)
30
20
Mixed venous
Assumed critical PO2
NEUROLOGIC SYNDROMES
Loss of consciousness · VO2max
10 Man on summit PB 253 torr DMO2 100 mL/min/torr 0 0
200
400
600
800
1000
1200
Oxygen uptake (mL O2/min) FIGURE 1-9 Calculated changes in the PO2 of alveolar gas and arterial and mixed venous blood as oxygen uptake is increased for a climber on the summit of Mt Everest. Unconsciousness develops at a mixed venous PO2 of 15 mm Hg. PB, Barometric pressure; DMO2, muscle dif 2max , maximum oxygen consumption. (Modified fusing capacity; VO from West JB: Climbing Mt. Everest without oxygen: An analysis of maximal exercise during extreme hypoxia, Respir Physiol 52:265, 1983.)
occurring above 4000 m (13,123 feet), acclimatization at an intermediate altitude is recommended. Highly anaerobic events at intermediate altitudes require only arrival at the time of the event, although mountain sickness may become a problem. The benefits of training at high altitude for subsequent performance at or near sea level depend on choosing the training altitude that maximizes the benefits and minimizes the “detraining” inevitable when maximal oxygen uptake is limited (altitude greater than 1500 to 2000 m [4921 to 6562 feet]). Hence, data from training above 2400 m (7874 feet) have shown no increase in subsequent sea level performance. Also, intermittent exposures to hypoxia seem to have no benefit.251,540 Runners returning to sea level after 10 days’ training at 2000 m (6562 feet) had faster running times and an increase in aerobic power, plasma volume, and hemoglobin concentration.19 Today the “live high–train low” approach pioneered by Levine and Stray-Gundersen294,513 has been adopted by many endurance athletes. The optimal dose for specific sports is still being worked out,570 but overall, endurance athletes believe and the science supports a small, but significant improvement in sea level performance after participating in a live high–train low training camp.514 The benefit appears to be due to enhanced erythropoietin production and increased red cell mass, which requires adequate iron stores and thus usually iron supplementation.328,443,512 Some individuals do not respond to live high–train low, perhaps related to genetic polymorphisms and the inability to increase erythropoietin levels sufficiently to raise red cell mass and thus increase oxygen-carrying capacity.79,247
High-Altitude Syndromes High-altitude syndromes are illnesses attributed directly to hypobaric hypoxia, even if exact mechanisms are unclear. Clinically and pathophysiologically these syndromes overlap. Rapidity of onset of hypoxia is crucial; for example, sudden exposure to extreme altitude may result in death from acute hypoxia (asphyxia), whereas more gradual ascent to the same altitude may result in AMS or no illness at all. Where symptoms of acute hypoxia end and AMS begins is vague, as reflected in the classic
Neurologic syndromes reflect both nervous system sensitivity to hypoxia and effects of compensatory mechanisms. Although brain adenosine triphosphate (ATP) production and overall metabolism remain intact during moderate hypoxia, impaired synthesis of neurotransmitters can produce cerebral symptoms such as lassitude, malaise, and cognitive defects. Compensatory cerebral vasodilation at altitude appears to be the trigger for altitude headache and contributes to development of AMS and HACE. However, much of the pathophysiology of AMS and HACE remains a mystery. Focal neurologic deficits without cerebral edema are also difficult to explain; cerebral artery spasm and watershed hypoxia have both been invoked. Understanding the exact etiology of these neurologic syndromes will parallel advances in neuroscience; the emphasis in altitude illness is finally and appropriately on the brain.438
ACUTE CEREBRAL HYPOXIA Acute, profound hypoxia, although of greatest interest in aviation medicine, may also occur on terra firma when ascent is too rapid or when hypoxia abruptly worsens. Carbon monoxide poisoning, pulmonary edema, sudden overexertion, sleep apnea, or a failed oxygen delivery system may rapidly exaggerate hypoxemia. Unacclimatized persons will lose consciousness from acute hypoxia at SaO2 of 40% to 60% or a PaO2 of less than about 30 mm Hg or mixed venous PO2 of 15 mm Hg. Tissandier, the sole survivor of the flight of the balloon Zenith in 1875, gave a graphic description of the effects of acute hypoxia: But soon I was keeping absolutely motionless, without suspecting that perhaps I had already lost use of my movements. Towards 7500 m [24,606 feet], the numbness one experiences is extraordinary. The body and the mind weaken little by little, gradually, unconsciously, without one’s knowledge. One does not suffer at all; on the contrary. One experiences inner joy, as if it were an effect of the inundating flood of light. One becomes indifferent; one no longer thinks of the perilous situation or of the danger; one rises and is happy to rise. Vertigo of the lofty regions is not a vain word. But as far as I can judge by my personal impression, this vertigo appears at the last moment; it immediately precedes annihilation—sudden, unexpected, irresistible. I wanted to seize the oxygen tube, but could not raise my arm. My mind, however, was still very lucid. I was still looking at the barometer; my eyes were fixed on the needle which soon reached the pressure number of 280, beyond which it passed. I wanted to cry out “We are at 8,000 meters.” But my tongue was paralyzed. Suddenly I closed my eyes and fell inert, completely losing consciousness.54 The ascent to over 8000 m (26,247 feet) took 3 hours, and the descent less than 1 hour. When the balloon landed, Tissandier’s two companions were dead. The prodigious work that Paul Bert conducted in an altitude chamber during the 1870s showed that lack of oxygen, rather than an effect of isolated hypobaria, explained the symptoms experienced during rapid ascent to extreme altitude. There exists a parallelism to the smallest details between two animals, one of which is subjected in normal air to a 9
CHAPTER 1 High-Altitude Medicine and Physiology
experiments of Bert.54 In terms of altitude illness, the general concept of a spectrum of illness with a common underlying pathogenesis is well accepted and provides a useful framework for discussion. For the neurologic syndromes, the spectrum progresses from high-altitude headache to AMS to high-altitude cerebral edema (HACE). In the lungs, the spectrum includes pulmonary hypertension, interstitial edema, and HAPE. These problems all occur within the first few days of ascent to a higher altitude, have many common features, and respond to descent and/or oxygen. Longer-term problems of altitude exposure include high-altitude deterioration in sojourners and chronic mountain sickness in high-altitude residents.
40
PART 1 MOUNTAIN MEDICINE
progressive diminution of pressure to the point of death, while the other breathes, also to the point of death, under normal pressure, an air that grows weaker and weaker in oxygen. Both will die after having presented the same symptoms.54 Bert goes on to describe the symptoms of acute exposure to hypoxia: It is the nervous system which reacts first. The sensation of fatigue, the weakening of the sense perceptions, the cerebral symptoms, vertigo, sleepiness, hallucinations, buzzing in the ears, dizziness, pricklings … are the signs of insufficient oxygenation of central and peripheral nervous organs. … The symptoms … disappear very quickly when the balloon descends from the higher altitudes, very quickly also … the normal proportion of oxygen reappears in the blood. There is an unfailing connection here.54 Bert was also able to both prevent and immediately resolve symptoms by breathing oxygen. Modern studies of acute hypoxic exposure use the measurement of time of useful consciousness; that is, the time until a subject can no longer take corrective measures, such as putting on an oxygen mask. With exposure to 8500 m (27,887 feet), that time is 60 seconds during moderate activity and 90 seconds at rest. Acute hypoxia can be quickly reversed by immediate administration of oxygen, rapid pressurization or descent, or correction of an underlying cause, such as relief of apnea, removal of a carbon monoxide source, repair of an oxygen delivery system, or cessation of overexertion. Hyperventilation increases time of useful consciousness during severe hypoxia.
HIGH-ALTITUDE HEADACHE The term high-altitude headache (HAH) has been used in the literature for decades, and studies directed toward the pathophysiology and treatment of HAH have been reported. Obviously these are to an extent also studies of AMS. Headache lends itself to investigation better than do some other symptoms, because headache scores have been well validated.244 Headache is generally the first unpleasant symptom consequent to altitude exposure and is sometimes the only symptom.214 It may or may not be the harbinger of AMS, which is defined as the presence of headache plus at least one of four other symptoms, in the setting of an acute altitude gain.435 One could even argue that it is the headache itself that causes other symptoms such as anorexia, nausea, lassitude, and insomnia, as is commonly seen in migraine or tension headaches, and that mild AMS is essentially due to headache. The International Headache Society206 has defined high-altitude headache as headache with at least two of the following characteristics: (1) bilateral; (2) frontal or frontotemporal; (3) dull or pressing quality; (4) mild or moderate intensity; and (5) aggravated by exertion, movement, straining, coughing, or bending. In addition, the headache must occur with an ascent to altitude greater than 2500 m (8202 feet), develop within 24 hours after ascent, and resolve within 8 hours after descent. Recent studies have attempted to characterize the clinical features and incidence of headache at altitude (Table 1-4). Silber and co-workers496 found that 50 of 60 trekkers (83%) in Nepal up to 5100 m (16,732 feet) developed at least one headache when over 3000 m (9843 feet). Older persons were less susceptible; women and those with headaches in daily life had more severe headaches, but no more headaches than others. Of those with headache, 52% did not have AMS by the Lake Louise criteria. The clinical features were widely variable. In general, the headaches were bilateral, generalized, dull, exacerbated by exertion or movement, often occurring at night, and resolved within 24 hours. Thus the headaches had some features of increased intracranial pressure (ICP). Persons with history of migraine did not have a higher incidence of headache. Various medications alleviated the headaches, especially mild ones, 70% of the time. Serrano-Duenas489 also described in detail HAH in 98 climbers in the Andes. Persons with history of primary headache were excluded. He found the following characteristics: holocranial, 65.6%; pulsatile-burst type quality, 75.3%; oscillating evolution, 10
TABLE 1-4 Clinical Characteristics of Headache Characteristic Location Global Frontal Hemi-cranial Occipital Change side Quality Pulsatile-burst Pressing/tightening Burning Dull Evolution Oscillate Disappear Diminish Increase Equal Break out in Elements Worsening Exercise Sudden movements Valsalva maneuver Light Elements Relieving Rest Analgesics Darkness Activity Concurrent Symptoms Anorexia Irritability Nausea Vomiting Apathy Gastric Malaise Somnolence Dysphasia Feelings Pessimism Anxiety Fear Isolation Strangeness
Percent Reporting 65.6 18.9 8.7 3.6 3.2 75.3 14.8 5.1 4.8 36.7 18.1 17.8 10.4 10.4 6.6 49.5 30.2 13.8 6.5 41.8 39 10.2 9 26.8 26.5 16.3 9.7 7.1 6.1 5.7 1.8 33.2 29.5 23.4 11.2 2.7
Modified from Serrano-Duenas M: High-altitude headache: A prospective study of its clinical characteristics, Cephalalgia 25:1110, 2005.
36.7%; increasing with exercise, 49.5%; relieved by rest, 41.8%; concurrent symptoms referred to: anorexia, 26.8%, irritability, 26.5%, and finally pessimism and anxiety feelings, 33.2% and 29.5%, respectively. Headaches were worse after a night’s sleep, more common in men, were of moderate intensity, and responded to analgesics. In general, the literature suggests that HAH can be prevented by the use of nonsteroidal antiinflammatory drugs65,72,157 and acetaminophen204 as well as the drugs commonly used for prophylaxis of AMS, acetazolamide and dexamethasone. Some agents appear more effective than do others, with ibuprofen and aspirin apparently superior to naproxen.65,70,73 A serotonin agonist (sumatriptan, a 5-HT1 [serotonin type 1] receptor agonist) was reported to be effective for HAH prevention and/or treatment in some studies,69,243,544 but not in others.28 Flunarizine, a specific calcium antagonist used for treatment of migraine, was not effective in one study.44 Interestingly, oxygen is often immediately effective for HAH (within 20 minutes) in subjects with and without AMS, indicating a rapidly reversible mechanism of the headache.26,191 The response to many different agents might reflect multiple components of the pathophysiology, or merely the nonspecific nature of analgesics. As Sanchez del Rio and Moskowitz463 have
Hypothalamus Brainstem
Autonomic response
CNS processing
High-altitude headache
Lower threshold for pain Trigeminovascular system activation
Hypoxia
eNOS upregulation
ACUTE MOUNTAIN SICKNESS Epidemiology and Risk Factors Although the syndrome of AMS has been recognized for centuries, modern rapid transport and proliferation of participants in mountain sports have increased the number of victims and therefore public awareness (see Table 1-1). The incidence and severity of AMS depend on the rate of ascent and the altitude attained (especially the sleeping altitude), duration of altitude exposure, level of exertion, recent altitude exposure, and inherent physiologic (genetic) susceptibility.440,475 For example, AMS is more common on Mt Rainier because of the rapid ascent, whereas high-altitude pulmonary or cerebral edema is uncommon because of the short stay (less than 36 hours). Persons with a demonstrated susceptibility to AMS had twice the incidence of AMS compared with nonsusceptibles, and this was independent of rate of ascent.475 The basis for inherent susceptibility is still unknown, but obviously depends on genetic factors. Acclimatization induced by recent altitude exposure can be protective; 4 days or more in the previous 2 months above 3000 m (9843 feet) reduced susceptibility to AMS on ascent to 4559 m (14,957 feet) by one-half, which was as effective as slow ascent475 (Figure 1-11). It also appears that protective effects of acclimatization persist after descent to low altitude. AMS was essentially absent in those who acclimatized to high altitude, returned to low altitude for 7 days, and were then reexposed to 4300 m (14,108 feet) in a hypobaric chamber.317 In addition, ventilation, SaO2, and exercise performance at altitude were maintained for at least 7 days,46,317,377 with some enhanced physical performance retained for several weeks.59,60,141,273,274 Recent epidemiologic studies suggest that protection from AMS may persist for months.475,586 Retention of the HVR might explain these results;305,433 yet studies showed that HVR returned to preascent values 7 days after descent.377 Compared with persons living at a lower altitude, residents at 900 m (2953 feet) or above reduced the incidence of AMS from 27% to 8% when ascending to between 2000 and 3000 m (6562 and 9843 feet) in Colorado.214 Age has an influence on incidence, with those over 50 years old somewhat less vulnerable.439,496 In a large study in Colorado, those over 60 had one-half the
incidence of AMS as those under 60 years of age. In contrast, a study of 827 mountaineers in Europe showed no influence of age on susceptibility.475 Perhaps different populations and physical activity explain the differing results. No study has ever shown older people to be more susceptible. Children from 3 months to puberty studied in Colorado had the same incidence as did young adults.534,592 A small study of tourists in Chile, however, found lower oxygen saturation and higher AMS in the 6- to 48-month age-group at 4440 m (14,567 feet).369 The largest study of children to date, of Han Chinese after ascent to Tibet, showed essentially the same incidence of AMS in 464 children as in 5335 adults, 34% and 38%, respectively.580 Women apparently have the same442,464,475 or a slightly greater incidence of AMS,214,546 but may be less susceptible to pulmonary edema.99,506 There appears to be no relation between AMS and the menstrual cycle.424 Most studies show no relation between physical fitness and susceptibility to AMS. However, obesity seems to increase the odds of developing AMS.154,214 Neither smoking nor the use of oral contraceptives increases risk for AMS.214,259,391 In summary, the most important variables related to AMS susceptibly are genetic predisposition, altitude of residence, altitude reached, rate of ascent, and prior recent altitude exposure. 70% 60%
Prevalence of AMS
pointed out, different inciting factors for headache may result in a final common pathway, such that the response to different therapies is not necessarily related to the initial cause of the headache. They have provided a useful multifactorial concept of the pathogenesis of HAH, based on current understanding of headaches in general.463 They suggest that the trigeminovascular system is activated at altitude by both mechanical and chemical stimuli (vasodilation, nitric oxide [NO] and other noxious agents), and in addition, the threshold for pain is likely altered at high altitude (Figure 1-10).463 If AMS and especially HACE ensue, then altered intracranial dynamics may also play a role, via compression or distension of pain-sensitive structures. A recent study provided evidence against sustained trigeminovascular activity,14 but more study will hopefully bring better understanding of the pathophysiology of these often debilitating headaches, and new treatments as well.
↑ NO
Nonsusceptible Susceptible
50% 40% 30% 20% 10% 0% Either ascent Ascent <4 days >3 days or and preexposure preexposure <5 days ≥5 days Rate of ascent and pre-exposure
Ascent >3 days and preexposure ≥5 days
FIGURE 1-11 The prevalence of acute mountain sickness (AMS) and 95% confidence intervals in nonsusceptible (blue bars) and susceptible (red bars) mountaineers in relation to the state of acclimatization defined as slow ascent (more than 3 days), fast ascent (3 days or less), preexposed (5 days or more above 3000 m [9843 feet] in the preceding 2 months), and not preexposed (4 days or less above 3000 m [9843 feet] in the preceding 2 months). (Reprinted from Schneider M, Bernasch D, Weymann J, et al: Acute mountain sickness: Influence of susceptibility, preexposure, and ascent rate, Med Sci Sports Exerc 34:1886, 2002.)
11
CHAPTER 1 High-Altitude Medicine and Physiology
FIGURE 1-10 Proposed pathophysiology of high-altitude headache. CNS, Central nervous system; eNOS, endothelial nitric oxide synthase; NO, nitric oxide. (Modified from Sanchez del Rio M, Moskowitz MA: High altitude headache. In Roach RC, Wagner PD, Hackett PH, editors: Hypoxia: Into the next millennium, New York, 1999, Plenum/Kluwer Academic Publishing, pp 145-153.)
PART 1 MOUNTAIN MEDICINE
TABLE 1-5 Clinical Characteristics of High-Altitude Illnesses Clinical Classification HAH
Mild AMS
Moderate to Severe AMS
HACE
Symptoms
Headache only
Headache plus one or more symptoms (nausea/vomiting, fatigue/lassitude, dizziness or difficulty sleeping) Symptoms of moderate to severe intensity
±Headache Worsening of symptoms seen in moderate to severe AMS
LL-AMS score* Physical signs
1-3, headache only None
Headache plus one more symptom (nausea/ vomiting, fatigue/ lassitude, dizziness or difficulty sleeping) All symptoms of mild severity 2-4 None
Findings
None
None
Pathophysiology
Unknown; cerebral vasodilation, trigeminovascular system?†
Unknown; same as HAH?
Antidiuresis Slightly increased body temperature Slight desaturation Widened A-a gradient Elevated ICP White matter edema (CT, MRI) Vasogenic edema; cytotoxic edema?
5-15 None
Ataxia Altered mental status HAPE common: positive chest radiograph, rales, dyspnea at rest Elevated ICP White matter edema (CT, MRI) Advanced vasogenic cerebral edema; cytotoxic edema?
AMS, Acute mountain sickness; CT, computed tomography; HACE, high-altitude cerebral edema; HAH, high-altitude headache; HAPE, high-altitude pulmonary edema; ICP, intracranial pressure; MRI, magnetic resonance imaging. *The self-reported Lake Louise AMS score. † See Figures 1-10 and 1-12.
Diagnosis Diagnosis of AMS is based on the setting, symptoms, physical findings, and exclusion of other illnesses. The setting is generally rapid ascent of unacclimatized persons to 2500 m (8202 feet) or higher from altitudes below 1000 m (3281 feet). For partially acclimatized persons, abrupt ascent to a higher altitude, overexertion, use of respiratory depressants, and perhaps onset of infectious illness376 are common contributing factors. The cardinal symptom of early AMS is headache, followed in incidence by fatigue, dizziness, and anorexia.214,500 The headache is usually throbbing, bitemporal, typically worse during the night and on awakening, and made worse by the Valsalva maneuver or stooping over (see High Altitude Headache, earlier). A good appetite is unusual, and nausea is common. These initial symptoms are strikingly similar to an alcohol hangover. Frequent awakening may fragment sleep, and periodic breathing often produces a feeling of suffocation. Although sleep disorder is nearly universal at high altitude, also affecting those without AMS, these symptoms may be exaggerated during AMS. Affected persons commonly complain of a deep inner chill, unlike mere exposure to cold temperature, accompanied by facial pallor. Other symptoms may include vomiting, dyspnea on exertion, and irritability. Lassitude can be disabling, with the victim too apathetic to contribute to his or her own basic needs. Pulmonary symptoms vary considerably. Everyone experiences dyspnea on exertion at high altitude; dyspnea at rest is distinctly abnormal, however, and presages HAPE rather than AMS. Cough is also extremely common at high altitude and not associated with AMS. Recent work suggests that altitude hypoxia actually lowers the cough threshold, as measured with an inhaled citric acid stimulus.333 However, any pulmonary symptom mandates careful examination for pulmonary edema. Specific physical findings are lacking in mild AMS. A higher heart rate has been noted in those with AMS,34,391 but Singh and associates500 noted bradycardia (heart rate less than 66 beats/min) in two-thirds of 1975 soldiers with AMS. Blood pressure is normal, but postural hypotension may be present. Occasionally, localized rales may be present,323 but this has also been observed in those without AMS.187 A slight increased body temperature with AMS may be present but is not diagnostic.321 Peripheral oxygen saturation as measured by pulse oximetry correlated poorly with presence of AMS during rapid ascent391,439,450 but was related to AMS during trekking.39 SaO2 at altitude on Denali was predictive of developing AMS on further ascent.436 Overall, pulse oximetry is 12
of limited usefulness in diagnosing AMS. Funduscopic examination reveals venous tortuosity and dilation; retinal hemorrhages may or may not be present and are not diagnostic. They are more common in AMS than non-AMS subjects at 4243 m (13,921 feet).187 Absence of the normal altitude diuresis, evidenced by lack of increased urine output and retention of fluid, is an early finding in AMS, although not always present.35,188,442,500,528 More obvious physical findings develop if AMS progresses to HACE. AMS displays no neurologic findings, whereas HACE is an encephalopathy (see High-Altitude Cerebral Edema, later). It is clinically useful to classify AMS as mild or moderate to severe on the basis of symptoms (Table 1-5). Importantly, AMS can herald the beginning of life-threatening cerebral edema. Differential Diagnosis Given the nonspecific nature of the symptoms, AMS is commonly confused with other conditions (Box 1-3). AMS is most commonly misdiagnosed as a viral flulike illness, hangover, exhaustion, dehydration, or medication or drug effect. Unlike an infectious illness, uncomplicated AMS is not associated with fever and myalgias. Hangover is excluded by the history. Exhaustion may cause lassitude, weakness, irritability, and headache and may therefore be difficult to distinguish from AMS. Dehydration, which causes weakness, decreased urine output, headache, and nausea, is commonly confused with AMS. Response to fluids BOX 1-3 Differential Diagnosis of High-Altitude
Illnesses
Acute mountain sickness and high-altitude cerebral edema
High-altitude pulmonary edema
Dehydration, exhaustion, viral or bacterial infection, alcohol hangover, hypothermia, carbon monoxide poisoning, migraine, hyponatremia, hypoglycemia, diabetic ketoacidosis, CNS infection, transient ischemic attack, arteriovenous malformation, stroke, seizures, brain tumors, ingestion of toxins or drugs, acute psychosis Asthma, bronchitis, pneumonia, mucus plugging (secondary to previous), hyperventilation syndrome, pulmonary embolus, heart failure, myocardial infarction
CNS, Central nervous system.
↓O2 vasodilation
Acute hypoxic ventilatory ↓CO2 response vasoconstriction ←→
Ca2+
sensitivity NO→impaired →relaxation/vasodilation
↑Ca2+ No release
Endothelium Elastic lamina Smooth muscle
Other molecules that may be involved: Acetylcholine Substance P Prostaglandins
Microhemorrhage
↑K+
Raised hydrostatic pressure
Venous
Capillary and blood-brain barrier
Arteriole
CHAPTER 1 High-Altitude Medicine and Physiology
Artery
NO
HIF-1α not broken down
Hypoxemia
Raised venous pressure
Free radical formation
Basement membrane damage Na+/K+ Upregulation ATPase failure of VEGF →intracellular Edema→↑ICP edema Adenosine →hypoxic vasodilation
Headache
Capillary basement membrane damage and angiogenesis Mechanical mediator PO2/PCO2 mediator Chemical mediator
Vasodilation→pain Pain fibers of trigeminal nerve→trigeminovascular system
FIGURE 1-12 Proposed pathophysiology of acute mountain sickness. HIF, Hypoxia-inducible factor; ICP, intracranial pressure; NO, nitric oxide; VEGF, vascular endothelial growth factor. (Modified from Wilson MH, Newman S, Imray CH: The cerebral effects of ascent to high altitudes, Lancet Neurol 8:175, 2009.)
helps to differentiate the two. AMS is not improved by fluid administration alone, and body hydration does not influence susceptibility to AMS (contrary to conventional wisdom).11 Hypothermia may manifest as ataxia and mental changes. Sleeping medication can cause ataxia and mental changes, but soporifics may also precipitate high-altitude illness because of increased hypoxemia during sleep. Migraine may be very difficult to distinguish from AMS. A trial of oxygen breathing or descent can be helpful to discriminate these other conditions from AMS. Pathophysiology The basic cause of AMS is hypoxemia, but the syndrome is different from acute hypoxia. Because symptoms are somewhat worse with hypobaric hypoxia than with normobaric hypoxia, hypobaria apparently also plays a minor role, most likely through its effect on fluid retention.240,261,303,304,441 Because of a time lag in onset of symptoms after ascent and lack of immediate or complete reversal of all symptoms with oxygen, AMS is thought to be secondary to the body’s responses to modest hypoxia. In addition, even though an altitude of 2500 to 2700 m (8202 to 8858 feet) presents only a minor decrement in arterial oxygen transport (SaO2 is still above 90%), AMS is common and some individuals may become desperately ill. Some aspects of AMS pathophysiology are clear. Findings documented in mild to moderate AMS include relative hypoventilation,336,366 impaired gas exchange (interstitial edema),171,286 fluid retention and redistribution,35,442,528 and increased sympathetic
drive.31,34 In mild to moderate AMS, limited data show that ICP or cerebrospinal fluid (CSF) pressure is not elevated at rest.17,205,579 In contrast, increased ICP and cerebral edema are documented in severe AMS, reflecting the continuum from advanced AMS to HACE.220,276,337,500,573 The known, well-established findings in AMS are reviewed extensively elsewhere.179,233,240 The remainder of this section focuses on remaining questions and new work in the quest to find the cause of AMS. We proposed more than a decade ago that moderate to severe AMS was caused by brain swelling leading to elevated ICP via a compromised buffering capacity. This hypothesis has not yet been directly tested. We now examine the data on brain swelling, ICP, and cranial buffering capacity in AMS. Brain Swelling in AMS. For decades, clinicians have postulated that AMS is a mild form of cerebral edema. Although this appears true for moderate to severe AMS, it now seems unlikely that mild AMS, or the headache alone, is due to edema (see High-Altitude Headache, earlier). Persons with moderate to severe AMS or HACE display elevated ICP and white matter edema on brain imaging in most but not all studies,144 whereas those with mild AMS do not.* Recent MRI studies have demonstrated that brain swelling occurs in all subjects ascending rapidly to moderate altitude, regardless
*References 197, 220, 276, 295, 337, 500.
13
PART 1 MOUNTAIN MEDICINE
of the presence of AMS, and is due to both vasodilation and minor vasogenic edema. In addition, there may be an intracellular fluid shift as evidenced by low apparent diffusion coefficient. Although this was greater in those with AMS, the volumetric changes were minor and unlikely to result in increased ICP without contributing factors.144,239,252,372,481 In summary, no gross elevation in brain volume has been found yet in mild AMS or headache alone, but elevated brain volume is almost universally observed in moderate to severe AMS and HACE. Intracranial Pressure and AMS. A fascinating story was recently reported in which a neurosurgeon measured ICP changes from a self-implanted ICP monitoring bolt in himself and in two others.572 They demonstrated that ICP remained normal at rest at all altitudes (studied from sea level to 5030 m [16,503 feet]); however, in the single subject with AMS, there was a dramatic increase in ICP even on minimal exertion. This study is consistent with recent indirect assessment of elevated ICP in AMS based on optic nerve sheath diameter.138,523 In addition, a study that measured opening lumbar pressure revealed significant elevations in AMS subjects compared with control or after AMS resolved.500 In contrast, one recent study in normobaric hypoxia reported no elevation of ICP in AMS when measured indirectly by repeat lumbar puncture.252 The evidence that ICP is elevated in mild AMS is limited and not compelling. Stronger evidence suggests that perhaps intracranial compliance is altered,275 and that although ICP might not be elevated at rest, it rises abruptly with isometric maneuvers such as lifting a pack, with Valsalva, or even with turning the head, which slightly elevates venous pressure.205,572 Altered compliance is consistent with the tight-fit hypothesis (see below). The Tight-Fit Hypothesis and AMS. Ross457 hypothesized in 1985 that persons with smaller intracranial and intraspinal CSF capacity would be disposed to develop AMS, because they would not tolerate brain swelling as well as those with more “room” in the craniospinal axis. It is displacement of CSF through the foramen magnum into the spinal canal that is the first compensatory response to increased brain volume, followed by increased CSF absorption and decreased CSF formation. Studies have shown that the increase in ICP for a given increase in brain volume is directly related to the “tightness” of the brain in the cranium (the brain volume: intracranial volume ratio) and to the volume of the spinal canal.492 Thus, the greater the initial CSF volume, the more accommodation that can take place in response to brain edema. Increases in volume are “buffered” by CSF dynamics. In light of our present understanding of increased brain volume on ascent to altitude, his hypothesis is still very attractive. Preliminary data that showed a relationship of preascent ventricular size or brain volume: cranial vault ratios and susceptibility to AMS support this hypothesis,182,252,572,593 as do the studies showing elevated ICP in moderate to severe AMS.220,276,337,500,573 The idea deserves further study. New Concepts. New, potentially important work is under way to understand the potential role of inflammatory mediators, free radicals, and even HIF-modulated reactions in the pathophysiology of AMS.14,16 Progress is hampered by the technical difficulty of some of these approaches, by lack of an animal model, and by the unresolved status of the basic pathophysiology. A potentially unifying hypothesis, with several novel ideas, is presented in Figure 1-12. In this schema, mechanical factors increase intravascular pressure and hence can cause vasogenic edema and vessel wall damage. This pressure can act in the artery (increased hydrostatic pressure associated with increased flow) or vein (if there is venous outflow obstruction, as in benign intracranial hypertension, for example). The partial pressures of oxygen and carbon dioxide are thought to have direct vasoactive properties, with hypoxemia causing vasodilation and hypocarbia causing vasoconstriction. A balance between these is mediated by the hypoxic and CO2 ventilatory responses. Cytotoxic edema is attributed to direct hypoxia-induced Na+/K+ ATPase failure. Many chemical mediators have been implicated. Free radical formation could directly damage the blood–brain barrier, causing vasogenic edema. Accumulation of HIF-1α and subsequent upregulation of 14
vascular endothelial growth factor (VEGF) could contribute to further blood–brain barrier damage and edema. Neuronally mediated adenosine release also causes vasodilation. Vessel dilation has been implicated in activating the trigeminovascular system, causing headache. An important element of HACE is microhemorrhage formation, caused by vessel damage from chemical mediators or cytokines or by damage through increased hydrostatic pressure.253 Natural Course of Acute Mountain Sickness The natural history of AMS varies with initial altitude, rate of ascent, and clinical severity. Symptoms can start within 2 hours after arrival and rarely if ever start after 36 hours at a given altitude. AMS usually resolves over the next 24 to 48 hours. The more rapid the ascent, and the higher the altitude, the more likely that symptoms will appear sooner and be worse. Singh and associates500 followed the illness in soldiers airlifted to altitudes of 3300 to 5500 m (10,827 to 18,045 feet). Incapacitating illness lasted 2 to 5 days, but 40% still had symptoms after 1 week and 13% after 1 month. Nine soldiers failed to acclimatize in 6 months and were considered unfit for duty at high altitude.500 Chinese investigators report that a percentage of lowland Han Chinese stationed on the Tibet Plateau cannot tolerate the altitude because of persistent symptoms and must be relocated to the plains.583 Persistent anorexia, nausea, and headache may afflict climbers at extreme altitude for weeks and can be considered a form of persistent AMS. The natural history of AMS in tourists who sleep at more moderate altitudes is much more benign. Duration of symptoms at 2700 m was 15 hours, with a range of 6 to 94 hours.361 Most individuals treat or tolerate their symptoms as the illness resolves over 1 to 3 days while acclimatization improves, but some persons with AMS seek medical treatment or are forced to descend if symptoms persist. A small percentage of those with AMS (3.4% at 4243 m [13,921 feet]) go on to develop cerebral edema, especially if ascent continues in spite of illness. Although 50% of persons with HAPE have AMS, no study has documented how many with AMS develop HAPE. Treatment Management of AMS is based on severity of illness at presentation, logistics, terrain, and experience of the caregiver. Early diagnosis is key, because treatment in the early stages of illness is easier and more successful (Box 1-4). Proceeding to a higher sleeping altitude in the presence of symptoms is contraindicated. The victim must be carefully monitored for progression of illness. If symptoms worsen despite 24 hours of acclimatization or treatment, descent is indicated. The two indications for immediate descent are neurologic findings (ataxia or change in consciousness) and pulmonary edema. Mild AMS can be treated by halting the ascent and waiting for acclimatization to improve, which can take from 12 hours to 3 or 4 days. Acetazolamide (250 mg twice a day orally, or as a single dose) speeds acclimatization and thus terminates the illness if given early.171,326 Symptomatic therapy includes analgesics such as aspirin (500 or 650 mg), acetaminophen (650 to 1000 mg), ibuprofen65 or other nonsteroidal antiinflammatory drugs, or codeine (30 mg) for headache. Ondansetron 4 mg orally disintegrating tablets every 4 hours as necessary is useful for nausea and vomiting. Persons with AMS should avoid alcohol and other respiratory depressants because of possible exaggerated hypoxemia during sleep. Descent to an altitude lower than where symptoms began effectively reverses AMS. Although descent should be as far as necessary for improvement, 500 to 1000 m (1640 to 3281 feet) is usually sufficient. Exertion should be minimized. Oxygen, if available, is particularly effective (and supply is conserved) if given in low flow (0.5 to 1 L/min by mask or cannula) during the night. Hyperbaric chambers, which simulate descent, have been used to treat AMS and aid acclimatization. They are effective and require no supplemental oxygen. Lightweight (less than 7 kg) fabric pressure bags inflated by manual air pumps are now being used on mountaineering expeditions and in mountain clinics (Figure 1-13). An inflation of 2 psi is roughly equivalent to a drop in altitude of 1600 m (5249 feet); the exact equivalent depends on initial altitude.257,437 A few hours of pressurization
High-Altitude Headache and Mild Acute Mountain Sickness • Stop ascent, rest, acclimatize at same altitude • Symptomatic treatment as necessary with analgesics and antiemetics • Consider acetazolamide, 125 to 250 mg bid, to speed acclimatization • OR descend 500 m (1640 feet) or more Moderate to Severe Acute Mountain Sickness • Low-flow oxygen, if available • Acetazolamide, 125 to 250 mg bid, with or without dexamethasone, 4 mg PO, IM, or IV q6h • Hyperbaric therapy • OR immediate descent High-Altitude Cerebral Edema • Immediate descent or evacuation • Oxygen, 2 to 4 L/min • Dexamethasone, 8 mg PO, IM, or IV, then 4 mg q6h • Hyperbaric therapy High-Altitude Pulmonary Edema • Minimize exertion and keep warm • Immediate descent or hyperbaric therapy • Oxygen, 4 to 6 L/min until improving, then 2 to 4 L/min • If above unavailable, one of the following: • Nifedipine, 30 mg extended release q12h • Sildenafil 50 mg q8h • Tadalafil 10 mg q12h • Consider inhaled β-agonist Periodic Breathing • Acetazolamide, 62.5 to 125 mg at bedtime as needed
hydrochlorothiazide, and other diuretics have not yet been evaluated for treatment (see Prevention, later). The steroid betamethasone was initially reported by Singh and co-workers500 to improve symptoms of soldiers with severe AMS. Subsequent studies have found dexamethasone to be effective for treatment of all degrees of AMS.140,196,262 Hackett and colleagues196 used 4 mg orally or intramuscularly every 6 hours, and Ferrazinni and associates140 gave 8 mg initially, followed by 4 mg every 6 hours. Both studies reported marked improvement within 12 hours, which was the first postdrug assessment, but clinical experience suggests improvement of AMS within 4 hours. There were no significant side effects. Symptoms increased when dexamethasone was discontinued after 24 hours.196 Clinicians debate whether the use of dexamethasone should also mandate descent. Is it safe to continue to ascend after treatment with dexamethasone or while taking the medication? In reality, people do, and problems seem to be few. In our opinion, dexamethasone use should be limited to less than 72 hours to minimize side effects. This generally is sufficient time to descend, or to better acclimatize, with or without acetazolamide. The mechanism of action of dexamethasone is unknown; it does not affect oxygen saturation, fluid balance, or periodic breathing.295 The drug blocks the action of VEGF,476 diminishes the interaction of endothelium and leukocytes (thus reducing inflammation),167 and may also reduce cerebral blood flow.250 Dexamethasone seems to not improve acclimatization, because some symptoms recur when the drug is withdrawn. Therefore an argument could be made for using dexamethasone to relieve symptoms and acetazolamide to speed acclimatization.52 Prevention Prevention strategy is based on risk assessment311 (Table 1-6). Graded ascent is the surest and safest method of prevention, although particularly susceptible individuals may still become ill. TABLE 1-6 Risk Categories for Acute Mountain
Sickness
IM, Intramuscularly; IV, intravenously; PO, orally.
result in symptomatic improvement and can be an effective temporizing measure while awaiting descent or the benefit of medical therapy.257,375,398,444,532 Long-term (12 hours or more) use of these portable devices is necessary to resolve AMS completely. Acetazolamide is of unquestionable prophylactic value and is now commonly and successfully used to treat AMS as well, although data supporting this are minimal.171,326 Singh and colleagues500 successfully used furosemide (80 mg twice a day for 2 days) to treat 446 soldiers with all degrees of AMS; it has not since been studied for treatment. Furosemide induced a brisk diuresis, relieved pulmonary congestion, and improved headache and other neurologic symptoms.500 Spironolactone,
Risk Category Low
Moderate
High
FIGURE 1-13 A fabric hyperbaric pressure bag being used on Mt Everest for treatment of severe altitude illness. Two psi pressure is equivalent to a drop of approximately 1600 m (5249 feet) in altitude.
Description Individuals with no prior history of altitude illness and ascending to <2800 m (9186 feet) Individuals taking >2 days to arrive at 2500-3000 m (8202-9843 feet) with subsequent increases in sleeping elevation <500 m (1640 ft)/day and an extra day for acclimatization every 1000 m (3281 feet) Individuals with prior history of AMS and ascending to 2500-2800 m (8202-9186 feet) in 1 day No history of AMS and ascending to >2800 m (9186 feet) in 1 day All individuals ascending >500 m (1640 ft)/day (increase in sleeping elevation) at altitudes above 3000 m (9843 feet) but with an extra day for acclimatization every 1000 m (3281 feet) History of AMS and ascending to >2800 m (3281 feet) in 1 day All individuals with a prior history of HAPE or HACE All individuals ascending to >3500 m (11,483 feet) in 1 day All individuals ascending >500 m (1640 ft)/day (increase in sleeping elevation) above >3000 m (9843 feet) without extra days for acclimatization Very rapid ascents (e.g., <7-day ascents of Mt Kilimanjaro)
Modified from Luks AM, McIntosh SE, Grissom CK, et al: Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness, Wilderness Environ Med 21:146, 2010. AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema. Notes: Altitudes listed in the table refer to the altitude at which the person sleeps. Ascent is assumed to start from elevations <1200 m (3937 feet). The risk categories described above pertain to unacclimatized individuals.
15
CHAPTER 1 High-Altitude Medicine and Physiology
BOX 1-4 Field Treatment of High-Altitude Illness
PART 1 MOUNTAIN MEDICINE
Carbonic anhydrase
CO2 + H2O <==> H2CO3 <==> H+ + HCO3 FIGURE 1-14 Action of acetazolamide to block carbonic anhydrase (shown in a molecular ribbon diagram) and thus slow the hydration of carbon dioxide.
Current recommendations are to avoid abrupt ascent from low altitude to sleeping altitudes greater than 2800 m (9186 feet) in 1 day, to spend 2 to 3 nights at 2500 to 3000 m (8202 to 9843 feet) before going higher, to not advance sleeping altitude more than 500 m (1640 ft)/day, and to take an extra night for acclimatization every 1000 m if continuing ascent.311 However, a recent study on Aconcagua reinforced the notion that individual susceptibility is a key factor, and that persons who are resistant to AMS can proceed much more quickly on the mountain safely.405 Day trips to higher altitude, with a return to lower altitude for sleep, aid acclimatization. Alcohol and sedative-hypnotics are best avoided on the first 2 nights at high altitude. Whether a diet high in carbohydrates reduces AMS symptoms is controversial.96,203,530 Exertion early in altitude exposure contributes to altitude illness,440 whereas limited exercise seems to aid acclimatization. Because altitude exposure in the previous weeks is protective, a faster rate of ascent may then be possible.475,586 Acetazolamide Prophylaxis. Acetazolamide is the drug of choice for prophylaxis of AMS. A carbonic anhydrase inhibitor, acetazolamide slows the hydration of carbon dioxide (Figure 1-14).
The effects are protean, involving particularly red blood cells, the brain, lungs, and kidneys. By inhibiting renal carbonic anhydrase, acetazolamide reduces reabsorption of bicarbonate and sodium and thus causes a bicarbonate diuresis and metabolic acidosis, beginning within 1 hour after ingestion. This rapidly enhances ventilatory acclimatization, increasing oxygenation. Importantly, the drug maintains oxygenation during sleep and prevents periods of extreme hypoxemia (see Figure 1-6).192,525,529 Because of acetazolamide’s diuretic action, it counteracts the fluid retention of AMS. It also diminishes nocturnal antidiuretic hormone secretion86 and decreases CSF production and volume and possibly CSF pressure.488 Acetazolamide also impacts brain aquaporin channels, possibly preventing water transport into the brain.533 Which of these effects is most important in preventing AMS is unclear. Numerous studies taken together indicate that acetazolamide is approximately 75% effective in preventing AMS in persons rapidly transported to altitudes of 3000 to 4500 m (9843 to 14,764 feet).132 Acetazolamide prophylaxis should be considered for persons with moderate to severe risk, as indicated in Tables 1-6 and 1-7. The ideal dose of acetazolamide for prevention is debated. Many studies have shown that 250 mg twice a day or 3 times a day was effective, as well as 500 mg in sustained action capsule taken every 24 hours.* To reduce the side effects, especially paresthesias, clinicians have more recently been using smaller doses (125 mg twice a day),348 and a number of studies now support this.37,77,548 Renal carbonic anhydrase is blocked with 5 mg/kg/ day, and this may be the maximum dose required, both in children and adults. Duration of medication use varies; the standard advice is to start 24 hours before ascent. Most clinicians recommend continuing for at least the first 2 days at high altitude, and longer if there is continuing gain in altitude. Acetazolamide can also be taken episodically, to speed acclimatization at any point while gaining altitude or to treat mild AMS. There is no rebound when discontinued. Although the danger of altitude illness passes after a few days of acclimatization, acetazolamide may still be useful to promote more effective sleep. Acetazolamide has side effects, most notably peripheral paresthesias and polyuria, and less commonly nausea, drowsiness, impotence, and myopia. Because it inhibits the instant hydration of carbon dioxide on the tongue, acetazolamide allows carbon dioxide to be tasted and can ruin the flavor of carbonated beverages, including beer. The issue of sulfonamide allergy and acetazolamide was recently reviewed.263 As a nonantibiotic sulfonamide drug, acetazolamide is usually tolerated well by persons with a history of sulfa antibiotic allergy; approximately 10% may have an allergic reaction.517 In persons without a history *References 83, 156, 170, 186, 286, 421, 575.
TABLE 1-7 Recommended Dosages for Medications Used in the Prevention and Treatment of Altitude Illness Medication
Indication
Route
Dosage
Acetazolamide
AMS, HACE prevention
Oral
AMS treatment*
Oral
AMS, HACE prevention
Oral
AMS, HACE treatment
Oral, IV, IM
HAPE HAPE HAPE HAPE HAPE
Oral Oral Oral Oral Inhaled
125 mg twice per day Pediatric dose: 2.5 mg/kg q12h 250 mg twice per day Pediatric dose: 2.5 mg/kg q12h 2 mg q6h or 4 mg q12h Pediatrics: should not be used for prophylaxis AMS: 4 mg q6h HACE: 8 mg once then 4 mg q6h Pediatric dose: 0.15 mg/kg/dose q6h up to 4 mg 30 mg SR version q12h 30 mg SR version q12h 10 mg twice per day 50 mg q8h 125 mcg twice per day*
Dexamethasone
Nifedipine Tadalafil Sildenafil Salmeterol
prevention treatment prevention prevention prevention
Modified from Luks AM, McIntosh SE, Grissom CK, et al: Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness, Wilderness Environ Med 21:146, 2010. AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema; IM, intramuscular; IV, intravenous; SR, sustained release. *Should not be used as monotherapy and should only be used in conjunction with oral medications.
16
Dexamethasone Prophylaxis. Dexamethasone effectively prevents AMS. Two mg every 6 hours or 4 mg every 12 hours was sufficient for sedentary subjects,250 but for exercising subjects at or above 4000 m (13,123 feet), this was insufficient,51,196,446 and 4 mg every 6 hours was necessary to prevent AMS.447 The initial chamber study in 1984 was with sedentary subjects.250 The drug reduced the incidence of AMS from 78% to 20%, comparable with previous studies with acetazolamide. Dexamethasone was not as effective in exercising subjects on Pike’s Peak,446 but subsequent work has shown effectiveness comparable with acetazolamide.42,132,295,360,594 The combination of acetazolamide and dexamethasone proved superior to dexamethasone alone.594 Because of potential serious side effects and the rebound phenomenon, dexamethasone is best reserved for treatment rather than for prevention of AMS, or used for prophylaxis when necessary in persons intolerant of or allergic to acetazolamide. Other Agents for AMS Prevention. Studies with Ginkgo biloba have had inconsistent results. Four studies had positive results, ranging from 100% to 50% reduction in AMS when given either 5 days or 1 day before ascent.158,318,368,451 Three studies were negative, two of which were follow-up studies by investigators with positive results previously.83,156,288 Conflicting results can possibly be explained by differences in dosing, duration of pretreatment, and varying rates of ascent, but most likely, they are due to differences in preparations of ginkgo.289 Ginkgo biloba is a complicated plant extract whose active ingredient in terms of preventing AMS is unknown. Even in the “standardized” preparations (24% flavonoids and 6% terpene ginkolides), the amounts of specific chemicals can vary considerably. Until the active ingredient is discovered and standardized, results with ginkgo will continue to be mixed. Meanwhile, because the product is very safe, nonprescription, inexpensive, and can be helpful, it is reasonable to consider its use. Acetazolamide, however, is likely the superior agent. Spironolactone,245,285 naproxen, calcium channel blockers, antacids, and medroxyprogesterone acetate have shown ineffectiveness for AMS prevention. Bailey and Davies15 tested an antioxidant “cocktail” for prevention of AMS. They reasoned that free-radicalmediated damage to the blood–brain barrier might play a role in the pathophysiology. They preloaded nine subjects with daily L-ascorbic acid, DL-α-tocopherol acetate and α-lipoic acid, and nine subjects with placebo for 3 weeks, and then during a 10-day trek to the Mt Everest base camp. Those on antioxidants had a slightly lower AMS score and higher arterial oxygen saturation and better appetite.15 A recent study failed to confirm any benefit of antioxidant therapy for preventing AMS.18 In spite of these marginal findings in field studies, some clinicians propose that regional changes in redox state in the brain can lead to focal blood–brain barrier disruption and vasogenic edema. See Bärtsch and associates25 for a detailed discussion of the antioxidant hypothesis.
HIGH-ALTITUDE CEREBRAL EDEMA HACE is an uncommon but deadly condition, usually occurring in those with AMS or HAPE. Although HACE is most common over 3000 m (9843 feet), it has been reported at altitudes as low as 2100 m (6890 feet).115 Reliable estimates of incidence range from 0.5% to 1% in unselect high-altitude visitors,33,186 but was 3.4% in those who had developed AMS.186 In Chinese railway workers at 4500 to 4900 m (14,764 to 16,076 feet), incidence was 0.5%. HACE occurs in 13% to 20% of persons with HAPE152,211,232 and in up to 50% of those who die from HAPE. In addition, HAPE is very common in those diagnosed with HACE; one series
from Colorado reported that 11 of 13 with a primary diagnosis of HACE also had HAPE. Pure cerebral edema, without pulmonary edema, appears to be uncommon at lower altitudes, but accounted for 54 of 66 HACE cases in Tibet.582 The mean altitude at onset was 4730 m (15,518 feet)in one survey, but was lower (3920 m [12,861 feet]) when associated with HAPE.233 Data are insufficient to draw any conclusions regarding effects of gender, age, preexisting illness, or genetics on susceptibility to HACE. Clinically and pathophysiologically, advanced AMS and HACE are similar, so that a distinction between them is inherently blurred. See our review190 and the recent series reported by Wu and associates582 for a more complete discussion. Clinical Presentation HACE is an encephalopathy, whereas AMS is not. The hallmarks of HACE are ataxic gait, severe lassitude, and altered consciousness, including confusion, impaired mentation, drowsiness, stupor, and coma. Headache, nausea, and vomiting are frequent, but not always present. Hallucinations, cranial nerve palsy, hemiparesis, hemiplegia, seizures, and focal neurologic signs have also been reported.118,199,220,500,582 Seizures are distinctly uncommon. Retinal hemorrhages are common but not diagnostic. The progression from mild AMS to unconsciousness may be as fast as 12 hours but usually requires 1 to 3 days; HACE can develop more quickly in persons with HAPE. Arterial blood gas study or pulse oximetry often reveals exaggerated hypoxemia. Clinical examination and chest radiography may reveal pulmonary edema. Laboratory studies and lumbar puncture are useful only to rule out other conditions. Computed tomography (CT) may show compression of sulci and flattening of gyri, and attenuation of signal more in the white matter than gray matter. MRI is more revealing, with a characteristic high T2 signal in the white matter, especially the splenium of the corpus callosum, and most evident on diffusion-weighted images.197,578,582 The following case report from Mt McKinley illustrates a typical clinical course of HACE in conjunction with HAPE. CLINICAL PRESENTATION H.E. was a 26-year-old German lumberjack with extensive mountaineering experience. He ascended to 5200 m (17,060 feet) from 2000 m (6562 feet) in 4 days and attempted the summit (6194 m [20,322 feet]) on the fifth day. At 5800 m (19,029 feet) he turned back because of severe fatigue, headache, and malaise. He returned alone to 5200 m (17,060 feet), stumbling on the way because of loss of coordination. He had no appetite and crawled into his sleeping bag too weak, tired, and disoriented to undress. He recalled no pulmonary symptoms. In the morning H.E. was unarousable, slightly cyanotic, and noted to have Cheyne-Stokes respirations. After 10 minutes on high-flow oxygen, H.E. began to regain consciousness, although he was completely disoriented and unable to move. A rescue team lowered him down a steep slope, and on arrival at 4400 m (14,436 feet) 4 hours later, he was conscious but still disoriented, able to move extremities but unable to stand. Respiratory rate was 60 breaths/min, and heart rate was 112 beats/min. Papilledema and a few rales were present. SaO2 was 54% on room air (normal is 85% to 90%). On a nonrebreather mask with 14 L/min oxygen, the SaO2 increased to 88% and the respiratory rate decreased to 40 breaths/min. Eight milligrams of dexamethasone were administered intramuscularly at 4:20 PM and continued orally, 4 mg every 6 hours. At 5:20 PM, H.E. began to respond to commands. The next morning H.E. was still ataxic but was able to stand, take fluids, and eat heartily. He was evacuated by air to Anchorage (sea level) at 12:00 PM. On admission to the hospital at 3:30 PM, roughly 36 hours after regaining consciousness, H.E. was somewhat confused and mildly ataxic. Arterial blood gas studies on room air showed a PO2 of 58 mm Hg, pH of 7.5, and PCO2 of 27 mm Hg. Bilateral pulmonary infiltrates were present on the chest radiograph. Magnetic resonance imaging of the brain revealed white matter edema, primarily of the corpus callosum (Figures 1-15 and 1-16). On discharge the next morning, H.E. was oriented, bright, and cheerful and had very minor ataxia and clear lung fields. 17
CHAPTER 1 High-Altitude Medicine and Physiology
of allergy to sulfa antibiotic, the incidence of hypersensitivity reaction to a sulfonamide nonantibiotic was 1.6%.517 The same analysis concluded that persons who are penicillin allergic are actually more likely to react to drugs like acetazolamide than those who are sulfa allergic. Nonetheless, it is wise to be cautious in persons with a history of allergy, especially anaphylaxis to either sulfa or penicillin. Many experts recommend a trial dose of the medication well before the altitude sojourn, to determine if the drug is tolerated well. Although the usual allergic reaction is a rash starting a few days after ingestion, anaphylaxis to acetazolamide does rarely happen.
PART 1 MOUNTAIN MEDICINE
Pathophysiology
FIGURE 1-15 Magnetic resonance image of a patient with highaltitude cerebral edema. Increased T2 signal in splenium of corpus callosum (arrow) indicates edema. (Reprinted from Hackett PH, Yarnell PR, Hill R, et al: High-altitude cerebral edema evaluated with magnetic resonance imaging: Clinical correlation and pathophysiology, JAMA 280:1920, 1998.)
The pathophysiology of HACE is a progression of the same mechanism as advanced AMS (see Acute Mountain Sickness, Pathophysiology, and Figure 1-12) and appears to be vasogenic edema. In cases similar to this, lumbar punctures have revealed elevated CSF pressures, often more than 300 mm H2O,220,573 evidence of cerebral edema on CT scan and MRI,197,272 and gross cerebral edema on necropsy.117,118 Small petechial hemorrhages were also consistently found on autopsy, and venous sinus thromboses were occasionally seen.117,118 Well-documented cases have often included pulmonary edema that was not clinically apparent. Whereas the brain edema of reversible HACE is most likely vasogenic, as the spectrum shifts to severe, end-stage HACE, then gray matter (presumably cytotoxic) edema develops as well, culminating in brain herniation and death. As Klatzo271 has pointed out, as vasogenic edema progresses, the distance between brain cells and their capillaries increases, so that nutrients and oxygen eventually fail to diffuse and the cells are rendered is chemic, leading to intracellular (cytotoxic) edema. Raised ICP produces many of its effects by decreasing cerebral blood flow, and brain tissue also becomes ischemic on this basis.344 Focal neurologic signs caused by brainstem distortion and by extraaxial compression, as in third and sixth cranial nerve palsies, may develop,452 making cerebral edema difficult to differentiate from primary cerebrovascular events. The most common clinical presentation, however, is change in consciousness associated with ataxia, without focal signs.582,589
1
2
3
4
5
6
FIGURE 1-16 Magnetic resonance imaging (MRI) scans of patient with high-altitude cerebral edema (HACE). A fluid-attenuated inversion recovery (FLAIR) (1) shows an areal lesion of the corpus callosum—confirmed by diffusion-weighted imaging (DWI) (2), with increased values in apparent diffusion coefficient (ADC) (3), indicating increased water diffusivity compatible with vasogenic edema; in combination, the characteristic MRI pattern consistent with HACE (1 to 3) that persists 6 weeks after the event. A novel finding relates to the multiple patchy hypointensities that correspond to multiple microhemorrhages (arrows) displayed on the T2* images (4 to 6). The right frontal meningioma (visible on FLAIR [1]; [arrowhead]) is an incidental finding. (Reprinted from Kallenberg K, Dehnert C, Dorfler A, et al: Microhemorrhages in nonfatal high-altitude cerebral edema, J Cereb Blood Flow Metab 28:1635, 2008.)
18
STROKE
Given the sporadic nature and generally remote location of this disorder, it is not surprising that there are no controlled trials regarding treatment of HACE. All experts agree that successful treatment requires early recognition. At the first sign of ataxia or change in consciousness, descent should be started, dexamethasone (4 to 8 mg intravenously, intramuscularly, or orally initially, followed by 4 mg every 6 hours) administered, and oxygen (2 to 4 L/min by vented mask or nasal cannula) applied if available (see Box 1-4). Oxygen can be titrated to maintain SaO2 at greater than 90% if oximetry is available. Comatose patients require additional airway management and bladder drainage. Attempting to decrease ICP by endotracheal intubation and hyperventilation is a reasonable approach, although these patients are already alkalotic and overhyperventilation could result in disastrous cerebral ischemia. Loop diuretics such as furosemide (40 to 80 mg) or bumetanide (1 to 2 mg) may reduce brain hydration, and have been used successfully,116,500 but an adequate intravascular volume to maintain perfusion pressure is critical. Hypertonic solutions of saline, mannitol, or oral glycerol have been suggested, but rarely used in the field. Controlled studies are lacking, but empirically the response to corticosteroids and oxygen seems excellent if they are given early in the course of the illness and disappointing if they are not started until the victim is unconscious. Coma may persist for days, even after evacuation to low altitude, but other causes of coma must be considered and ruled out by appropriate evaluation.220 The average duration of hospital stay in one series of patients with severe HACE was 5.6 days, and average time to full recovery was 2.4 weeks, with a range of 1 day to 6 weeks.197 Two patients of the 44 in the series by Dickinson118 remained in coma for 3 weeks. Sequelae lasting weeks are common;197,220 longer-term follow-up has been limited, but presumed permanent impairment has been reported.190,220 In the Chinese series of 66 patients, HACE was diagnosed early, and descent was uniformly successful. Ataxia resolved in all but one within 7 days, and only one patient had long-term sequelae, clonic convulsions affecting the left hand.582 Prevention of HACE is the same as for AMS and HAPE.
The occurrence of stroke in a young, fit person at high altitude is uncommon but tragic. A number of case reports have described climbers with resultant permanent dysfunction.85,219,505 Indian soldiers at extreme altitude have a high incidence of stroke.249 Cerebral venous thrombosis manifests more insidiously, and diagnosis is often delayed.* Factors contributing to stroke may include polycythemia, dehydration, increased ICP if AMS is present, increased cerebrovenous pressure, cerebrovascular spasm, and familial thrombophilia.38 Stroke may be confused with HACE. Neurologic symptoms, especially focal abnormalities without AMS or HAPE that persist despite treatment with oxygen, corticosteroids, and descent, suggest a cerebrovascular event and mandate careful evaluation with a complete neurologic workup.
FOCAL NEUROLOGIC CONDITIONS WITHOUT AMS OR CEREBRAL EDEMA Various localizing neurologic signs, transient in nature and not necessarily occurring in the setting of AMS, suggest migraine, cerebrovascular spasm, transient ischemic attack (TIA), local hypoxia without loss of perfusion (watershed effect), or focal edema.41 Cortical blindness is one such condition. Hackett and colleagues194 reported six cases of transient blindness in climbers or trekkers with intact pupillary reflexes, which indicated that the condition was due to a cortical process. Treatment with breathing of either carbon dioxide (a potent cerebral vasodilator) or oxygen resulted in prompt relief, suggesting that the blindness was due to inadequate regional circulation or oxygenation. Descent effected relief more slowly. Other conditions that could be attributed to spasm or “TIA” have included transient hemiplegia or hemiparesis, transient global amnesia, unilateral paresthesias, aphasia, and scotoma.* The true mechanism of these focal findings is unknown and may be multifactorial. Young, healthy altitude sojourners are unlikely to have TIA syndrome from cerebrovascular disease. Other neurologic complications at altitude include globus pallidum lesions, which were considered complications of AMS or HACE and reported to lead to Parkinson’s disease.248,355,495,527,543 Although these deficits were related to high altitude, whether altitude illness was truly the proximate cause of these lesions is unclear. The globus pallidum is sensitive to hypoxia, especially from carbon monoxide poisoning, and can also be damaged by ischemia.
*References 36, 41, 57, 78, 299, 576, 597.
CLINICAL PRESENTATION E.H., a 42-year-old male climber on a Mt Everest expedition, awoke at 8000 m (26,247 feet) with dense paralysis of the right arm and weakness of the right leg. On descent the paresis cleared, but at base camp (5000 m [16,404]) severe vertigo developed, along with extreme ataxia and weakness. Neurologic consultation on return to the United States resulted in a diagnosis of multiple small cerebral infarcts, but none was visible on CT scan of the brain. The hematocrit value 3 weeks after descent from the mountain was 70%. Over the next 4 years signs gradually improved, but mild ataxia, nystagmus, and dyslexia persist. The focal and persistent nature of the cerebral symptoms and signs, although multiple, indicates a cerebrovascular, rather than an intracranial, pressure etiology. The hematocrit value on the mountain was greater than 70%, high enough for increased viscosity and microcirculatory sludging to contribute to ischemia and infarction. No familial thrombophilia was detected. Treatment of stroke is supportive. Oxygen and corticosteroids may be worthwhile to treat any AMS or HACE component. Immediate evacuation to a hospital is indicated. Persons with TIAs at high altitude should probably be started on aspirin therapy and proceed to a lower altitude. Oxygen may quickly abort cerebrovascular spasms and will improve watershed hypoxic events. When oxygen is not available, rebreathing to raise alveolar PCO2 may be helpful by increasing cerebral blood flow.
COGNITIVE CHANGES AT HIGH ALTITUDE If cerebral oxygen consumption is constant, what causes the well-documented, albeit mild, cognitive changes at high altitude? The cognitive changes may be related to specific neurotransmitters. For example, tryptophan hydroxylase in the serotonin synthesis pathway has a high requirement for oxygen (Michaelis constant [Km] = 37 mm Hg).95,160 Tyrosine hydroxylase, in the dopamine pathway, is also oxygen sensitive. Gibson and Blass160 suggested that a decrease in acetylcholine activity during hypoxia might explain the lassitude. In a fascinating study, Banderet and Lieberman21 showed that increased dietary tyrosine reduced mood changes and symptoms of environmental stress in subjects at simulated altitude. Further work with neurotransmitter agonists and antagonists will help shed light on their role in cognitive dysfunction at altitude and could lead to new pharmacologic approaches to improve neurologic function.
HIGH-ALTITUDE PULMONARY EDEMA The most common cause of death related to high altitude, HAPE is completely and easily reversed if recognized early and treated properly. Undoubtedly HAPE was misdiagnosed for centuries, as evidenced by frequent reports of young, vigorous men suddenly dying of “pneumonia” within days of arriving at high altitude. The death of Dr. Jacottet, “a robust, broad-shouldered young man,” on Mt Blanc in 1891 (he refused descent so that he could *References 177, 256, 460, 505, 538, 597.
19
CHAPTER 1 High-Altitude Medicine and Physiology
Treatment
PART 1 MOUNTAIN MEDICINE
“observe the acclimatization process” in himself) may have provided the first autopsy of HAPE. Angelo Mosso wrote, From Dr. Wizard’s post-mortem examination . . . the more immediate cause of death was therefore probably a suffocative catarrh accompanied by acute edema of the lungs. . . . I have gone into the particulars of this sorrowful incident because a case of inflammation of the lungs also occurred during our expedition, on the summit of Monte Rosa, from which, however, the sufferer fortunately recovered.374 On an expedition to K2 (Karakorum Range, Pakistan) in 1902, Alistair Crowley101 described a climber “suffering from edema of both lungs and his mind was gone.” In the Andes, physicians were familiar with pulmonary edema peculiar to high altitude,238,301 but it was not until Hultgren and Spickard226 and Houston218 offered their observations that the English-speaking world became aware of high-altitude pulmonary edema (see Rennie422 for a review). Hultgren and colleagues237 then published hemodynamic measurements in persons with HAPE, demonstrating that it was a noncardiogenic edema. Since that time, many studies and reviews have been published, and HAPE is still the subject of intense investigation. The reader is referred to recent reviews.* Individual susceptibility, rate of ascent, altitude reached, degree of cold,419 physical exertion, and certain underlying medical conditions are all factors determining the prevalence of HAPE. The incidence varies from approximately 1 in 10,000 skiers at moderate altitude in Colorado to 1 in 50 climbers on Mt McKinley (6194 m [20,322 feet]) and up to 6% of mountaineers in the Alps ascending rapidly to 4559 m (14,957 feet).29 Hultgren and associates235 reported 150 cases of HAPE over 39 months at a Colorado ski resort at 2928 m (9606 feet). Some regiments in the Indian Army had a much higher incidence of HAPE (15%) because of very rapid deployment to the extreme altitude of 5500 m (18,045 feet)501 (see Table 1-1). Wu and colleagues582 reported HAPE in 0.5% of Chinese railway workers at 4000 to 4900 m (13,123 to 16,076 feet). Persons with previous HAPE had a 60% attack rate when they went to 4559 m (14,957 feet) in 36 hours, but with slower ascent, some of the same individuals climbed over 7000 m (22,966 feet) without illness.24,30 HAPE appears to be less common in women.99,232,506 Whether all persons are capable of developing HAPE (with a very rapid ascent to a sufficiently high altitude and with heavy exercise) is arguable.32 Likewise, some studies suggest that many persons contract subclinical extravascular lung water,100 whereas others contradict this.111 Even well-acclimatized individuals with a sudden push to a higher altitude can succumb to HAPE.100 Nonetheless, a population of HAPE-susceptible persons with unique physiologic characteristics has been described (see HAPE Susceptibility, later). These individuals represent the small percentage of people who develop HAPE when others in the same circumstances do not. HAPE in children is associated as well with antecedent viral infections, trisomy 21, and underlying congenital cardiovascular malformations, such as unilateral absence of the pulmonary artery.105 CLINICAL PRESENTATION D.L., a 34-year-old man, was in excellent physical condition and had been on numerous high-altitude backpacking trips, occasionally suffering mild symptoms of AMS. He drove from sea level to the trailhead and hiked to 3050 m (10,007 feet) sleeping altitude the first night of his trip in the Sierra Nevada. He proceeded to 3700 m (12,139 feet) the next day, noticing more dyspnea on exertion when walking uphill, a longer time than usual to recover when he rested, and a dry cough. He complained of headache, shivering, dyspnea, and insomnia the second night. The third day the group descended to 3500 m (11,483 feet) and rested, primarily for D.L.’s benefit. That night, D.L. was unable to eat, noted severe dyspnea, and suffered
*References 32, 109, 307, 320, 467, 472, 477, 515.
20
coughing spasms and headache. On the fourth morning D.L. was too exhausted and weak to get out of his sleeping bag. His companions noted that he was breathless, cyanotic, and ataxic but had clear mental status. A few hours later he was transported by helicopter to a hospital at 1200 m (3937 feet). On admission he was cyanotic, his oral temperature was 37.8° C (100° F), blood pressure 130/76 mm Hg, heart rate 96 beats/min, and respiratory frequency 20 breaths/min. Bilateral basilar rales to the scapulae were noted. Findings of cardiac examination were reported as normal. Romberg and finger-to-nose tests revealed 1+ ataxia. Arterial blood gas studies on room air revealed PO2 24 mm Hg, PCO2 28 mm Hg, and pH 7.45. The chest radiograph showed extensive bilateral patchy infiltrates (Figure 1-17, C ). D.L. was treated with bed rest and supplemental oxygen. On discharge to his sea level home 3 days later, the pulmonary infiltrates and rales had cleared, although blood gas values were still abnormal: PO2 76 mm Hg, PCO2 30 mm Hg, and pH 7.45. He had an uneventful, complete recovery at home. D.L. was advised to ascend more slowly in the future, staging his ascent with nights spent at 1500 m (4921 feet) and 2500 m (8202 feet). He was taught the early signs and symptoms of HAPE and advised on pharmacologic prophylaxis. This case illustrates typical aspects of HAPE. Victims are frequently young, fit males who ascend rapidly from sea level and may not have previously suffered HAPE even with repeated altitude exposures; the particular ascent may have been faster than previously. HAPE usually occurs within the first 2 to 4 days of ascent to higher altitudes (above 2500 m [8202 feet]), most commonly on the second night.180 Decreased exercise performance and increased recovery time from exercise are the earliest indications of HAPE. The victim suffers fatigue, weakness, and dyspnea on exertion, especially when walking uphill; he or she often ascribes these nonspecific symptoms to various other causes. Signs of AMS are present about 50% of the time.232 A persistent dry cough develops. Nail beds and lips become cyanotic. The condition typically worsens at night, and tachycardia and tachypnea develop at rest. Increasing respiratory distress heralds to the victim the development of a serious condition. In contrast to the usual 1- to 3-day gradual onset, HAPE may strike abruptly, especially in a sedentary person who may not notice the early stages.552 Orthopnea is uncommon (7%). Pink or blood-tinged, frothy sputum is a very late finding. Hemoptysis was present in 6% of victims in one series.235 Severe hypoxemia may produce cerebral edema with mental changes, ataxia, decreased level of consciousness, and coma. Hultgren and colleagues235 reported an incidence of HACE of 14% in those with HAPE at ski resorts. On admission to the hospital, the victim does not generally appear as ill as expected based on arterial blood gas and radiographic findings. Elevated temperature up to 38.5° C (101.3° F) is common. Tachycardia correlates with respiratory rate and severity of illness.237 Rales may be unilateral or bilateral and usually originate from the right middle lobe. Concomitant respiratory infection is sometimes present. Pulmonary edema may manifest with predominantly neurologic manifestations and minimal pulmonary symptoms and findings, most likely in persons with low HVR. Cerebral edema, especially with coma, may obscure the diagnosis of HAPE.189 Pulse oximetry or chest radiography confirms the diagnosis. Differential diagnosis includes pneumonia, bronchitis, mucus plugging, pulmonary embolism or infarct, heart failure, acute myocardial infarction, and sometimes asthma (see Box 1-3). Complications include infection, cerebral edema, pulmonary embolism or thrombosis, and such injuries as frostbite or trauma secondary to incapacitation.24,189,233 Hemodynamics Hemodynamic measurements by catheter show elevated pulmonary artery pressure and pulmonary vascular resistance, low to normal pulmonary wedge pressure, and low to normal cardiac output and systemic arterial blood pressure.234,403 Echocardiography demonstrates high pulmonary artery pressure, tricuspid regurgitation, normal left ventricular systolic function, somewhat
CHAPTER 1 High-Altitude Medicine and Physiology
A
B
C
D
FIGURE 1-17 A, Typical radiograph of high-altitude pulmonary edema (HAPE) in a 29-year-old female skier at 2450 m (8038 feet). B, The same patient 1 day after descent and oxygen administration, showing rapid clearing. C, Bilateral pulmonary infiltrates on radiograph of a patient with severe HAPE after descent (case presented in text). D, Ventilation and perfusion scans in a person with congenital absence of right pulmonary artery after recovery from HAPE.
abnormal diastolic function,7 and variable right-sided heart findings of increased atrial and ventricular size.193,393 The electrocardiogram (ECG) usually reveals sinus tachycardia. Changes consistent with acute pulmonary hypertension, such as right axis deviation, right bundle branch block, voltage for right ventricular hypertrophy, and P-wave abnormalities, have been described.24,232 Atrial flutter has been reported, but ventricular arrhythmias have not. Laboratory Studies Kobayashi and colleagues272 reported clinical laboratory values in 27 patients with HAPE that showed mild elevations of hematocrit and hemoglobin, probably secondary to intravascular volume depletion and perhaps plasma leakage into the lungs. Elevation of peripheral white blood cell count is common but is rarely above 14,000 cells/mL3. Serum concentration of creatine
phosphokinase (CPK) is increased, mostly due to skeletal muscle damage, although in two patients, CPK isoenzymes showed brain fraction levels of 1% of total, which may have indicated brain damage.272 An unpublished study in Colorado has found normal brain natriuretic peptide (BNP) values in patients with HAPE (S. Gallagher, personal communication). Arterial blood gases consistently reveal respiratory alkalosis and marked hypoxemia, more severe than expected for the patient’s clinical condition. Because respiratory or primary metabolic acidosis has not been reported, arterial blood gas studies are unnecessary if noninvasive pulse oximetry is available to measure arterial oxygenation. At 4200 m (13,780 feet) on Mt McKinley, the mean value of PaO2 in HAPE was 28±4 mm Hg. Values as low as 24 mm Hg in HAPE are not unusual. Arterial oxygen saturation values in HAPE subjects at 4300 m (14,108 feet) ranged from 40% to 70%, with a mean of 56% ± 8%.480 At 2928 m (9606 feet), mean 21
PART 1 MOUNTAIN MEDICINE
SaO2 was 74%.235 Arterial acid–base values may be misleading in patients taking acetazolamide, because this drug produces significant metabolic acidosis. Radiographic Findings The radiographic findings in HAPE have been described in original reports.237,330,554,555 Findings are consistent with noncardiogenic pulmonary edema, with generally normal heart size and left atrial size, and no evidence of pulmonary venous prominence, such as Kerley lines. The pulmonary arteries increase in diameter.555 Infiltrates are commonly described as fluffy and patchy with areas of aeration between infiltrates and in a peripheral rather than central location. Infiltrates may be unilateral or bilateral, with a predilection for the right middle lung field, which corresponds to the usual area of rales. Pleural effusion is rare. Radiographic findings generally correlate with illness severity and degree of hypoxemia. A small right hemithorax, absence of pulmonary vascular markings on the right, and edema confined to the left lung are criteria for diagnosis of unilateral absent pulmonary artery.185 Radiographic findings of HAPE are presented in Figure 1-17. Clearing of infiltrates is generally rapid once treatment is initiated. Depending on severity, complete clearing may take from 1 to several days. Infiltrates are likely to persist longer if the patient remains at high altitude, even if confined to bed and receiving oxygen therapy. Radiographs taken within 24 to 48 hours of return to low altitude may still be able to confirm diagnosis of HAPE. Recently, an ultrasound technique known as “comet-tail” scoring, previously validated in cardiogenic pulmonary edema, has been used to evaluate extravascular lung water at high altitude, which in the right setting might indicate clinical or subclinical pulmonary edema. The comet-tail artifacts are created by microreflections of the ultrasound beam within interlobular septa thickened by the presence of increased lymphatic fluid consistent with interstitial and/or alveolar edema. Eleven patients at 4240 m (13,911 feet) with a clinical diagnosis of HAPE underwent chest ultrasound examinations using this technique.137 Seven patients with no evidence of HAPE or other altitude illness served as control subjects. HAPE patients had much higher comet-tail scores and lower oxygen saturation than did control subjects, and scores decreased as HAPE cleared. The comet-tail technique seemed to be able to recognize and monitor the degree of pulmonary edema in HAPE. Although an ultrasound machine is rarely available in the wilderness, this technique might prove to be a valuable research tool, and it offers easy repeated measurements while avoiding radiation.313 Recently, investigators successfully used a satellite telemedical connection with a remote expert to guide thoracic ultrasound examinations at Advanced Base Camp on Mt Everest; high-quality images were obtained that verified increases in lung water.394 Another group, also in Nepal, used the technique while trekking up to 4700 m (15,420 feet) and found a high prevalence of extravascular lung water, but no association with estimated pulmonary artery pressure.409 This technique may lend itself well to answering the question of whether the oft-reported increase in extravascular lung water on ascent to high altitude and in AMS is actually a precursor to HAPE. Pathologic Findings More than 20 autopsy reports of persons who died of HAPE have been published.* Of those whose cranium was opened, more than one-half had cerebral edema. All lungs showed extensive and severe edema, with bloody, foamy fluid in the airways. Lung weights were two to four times normal. The left side of the heart was normal. The right atrium and main pulmonary artery were often distended. Proteinaceous exudate with hyaline membranes was characteristic. All lungs had areas of inflammation with neutrophil accumulation. The diagnosis of bronchopneumonia was common, although bacteria were not noted. Pulmonary veins, the left ventricle, and the left atrium were generally not dilated, in contrast to the right ventricle and atrium. Most reports mention *References 12, 117, 380, 500, 501, 573.
22
capillary and arteriolar thrombi and alveolar fibrin deposits, as well as microvascular and gross pulmonary hemorrhage and infarcts. The autopsy findings thus suggest a protein-rich, permeability type of edema with thrombi or emboli. Confirmation of HAPE as a permeability edema was obtained by analysis of alveolar lavage fluid by Schoene and associates.478,480 These clinicians found a 100-fold increase in lavage fluid protein levels in patients with HAPE compared with well control subjects and patients with AMS.480 The lavage fluid also had a low percentage of neutrophils, in contrast to findings in adult respiratory distress syndrome. Further evidence for a permeability edema was a 1:1 ratio of aspirated edema fluid protein to plasma protein level found by Hackett and colleagues.184 In addition, the lavage fluid contained vasoactive eicosanoids and complement proteins, indicative of endothelium–leukocyte interactions. More recent research using repeated bronchoalveolar lavage as HAPE was developing found that inflammation was absent early on, suggesting that inflammation is a response to the alveolar damage, rather than an initiating event.531 Mechanisms of High-Altitude Pulmonary Edema An acceptable explanation for HAPE must take into account three well-established facts: excessive pulmonary hypertension, highprotein permeability leak, and normal function of the left side of the heart. A mechanism consistent with these facts is failure of capillaries secondary to overperfusion and capillary hypertension (Figure 1-18). Role of Pulmonary Hypertension. Excessive pulmonary artery pressure (PAP) is the sine qua non of HAPE; no HAPE has been reported without pulmonary hypertension. All persons ascending to high altitude or otherwise enduring hypoxia, however, have some elevation of PAP. The hypoxic pulmonary vasoconstrictor response (HPVR) is thought to be useful in humans at sea level because it helps match perfusion with ventilation. When local areas of the lungs are poorly ventilated because of infection or atelectasis, for example, the HPVR Altitude hypoxia HVR, sleep, and exercise ↓ PaO2
Uneven HPV
↑ Sympathetic activity
Exercise PHTN
Pulmonary and peripheral venous constriction
Overperfusion
↑ Pcap
↑ Pulmonary blood volume
Capillary stress failure
Capillary leak
↓ Alveolar Na and H2O clearance
High-altitude pulmonary edema FIGURE 1-18 Proposed pathophysiology of high-altitude pulmonary edema. HPV, Hypoxic pulmonary vasoconstriction; HVR, hypoxic ventilatory response; PaO2, arterial partial pressure of oxygen; Pcap, capillary pressure; PHT, pulmonary hypertension.
Overperfusion and Capillary Leak. To explain how pulmonary hypertension might lead to edema, Hultgren suggested that in those who develop HAPE, the hypoxic pulmonary vasoconstriction is uneven and the delicate microcirculation in an unconstricted (relatively dilated) area is subjected to high pressure and flow, leading to leakage (edema). The unevenness could be due to anatomic characteristics, such as distribution of muscularized arterioles, or to functional factors, such as loss of HPVR in severely hypoxic regions.227 Uneven perfusion is suggested clinically by the typical patchy radiographic appearance and is supported by lung scans and MRI imaging during acute hypoxia showing uneven perfusion in persons with a history of HAPE.215,553 Persons born without a right pulmonary artery are highly susceptible to HAPE (see Figure 1-17, D),185 supporting the concept of overperfusion of a restricted vascular bed as a cause of edema, because the entire cardiac output flows into one lung. Other causes of overperfusion of the pulmonary circulation that predispose to HAPE include left-to-right shunts such as atrial septal defect, ventricular septal defect, and patent ductus arteriosus. Rapid reversibility of the illness and response to vasodilators are also consistent with this mechanism. When hydrostatic pressure is reduced, alveolar fluid is quickly reabsorbed. Other factors contributing to increased hydrostatic pressure, such as exercise or high salt load with subsequent hypervolemia, also may play a role in HAPE. The authors have several times observed onset of HAPE after large salt intake. Some studies have also suggested roles for pulmonary venous constriction, which would contribute to increased capillary hydrostatic pressure.193,325 The end result of overperfusion and increased capillary pressure325 is distension, increased filtration of fluid, and even rupture of the capillary–alveolar membrane, termed “stress failure,”567,568 with subsequent leakage of cells and proteins. Alveolar Fluid Balance. Fluid filtration into the interstitial and alveolar space, reabsorption back across the epithelial membrane, and clearance of interstitial fluid by lymph result in a dynamic balance that generally prevents alveolar flooding. On ascent to altitude, the hydrostatic pressure gradient for filtration is increased. As might be expected, multiple lines of evidence suggest that extravascular lung water is increased at altitude.100,169,409,557 Despite this, frank alveolar flooding is uncommon. This may well be due to differences in hydrostatic pressure in persons resistant and susceptible to HAPE. However, persons who contract HAPE appear to also have impaired ability to clear alveolar fluid. On a constitutive (genetic) basis, HAPE subjects have lower activity of the epithelial sodium channel and therefore reduced ability to transport sodium across the epithelium back into the interstitial space.329,466,468 (It is the sodium gradient across the epithelium that determines movement of water from alveoli.) In addition, epithelial sodium transport is diminished by hypoxia per se, so that those with already impaired function become more impaired at altitude. How large a role this mechanism plays in HAPE is uncertain216 (see Figure 1-18). Control of Ventilation. As in AMS, persons with HAPE had a lower HVR than did persons who acclimatized well,195,336 but not
all persons with a low HVR become ill. Thus, low HVR appears to play a permissive, rather than causative, role in HAPE, whereas a brisk HVR appears to be protective. Persons who hypoventilate are more hypoxemic and presumably suffer greater pulmonary hypertension. Possibly more important, low HVR may permit episodes of extreme hypoxemia during sleep (see Figure 1-7).180,195 In addition, a low HVR may allow further ventilatory depression through central nervous system (CNS) suppression (hypoxic ventilatory depression). Such persons, when given oxygen, show a “paradoxical” increase in ventilation.195 Despite correlation of HAPE with low HVR, its value as a sea level predictor is poor.110 HAPE Susceptibility Persons susceptible to HAPE (HAPE-s) show at sea level abnormal rise of PAP and pulmonary vascular resistance during hypoxic challenge at rest and during exercise and even during exercise in normoxia, suggesting overreactivity of the pulmonary circulation to both hypoxia and exercise.131,175,258 Part of this reactivity may be related to greater alveolar hypoxemia secondary to lower HVR,195,212,338 but other factors have been uncovered. Microneurographic recordings from the peroneal nerve during hypoxia established a direct link in HAPE-s between the rise in PAP and greater sympathetic activation,126 indicating that sympathetic overactivation might contribute to HAPE. Smaller and less distensible lungs have been noted in HAPE-s, which might limit the ability to accommodate increased flow by vascular recruitment and thus result in a higher vascular resistance.131,212,508 Another characteristic of HAPE-s is abnormal endothelial function, as evidenced by reduced NO synthesis during hypoxia50,74,474 and during HAPE,125 and higher levels of endothelin, a potent pulmonary vasoconstrictor.470,509 The importance of reduced NO is reinforced by studies showing improvement in pulmonary hemodynamics when either NO or a phosphodiesterase (PDE)-5 inhibitor was given to HAPE subjects9,159,322,474 (Figure 1-19). As mentioned previously, HAPE-s also are characterized by impairment of respiratory transepithelial sodium and water transport, making it more difficult to reabsorb alveolar fluid.469,473 Patent foramen ovale (PFO) also has been observed to be more common among HAPE-susceptible than among HAPEresistant adult mountaineers.6,311 Since the initial report of Levine and co-workers,293 the association of PFO and HAPE has been confirmed, but cause and effect have not been established.6 Allemann and associates6 performed a case-control study of 16 HAPE-susceptible participants and 19 mountaineers resistant to HAPE. Presence of PFO was determined by transesophageal echocardiography and estimated pulmonary artery pressure by Doppler echocardiography at low (550 m [1804 feet]) and high altitude (4559 m [14,957 feet]). The frequency of PFO was more than four times higher in HAPE-susceptible than in HAPE-resistant participants, both at low altitude (56% versus 11%) and high altitude (69% versus 16%). At high altitude, SaO2 before the onset of pulmonary edema was significantly lower in HAPE-susceptible participants than in the control group (73% versus 83%). Also, in the HAPE-susceptible group, participants with a large PFO had more severe arterial hypoxemia (65% versus 77%) than did those with smaller or no PFO. The authors speculated that at high altitude a large PFO may contribute to exaggerated arterial
Nitric oxide—overview Hypoxia
eNOS
L-arginine
NO
cGMP
Vascular muscle relaxation
PDE-5 inhibitor
Degradation by PDE-5
FIGURE 1-19 The nitric oxide pathway and action of phosphodiesterase-5 inhibitors. In the presence of an inhibitor c-GMP, the second messenger of nitric oxide is not degraded, and vasodilation is therefore enhanced. c-GMP, guanosine monophosphate; eNOS, endothelial nitric oxide synthase NO, nitric oxide; PDE, phosphodiesterase.
23
CHAPTER 1 High-Altitude Medicine and Physiology
directs blood away from those areas to well-ventilated regions. In the setting of global hypoxia, as occurs with ascent to high altitude, HPVR is presumably diffuse and all areas of the lung constrict, causing a restricted vascular bed and an increase in PAP, which is of little if any value for ventilation–perfusion matching at high altitude. The degree of HPVR varies widely among individuals (as well as among species), and is most likely an inherent trait. HAPE-susceptible persons have a greater increase in PAP than do persons who are not susceptible (see HAPE Susceptibility, later). Although other factors, such as the vigor of the ventilatory response and subsequent alveolar PO2, may help determine the ultimate degree of pulmonary hypertension, HPVR appears to be the dominant factor. Because all persons with HAPE have excessive pulmonary hypertension, but not all those with excessive pulmonary hypertension have HAPE, it appears that pulmonary hypertension is necessary but in and of itself is not the cause of HAPE.
PART 1 MOUNTAIN MEDICINE
hypoxemia and facilitate HAPE.6 Others pointed out, however, that the greater hypoxemia may have been due to subclinical pulmonary edema,139 or that a PFO was a marker of a reactive pulmonary vascular bed.108 HAPE-s are known to have exaggerated pulmonary pressure response to exercise at sea level, for example, which could maintain an open shunt. Because occurrence of PFO is so common in the general population, more compelling evidence is required before suggesting that PFO is a predisposing factor to HAPE, and that those with PFO should consider closure of the defect before significant altitude exposure, or as a result of an episode of HAPE, as some have recommended.82 Genetics of HAPE The first major genetic studies in lowlanders visiting high altitudes have focused on HAPE because it is the most fully understood pathophysiologic process occurring in lowlanders visiting high altitudes.* Although many characteristics of HAPE-susceptible persons are apparently genetically determined, actual genetic studies are conflicting and difficult to interpret. Good evidence for a genetic component to HAPE susceptibility comes from study of major human leukocyte antigen (HLA) alleles in 28 male and 2 female subjects with a history of HAPE compared with HLA alleles in 100 healthy volunteers.201 The HLA-DR6 and HLA-DQ4 antigens were associated with HAPE, and HLA-DR6 with pulmonary hypertension. These findings suggest that immunogenetic susceptibility may underlie development of HAPE, at least in some cases. Given the importance of endothelial function in HAPE, investigators have looked at gene polymorphisms for endothelial nitric oxide synthase (eNOS). Two recent studies have established a link between HAPE-s and the Glu298Asp alleles of the eNOS gene in Japanese and Indian subjects.2,123 An additional study of NOS3-related gene polymorphisms that could explain decreased NO synthesis found no relation to HAPE-s.563 This may be explained by racial differences or by the specific processes encoded by the different gene fragments. The insertion–deletion polymorphism of the angiotensin-converting enzyme (ACE) gene has also garnered attention, because the renin-aldosterone-angiotensin system is known to be activated in HAPE,34 and the ACE gene has also been linked to performance at altitude.362 The insertion–deletion polymorphism was not associated with HAPE susceptibility in populations of Indians, Japanese, and whites.112,217,280 However, one variant of the angiotensin receptor gene was correlated with HAPE susceptibility in Japanese.217 In summary, gene polymorphisms coding for the angiotensin receptor and endothelial NO distinguish HAPE-s from HAPEresistant subjects. In the near future, single nucleotide polymorphism scanning techniques as well as RNA gene expression techniques will be used to explore the genetic contributions to high-altitude physiology and pathophysiology. The search continues for a genetic basis for HAPE susceptibility.† Treatment Treatment choices for HAPE depend on severity of illness and logistics. As with all high-altitude illnesses, early recognition is key to successful outcome (see Box 1-4). In the wilderness, where oxygen and medical expertise may be unavailable, persons with HAPE need to be urgently evacuated to lower altitude. However, because of augmented pulmonary hypertension and greater hypoxemia with exercise, exertion must be minimized. Early HAPE responds rapidly to descent of only 500 to 1000 m (1640 to 3281 feet), and the victim may be able to reascend slowly 2 or 3 days later. In high-altitude locations with oxygen supplies, bed rest with supplemental oxygen may suffice, but severe HAPE may require high-flow oxygen (4 L/min or more) for more than 24 hours. Hyperbaric therapy with a fabric pressure bag (2 psi) is equivalent to low-flow oxygen and can help conserve oxygen supplies.437 Oxygen immediately increases arterial oxygenation and reduces pulmonary artery pressure, heart rate, respiratory rate, *References 3, 200, 306, 363, 412, 413, 458, 502, 510, 536, 558, 596. † References 3, 122, 200, 306, 363, 373, 412, 413, 458, 502, 510, 536, 558, 596.
24
and symptoms. When descent is not possible, oxygen (or a hyperbaric bag) can be lifesaving. Rescue groups should make delivery of oxygen to the victim, by airdrop if necessary, the highest priority if descent is slow or delayed. If oxygen is not available, immediate descent is lifesaving. Waiting for a helicopter or rescue team has too often proved fatal. Because cold stress elevates PAP, the victim should be kept warm.80 The use of a mask providing resistance on expiration (expiratory positive airway pressure [EPAP]) was shown to improve gas exchange in HAPE, and this or continuous positive airway pressure (CPAP) may be useful as a temporizing measure.479 The same is accomplished with pursed-lip breathing. An unusual case report suggested that a climber may have saved his partner’s life by postural drainage to expel airway fluid.56 Drugs are of limited necessity in HAPE, because oxygen and descent are so effective.311 Medications that reduce pulmonary blood volume, PAP, and pulmonary vascular resistance are physiologically rational to use when oxygen is not available or descent delayed. Singh and associates500 reported good results with furosemide (80 mg every 12 hours), and greater diuresis and clinical improvement occurred when 15 mg parenteral morphine was given with the first dose of furosemide. Their use, however, has been eclipsed by recent results with vasodilators. The calcium channel blocker nifedipine (30 mg slow release every 12 to 24 hours) was effective in reducing pulmonary vascular resistance and PAP during HAPE and slightly improved arterial oxygenation.30 Clinical improvement, however, was not dramatic. Nifedipine is well tolerated and unlikely to cause significant hypotension in healthy persons and avoids the danger of CNS depression from morphine and possible hypovolemia from diuretics. Clinical improvement is much better, however, with oxygen and descent than with any medication. NO, a potent pulmonary vasodilator, improves hemodynamics in HAPE but is rarely available, and in any event is usually given with oxygen. The PDE-5 inhibitors, which increase cyclic guanosine monophosphate (c-GMP) to produce pulmonary vasodilation during hypoxia159,425,427 (see Figure 1-19), have shown value for prevention of HAPE322 but have not yet been studied for treatment. Whether these agents will prove to be more effective than nifedipine for treatment is unknown. A theoretic advantage is that the PDE-5 inhibitors produce less systemic vasodilation. Nifedipine, and perhaps other vasodilators, might be useful adjunctive therapy but is not a substitute for definitive treatment (see Box 1-4 and Table 1-7).178,311 β-Agonists may also have an adjunctive role but should not be considered for monotherapy.311 After evacuation of the victim to a lower altitude, hospitalization may be warranted for severe cases. Treatment consists of bed rest and oxygen sufficient to maintain SaO2 greater than 90%; medications are rarely necessary. Rapid recovery is the rule.599 Antibiotics are indicated for infection when present. Occasionally pulmonary artery catheterization or Doppler echocardiography is necessary to differentiate cardiogenic from high-altitude pulmonary edema. Endotracheal intubation and mechanical ventilation are rarely needed. A HAPE victim demonstrating unusual susceptibility, such as onset of HAPE despite adequate acclimatization or onset below 2750 m (9022 feet), might require further investigation, such as echocardiography, to rule out an intracardiac shunt or preexisting pulmonary hypertension. In children, undiagnosed congenital heart disease is worth considering105 (Figure 1-20). Hospitalization until blood gas values are completely normal is not warranted; all persons returning from high altitude are at least partially acclimatized to hypoxemia, and hypocapnic alkalosis persists for days after descent. Distinct clinical improvement, radiographic improvement over 24 to 48 hours, and PaO2 of 60 mm Hg or SaO2 greater than 90% are adequate discharge criteria. Patients are advised to resume normal activities gradually and are warned that 1 to 2 weeks may be required to recover complete strength. Physicians should recommend preventive measures, including graded ascent with adequate time for acclimatization, and should provide instruction on use of acetazolamide, nifedipine, or PDE-5 inhibitors for future ascents. An episode of HAPE is not a contraindication to subsequent high-altitude exposure, but education to ensure proper preventive measures and recognition of early symptoms is critical.
FIGURE 1-20 Chest radiograph of severe high-altitude pulmonary edema (HAPE) in a 4-year-old girl with a small previously undiagnosed patent ductus arteriosus that predisposed her to HAPE.
Prevention The preventive measures previously described for AMS also apply to HAPE: graded ascent, time for acclimatization, low sleeping altitudes, and avoidance of alcohol and sleeping pills.311 Exertion may contribute to onset of HAPE, especially at moderate altitude. Reports from North America at 2500 to 3800 m (8202 to 12,467 feet) have included hikers, climbers, and skiers, all of whom were exercising vigorously. Menon and colleagues346 clearly showed that sedentary men taken abruptly to higher altitude were just as likely to become victims of HAPE. Prudence dictates not overexerting for the first 2 days at altitude. Considerable clinical experience suggests that acetazolamide prevents HAPE in persons with a history of recurrent episodes. Recent animal work showing that acetazolamide blocks hypoxic pulmonary hypertension supports this practice49,213 as does the fact that acetazolamide speeds acclimatization. Nifedipine (20 mg slow release every 8 hours) prevented HAPE in subjects with a history of repeated episodes.30 The drug should be carried by such individuals and started at the first signs of HAPE or, for an abrupt ascent, started when leaving low altitude. The PDE-5 inhibitors sildenafil and tadalafil effectively block hypoxic pulmonary hypertension and therefore will prevent HAPE.320 Tadalafil 10 mg every 12 hours prevented HAPE with rapid ascent in HAPEsusceptible subjects.322The optimal dose has not been established; regimens for sildenafil have varied from a single dose of 50 or 100 mg just before exposure for acute studies159,425 to 40 mg 3 times a day for 2 to 6 days at altitude,404,427 and for tadalafil 10 mg every 12 hours was effective.145,322 Most recently, and rather surprisingly, dexamethasone was also found effective in preventing HAPE in susceptible subjects. Maggiorini and co-workers322 gave 8 mg dexamethasone every 12 hours, starting 2 days before exposure, and found it as effective as tadalafil in reducing PAP and preventing HAPE. Dexamethasone has many actions in the lungs; which particular action(s) explains this observed effect is unknown.32 As these studies demonstrate, any agent that blocks hypoxic pulmonary hypertension will block onset of HAPE, reinforcing the concept of pulmonary hypertension as the sine qua non of high altitude pulmonary edema. Problems of Lifelong or Long-Term Residents of High Altitude Reentry Pulmonary Edema. In some persons who have lived for years at high altitude, HAPE develops on reascent from a trip to low altitude.128 Clinicians have suggested that the incidence of HAPE on reascent of altitude residents may be higher than that during initial ascent by flatlanders,34,229 but data on true incidence are difficult to obtain. Children and adolescents are more susceptible than adults.128 Hultgren228 found HAPE prevalence in Peruvian natives of 6.4 per 100 exposures in the 1- to 20-year age-group, and 0.4 per 100 exposures in persons over 21 years.
Chronic Mountain Sickness. In 1928 Carlos Monge359 described a syndrome in Andean high-altitude natives that was characterized by headaches, insomnia, lethargy, plethoric appearance, and polycythemia greater than expected for the altitude. Known variously as Monge’s disease, chronic mountain polycythemia, or chronic mountain sickness, the condition has now been recognized in all high-altitude areas of the world.279,358,402 Lowlanders who relocate to high altitude and native residents are susceptible. Chinese investigators reported that 13% of lowland Chinese males and 1.6% of females who had relocated to Tibet developed excessive polycythemia (hemoglobin level greater than 20 g/dL).588 The incidence in Leadville, Colorado, is also high in men over 40 years of age and distinctly low in women.278 The increased hematopoiesis is apparently related to greater hypoxic stress, which may be due to a number of causes, such as lung disease, sleep apnea syndromes, and idiopathic hypoventilation. A diagnosis of “pure” chronic mountain polycythemia excludes lung disease and is characterized by relative alveolar hypoventilation, excessive nocturnal hypoxemia, and respiratory insensitivity to hypoxia.292,358 Some studies suggest that even for the degree of hypoxemia, the red blood cell mass is excessive, implying excessive amounts or overactivity of erythropoietin.574 The new international guidelines propose a hemoglobin value greater than 21 g/dL for males and 19 g/dL for females as essential for the diagnosis, as well as residence above 2500 m (8202 feet) and absence of lung disease.292 The reader is referred to recent reviews for in-depth information.357,418,420,584 In addition, an international consensus group has recently published papers on the definition and scoring of chronic mountain sickness.291 Therapy of CMS is routinely successful. Descent to a lower altitude is the definitive treatment. The syndrome reappears after return to high altitude. Supplemental oxygen during sleep is valuable. Phlebotomy is a common practice and provides sub jective improvement, although without significant objective changes.574 The respiratory stimulants medroxyprogesterone acetate (20 to 60 mg/day)277 and acetazolamide (250 or 500 mg/ day)429 have also been shown to reduce hematocrit value by improving oxygenation. Acetazolamide (250 mg) increased nocturnal arterial O2 saturation by 5%, decreased mean nocturnal heart rate by 11%, the number of apnea/hypopnea episodes during sleep by 74%, and hematocrit by 7%.429 The response to acetazolamide emphasizes the contribution of hypoventilation and nocturnal desaturation to chronic mountain sickness. Another approach was based on the knowledge that ACE inhibitors blunt hypoxia-mediated erythropoietin release. Plata and associates406 showed that 5 mg/day of enalapril for 2 years reduced hemoglobin concentration, packed cell volume, proteinuria, and need for phlebotomy. Pulmonary hypertension and right heart failure may also occur in persons with CMS. Symptomatic High-Altitude Pulmonary Hypertension. Children living at high altitude may be at risk for symptomatic highaltitude pulmonary hypertension (SHAPH).388 This problem has been identified in South America, North America, and Asia, with a predilection in populations not genetically adapted to altitude. Other names for this affliction previously have included “pediatric high-altitude heart disease” and “subacute infantile mountain sickness.” The underlying pathophysiology is pulmonary 25
CHAPTER 1 High-Altitude Medicine and Physiology
The phenomenon has been observed most often in Peru, where high-altitude residents can return from sea level to high altitude quite rapidly. Cases have also been reported throughout Colorado,482 but reports are conspicuously rare from Nepal and Tibet,581 perhaps because Himalayan highlanders are better adapted or because very rapid return back to high altitude has not been readily available,587 although that is changing. Wu581 reported a 37-year-old Tibetan man with chronic mountain sickness who developed reentry HAPE and suggested that similar cases may have been missed previously. Severinghaus490 has postulated that increased muscularization of pulmonary arterioles that develops with chronic high-altitude exposure generates an inordinately high PAP on reascent, causing the edema. Whether uneven pulmonary vasoconstriction is present has not been investigated. Changes in fluid balance with descent and reascent might also play a role.581
PART 1 MOUNTAIN MEDICINE
hypertension resulting in hypertrophy and dilation of the right ventricle with eventual right-sided congestive heart failure. Clinically these children have poor growth, fatigue, irritability, dyspnea, and cyanosis or pallor. On physical examination, as the illness advances, hepatomegaly and leg edema signal right-sided heart failure. Blood gases or pulse oximetry reveal exaggerated hypoxemia. Chest radiograph shows cardiomegaly and enlarged main pulmonary artery and sometimes infiltrates. Echocardiography usually confirms the diagnosis, although ECG and cardiac catheterization can also be useful. Right ventricular hypertrophy, right atrial dilation, and persistence of PFO and patent ductus arteriosus may also be noted. Definitive treatment is relocation to a lower altitude. Other but inferior therapies include supplemental oxygen, diuretics, and pulmonary vasodilators such as calcium channel blockers, PDE-5 inhibitors, and NO and prostaglandin inhibitors.292
CHILDREN AT HIGH ALTITUDE Children born at high altitude in North America appear to have a higher incidence of complications in the neonatal period than do their lower-altitude counterparts.386 In populations better adapted to high altitude over many generations, neonatal transition has not been as well scrutinized, but there does appear to be some morbidity.388,571 High-altitude residence does not clearly impact eventual stature, but growth and development are slowed. In the developing world, confounding factors such as nutrition and socioeconomic status make these issues difficult to assess. Children residing at high altitude are more likely to develop pulmonary edema on return to their homes from a low-altitude sojourn than are lowland children on induction to high altitude. Some of these children may have preexisting pulmonary hypertension of various etiologies.105 Lowland children traveling to high altitude are just as likely to suffer AMS as are adults.408 No data indicate that children are more susceptible to altitude illness, although diagnosis can be more difficult in preverbal children.591 Despite this somewhat reassuring fact, very conservative recommendations are made regarding taking children to high altitude; it should be made clear that these opinions are not based on science.40,407 Durmowicz and colleagues128 showed that children with respiratory infections were more susceptible to HAPE, as are children with Down syndrome, past repair of congenital shunts, following chemotherapy, and other problems. Children can be given acetazolamide or dexamethasone as necessary for AMS/HACE.129 The dosage of acetazolamide for prevention or treatment of AMS in children is 5 mg/kg/day in divided doses (see Table 1-7). See Pollard and associates408 for an excellent consensus document on children at altitude, and excellent recent reviews.129,388,591 Healthy newborn term infants born to lowland mothers should probably avoid sleeping altitudes greater than 2500 m (8202 feet) for the first 4 to 6 weeks of life because of concern regarding cardiopulmonary transition rather than for altitude illness.387 Infants with viral infections, neonatal intensive care unit stay, transient oxygen treatment, Down syndrome, or any pulmonary condition or cardiac defect should be carefully evaluated by a physician regarding altitude exposure. For all infants going to altitude, pulse oximetry monitoring should be considered. Parents need to be aware of potential problems at altitude, including symptoms of AMS unique to infants.387
Other Medical Concerns at High Altitude CARBON MONOXIDE Carbon monoxide poisoning is a danger at high altitude, where field shelters are designed to be small and windproof. Cooking inside closed tents and snow shelters during storms is a particular hazard.* The effects of carbon monoxide and high-altitude hypoxia are additive. A reduction in oxyhemoglobin caused by *References 146, 264, 290, 453, 535, 542.
26
carbon monoxide increases hypoxic stress, rendering a person at a “physiologically higher” altitude, which may precipitate AMS. Because of preexisting hypoxemia, smaller amounts of carboxyhemoglobin produce symptoms of carbon monoxide poisoning. These two problems may coexist. Immediate removal of the victim from the source of carbon monoxide and forced hyperventilation, preferably with supplemental oxygen, rapidly reverse carbon monoxide poisoning.
HIGH-ALTITUDE DETERIORATION The world’s highest human habitation is at approximately 5500 m (18,045 feet). Above this altitude, deterioration outstrips the ability to acclimatize.265 The deterioration is more rapid the higher one goes above the maximum point of acclimatization. Above 8000 m (26,247 feet), deterioration is so rapid that without supplemental oxygen, death can occur in a matter of days. Life-preserving tasks such as melting snow for water may become too difficult, and death may result from dehydration, starvation, hypothermia, and especially neurologic and psychiatric dysfunction.142 Loss of body weight due to anorexia and malabsorption is a prominent feature during expeditions to extreme high altitude. Pugh410 reported 14 to 20 kg (30.9 to 44 lb) body-weight losses in climbers on the 1953 British Mt Everest Expedition. Nearly 30 years later, with improvement in food and cooking techniques, climbers on the American Medical Research Expedition to Mt Everest still lost an average of 6 kg (13.2 lb).61 This was due in part to 49% decrease in fat absorption and 24% decrease in carbohydrate absorption. During OEII, in which the “climbers” were allowed to eat foods of their choosing ad libitum, they still suffered large weight losses: 8 kg (17.6 lb) overall, including 3 kg (6.6 lb) of fat and 5 kg (11 lb) of lean body weight (muscle).221,455 At 4300 m (14,108 feet), weight loss was attenuated by adjusting caloric intake to match caloric expenditure.75 In fact, recent work supports hypoxic exposure as a treatment for obesity.298,381,414,593 Thus, significant weight loss with prolonged exposure to high altitude may be overcome with adequate caloric intake, but decreased appetite is a problem.260,541 At very high altitudes, an increase in caloric intake may not be sufficient to completely counteract the severe anorexia and weight loss because other mechanisms may come into play. At extreme altitude, Ryn459 reported an incidence of acute organic brain syndrome in 35% of climbers going above 7,000 m (22,966 feet), in association with high-altitude deterioration. This syndrome, which features impaired judgment or even psychosis, could directly threaten survival.
HIGH-ALTITUDE SYNCOPE Syncope within the first 24 hours of arrival occurs occasionally at moderate altitude382,383 but is not observed in mountaineers at higher altitudes; it is a problem of acute induction to altitude.370 The mechanism is an unstable cardiovascular control system, and it is considered a form of neurohumoral (or neurocardiogenic) syncope.149 An unstable state of cerebral autoregulation may also play a role.595 These events appear to be random and seldom occur a second time. Preexisting cardiovascular disease is not a factor in most cases. Postprandial state and alcohol ingestion seem to be contributing factors. Altitude syncope has no direct relation to high-altitude illness.41
ALCOHOL AT HIGH ALTITUDE Two questions regarding alcohol are frequently asked: (1) does alcohol affect acclimatization, and (2) does altitude potentiate the effects of alcohol? Epidemiologic research indicated that 64% of tourists ingested alcohol during the first few days at 2800 m (9186 feet).214 The effect of alcohol on altitude tolerance and acclimatization might therefore be of considerable relevance. Roeggla and co-workers449 determined arterial blood gases 1 hour after ingestion of 50 g of alcohol (equivalent to 1 L of beer) at 171 m (561 feet) and again after 4 hours at 3000 m (9843 feet). A placebo-controlled, double-blinded paired design was used. For the 10 subjects, alcohol had no effect on ventilation at the low altitude, but at high altitude it depressed ventilation, as gauged
THROMBOSIS: COAGULATION AND PLATELET CHANGES Autopsy findings in deaths due to altitude illness of widespread thrombi in the brain and lungs, as well as the impression that thrombosis is greater at altitude,249 have led to many investigations of the clotting mechanism at high altitude. For a review, see Grover and Bärtsch.173 Although changes in platelets and coagulation have been observed in rabbits, mice, rats, calves, and humans on ascent to high altitude,207 these are generally in vitro and with very rapid ascent. In vivo studies using more realistic ascent profiles up to 4500 m (14,764 feet) in the mountains, and higher in chambers, have generally not found changes in coagulation and fibrinolysis,173 but this is still an area of active study.62,549 Although the increased incidence of thrombosis in soldiers and others at extreme altitude can be attributed to dehydration, polycythemia, and forced inactivity, there is some
evidence of enhanced fibrin formation with stay of a few weeks over 5000 m (16,404 feet).449 In addition, unexplained thrombosis is reported at moderate altitude of 4000 to 5000 m (13,123 to 16,404 feet)81,136 and at extreme altitude.8,267 As for thrombosis in HAPE, Singh and colleagues498 reported increased fibrinogen levels and prolonged clot lysis times during HAPE, attributed to a breakdown of fibrinolysis. These authors also reported thrombotic, occlusive hypertensive pulmonary vascular disease in soldiers who had recently arrived at extreme altitude.497 A series of experiments by Bärtsch and colleagues,27,173 however, carefully examined this issue in well subjects and in those with AMS and HAPE. They concluded that HAPE is not preceded by a prothrombotic state and that only in “advanced HAPE” is there fibrin generation, which abates rapidly with oxygen treatment. They considered the coagulation and platelet activation as an epiphenomenon rather than as an inciting pathophysiologic factor and likely due to inflammation from structural damage to the capillaries or the extreme hypoxemia. A difficult clinical question is whether ascent to altitude might result in thrombosis in persons with familial thrombophilia, such as factor V Leiden, a common anomaly, or protein C deficiency, antiphospholipid syndrome, or others. Such cases have been reported,8,38,58,255,267,379 although cause and effect cannot be established with certainty. In addition, persons with a past history of deep vein thrombosis or pulmonary embolism wonder if they are at increased risk at high altitude, as do women on hormonal contraceptives. Unfortunately, the literature does not provide guidance for these individuals. Some experts empirically recommend daily aspirin during altitude exposure for such patients, and this seems to be a safe suggestion. Others have raised the possibility that aspirin therapy might cause or exacerbate retinal hemorrhages at high altitude. Although no study has investigated this at altitude, research from patients with diabetic retinopathy has shown no danger of increased hemorrhages from aspirin.22 In addition, a retinal hemorrhage in a climber was treated with aspirin, and the hemorrhage resolved.284
PERIPHERAL EDEMA Edema of the face, hands, and ankles at high altitude is common, especially in females. Incidence of edema in at least one area of the body in trekkers at 4200 m (13,780 feet) was 18% overall, 28% in females, 14% in males, 7% in asymptomatic trekkers, and 27% in those with AMS.187 Although not a serious clinical problem, edema can be bothersome. The presence of peripheral edema demands examination for pulmonary and cerebral edema. In the absence of AMS, peripheral edema is effectively treated with a diuretic. Treatment of accompanying AMS by descent or medical therapy also results in diuresis and resolution of peripheral edema. The mechanism is presumably similar to fluid retention in AMS but may also be merely due to exercise.350
IMMUNOSUPPRESSION Mountaineers have observed that infections are common at high altitude, slow to resolve, and often resistant to antibiotics.376 On the American Medical Research Expedition to Mt Everest in 1981, serious skin and soft tissue infections developed. “Nearly every accidental wound, no matter how small, suppurated for a period of time and subsequently healed slowly.”465 A suppurative hand wound and septic olecranon bursitis did not respond to antibiotics but did respond to descent to 4300 m (14,108 feet) from the 5300 m (17,388 feet) base camp. Nine of 21 persons had significant infections not related to the respiratory tract. Most highaltitude expeditions report similar problems. Data from OEII indicated that healthy individuals are more susceptible to infections at high altitude because of impaired T lymphocyte function; this is consistent with previous Russian studies in humans and animals.345 In contrast, B cells and active immunity are not impaired. Therefore resistance to viruses may not be impaired, whereas susceptibility to bacterial infection is increased. The degree of immunosuppression is similar to that seen with trauma, burns, emotional depression, and space flight. The mechanism may be related, at least in part, to release of 27
CHAPTER 1 High-Altitude Medicine and Physiology
by decreased PaO2 (from 69 to 64 mm Hg) and increased PCO2 (from 32.5 to 34 mm Hg). Whether this degree of ventilatory depression would contribute to acute mountain sickness and whether repeated doses would have greater effect was not tested. Nonetheless, the authors argue that alcohol might impede ventilatory acclimatization and should be used with caution at high altitude. Conventional wisdom proffers an additive effect of altitude and alcohol on brain function. McFarland,341 who was concerned about the interaction in aviators, wrote, “…the alcohol in two or three cocktails would have the physiologic action of four or five drinks at altitudes of approximately 10,000 to 12,000 feet.” Also, “Airmen should be informed that the effects of alcohol are similar to those of oxygen want and that the combined effects on the brain and the CNS are significant at altitudes even as low as 8,000 to 10,000 feet.”341 His original observations were made on two subjects in the Andes in 1936. He found that blood alcohol levels rose more rapidly and reached higher values at altitude but noted no interactive effect of alcohol and altitudes of 3810 and 5335 m (12,500 and 17,503 feet).342 Most subsequent studies refuted the increased blood alcohol concentration data except at the highest altitudes, over 5450 m (17,881 feet). Higgins and associates, 209,210 in a series of chamber studies, found blood alcohol levels were similar at 392 and 3660 m (1286 and 12,008 feet), and they noted no synergistic effects of alcohol and altitude. Lategola and colleagues287 found that blood alcohol uptake curves were the same at sea level and 3660 m (12,008 feet), and that performance on math tests showed no interaction between alcohol and altitude. In another study of 25 men, performance scores were similar at sea level and at a simulated 3810 m (12,500 feet) altitude, with blood alcohol level of 88 mg%.93 Performance was not affected by hypoxia, only by alcohol, and older subjects were more affected. When more demanding tasks were tested, Collins92 found that a blood alcohol level of 91 mg% affected performance, as did an altitude of 3660 m (12,008 feet) during night sessions when the subjects were sleep deprived, but there was no significant altitude–alcohol interaction. In the one study in which Collins and co-workers94 were able to discern some altitude effect, there was a simple additive interaction of altitude (hypoxic gas breathing) and alcohol. He concluded that performance decrements due to alcohol may be increased by altitudes of 3660 m (12,000 feet) if subjects are negatively affected by that altitude without alcohol. All of these aviation-oriented studies used acute hypoxia equivalent to no more than 3500 m (11,483 feet). Perhaps the highest altitude (without supplemental oxygen) at which alcohol was studied was 4350 m (14,272 feet), on the summit of Mt Evans in Colorado. Freedman and associates148 found that alcohol affected auditory evoked potentials the same as in Denver; that is, no influence of altitude was detectable. In summary, the limited data on blood gases at altitude after alcohol ingestion support the popular notion that alcohol could slow ventilatory acclimatization and therefore might contribute to AMS. Considerable data at least up to 3660 m (12,000 feet), however, refute the belief that altitude potentiates the effect of alcohol. How altitude and alcohol might interact during various stages of acclimatization in individuals at higher altitudes is still unknown.
PART 1 MOUNTAIN MEDICINE
adrenocorticotropic hormone, cortisone, and β-endorphins, all of which modulate the immune response.135,354 Intense ultraviolet exposure has also been shown to impair immunity. Persons with serious infections at high altitude may need oxygen or descent for effective treatment. Impaired immunity because of altitude should be anticipated in situations where infection could be a complication, such as trauma, burns, and surgical and invasive procedures.
HIGH-ALTITUDE PHARYNGITIS, BRONCHITIS, AND COUGH Sore throat, chronic cough, and bronchitis are nearly universal in persons who spend more than 2 weeks at an extreme altitude (over 5500 m [18,045 feet]).84,300,333,370 All 21 members of the 1981 American Medical Research Expedition to Mt Everest suffered these problems.465 Only two of eight subjects in OEII (where the temperature was greater than 21° C [69.8° F] and relative humidity was greater than 80%) developed cough, and only above 6500 m (21,325 feet). Only four had sore throat. Acute hypoxia directly lowers the cough threshold, thus exacerbating high-altitude cough.334 Other factors are at play.332 In the field, these problems usually appear without fever or chills, myalgia, lymphadenop athy, exudate, or other signs of infection. The increase in ventilation, especially with exercise, forces obligate mouth breathing at altitude, bypassing the warming and moisturizing action of the nasal mucous membranes and sinuses. Movement of large volumes of dry, cold air across the pharyngeal mucosa can cause marked dehydration, irritation, and pain, similar to pharyngitis. Vasomotor rhinitis, quite common in cold temperatures, aggravates this condition by necessitating mouth breathing during sleep. For this reason, decongestant nasal spray is one of the most coveted items in an expedition medical kit. Other countermeasures include forced hydration, hard candies, lozenges, and steam inhalation. High-altitude bronchitis can be disabling because of severe coughing spasms. Cough fractures of one or more ribs are not rare.300 Purulent sputum is common. Response to antibiotics is poor; most victims resign themselves to taking medications such as codeine and do not expect a cure until descent. Bronchitis developed in 13 of 19 climbers above 4300 m (14,108 feet) on Aconcagua.415 Mean sputum production was 6 teaspoons per day. All reported that onset was after a period of excessive hyperventilation associated with strenuous activity. Although an infectious etiology is possible, experimental evidence suggests that respiratory heat loss results in purulent sputum and sufficient airway irritation to cause persistent cough.340 This is supported by the beneficial effect of steam inhalation and lack of response to antibiotics. Many climbers find that a thin balaclava, porous enough for breathing, traps some moisture and heat and effectively prevents or ameliorates the problem. Many climbers with high-altitude cough use inhaled fluticasone and salmeterol or similar inhaled agents and report success; studies of these medications are underway. Differential diagnosis of persistent cough in these conditions can be difficult.162
HIGH-ALTITUDE RETINOPATHY AND ULTRAVIOLET KERATITIS See Chapter 28.
Common Medical Conditions and High Altitude Persons with certain preexisting illnesses might risk adverse effects on ascent to high altitude, due either to exacerbation of illnesses or to illnesses that impact acclimatization and susceptibility to altitude illness. Certain populations also require special consideration, such as the very young, the pregnant and older adults. This section presents an overview of current knowledge regarding these issues. Despite the importance of the interaction of altitude and common medical conditions, research has so far been limited. See the original review by Hackett183 and updated recent reviews for more detailed discussions.315,349,448,585 28
BOX 1-5 Advisability of Exposure to High and Very
High Altitude for Common Conditions (Without Supplemental Oxygen)
Probably No Extra Risk • Young and old • Fit and unfit • Mild obesity • Diabetes • After coronary artery bypass grafting (without angina) • Mild chronic obstructive pulmonary disease (COPD) • Asthma • Low-risk pregnancy • Controlled hypertension • Controlled seizure disorder • Psychiatric disorders • Neoplastic diseases • Inflammatory conditions Caution • Infants <6 weeks old • Moderate COPD • Asymptomatic pulmonary hypertension • Compensated congestive heart failure (CHF) • Morbid obesity • Sleep apnea syndromes • Troublesome arrhythmias • Stable angina/coronary artery disease • High-risk pregnancy • Sickle cell trait • Cerebrovascular diseases • Space-occupying brain lesions • Any cause for restricted pulmonary circulation • Seizure disorder (not on medication) • Radial keratotomy • Recent myocardial infarction or stroke Contraindicated • Sickle cell anemia (with history of crises) • Severe COPD • Symptomatic pulmonary hypertension • Uncompensated CHF • Unstable coronary or cerebrovascular disease
Conditions that can be aggravated by high-altitude exposure are listed in Box 1-5.
RESPIRATORY DISEASES Chronic Lung Disease Although oxygen saturation remains above 90% in a normally acclimatizing, healthy, and awake person until over 3000 m (9843 feet) (see Figure 1-1), persons with hypoxemic lung disease reach this threshold at a lower altitude that depends on the baseline blood oxygen values. As a result, these persons might have altitude-related problems at lower altitudes than would healthy individuals. Improved airflow will result from decreased air density at high altitude, but hypoxemia, pulmonary hypertension, disordered control of ventilation, and sleep-disordered breathing could all become worse. Unfortunately, few data are available to guide the clinician advising such a person undertaking a trip to altitude.89,314,516 Most literature addresses prediction of blood gas values at 2500 m (8202 feet), the maximum allowable cabin altitude in commercial aircraft. Ascent to terrestrial high altitude, of course, involves much longer time periods and often at higher altitudes. Thus, the clinical usefulness of these studies is limited. Hypoxic gas breathing at sea level, as in the High Altitude Simulation Test, can predict oxygenation at high altitude, but this does
Cystic Fibrosis Children with cystic fibrosis have been reported to do poorly at high altitude,507 and hypoxic testing has also tried to predict the need for supplemental oxygen upon ascent in this condition.143,254,390,454 As with COPD, such tests are not particularly useful and tend to underestimate the oxygen requirements, because they are done only during rest and while awake. Supplemental oxygen should be available for these children, and oxygen saturation monitoring might be desirable in certain circumstances. The physician should be liberal with the use of antibiotics and adjunctive therapy for exacerbations at high altitude, given the likely danger of greater hypoxemia and greater difficulty treating
infections at high altitude. Cystic fibrosis encompasses a wide range of pulmonary impairment; one patient with mild disease was able to hike to 5600 m (18,373 feet).89 Asthma The available literature suggests that asthmatics, both residents and sojourners, do well at moderate altitude, primarily because of decreased allergens and pollution.88,89,224,560,585 Indeed, high altitude as a treatment for asthma has been popular in Europe for many decades. The effect is comparable with high doses of inhaled corticosteroids.89 However, because altitude exposure often includes exercise (and cold), asthmatics with exerciseinduced bronchospasm (EIB), rather than allergic asthma, might have problems at altitude. Matsuda and colleagues335 investigated the effect of altitude on 20 asthmatic children with EIB in a hypobaric chamber simulating 1500 m (4921 feet), with the temperature and humidity held constant. Except for the increased respiratory rate during exercise, as expected, all other physiologic variables were unchanged compared with those at sea level. The authors concluded that the modest altitude of 1500 m (4921 feet) does not exacerbate exercise-induced asthma. Berntsen and coworkers53 reported similar results at 2500 m (8202 feet). Durand and associates, 127 however, found that 50% of highly trained ski mountaineers in the Alps developed EIB during racing, and that only one-fourth had been previously diagnosed with EIB. Whether this occurs with such frequency in nonelite athletes at lesser exercise intensities requires investigation. Given the frequency of exercise dyspnea at high altitude, EIB should always be considered by the clinician. Golan and colleagues163 screened travelers and found 147 asthmatics who trekked to high altitude. Risk factors for an asthma attack at altitude were use of inhaled bronchodilators more than 3 times a week before travel and intensive physical exertion during the trek. A small but careful study was done with 11 asthmatics who were in stable condition with normal respiratory function at sea level. Cogo and colleagues87 tested both methacholine challenge and hyperosmolar aerosol at sea level and multiple altitudes up to 5050 m (16,568 feet). At no altitude was there an increase in bronchial responsiveness, and at the highest altitude, there was a decrease. They concluded that the positive aspects of high altitude prevailed over potential negative factors for asthmatics and attributed the benefit to the increase in circulating catecholamines found in their subjects. In the presence of bronchoconstriction at high altitude, however, hypoxemia is likely to be greater than at low altitude, and for this reason there could be an association between asthma and HAPE or AMS. Reassuringly, no such relationship has yet been reported.224,511 Mirrakhlmov353 investigated the effect of acetazolamide in 16 asthmatic patients taken to 3200 m (10,499 feet). Acetazolamide showed the same benefits as in nonasthmatics, with higher oxygen saturation and fewer AMS symptoms compared with the placebo control group. Seven of the eight asthmatics in the control group developed symptoms of AMS, a rather high incidence, but without a nonasthmatic control group for comparison, it is not known whether this incidence was abnormal. Persons with asthma ascending to high altitude should be advised to be at maximum function before ascent, to continue on their usual medications, including corticosteroids, and to have corticosteroids and bronchodilators with them in the event of an exacerbation.88 Because airway heat loss can be a trigger for bronchospasm, the use of an airway warming mask might be helpful but is unproved.456 In summary, the available data, although limited, suggest that high altitude does not exacerbate asthma, and it actually improves allergic asthma. Further work needs to determine if asthma might have any influence on susceptibility to AMS and HAPE; anecdotally, this does not seem to be the case. Although it seems likely that a severe asthma attack at high altitude would be more dangerous than at low altitude, no data are available to answer this question. Although caution and adequate preparation are necessary, asthma is not a contraindication to high-altitude travel. Pulmonary Vascular Disorders Because of the danger of HAPE, pulmonary hypertension (PHT) of any etiology is at least a relative contraindication to 29
CHAPTER 1 High-Altitude Medicine and Physiology
not always correlate with symptoms and is inconvenient.121 Sea level PO2 values of 68 and 72 mm Hg successfully classified more than 90% of the subjects with a PaO2 greater than 55 mm Hg at simulated altitudes of 1525 m (5003 feet) and 2440 m (8005 feet), respectively.165,166 Such predictions have been further refined with the addition of spirometry.120 A PaO2 of 55 mm Hg results in saturation of 90% at high altitude, where there is slight alkalosis. These data suggested that persons with PaO2 values lower than these at sea level might require supplemental oxygen at modest altitudes. The British Thoracic Society states that patients with resting SaO2 less than 92% at sea level should use supplemental oxygen during airplane flight, and presumably on ascent to altitude. However, in the only clinical studies to date, patients with moderate chronic obstructive pulmonary disease (COPD) did quite well at altitude.168,339 Graham and Houston168 found that eight subjects with COPD taken to 1920 m (6299 feet) had only minor symptoms on ascent, despite the fact that mean PaO2 declined from 66 mm Hg at sea level to 51 mm Hg while at rest and from 63 to 47 mm Hg with exercise. The patients did acclimatize with a drop in PCO2 and a corresponding increase in PaO2 over 4 days, the same response as seen in healthy persons. Matthys and associates339 studied 10 patients at simulated altitude of 2500 m (8202 feet). Mean PAP increased from 21 to 25 mm Hg, PaO2 decreased from 68 to 51 mm Hg at rest, and the only symptom was an increase in fatigue. The authors concluded that travel to this moderate altitude is safe for such patients. They speculated that these persons might have been partially acclimatized because of their hypoxic lung disease and were therefore less likely to develop AMS. Unfortunately, no further investigations with sicker patients or at higher altitudes have yet been reported. Persons with COPD who become hypoxic and uncomfortable at altitude should be treated with oxygen therapy. Oxygen should also be considered for those predicted to become severely hypoxemic.47 See Luks310 for a helpful discussion on determining need for oxygen in these patients. To adjust oxygen therapy at altitude for persons already on supplemental oxygen, FIO2 is increased by the ratio of higher to lower barometric pressure (see Table 1-3). Oxygen also improved hemodynamics (lowered blood pressure) and decreased pulsus paradoxus and pulse pressure in COPD patients at a simulated altitude of 2438 m (8000 feet).48 With the advent of simple and inexpensive pulse oximetry, patients can be counseled to monitor their oxygen saturation, determine the need for oxygen, and titrate their own oxygen use. All patients with lung disease contemplating a trip to high altitude should be aware of oxygen availability at their destination, as well as medical services. Nearly all resorts worldwide, for example, have oxygen concentrators or compressed gas cylinders that can be obtained for use in hotels or other accommodations. In North America, home oxygen companies honor prescriptions from physicians in any state, and oxygen is quite easily obtained. Interestingly, reports of persons with COPD developing altitude illness are absent from the literature. On the other hand, the issue has not been specifically addressed. Any degree of pulmonary hypertension might be expected to increase the likelihood of HAPE, and although this has been clearly demonstrated in other conditions (see High-Altitude Pulmonary Edema, earlier), it has not yet been reported with pulmonary hypertension associated with COPD. No research has yet addressed the use of medications such as acetazolamide or medroxyprogesterone in these patients to determine if respiratory stimulants might improve altitude tolerance.
PART 1 MOUNTAIN MEDICINE
high-altitude exposure. In addition, hypoxic pulmonary vasoconstriction will most likely exaggerate preexisting pulmonary hypertension, leading to greater symptoms.183,309 Many patients with pulmonary hypertension may not be diagnosed as such, and the clinician must have an awareness of conditions associated with PHT, including trisomy 21, congenital heart disease, unilateral absent pulmonary artery, granulomatous mediastinitis, and restrictive lung diseases, all of which have been associated with high-altitude pulmonary edema.185,312,431,539 Other conditions warranting caution include bronchopulmonary dysplasia, recurrent pulmonary emboli, mitral stenosis, kyphoscoliosis, and scleroderma with CREST syndrome. As Hultgren has observed, however, some patients with PHT are able to tolerate high altitude,231 and hypoxic gas breathing can be used to identify an individual’s response to hypoxia if clinically indicated.309 Persons with PHT who must travel to high altitude might benefit from calcium channel blockers, isoproterenol, and especially low-flow oxygen.309 A report by Naeije and associates378 highlighted the increased susceptibility to HAPE in those with pulmonary hypertension; a lowland woman with pulmonary hypertension secondary to fenfluramine developed two episodes of HAPE. The first episode was at 2300 m (7546 feet) and the second one at only 1850 m (6070 feet), with skiing up to 2350 m (7710 feet). Whether pulmonary hypertension is primary or secondary, patients should be made aware of the potential hazards of high altitude, including right heart failure and HAPE. Despite lack of firm data to guide clinicians, a reasonable approach is that persons with mean PAP greater than 35 mm Hg or systolic PAP greater than 50 mm Hg at baseline should probably avoid travel to altitudes greater than 2500 m (8202 feet). If such travel is undertaken, supplemental oxygen during the sojourn should be recommended. Patients with milder degrees of pulmonary hypertension may travel to altitudes less than 3000 m (9843 feet) but should consider prophylactic measures, including pulmonary vasodilators or supplemental oxygen.309
(p <0.01 between altitudes) with ratios of central to obstructive events of 0.1, 0.8, 1.0, 1.9, and 1.9 (p <0.01 between altitudes), respectively. Tracking performance during simulated driving was significantly impaired at 2590 m (8497 feet) compared with 490 m (1608 feet). Systolic blood pressure and cardiac arrhythmias were increased at altitude. In a report linking obesity–hypoventilation syndrome, OSA, and reduced peripheral chemosensitivity to hypoxia, Richalet and co-workers426 studied a 24-year-old man with Down syndrome who developed HAPE at 2000 m (6562 feet); he did not have pulmonary hypertension. These studies were all in patients without treatment and suggest that a trade-off of OSA for CSA is not a benefit in terms of oxygenation or adverse events, and that patients with OSA or CSA must be cautious when traveling to high altitude. In contrast, patients with sleep apnea treated at altitude with CPAP, oxygen, or acetazolamide (for central events) apparently do well. Patz and associates400 showed that CPAP pressure did not vary significantly in seven patients traveling between 3048 m (10,000 feet) and sea level. Average CPAP 95th percentile absolute pressure and mean CPAP absolute pressure were stable, using a ResMed Autoset autotitrating CPAP unit. Others have suggested that the hypobaria of high altitude can decrease the delivered pressure of CPAP machines that do not have pressurecompensating features, but such machines are no longer in use. For those not being treated with CPAP, but who exhibit hypoxemia during sleep at low altitude, the physician should provide supplemental nocturnal oxygen during an altitude sojourn. Because central apnea events are easily treated with acetazolamide, patients with sleep apnea going to altitude should be considered for acetazolamide therapy, regardless of CPAP use.1,161 See Table 1-8 for recommendations regarding sleep apnea and other ventilatory disorders.
Sleep Apnea, Sleep-Disordered Breathing Persons with snoring, sleep apnea syndrome, and sleep-disordered breathing who become mildly hypoxemic at sea level may become severely hypoxemic at high altitude. This could contribute to high-altitude illness and aggravate attendant problems such as polycythemia, pulmonary hypertension, systemic hypertension, cardiac arrhythmia, or insomnia. On the other hand, changes in ventilatory control and breathing secondary to altitude hypoxia might conceivably improve certain apnea syndromes. In general, the limited research available has shown that obstructive sleep apnea (OSA) tends to improve at altitude, but that central sleep apnea (CSA) can either develop or become worse. Burgess and colleagues68 demonstrated a decrease in obstructive events but a “conversion” to severe central events in five men with moderate OSA studied without CPAP. The obstructive respiratory disturbance index fell from 25.5/hr at 60 m (197 feet) to 0.5/hr at 2750 m (9022 feet), while the central respiratory disturbance index rose from 0.4/hr at 60 m (197 feet) to 78.8/hr at 2750 m (9022 feet). Mean sleep SaO2 fell from 94% at 60 m (197 feet) to 85% at 2750 m (9022 feet) simulated altitude.68 They attributed the decrease in OSA to increased upper airway tone and increased respiratory rate, and the increased CSA to hypocapnia during non-REM sleep. Similarly, a small study in Colorado showed that the apnea–hypopnea index decreased in patients with OSA not on CPAP living at high altitude when they went to lower altitudes, due primarily to a decrease in central events, while OSA events persisted.399 These observations were confirmed in a detailed study of 34 patients with OSA with median apnea–hypopnea index of 47.5 events per hour, residing above 600 m (1969 feet). They did the following: patients spent 1 day in Zurich (490 m [1608 feet]) and 4 days in the Swiss Alps at 1860 m (6102 feet) and 2590 m (8497 feet) (2 days each), during which their CPAP was discontinued.389 Daily evaluations included polysomnography, symptom questionnaires, physical examination, and driving simulator tests. Median oxygen saturations at 490 m (1608 feet) and in the first and second nights at 1860 and 2590 m (6102 and 8497 feet), respectively, were 94%, 90%, 90%, 86% and 87% (p <0.01 between altitudes). Corresponding median apnea–hypopnea index values were 47.5, 85.1, 74.6, 90.0, and 90.9 events per hour
Hypertension In healthy persons rapidly ascending to high altitude, the change in blood pressure, if any, is variable, depending on magnitude of hypoxic stress, cold, diet, exercise, and genetic factors. Most studies report a slight increase in blood pressure, associated with increased catecholamine activity and increased sympathetic activity.416 One well-controlled study showed an increase in blood pressure at 3500 m (11,483 feet) from a mean of 105/66 mm Hg at sea level to 119/77 mm Hg at 3 days, 111/75 mm Hg at 3 weeks, and back to 102/65 mm Hg on return to sea level.331 Pugh411 reported transient increases in blood pressure in athletes at the Olympics in Mexico City. Certain individuals, however, appear to have a pathologic response on induction to high altitude. For example, arterial hypertension develops in 10% of lowland Chinese who move to Tibet.494 The authors consider this a form of altitude maladaptation and treat the condition by returning the affected individuals to low altitude. After a period of at least 2 months, however, downregulation of adrenergic receptors results in attenuation of the initial blood pressure response. This mechanism is thought to be the reason that longterm residents of high altitude have lower blood pressure than do their sea level counterparts.230,445 Apparently for the same reason, chronic altitude exposure has also been shown to inhibit progression of hypertension.352 As for the effect of short-term altitude exposure on preexisting hypertension, studies have generated mixed results. In general, the response in hypertensives is similar to those without hypertension (i.e., a small increase in blood pressure, with an exaggerated response in some individuals). The greater the hypoxic stress (the higher the altitude), the greater the change in blood pressures. Altitudes less than 3000 m (9843 feet) seem to result in little if any change.439 Palatini and colleagues397 studied 12 normotensives and 12 untreated mild hypertensives with 24-hour ambulatory blood pressure monitoring at sea level, after 12 hours at 1210 m (3970 feet), and after 1.5 to 3 hours at 3000 m (9843 feet). The authors concluded that the increase of blood pressure in both normotensives and hypertensives was not important at 1200 m (3970 feet) but could become so at 3000 m (9843 feet). However, individual variability was great; the maximum change
30
CARDIOVASCULAR CONDITIONS
for Ventilatory Disorders
Obesity Hypoventilation • Counsel against high-altitude travel. • If high-altitude travel cannot be avoided, administer supplemental oxygen for daytime and nighttime use. • Counsel patients about the risks for and symptoms of AMS, and achieve prophylaxis with acetazolamide 125 mg or 250 mg bid. • In patients with preexisting CPAP prescription, travel to altitude with CPAP unit. Obstructive and Central Sleep Apnea • Travel to altitude with CPAP machine. • Consider acetazolamide 125-250 mg bid, or single dose at bedtime. • Continue preexisting nocturnal oxygen therapy; if so, acetazolamide not indicated. • Evaluate patients with daytime hypoxemia for PHT and, if present, achieve prophylaxis with nifedipine SR 30 mg bid. • Optimize heart-failure regimen for patients with central sleep apnea due to cardiomyopathy. Prior Carotid Artery Surgery • Avoid high-altitude travel in patients with preceding bilateral carotid body resection. • If travel cannot be avoided, administer supplemental oxygen. • Assess hypoxic ventilatory response in patients with prior history of carotid endarterectomy, and administer supplemental oxygen if response is suppressed. Neuromuscular Disorders • Screen for sleep-disordered breathing and, if present, treat with bilevel positive airway pressure at altitude. • Screen for baseline hypoventilation and, if present, travel to high altitude with bilevel positive airway pressure. • Administer nocturnal supplemental oxygen in patients with history of nocturnal desaturation. • Screen kyphoscoliosis patients for pulmonary hypertension and, if present, administer supplemental oxygen and prophylax with nifedipine SR 30 mg bid. • Counsel patients with bilateral diaphragmatic paralysis against high-altitude travel. If travel cannot be avoided, administer bilevel positive airway pressure. Modified from Luks AM, Swenson ER: Travel to high altitude with pre-existing lung disease, Eur Respir J 29:770, 2007. AMS, Acute mountain sickness; CPAP, continuous positive airway pressure, PHT, pulmonary hypertension.
was 17.4 mm Hg for systolic and 16.3 mm Hg for diastolic blood pressures. Two other studies were able to demonstrate a slightly greater blood pressure response in hypertensives compared with normotensives on ascent to 2572 m (8438 feet) and 3460 m (11,352 feet).113,471 Again, these authors also noted important individual variation, with some subjects increasing their systolic blood pressure by as much as 25 mm Hg at rest and 40 mm Hg during exercise, compared with sea level measurements. The important question of whether the blood pressure would continue to increase over the first 2 weeks at high altitude, as it does in normotensives, has not yet been addressed. At a more modest altitude, Halhuber and co-workers198 claimed a significant reduction in the blood pressure of 593 persons with hypertension after 14 days at 1700 to 2000 m (5577 to 6562 feet) in the Alps. A similar study of hypertensives at higher altitude will hopefully be accomplished. Patients receiving antihypertensive treatment should continue their medications while at high altitude. Because some persons may unpredictably become markedly hypertensive acutely,231 blood pressure monitoring should be considered, especially in those with labile hypertension or those who become symptomatic at altitude. Hypertension in short-term high-altitude sojourners for the most part should be considered transient and should not be treated, because it rarely reaches dangerously high levels and will resolve on descent. Given the large number of
hypertensive patients visiting ski resorts and trekking at high altitude, however, the occasional person with an exaggerated response will require treatment.231 Because the mechanism appears to be increased α-adrenergic activity, an α-blocker might be the best choice of therapy for these individuals. A preliminary report also suggested that nifedipine might be useful and superior to atenolol.114 The best medication, dosage, and duration still need to be determined. There is no evidence to date to suggest that hypertensive patients are more likely to develop high-altitude illnesses. Although requiring some caution, hypertension does not seem to be a contraindication to high-altitude exposure. Arteriosclerotic Heart Disease Lifelong residence at high altitude appears to offer some protection from coronary artery disease (CAD) and the attendant acute coronary artery events,351 perhaps in part because of increased myocardial vascularity. Other factors that might explain this finding, such as genetics, fitness, and diet have not been adequately evaluated. The effect of acute, transient exposure to high altitude on the healthy heart also appears to be benign. Various avenues of research have indicated that the healthy heart tolerates even extreme hypoxia quite well, all the way to the summit of Mt Everest (PaO2 less than 30 mm Hg). Numerous ECGs, echocardiograms, heart catheterizations, and exercise tests have failed to demonstrate any evidence of cardiac ischemia or cardiac dysfunction in healthy persons at high altitudes. This could partly be due to the marked reduction in maximal exercise with increasing altitude, which reduces maximal heart rate and myocardial oxygen demand, and also due to increased coronary blood flow. A person with CAD, however, may not have the same adaptive capacities. For example, diseased coronary arteries might have limited ability to vasodilate and might actually constrict, because of unopposed sympathetic activation.297 What then are the risks, and what should be the advice for persons with CAD considering a visit to high altitude? Surprisingly little literature is available to help the physician advise such persons. Does high altitude provoke acute coronary events or sudden death? In the United States., no evidence from state or county mortality statistics suggests an increased prevalence of acute coronary events in visitors to high-altitude locations. In Europe, Halhuber and associates198 reported an incidence of only 0.2% for myocardial infarction in 434 patients with CAD taken to altitudes between 1700 and 3200 m (5577 and 10,499 feet) for 4 weeks in the Alps. They also reported a very low incidence of sudden death in 151,000 vacationers in the Alps, 69,000 of whom were over age 40 years. In contrast are data from Austria claiming a higher rate of sudden cardiac death in the mountains, compared with the overall risk for sudden cardiac death.71 However, the altitudes were rather low (1000 to 2100 m [3281 to 6890 feet]), and no increased risk was evident in men who participated regularly in sports. The authors suggested that abrupt onset of exercise in sedentary men combined with altitude stress might induce cardiac sudden death, but whether altitude contributed at all is unclear. In summary, limited data suggest no increased risk for sudden cardiac death or myocardial infarction at altitudes up to 2500 m (8202 feet). Another important question is whether altitude will exacerbate stable ischemia. The slight increase in heart rate and blood pressure on initial ascent to altitude might exacerbate angina in persons with CAD, as described by Hultgren.231 One study evaluated nine men with stable exercise-induced angina by exercise treadmill test at 1600 m (5249 feet) (Denver) and within the first hour of arrival at 3100 m (10,171 feet).371 Cardiac work was slightly higher for a given workload at high altitude compared with low altitude, and as a result, the onset of angina was at a slightly lower workload. They found that a heart rate of 70% to 85% of the rate that produced ischemia at low altitude was associated with angina-free exercise at 3100 m (10,171 feet), and they suggested that angina patients at altitude adjust their activity level based on heart rate, at least on the day of arrival.371 Brammel and colleagues64 reported similar results and also suggested that those with angina need to reduce their activity at high altitude to avoid angina episodes. In a more recent study, Levine and co-workers297 investigated 20 men who were much older than those in the previous investigations (mean age 68 ± 3 years) and 31
CHAPTER 1 High-Altitude Medicine and Physiology
TABLE 1-8 Summary of Recommendations
PART 1 MOUNTAIN MEDICINE
performed symptom-limited exercise tests. With acute exposure to 2500 m (8202 feet), the double product (heart rate times systolic blood pressure) required to induce 1 mm ST depression was decreased about 5%, but after 5 days of acclimatization at 2500 m (8202 feet), this value was unchanged from sea-level. The degree of ischemia (maximal ST segment depression) was the same at sea level, with acute altitude exposure, and after 5 days at 2500 m (8202 feet). Also, no new wall motion abnormalities on echocardiography were seen at high altitude. Only one subject exhibited increased angina at altitude, and one person with severe coronary artery disease developed a myocardial infarction after maximal exercise at 2500 m (8202 feet). The authors concluded that coronary artery disease patients who are well compensated at sea level do well at a moderate altitude after a few days of acclimatization, but that acutely angina threshold may be lower and activity should be reduced.297 Finally, a study of 97 older adults visiting 2500 m (8202 feet), many with CAD and abnormal ECGs, found no new ECG changes and no events suggestive of ischemia. In contrast with the Levine study, these subjects did not do exhaustive exercise tests, but merely their usual activities, which included walking in the mountains.439 Taken altogether, these various investigations indicate that persons with CAD, including older adults, generally do well at the modest altitude of 2500 m (8202 feet), but that reducing their activities the first few days at altitude is wise. To address the question of whether altitude might provoke cardiac arrhythmia, Levine associates,297 in their study mentioned above, found that premature ventricular contractions (PVCs) increased 63% on acute ascent but returned to baseline after 5 days of acclimatization. A simultaneous rise in urine norepinephrine in these subjects indicated that sympathetic activation was the cause of the increased ectopy. They observed no increase in higher-grade ectopy, however, and no changes in signal-averaged ECG suggestive of a change in fibrillation threshold; in other words, the PVCs appeared benign. Halhuber and colleagues198 also found increased ectopy in their subjects and also no serious adverse events. In addition, Alexander5 described asymptomatic PVCs and ventricular bigeminy in himself while trekking to 5900 m (19,357 feet). Subsequent evaluation found no evidence of heart disease, and the event prompted him to thoroughly review the subjects of altitude, age, and arrhythmia. Although no dangerous arrhythmias have ever been reported in high-altitude studies, persons with troublesome or high-grade arrhythmias have not been evaluated upon ascent to high altitude. The available evidence would suggest that patients whose arrhythmias are well controlled on medication should continue the medication at altitude, whereas those with poorly controlled arrhythmias might do better to avoid visiting high altitude. In terms of advising persons with CAD or high likelihood of CAD about altitude exposure, the stress of high altitude on the coronary circulation appears to be minimal at rest but significant in conjunction with exercise. Ideally no one with known CAD or even risk factors for CAD should undertake unaccustomed exercise at any altitude, and especially at high altitude. Therefore advising an exercise program at sea level before exercising at altitude is prudent. The same technique of risk stratification that is commonly used at sea level can be applied for providing advice for high altitude.225 Using the standard recommendations, asymptomatic males over age 50 with no risk factors require no testing. For asymptomatic males over age 50 with risk factors, an exercise test is recommended to determine risk status before exercising at high altitude, and then further evaluation as indicated. Patients with previous myocardial infarction, bypass surgery, or angioplasty are considered high risk only if they have a strongly positive exercise treadmill test. Patients with multiplevessel bypass grafts who were asymptomatic and with normal exercise tests at sea level have successfully visited altitudes over 5000 m (16,404 feet). High-risk patients may require coronary angiography to establish appropriate management. Alexander4 has proposed different criteria for those with CAD at high risk at altitude: an ejection fraction of less than 35% at rest, a fall in exercise systolic blood pressure, ST-segment depression greater than 2 mm at peak heart rate, and high-grade ventricular ectopy. For these persons, he recommends ascent to no more than 2500 m (8202 feet) and proximity to medical care. Both sets of 32
recommendations, while reasonable, need to be validated with outcome studies. Heart Failure Although information on the effect of high altitude on heart failure is scant, physicians in resort areas have noted a tendency toward acute decompensation in those with a history of heart failure within 24 hours of arrival. Those with CAD and low ejection fractions (less than 45%), but without active heart failure, actually did quite well, as gauged by exercise tests during acute exposure to 2500 m (8202 feet).134 Compared with 23 control subjects, the decrement in exercise performance was similar, and no complications or signs of ischemia developed. Although these results are encouraging for such patients, they made no observations past the first few hours at altitude. One concern is that persons with heart failure might be more likely to retain fluid at altitude, especially if AMS were to develop, and that this could aggravate heart failure. Supporting this notion, Alexander4 found that ejection fraction declined at altitude during an exercise study in patients with angina, with an increase in end-diastolic and systolic volume as measured by two-dimensional echocardiography. Ventricular contractility was not depressed, however, and these changes were attributed to fluid overload. Patients with heart failure need to be informed about possible consequences of high-altitude exposure. In particular, they need to avoid acute mountain sickness, which is associated with fluid retention, continue their regular medications, and be prepared to increase their diuretic should symptoms of failure exacerbate. Acetazolamide prophylaxis may be useful to consider in terms of speeding acclimatization, inducing diuresis, and preventing AMS, but its efficacy in these patients remains untested.
OBESITY The interaction of obesity and altitude has recently received much attention. A small study suggested increased susceptibility to AMS in mildly obese men,154 possibly because of lower nocturnal oxygen saturation that was present despite greater than normal hypoxic and hypercapnic chemosensitivity.155 Another larger study examined men with metabolic syndrome (obesity, hypertension, diabetes, and hyperlipidemia) with a 3-week stay at 1700 m (5577 feet) and found normal altitude responses and a loss of body fat.176 In fact, recent work supports hypoxic exposure as a treatment for obesity.298,381,414,493 However, obese men and women (mean body mass index 47.1 kg/m2) who were permanent residents at a mean altitude of 2448 m (8031 feet) had a 96% incidence of systolic pulmonary artery hypertension (>30 mm Hg), which was related to alveolar hypoventilation.545 These residents with obesity–hypoventilation syndrome are at increased risk for developing right heart failure. Tourists with obesity–hypoventilation are at risk for AMS and HAPE.314,426 Because of the high risk for altitude illness or aggravation of pulmonary hypertension and decompensation of the right ventricle, these patients should probably avoid high-altitude travel. See recommendations in Table 1-8.
SICKLE CELL DISEASE Sickle cell crisis is a well-recognized complication of high-altitude exposure.147 Even the modest altitude of a pressurized aircraft (1500 to 2000 m [4921 to 6562 feet]) causes 20% of persons with hemoglobin SC and sickle-thalassemia genetic configuration to have a vasoocclusive crisis.327 High-altitude exposure may precipitate the first vasoocclusive crisis in persons previously unaware of their condition. Persons with sickle cell anemia and a history of vasoocclusive crises are advised to avoid altitudes over 1800 m (5906 feet) unless they are taking supplemental oxygen. Persons with sickle cell disease who live at high altitude in Saudi Arabia have twice the incidence of crises, hospitalizations, and complications as do Saudis at low altitude. Splenic infarction syndrome has been reported more commonly in persons with sickle cell trait than in those with sickle cell anemia, probably because sickle cell disease produces autosplenectomy early in life. Frequent reports in the literature emphasize the need to consider splenic syndrome caused by sickle cell trait in any
person with left upper quadrant pain, even at an altitude of only 1500 m (4921 feet).283,327 A number of authors have suggested that nonblack persons with the trait may be at greater risk for splenic syndrome at high altitude than are black persons.283 Treatment of splenic syndrome consists of intravenous hydration, oxygen, and travel to a lower altitude.537 The overall incidence of problems in persons with the trait is low, however, and no special precaution other than recognition of the splenic syndrome is recommended. The U.S. Army, for example, does not consider soldiers with the trait unfit for duty at high altitude.119
PREGNANCY In high-altitude natives, pregnancy-associated hypertension is four times more common than in low-altitude pregnancies, preeclampsia is more common, and full-term infants are small for gestational age.364,367 These problems raise the issue of whether short-term altitude exposure may also pose a risk. So far, there is no evidence that these problems or others, such as spontaneous abortion, abruptio placentae, or placenta previa, can result from a sojourn to high altitude.385 Unfortunately, however, few data exist on the influence of a high-altitude visit during pregnancy on the mother and the fetus. For moderate altitude, the research to date has been reassuring.222,223 Artal and associates13 studied seven sedentary women at 34 weeks’ gestation. Maximal and submaximal exercise tests were completed at sea level and 1829 m (6000 feet) after 2 to 4 days of acclimatization. They reported the expected decrease in maximal aerobic work but found no difference from sea level in fetal heart rate responses or in maternal lactate, epinephrine, and norepinephrine levels. Although this study was in a small number of subjects, the authors concluded that it is safe for third-trimester women to engage in brief bouts of exercise at moderate altitude. A similar conclusion was reached in a study of 12 pregnant subjects who exercised after ascent to 2225 m (7300 feet). The authors did not discover any abnormal fetal heart rate responses and considered exercise at altitude benign for both mother and fetus.43 Huch222 also concluded that short-term exposure to altitude with exercise was safe during pregnancy. In summary, available data, though limited, indicate that short-term exposure to altitudes up to
2500 m (8202 feet) with exercise is safe for a lowland woman with a normal pregnancy. Another avenue of research has been alteration of blood gases during pregnancy. Human and animal studies with acute hypoxic challenge, as well as oxygen-breathing studies, have drawn two conclusions: (1) that a compromised placental–fetal circulation could be unmasked at high altitude, and (2) that a fetus with a normal placental–fetal circulation seems to tolerate a level of acute hypoxia far exceeding that incurred by moderate altitude exposure.23,97,432 Based on available research, it seems prudent to recommend that only women with normal, low-risk pregnancies undertake sojourns to altitude. For these women, exposure to an altitude at which SaO2 will remain above 85% most of the time (up to 3000 m altitude) appears to pose no risk for harm. However, further study is needed to place these recommendations on a more solid scientific footing. Ultrasound or other assessment may be useful to rule out the more common complications before travel. It is not the altitude per se that determines whether the fetus becomes stressed, but rather it is maternal (and fetal) arterial oxygen transport. A woman with high-altitude pulmonary edema at 2500 m (8202 feet), for example, is much more hypoxemic than is a healthy woman at 5,000 m (16,404 feet). Therefore a strategy for preventing altitude illness, especially pulmonary edema, must be explained and implemented. Similarly, elevated carboxyhemoglobin from smoking, lung disease, and other problems of oxygen transport will render the pregnant patient at altitude more hypoxemic and physiologically at a higher altitude. Consideration of a high-altitude sojourn in the developing world or in a wilderness setting raises other issues that may be more important than the modest hypoxia. These include remoteness from medical care should a problem arise, quality of available medical care, use of medications for such important risks as malaria and traveler’s diarrhea (many of which are contraindicated in pregnancy), and the risks for trauma.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 2
AVALANCHES COLIN K. GRISSOM, MARTIN I. RADWIN, DALE ATKINS, AND SCOTT E. MCINTOSH
An avalanche is a mass of snow that slides down a mountainside. In the United States, approximately 100,000 avalanches occur annually, of which about 100 cause injuries, death, or the destruction of property. According to a database of reported incidents from 1999-2000 to 2008-2009, about 350 people per year are caught or otherwise involved in avalanches.3 Of these, approximately 90 individuals are partly or wholly buried, 40 sustain injury, and 28 are killed. Average annual property damage varies tremendously, depending on the severity of the winter. From 1999 to 2009, damages as a result of avalanches ranged from a low of $30,000 to a high of $16.5 million (median = $265,000).4 This chapter describes the properties of the mountain snowpack that contribute to avalanche formation; avalanche safety techniques; rescue; and victim physiology and treatment.
Properties of Snow SNOW CLIMATES Snow cover is variable on both the broad geographic scale (i.e., Antarctic snow is quite different from snow found in the Cascade
Mountains of North America, which is quite different from the snow in the Southern Rocky Mountains of the United States) and the microscale (i.e., snow conditions may vary greatly from one side of a rock or tree to the other). All snow crystals are made of the same substance (i.e., water molecules), but local and regional environmental conditions control the type and character of the snow that is found at a given location. To better understand the geographic differences that affect avalanche initiation, it is helpful to consider some basic climate conditions. The character of the snow and the avalanche propensity in different mountain ranges around the world can be described as one of three types—maritime, continental, or transitional—on the basis of the average snow conditions of that particular region. Heavy snowfall and relatively mild temperatures characterize the maritime snow climate. The snow cover is deep and the new snow is dense as a result of moist ocean storms coming ashore at lower altitudes. Rain is common, and it is a significant cause of avalanches when it falls on deep fresh snow. Arctic air intrusions are uncommon but can occur each winter. In general, the
For online-only figures, please go to www.expertconsult.com
33
PART 1 MOUNTAIN MEDICINE
TABLE 2-1 Characteristics of Maritime, Transitional
(Intermountain), and Continental Snow Climates on the Basis of 15-Year Means
Type Maritime Transitional Continental
Total Precipitation (mm)
Air Temperature in ° C (° F)
Snow Depth (cm)
New Snow Density (kg/m3)
1286 854 550
−1.3° (29.7°) −4.7° (23.5°) −7.3° (18.9°)
186 170 113
120 (12%) 90 (9%) 70 (7%)
Data from Armstrong R, Armstrong B: Snow and avalanche climates of the Western United States: A comparison of maritime, intermountain and continental conditions. In Proceedings of the Davos Symposium. Davos, Switzerland, 1986, Swiss Avalanche Institute.
snowpack gains strength quickly with time in this snow climate. In North America, examples of maritime ranges include the Sierras, Cascade Mountains, and Coast Range of British Columbia. Far removed from coastal areas, the continental snow climate is characterized by low snowfall, cold temperatures, and higher altitudes. Snowfall is light and of low density, and wind is a key instigator of avalanches. Avalanche cycles are often the result of buried structural weaknesses that occur in shallow snowpacks and that may cause avalanche danger to persist for days, weeks, or even months. Avalanches that are released from these old, persistent, weak layers are a distinguishing trait of a continental climate. In this climate, especially during the early months of the winter, the shallow snow cover loses strength with time. Continental ranges include the Canadian Rocky Mountains, Southern Rocky Mountains, and Brooks Range. In between the maritime and continental regions is a transitional snow climate that, in North America, is often referred to as the “intermountain” snow climate. Many mountain regions in this class tend to exhibit intermediate features that reflect both of the other types of climates (Table 2-1). Examples of these mountain ranges include the Wasatch Range in Utah, Teton Range in Wyoming, and Columbia Mountains of British Columbia.
PHYSICAL PROPERTIES Although snow cover appears to be nothing more than a thick homogeneous blanket that covers the ground, it is in fact one of the most complex materials found in nature. It often exists concurrently in solid, liquid, and gaseous phases. Snow is highly variable; it may go through significant changes during relatively short periods as a result of environmental factors. At any single site, the seasonal snow cover varies from top to bottom and results in a complex layered structure, the study of which is referred to as stratigraphy. Individual layers may be quite thick or very thin, and they may vary greatly in strength and in their ability to adhere to one another. In general, thicker layers represent consistent conditions during one storm, when new snow crystals that fall are of the same type, when wind speed and direction vary little, and when temperature and precipitation are fairly constant. Thinner layers that are perhaps only millimeters in thickness often reflect conditions between storms. Examples include a melt-freeze crust or sun crust that is formed during fair weather or a hard wind crust that is formed during a period of strong winds. A brittle buried surface hoar layer represents what were once delicate feather-shaped crystals of surface hoar on the surface of the snow that were deposited from the moist atmosphere onto the cold snow surface during a clear night. These crystals are very fragile and weak; after they are buried by subsequent snowfalls, they may be a persistent and major contributor to avalanche formation. One property of snow is strength or hardness, which is of great importance in terms of avalanche formation. Snow can vary from light and fluffy, easy to shovel, and especially delightful to ski through to heavy and dense, impossible to penetrate with a shovel, and firm enough to make it very difficult for a skier to carve a turn. The arrangement of the ice skeleton (i.e., the lattice 34
of ice crystals within the snowpack) and the changing density (i.e., the mass per unit volume, which is typically represented as kg/m3) produce this wide range of conditions. In the case of snow, density is determined by the volume mixture of ice crystals and air. In general, the denser the snow layer, the harder and stronger it becomes, as long as it is not melting. The density of new snow can have a wide range of values. This depends on how closely the new snow crystals pack together, which is controlled by the shapes of the crystals. The initial crystals that fall from the atmosphere have a variety of shapes, and some pack more closely together than do others (Figure 2-1). For example, needles pack more closely than stellars; thus the density of snow made of compressed needles may be three to four times greater than that of snow composed of stellars. Wind can alter the shapes of new snow crystals and break them into much smaller pieces that pack very closely together to form wind slabs. Such slabs may possess a density that is five to ten times that of new stellars falling in the absence of wind. Because these processes occur at different times and locations at the surface of the snow cover and are buried by subsequent snowfalls, a varied heterogeneous layered structure results. Thus minor variations in atmospheric conditions can have an important influence on the properties of snow on the ground. After snow has been deposited on the surface, snow density increases as the snow layer compacts vertically as a result of the effects of gravity, weather, and crystal metamorphosis (i.e., settlement). Because an increase in density often equals an increase in strength, the rate at which this change occurs is important with respect to avalanche potential. Snow is composed predominantly of air pockets within an ice skeleton of crystals, and it is therefore highly compressible. In a typical layer of new snow, 85% to 95% of the volume is comprised of air pockets, and it can settle under its own weight. Individual ice crystals can move and slide past each other, and, because the force of gravity causes them to move slowly downward, the layer shrinks. A heavier snow layer or a warmer temperature speeds settlement. At the same time, the complex and intricate shapes that characterize the new snow crystals begin to change. They become more rounded and suitable for closer packing. Intricate crystals (e.g., stellars) possess a shape that is naturally unstable and that changes quickly. New snow crystals have a large surface area– to–volume ratio and are composed of a crystalline solid that is close to its melting point. In this regard, snow crystals are unique among the materials that are found in nature. Surface energy physics dictate that this unstable condition will lead to a change in the crystalline shape toward an energy equilibrium; in other words, the warmer the temperature, the faster the change. Under very cold conditions, the original shapes of the snow crystals are sometimes still recognizable after they have been in the snow cover for several days or even after a week or two. However, as temperatures warm and approach the melting point, such shapes disappear within a few hours to a day. Changes in the shape or texture of snow crystals are examples of metamorphism, which in geologic terms defines changes that result from the effects of temperature and pressure. As the crystal shapes simplify, they
F1
Plate
F6
Capped column
F2
Stellar crystal
F7
Irregular crystal
F3
Column
F8
Graupel
F4
Needle
F9
Ice pellet
F5
Spacial dentrite
F0
Hail
FIGURE 2-1 International classification of solid precipitation. (From the International Association of Scientific Hydrology, with permission.)
KINETIC METAMORPHISM
Ice grain
Water vapor Ice grain
Low temperature
Heat flow High temperature
FIGURE 2-4 In the temperature-gradient process, ice sublimates from the top of one grain, moves upward as water vapor, and then is deposited on the bottom surface of the grain above. If conditions allow this process to continue long enough, all of the original grains are lost as the recrystallization produces a layer of new crystals.
CHAPTER 2 AVALANCHES
can pack more closely together, thereby enhancing further settlement and strength (Figure 2-2, online). New snow metamorphic changes generally occur within hours to a few days. However, the structure of a seasonal snow cover changes over a period of weeks to months via other processes. Settlement, which may initially have been rapid, continues at a much slower rate. Other factors begin to exert dominant influences on metamorphism throughout the snowpack. These factors include the difference in temperature measured upward or downward in the snow layer, which is called the temperature gradient. Averaged diurnally, snow temperatures are generally coldest near the surface and warmest near the ground at the base of the snow cover, which creates a temperature gradient across a snow layer that is sandwiched between cold winter air and the relatively warm ground (Figure 2-3, online). The effect of temperature gradients is an ongoing dynamic process that can cross ice, large empty spaces filled with air, and dense snow. Warm air contains more water vapor than does cold air; this holds true for air that is trapped within the snow cover. The greater the amount of water vapor, the greater the pressure; therefore both a pressure gradient and temperature gradient exist through the snow cover. When a pressure difference exists, the difference naturally tends to equalize, just as adjacent high and low atmospheric pressure centers cause the movement of air masses. Pressure differences within snow cause vapor to move upward through the snow layers. The air within the layers of the snow cover (i.e., in the pore spaces between grains) is saturated with water vapor, with a relative humidity of 100%. When air moves from a warmer to a colder layer, the amount of water vapor that can be supported in the pore spaces diminishes. Some vapor changes to ice and is deposited on the surrounding ice grains. We witness a similar process when warm, moist air in a heated room comes in contact with a cold windowpane. The invisible water vapor is cooled to its freezing point, and some of the vapor changes state and is deposited as frost on the window. Figure 2-4 shows how the texture of the snow layer changes during this temperature-gradient process. Water molecules sublimate from the upper surfaces of a grain. The vapor moves upward along the temperature (and vapor) gradient and is deposited as a solid ice molecule on the underside of a colder grain above. This process will continue as long as a strong temperature gradient exists. If the gradient continues long enough, all grains in the snow layer are transformed from solid to vapor and back to solid again; in other words, they recrystallize. The new crystals are completely different in texture and shape from their initial form. They become loose, coarse crystals with faceting, straight sides, and sharp angles (also known as faceted crystals or sugar snow), and they may eventually evolve into a large, striated, hollow-cup form. Examples of these crystals are shown in Figure 2-5. This process is called temperature-gradient metamorphism
A
B FIGURE 2-5 A, Mature depth-hoar grains. Facets and angles are visible. Grain size, 3 to 5 mm (0.12 to 0.20 inch). B, Advanced temperature-gradient grains attain a hollow cup-shaped form. Size, 4 mm (0.16 inch). (Courtesy Doug Driskell.)
or kinetic metamorphism. Well-developed crystals that typically form at the basal layer of the snow cover are commonly known as depth hoar. Depth hoar and faceted crystals are of particular importance to avalanche formation, because these crystals are very weak, with little or no cohesion (bonding) at the grain contacts. They can form the weak layer that fails under a slab and causes an avalanche.
KINETIC METAMORPHISM In the presence of a strong temperature gradient (e.g., ≥1° C [1.8° F] per 10 cm [3.9 inches]), kinetic metamorphism can occur anywhere within a snowpack. Typically, temperature gradients are described as extending upward from the warm ground toward the colder snow surface; however, very strong temperature gradients on the order of 2° C (1.8° F) per centimeter or more (20° C [18° F] per 10 cm [3.9 inches]) can extend for a couple of centimeters from a warm melt-freeze crust into colder snow. Strong temperature gradients can exist in the upper 10 to 30 cm (3.9 to 11.8 inches) of the snowpack, which is often related to the effects of alternating incoming solar radiation (short-wave radiation) and outgoing radiational cooling (longwave radiation) resulting in near-surface facets. These coarse and poorly bonded loose crystals, which are typically 1 to 3 mm (0.04 to 0.12 inch) in size, have straight sides and sharp angles. Backcountry skiers often describe this snow as “recycled powder,” because it often forms on colder and northerly facing slopes with prolonged periods of cold and clear conditions. A temperature gradient forms because radiational cooling (which occurs often— but not exclusively—on clear nights) causes the surface snow to become very cold relative to the snow 10 to 30 cm (3.9 to 11.8 inches) below the surface, which changes more slowly and which may still be under the effects of daytime warming. In the colder temperatures of continental snow climates, strong temperature gradients often exist just above the warm ground and can persist for months when the snow cover remains shallow (typically <1 m [3.3 feet] deep). The persistent gradient and warm basal snow layer temperature can cause very large 35
PART 1 MOUNTAIN MEDICINE
and complex faceted grains to form as well-developed depth hoar. These large, cup-shaped crystals, which are typically 4 to 10 mm [0.16 to 0.39 inch] in size, are characterized by straight sides, sharp angles, and multiple layers of faceted faces. The grains can be described as looking like etched crystal glass, and their organized striations can make them sparkle. The strong temperature gradients that drive kinetic metamorphism are aided by low-density new snow, because the larger pore spaces allow for the easier migration of water vapor. Typical faceted crystals or grains, which were previously referred to as temperature-gradient snow, are commonly called squares. Depth hoar is reserved for well-developed, cup-shaped, and large faceted crystals. Any faceted layer in the snow cover can lead to a persistent weak layer, especially layers of larger grains, which are slower and more resistant to change or to gaining strength.
EQUILIBRIUM METAMORPHISM In the absence of a strong temperature gradient, a totally different type of snow texture develops. When the gradient is less than about 1° C (1.8° F) per 10 cm (3.9 inches), there are still vapor pressure differences, but upward movement of vapor through the snow layers occurs at a much slower rate. As a result, water vapor that is deposited on a colder grain tends to cover the total grain in a more homogeneous manner rather than showing the preferential deposition that is characteristic of faceted crystals. This process produces a grain with a smooth surface of a more rounded or oblong shape. Over time, vapor is deposited at the grain contacts (concavities) as well as over the remaining surface of the grain (convexities). Connecting bonds that are formed at the grain contacts give the snow layer strength over time (Figure 2-6, online). Bond growth, which is called sintering, yields a cohesive texture, which is in contrast to the cohesionless texture of depth hoar and other forms of faceted crystals. This type of grain has been referred to by various terms: equilibrium snow, equitemperature snow, equilibrium metamorphism, or simply rounds. These grains can generally be described as fine and well-sintered (bonded) snow. Such bonded and interconnected grains are shown in Figure 2-7. Weak temperature gradients and high-density new snow force water vapor molecules to form bonds and thus drives equilibrium metamorphism. The preceding paragraphs described the big picture in terms of what happens to snow layers after they have been buried by subsequent snowfalls. If the temperature layer is below freezing and no melting is taking place, one of the two processes described previously is occurring, or perhaps a transition exists between the two. Within the total snow cover, these metamorphic processes may occur simultaneously, but only one can take place within a given layer at a given time, depending upon the strength or weakness of the temperature gradient. Both processes accelerate with warmer snow temperature, because more water vapor is involved.
FIGURE 2-7 Bonded or sintered grains that result from equitem perature metamorphism. Grain size, 0.5 to 1 mm (0.02 to 0.04 inch). (Courtesy Doug Driskell.)
36
FIGURE 2-8 Loose snow or point-release avalanche. (Courtesy U.S. Department of Agriculture Forest Service.)
AVALANCHE TYPES There are two basic types of avalanche release. The first is a point-release avalanche or a loose snow avalanche (Figure 2-8). A loose snow avalanche involves cohesionless snow; it is initiated at a point, and it spreads out laterally as it moves down the slope to form a characteristic inverted “V” shape. A single grain or a clump of grains slips out of place and dislodges those below on the slope, which in turn dislodge others. The avalanche continues as long as the snow is cohesionless and the slope is steep enough. In dry snow, this type of avalanche usually involves only small amounts of near-surface snow. However, in wet snow, which is caused by warm air temperatures or rain, these avalanches can be very large and destructive. The second type of avalanche, the slab avalanche, requires a cohesive layer of stronger snow over a layer of weaker snow. The cohesive blanket of snow breaks away simultaneously over a broad area (Figure 2-9). A slab release can involve a range of snow thicknesses, from the near-surface layers to the entire snow cover down to the ground. Slab avalanches can occur in dry or wet snow. In contrast with a loose snow avalanche, a slab avalanche has the potential to involve very large amounts of snow. Because dry slab avalanches are responsible for 95% of U.S. fatal accidents, these avalanches receive the interest of researchers.4 The majority of the information in this chapter deals with
MECHANICAL PROPERTIES: HOW SNOW DEFORMS ON A SLOPE Almost all physical properties of snow can be easily seen or measured in the field. A snow pit provides a wealth of information about these properties, layer by layer, throughout the thickness of the snow cover; however even detailed knowledge of these properties does not provide all of the information that is necessary to evaluate avalanche potential. The current mechanical state of the snow cover must be considered. Unfortunately, for the average person, these properties are virtually impossible to directly measure. Mechanical deformation occurs within the snow cover just before its failure and the start of a slab avalanche. Snow cover has a tendency to settle simply from its own weight. When this occurs on level ground, the settlement is perpendicular to the ground, and the snow layer increases in density and gains in strength. The situation is not so simple when snow rests on a slope. The force of gravity is divided into two components: one that tends to cause the snow layer to shrink in thickness and a new component that acts parallel to the slope, which tends to pull the snow down the slope. Down-slope movement within the snow cover occurs at all times, even on gentle slopes. The speed of movement is slow, generally on the order of a few millimeters per day, but it can be up to millimeters per hour within new snow on steep slopes or with warming temperatures. The evidence of these forces is often clearly visible in the bending of trees and damage to structures built on snow-covered slopes. Although the movement is slow, when deep snow pushes against a rigid structure, the forces are significant, and even large buildings can be pushed off of their foundations. Snow deforms in a highly variable fashion, and is described as a viscoelastic material. Sometimes it deforms as if it were a liquid (viscous), and at other times it responds more like a solid (elastic). Viscous deformation implies continuous and irreversible flow. Elastic deformation implies that, after the force that is causing the deformation is removed, some part of the initial deformation is recovered. The elasticity of snow is not so obvious, primarily because the amount of rebound is very small as compared with those of more familiar materials.
FIGURE 2-9 Slab avalanche. (From the U.S. Department of Agriculture Forest Service; Williams K, Armstrong B: The snowy torrents, Jackson, Wyo, 1984, Teton Bookshop, with permission. Top courtesy Alexis Kelner.)
dry slab avalanches or dry loose snow avalanches. Because wet snow avalanches have received little research, relatively little is known about the processes that cause these avalanches. Recent research reaffirms the challenges to “observe, measure, and quantify the characteristics leading to wet snow avalanches.”32
SLAB AVALANCHE FORMATION To understand the conditions of snow cover that contribute to dry slab avalanche formation, it is essential to reemphasize that snow cover develops layer by layer. The layered structure is directly tied to the two ingredients that are essential to the formation of slab avalanches: the cohesive layer of snow and the weak layer beneath. If the snow cover is homogeneous from the ground to the surface, slab avalanche danger is low, regardless
Moderate to heavily rimed crystals
SLAB
a We
SLAB
SLAB
tr
bs
u ks
ate
Lightly rimed crystals
Warm, dense
Deposited by strong winds
a We
te
tra
bs
u ks
Cold, light
Deposited by light winds
st
ub
s ak
e rat
We
FIGURE 2-10 Snow-layer combinations that often contribute to avalanche formation.
37
CHAPTER 2 AVALANCHES
of the snow type. If the entire snow cover is sintered, dense, and strong, stability is very high. Even if the entire snow cover is composed of depth hoar, there is still no hazard from slab avalanches, because the cohesionless character precludes formation of a slab, which is one of the essential ingredients. Loose snow avalanches may still occur in this situation on steep slopes. The combination of a basal layer of depth hoar with a cohesive layer above provides the ingredients for slab avalanche danger. For successful evaluation of slab avalanche potential, information is needed about the entire snowpack and not just its surface. A hard wind slab at the surface may intuitively appear strong and safe. However, when it rests on a weaker layer that may be well below the surface, it may fail under the weight of a skier and be released as a slab avalanche. Many snow structure combinations can contribute to slab avalanche formation, but the prerequisite conditions are a cohesive layer over a weak layer sitting on a bed surface. Figure 2-10 describes other combinations that result in brittle or cohesive layers of snow on a weak layer.
PART 1 MOUNTAIN MEDICINE
Force
Snow
Viscous deformation
Elastic fracture FIGURE 2-11 Depending on prevailing conditions, snow may deform and stretch in a viscous or flowing manner, or it may respond more like a solid and thus fracture.
With regard to avalanche formation, it is important to know when snow acts primarily as an elastic material and when it responds more like a viscous substance. These conditions are shown in Figure 2-11. Laboratory experiments have shown that conditions of warm temperatures and the slow application of force favor viscous deformation. One sees examples of this as snow slowly deforms and bends over the edge of a roof or sags from a tree branch. In such cases, the snow deforms but does not crack or break. By contrast, when temperatures are very cold or when force is applied rapidly, snow reacts like an elastic material. If enough force is applied, it fractures. We think of such a substance as brittle; release of stored elastic energy causes fractures to move through the material. In the case of snow cover on a steep slope, forces associated with accumulating snow or the weight of a skier may increase until the snow fails. At that point, stored elastic energy is released and is made available to drive brittle fractures over great distances through the snow slab. The slab avalanche provides the best example of elastic deformation in snow cover. Although the deformation cannot actually be seen, evidence of the resultant brittle failure is clearly present in the form of the sharp, linear fracture line and crown face of the slab release (Figure 2-12). The crown face is almost always perpendicular to the bed surface, which is evidence that snow has failed in a brittle manner. To fully understand the slab avalanche condition or the stability of the snow cover, its mechanical state must be considered. Snow is always deforming in a down-slope fashion, but, throughout most of the winter, the strength of the snow is sufficient to prevent an avalanche. The snow cover is layered, and some layers are weaker than others. During periods of snowfall, blowing snow, or both, an additional load or weight is being applied to the snow in the starting zone, the snow is creeping
FIGURE 2-12 The consistent 90-degree angle between the crown face and the bed surface of the avalanche shows that slab avalanches result from an elastic fracture. (Courtesy A. Judson.)
38
faster, and these new stresses are beginning to approach the strength of the weakest layers. The weakest layer has a weakest point somewhere within its continuous structure. If the stresses caused by the load of the new snow or the weight of a skier reach the level at which they equal the strength of the weakest point, the snow fails completely at that point (Figure 2-13); this means that the strength at that point immediately goes to zero. This is analogous to what would happen if someone on a tugof-war team were to let go of the rope. If the remainder of the team was strong enough to make up for the lost member, not much would change immediately. The same situation exists with snow cover. If the surrounding snow has sufficient strength to make up for the fact that the strength at the weakest point has now gone to zero, nothing happens beyond perhaps a localized movement or collapse in the snow, which is often heard as a “whumpf” sound. If the surrounding snow is not capable of compensating, the area of snow next to the initial weak point fails, then at the next, and so forth, until a propagating chain reaction begins. As the initial crack forms in the now unstable snow, the elastic energy is released, which in turn drives the crack further and releases more elastic energy. The ability of snow to store elastic energy is essentially what allows large slab avalanches to occur. As long as the snow properties are similar across the avalanche starting zone, the crack will continue to propagate, thereby allowing entire basins that are many acres in area to be set in motion within a few seconds.
Avalanche Dynamics The topic of avalanche dynamics includes how avalanches move, how fast they move, and how far and with how much destructive power they travel. The science of avalanche dynamics is not well advanced, although much has been learned during the past few decades. Measured data for avalanche velocity and impact pressure are still lacking. Although any environmental measurement presents its own set of problems, it is clear that opportunities for making measurements inside a moving avalanche are extremely limited. Although avalanche paths exist in a variety of sizes and shapes, they all have three distinct parts with respect to dynamics (Figure 2-14). In the starting zone, which is usually the steepest part of the path, the avalanche breaks away, accelerates down the slope, and picks up additional snow. From the starting zone, the avalanche proceeds to the track, where it remains essentially constant and picks up little or no additional snow as it moves; the average slope angle becomes less steep, and frequently the snow cover is more stable than in the starting zone; however a significant amount of snow can be entrained into the avalanche from the track.40 Small avalanches often stop in the track. Larger avalanches travel down the track and into the runout zone, where the avalanche motion ends. Most avalanches stop quickly, within seconds, although very large avalanches tend to slowly decelerate across a gradual slope, such as an alluvial fan. As a general rule, the slope angle of starting zones is 30 to 45 degrees, the track is 20 to 30 degrees, and the runout zone is less than 20 degrees. Avalanches may appear to be turbulent rivers of snow with fluid-like characteristics; however avalanches are granular flows that move much more like a sliding block than water. Few actual measurements of avalanche velocities have been made, but enough data have been obtained to provide some typical values for the various avalanche types. For the highly turbulent dry powder avalanches, the velocities are commonly in the range of 34 to 45 m/s (75 to 100 mph), with rare examples in the range of 67 to 89 m/s (150 to 200 mph). Such speeds are possible for powder avalanches because large amounts of air in the moving snow greatly reduce the forces that result from internal friction. As the snow in the starting zone becomes dense, the terrain becomes less steep and movement becomes more flow-like, with typical velocities slowing to the range of 22 to 34 m/s (50 to 75 mph). During spring conditions, when the snow contains large amounts of liquid water, speeds may reach only about 11 m/s (25 mph). In most cases, the avalanche simply follows a path down the steepest route on the slope while being guided or channeled by
CHAPTER 2 AVALANCHES
A
B
C
FIGURE 2-13 Slab avalanche released by a skier. A skier is descending a slope (A) and causes the release of a slab of avalanche (B), but is able to ski off to the side to escape (C). (Courtesy R. Ludwig.)
terrain features. However the higher-speed avalanche may deviate from this path. Terrain features (e.g., the sidewalls of a gully) that would normally direct the flow of the avalanche around a bend may be overridden by a high-velocity powder avalanche (Figure 2-15). The slower-moving avalanches, which travel near the ground, tend to follow terrain features, thereby giving them somewhat predictable courses. Because avalanches can travel at very high speeds, the resultant impact pressures can be significant. Smaller and medium-size
events with impact pressures of 1 to 15 kilopascals have the potential to heavily damage wood-frame structures. Extremely large avalanches with impact pressures of more than 150 kilopascals possess the force to uproot mature forests and even to destroy structures that are made of concrete. Some reports of avalanche damage describe circumstances that cannot be easily explained simply by the impact of large amounts of fast-moving dense snow. Some observers have noted that as an avalanche passed, some buildings seemingly exploded, 39
PART 1 MOUNTAIN MEDICINE
of snow crystals can increase the air density by a factor of three or more. A powder cloud that is traveling at a moderate dry avalanche speed of 27 m/s (60 mph) could have the impact force of a 80-m/s (180-mph) wind, which is well beyond the destructive capacity of a hurricane.
Identifying Avalanche Terrain Starting zone
The essential ingredients of an avalanche—snow and a steepenough slope—are such that any mountain or even a small hillside can produce an avalanche if conditions are exactly right. To be a consistent producer of avalanches, a mountain and its weather must work in harmony. Track
SLOPE ANGLE
Runout zone
FIGURE 2-14 The three parts of an avalanche path: the starting zone, the track, and the runout zone. (Courtesy B. Armstrong.)
perhaps from some form of vacuum created by the fast-moving snow. Other reports have indicated that a structure was destroyed by the “air blast” preceding the avalanche, because there was no evidence of large amounts of avalanche debris in the area. This damage more likely resulted from the powder cloud, which may be composed of only a few inches of settled snow, yet which contributes significantly to the total impact force. The presence
Avalanches occur with greatest frequency on slopes of 30 to 45 degrees. These are the angles at which the balance between strength (i.e., the bonding of the snow trying to hold it in place) and stress (i.e., the force of gravity trying to pull it loose) is most critical. The easiest way to create high stress is to increase the slope angle; gravity works that much harder to stretch the snow out and to rip it from its underpinnings. A slope of 45 degrees produces many more avalanches than a slope of 30 degrees. On even steeper slopes (i.e., >45 degrees), the force of gravity wins; snow generally rolls or sloughs off, thus preventing the buildup of deep snowpacks. Exceptions exist, especially in maritime snow climates or when strong winds plaster damp snow onto steep slopes. Dry snow avalanches have occurred on slopes of 22 to 25 degrees, which is the angle of repose for granular round substances like sand; however these are rare, because snow grains are seldom round and seldom touch without forming bonds. Although an avalanche release requires a steep slope, it is possible to trigger an avalanche from shallow and even flat slopes at the bottom of steep slopes. A collapse in a persistent weak layer in these areas could send fractures upslope, thus releasing the avalanche. This is analogous to pulling a log out from the bottom of a wood pile. When snow is thoroughly saturated with water, a slush mixture is formed, and an avalanche can release on low-angle terrain. For example, a wet snow avalanche in Japan occurred on a beginner slope at a ski area. The slope was only 10 degrees, but the avalanche was large enough to kill seven skiers. This extreme situation applies only to a water-saturated snowpack, which behaves more like a liquid than a solid.
ORIENTATION
FIGURE 2-15 The large powder cloud associated with a fast-moving dry snow avalanche. (Courtesy R. Armstrong.)
40
Avalanches occur on slopes facing every point of the compass. Steep slopes are equally likely to face east, west, north, or south. In the northern hemisphere, certain factors cause more avalanches to occur on slopes that are facing north, northeast, and east than on those facing south through west; these relate to slope orientation with respect to sun and wind. In the southern hemisphere, more avalanches occur on east, southeast, and south-facing slopes. The sun angle in northern hemisphere winters causes south slopes to get much more sunshine and heating than do north slopes, which frequently leads to radically different snow covers. North slopes have deeper and colder snow covers, often with a substantial layer of depth hoar near the ground. South slopes usually carry a shallower and warmer snow cover that is laced with multiple ice layers that are formed on warm days between storms. Most ski areas are built on predominantly north-facing slopes to take advantage of deeper and longer-lasting snow cover. At high latitudes (e.g., in Alaska), the winter sun is so low on the horizon and the heat input to south slopes is so small that there are few differences in the snow covers of north and south slopes. The effect of the prevailing west wind at mid latitudes is important. Storms most often move west to east, and storm winds are most frequently from the western quadrant (i.e., southwest, west, or northwest). Storm winds pick up fallen snow and redeposit it on slopes that are facing away from the wind (i.e., northeast, east, and southeast slopes). These are the slopes that are most often overburdened with wind-drifted snow. The net
AVALANCHE TERRAIN PATHS The frequency with which a path produces avalanches depends on a number of factors, with slope steepness being a major one. The easiest way to create high stress is to increase the slope angle; gravity works that much harder to stretch out the snow and to rip it from its underpinnings. A slope of 45 degrees produces many more avalanches than does one of 30 degrees, however, specific terrain features are also important. Broad slopes that are curved into a bowl shape and narrow slopes that are confined to a gully efficiently collect snow. Those that have a curved horizontal profile, such as a bowl or gully, trap blowing snow that is coming from several directions; the snow drifts over the top and settles as a deep pillow. Alternatively, the plane-surfaced slope collects snow efficiently only if it is being blown directly from behind. A side wind scours the slope more than it loads the slope. The surface conditions of a starting zone often dictate the size and type of avalanche. A particularly rough ground surface (e.g., a boulder field) does not usually produce avalanches early in the winter, because it takes considerable snowfall to cover the ground anchors. After most of the rocks are covered, avalanches pull out in sections, with the area between two exposed rocks running one time and the area between another two other rocks running another. A smooth rock face or a grassy slope provides a surface that is usually too slick for snow to grip; therefore fulldepth avalanches are distinctly possible. If the avalanche does not run during the winter, it is likely to run to ground in the spring after melt water percolates through the snow and lubricates the ground surface.
VEGETATION Vegetation has a mixed effect on avalanche releases. Bushes provide anchoring support until they become totally covered; at that point, they may provide weak points in the snow cover, because air circulates around the bush and provides an ideal habitat for the growth of depth hoar. It is common to see that the fracture line of an avalanche has run from a rock to a tree to a bush, because these are all places of healthy depth hoar growth. A dense stand of trees can easily provide enough anchors to prevent avalanches. The reforestation of slopes that are devoid of trees as a result of logging, fire, or avalanche is an effective means of avalanche control. Scattered trees on a gladed slope offer little if any support to hold snow in place. Isolated trees may do more harm than good by providing concentrated weak points on the slope.
Factors That Contribute to Avalanche Formation The factors that contribute to avalanche release are terrain, weather, and snowpack. Terrain factors are fixed, but the states of the weather and of the snowpack change daily or even hourly. Precipitation, wind, temperature, snow depth, snow surface, weak layers, and settlement are all factors that determine whether an avalanche will occur.
SNOWFALL New snowfall is the event that leads to most avalanches. More than 80% of all avalanches run during or just after a storm. Fresh snowfall adds weight to existing snow cover. If the snow cover is not strong enough to absorb this extra weight, avalanche releases occur. The size of the avalanche is usually related to the amount of new snow. Snowfalls of less than 15 cm (6 inches) seldom produce avalanches. Snows of 15 to 30 cm (6 to 12 inches) usually produce a few small slides, and some of these harm skiers who release them. Snows of 30 to 60 cm (1 to 2 feet) produce avalanches of larger size that present considerable
threats to skiers and that pose closure problems for highways and railways. Snows of 60 to 120 cm (2 to 4 feet) are much more dangerous, and snowfalls of more than 120 cm (4 feet) produce major avalanches that are capable of large-scale destruction. These predictions are guidelines that are based on data and experience and must be considered with other factors to arrive at the true hazard. For example, a snowfall of 10 inches (25 cm) whipped by strong winds may be serious; a fall of 60 cm (2 feet) of feather-light snow in the absence of wind may produce no avalanches.
SNOWFALL INTENSITY The rate at which snowfall accumulates is almost as important as the amount of snow. A snowfall of 90 cm (3 feet) in one day is far more hazardous than the same amount of snow falling over the course of 3 days. As a viscoelastic material, snow can absorb slow loading by deforming or compressing. Under a rapid load, the snow cannot deform quickly enough and is more likely to crack, which is how slab avalanches begin. A snowfall rate of 2.5 cm (1 inch) or more per hour that is sustained for 10 hours or more is generally a red flag with regard to avalanche danger; the danger worsens if the snowfall is accompanied by wind.
RAIN The age of the surface snow is an important factor with regard to changes in stability when rain falls. Within hours of light rain falling on fresh or recent snow (i.e., from within several days), avalanching can occur for reasons that are not well understood. The rain somehow causes a loss of strength in the new snow. Significant rain (usually about 2.5 cm [1 inch]) falling on an old snow surface (i.e., several days old or older) produces few or no avalanches. Despite the apparent addition of weight caused by rain (2.5 cm [1 inch] of rain is the equivalent in weight to 25 to 30 cm [10 to 12 inches] of snow), the rain tends to drain down through the older snow grains and invariably freezes into an ice crust, which adds strength to the snow cover. At a later time, the smooth crust could become a sliding layer beneath new snowfall. Heavy rain (usually >2.5 cm [1 inch]) greatly weakens the snow cover. It adds weight to the snowpack, but it adds no internal strength of its own (in the form of a skeleton of ice, as new snow would create); it dissolves bonds between snow grains as it percolates through the top snow layers, thus reducing strength even further.
NEW SNOW DENSITY AND CRYSTAL TYPE A layer of fresh snow contains only a small amount of solid material (ice); the majority of the volume is occupied by air. It is convenient to refer to snow density as a percentage of the volume occupied by ice. New snow densities usually range from 7% to 12%, depending on the snow climate. In the high elevations of Colorado, 7% is an average value; in the more maritime climates of the Sierras and the Cascades, 12% is a typical value. Density becomes an important factor in avalanche formation when it varies from average values. Avalanche danger increases when heavier, more-dense snow falls on lighter, less-dense snow, which can occur from storm to storm or even within a single storm (sometimes called an upside-down storm). Wet snowfalls or falls of heavily rimed crystals (e.g., graupel) may have densities of 20% or more. Graupel is a type of snowflake that has been transformed into a pellet of soft ice because of riming inside a cloud. A layer of heavier-than-normal snow presents a danger because of excess weight. Snowfall that is much lighter than normal (e.g., 2% to 4%) can also present a dangerous situation. If the low-density layer quickly becomes buried by snowfall of normal or high density, a weak layer has been introduced into the snowpack. By virtue of low density, the weak layer has a marginal ability to withstand the weight of layers above, thereby making it susceptible to collapse. Storms that begin with low temperatures but then warm up produce an unstable layer of weak, light snow beneath a stronger, heavier layer, thereby acting as a slab and thus as one of the necessary ingredients for an avalanche. 41
CHAPTER 2 AVALANCHES
effect of sun and wind is to cause more avalanches on northfacing through east-facing slopes.
PART 1 MOUNTAIN MEDICINE
Density is closely linked to crystal type. Snowfalls that consist of graupel, fine needles, and columns can accumulate at high densities. Snowfalls of plates, stellars, and dendritic forms account for most of the lower densities.
WIND SPEED AND DIRECTION Wind can transport snow into avalanche starting zones at rates that are much greater than can snow falling from clouds. Wind drives fallen snow into drifts and cornices from which avalanches begin. Winds pick up snow from exposed windward slopes and drive it onto adjacent leeward slopes, where it is deposited into sheltered hollows and gullies; this can quickly turn a 1-foot snowfall into a 3-foot drift in a starting zone. The rate at which blowing snow collects in bowls and gullies can be impressive. In one test at Berthoud Pass, Colorado, the wind deposited snow in a gully at a rate of 45 cm (18 inches) per hour. A speed of 7 m/s (15 mph) is sufficient to pick up freshly fallen snow. Higher speeds are required to dislodge older snow. Speeds of 9 to 22 m/s (20 to 50 mph) are the most efficient for transporting snow into avalanche starting zones. Speeds of more than 22 m/s (50 mph) can create spectacular banners of snow streaming from high peaks, but much of this snow is lost to sublimation in the air or is deposited far down the slope away from the avalanche starting zone. Winds also increase the avalanche potential, because blowing snow is denser after deposition than before transport. This is because snow grains are subjected to harsh treatment in their travels; each collision with another grain knocks off arms and rounds sharp angles, thereby reducing the grain’s size and allowing the pieces to settle and pack together into a denser layer. The net result of wind is to fill avalanche starting zones with additional, heavier, and more cohesive snow than if the wind had not blown.
TEMPERATURE The role of temperature in snow metamorphism occurs over a period of days, weeks, and even months. The influence of temperature on the mechanical state of the snow cover is more acute, with changes occurring in minutes to hours. The actual effect of temperature is not always easy to interpret; whereas an increase in temperature may contribute to the stabilization of the snow cover in one situation, it might at another time lead to avalanche activity. In several situations, an increase in temperature clearly produces an increase in avalanche potential. In general, these conditions include a rise in temperature during a storm or immediately after a storm or a prolonged period of warm, fair weather such as occurs with spring conditions. In the first example, the temperature at the beginning of a snowfall may be well below freezing, but, as the storm progresses, the temperature increases. As a result, the initial layers of new snow are light, fluffy, low density, and relatively low in strength, whereas the later layers are warmer, denser, and stiffer. Thus, the essential ingredient for a slab avalanche is provided within the new snow layers of the storm: a cohesive slab resting on a weak layer. If the temperature continues to rise, the falling snow turns to rain; this situation is not uncommon in lower-elevation coastal mountain ranges. When this happens, avalanches are almost certain; as the rain falls, additional weight is added to the avalanche slope, but no additional strength is provided as it is whenever a new layer of snow accumulates. The second example may occur after an overnight snowstorm that does not produce an avalanche on the slope of interest. By morning, the precipitation stops, and clear skies allow the morning sun to shine directly on the slopes. The sun rapidly warms the cold, low-density, new snow, which begins to deform and creep down slope. The new snow layer settles, becomes denser, and gains strength. At the same time, it is stretched downhill, and some of the bonds between the grains are pulled apart; thus the snow layer becomes weaker. If more bonds are broken by stretching than are formed by settlement, there is not enough strength to hold the snow on the slope, and an avalanche occurs. 42
In these first two examples, the complete snow cover generally remains at temperatures that are below freezing. A third example occurs when a substantial amount of the winter’s snow cover is warmed to the melting point. During winter, sun angles are low, days are short, and air temperatures are cold enough that the small amount of heat gained by the snow cover during the day is lost during the long cold night. As spring approaches, this pattern changes, and eventually enough heat is available at the snow surface during the day to cause some melt. This melt layer refreezes again that night, but the next day more heat may be available, so eventually a substantial amount of melting occurs and melt water begins to move down through the snow cover. As melt water percolates slowly downward, it melts the bonds that attach the snow grains, and the strength of the layers decreases. At first the near-surface layers are affected, with the midday melt reaching only as far as the uppermost few inches and with little or no increase in avalanche hazard. If warm weather continues, the melt layer becomes thicker, and the potential for wet snow avalanches increases. The conditions that are most favorable for wet slab avalanches occur when the snow structure provides the necessary layering. When melt water encounters an ice layer or an impermeable crust—or, in some cases, a layer of weak depth hoar—wet slab avalanches are likely to occur.
DEPTH OF SNOW COVER Of the snowpack factors that contribute to avalanche formation, the depth of the snow cover is the most basic. When the early winter snowpack covers natural anchors (e.g., rocks, bushes), the start of the avalanche season is at hand. However a word of caution is necessary for backcountry travelers in the weak, depth-hoar–prone, continental snow climate. The early winter avalanche danger starts not when the natural anchors are covered but when the snow fills in the spaces between the obvious anchors. North-facing slopes are usually covered before other slopes. A scan of the terrain usually suffices to discern this clue, but another method can be used to determine the time of the first significant avalanches. Long-term studies show a relationship between snow depth at a study site and avalanche activity. For example, along Red Mountain Pass, Colorado, it is unlikely that an avalanche large enough to reach the highway will run until close to 90 cm (3 feet) of snow covers the ground at the University of Colorado’s snow study site. At Alta, Utah, when 130 cm (52 inches) of snowpack has built up, the first avalanche to cover the road leading from Salt Lake City can be expected.
WEAK LAYERS Any layer that is susceptible to failure and fracture as a result of the overburden of additional weight is a weak link. Of the snowpack contributory factors, this is the most important, because a weak layer is essential to every avalanche. Fracture in the weak layer propagates along what is called the failure plane, sliding surface, or bed surface. The most troubling layers are called persistent weak layers, which are usually made of snow crystals and include larger faceted snow, depth hoar, and surface hoar. These crystals are slow to change shape and gain strength, so they may persist for days, weeks, months, or even all season. One common weak layer is an old snow surface that offers a poor bond for new snow. Another weak layer that forms on the snow surface is hoar frost or surface hoar (see Physical Properties, earlier). On clear and calm nights, this hoar forms a layer of feathery, sparkling flakes that grow on the snow surface. The layer can be a major contributor to avalanche formation when it is buried by snowfall as a result of its frequent persistence in the snowpack. Many avalanches have been known to release from a buried layer of surface hoar, and sometimes this layer is more than 1 month old and 180 cm (6 feet) or more below the surface. A weak layer that is almost always found deep within the snowpacks that blanket the Colorado Rocky Mountains (continental snowpack) is large temperature-gradient snow (facets) or depth hoar. One way to decide whether a temperature-gradient layer is near its collapse point is to test the strength of the
Safe Travel in Avalanche Terrain The first major decision that is often faced in backcountry situations is whether to avoid or confront a potential avalanche hazard. A group that is touring with no particular goal in mind will probably not challenge avalanches. For this group, education to recognize and avoid avalanche terrain is sufficient. At the other extreme, mountaineering expeditions that have specific goals and that are willing to wait out dangerous periods or take severe risks to accomplish their objective need considerably more information. Traveling safely in avalanche terrain requires special preparations, including education and the carrying of safety and rescue equipment. The group should have the skills required to anticipate and react to an avalanche.
IDENTIFYING AVALANCHE TERRAIN Because most avalanches release on slopes of 30 to 45 degrees, judging angle is a prime skill for the recognition of potential avalanche areas. An inclinometer can be used to measure slope angles. Some compasses are also equipped for this purpose; a second needle and a graduated scale in degrees can be used to measure slope angles. A ski pole may be used to judge approximate slope angle. When dangled by its strap, the pole becomes a plumb line from which the slope angle can be “eyeballed.” Evidence of fresh avalanche activity (i.e., the presence of fracture lines and the rubble of avalanche snow on the slope or at the bottom) identifies avalanche slopes. Other clues are swaths of missing trees or trees that are bent downhill or damaged, especially with the uphill branches removed. Above the tree line, steep bowls and gullies are almost always capable of producing avalanches.
ROUTE FINDING Good route-finding techniques are necessary for safe travel in avalanche terrain (Figure 2-16). Route finding in avalanche country should not only avoid avalanches but should also be efficient and take into account the abilities and desires of the group to choose a route that is not overly technical, tiresome, or
time consuming. The safest way to avoid avalanches is to travel above or below and at a distance from them. When taking a route above avalanche terrain, the traveler should choose a ridgeline that is above the avalanche starting zones. It is safest to travel the windward side of the ridge. The snow cover is usually thinner and wind packed, with rocks sticking through; this does not make for the most pleasant skiing, but it is safe. Cornice collapses present a very real hazard; they should be avoided by staying on the roughened snow toward the windward side. When ascending a potential avalanche path, a safe route (e.g., a dense forested area that is well anchored, a low-angle approach) should be selected. Skiers who are taking a route in the valley below avalanche terrain should not linger in the runouts of avalanche paths. Although it is unlikely that a skier who is traveling along the valley could trigger an avalanche high up on the slope, it is possible to trigger an avalanche from below if one is traveling close to the compression zone, thereby initiating a fracture that propagates upward. Slopes of 30 degrees or more should be approached with caution. By climbing, descending, and traversing only in gentle terrain, avalanche risk can be avoided.
CROSSING AVALANCHE SLOPES Travel through avalanche country always involves risk, but certain travel techniques can minimize that risk. Proper travel techniques might not prevent an avalanche release but can improve the odds of survival. The timing of a trip has a lot to do with safety. Most avalanches occur during and just after storms. Waiting a full day after a storm has ended can allow the snowpack to react to the new snow load and to gain strength. Before crossing or venturing onto a potential avalanche slope, the skier, hiker, or snowmobiler should tighten up clothing; zip up zippers; and put on a hat, gloves, and goggles. Backpacks should be worn normally, because they may afford protection from back trauma and because the items necessary for survival after a rescue can be stored inside. If the use of a large mountaineering pack will cause a person to be top heavy and more likely to fall, another route should be considered. The skier should remove pole wrist straps and ski runaway straps, because poles and skis attached to the victim hinder extremity motions and only serve to drag the victim under. A person who is wearing a rescue beacon should always be certain that it is transmitting. When crossing potential avalanche slopes, it is always better to cross as high or as low as possible and to avoid the middle. All persons should traverse in the same track. This not only reduces the amount of work required but also disturbs less snow, which lowers the chance of avalanche release. Should the slope fracture when individuals are crossing high, most of the sliding snow will be below, and the chance of staying on the surface of the moving avalanche will be greater. Invariably the person who is highest on the slope runs the least risk of being buried. A person who must climb or descend an avalanche path should keep close to its sides. Should the slope fracture, escaping to the side improves the chance of survival. Only one person at a time should cross, climb, or descend an avalanche slope; all other members should watch from a safe location. Two commonsense principles lie behind this advice. First, only one group member is exposed to the hazard, thereby leaving the others available as rescuers. Second, less weight is put on the snow. Snowmobilers all too often fall prey to multivictim accidents, because an additional rider will drive up a steep slope to help a friend who is stuck near the starting zone. Skiers, snowboarders, climbers, and snowmobilers should never drop their guard on an avalanche slope. They should stop only at the edge of the slope or beneath a point of protection (e.g., a rock outcropping); they should not stop in the middle of a slope or in the runout zone. It is not uncommon for the second, third, or even tenth person traversing or traveling down a slope to trigger the avalanche. Trouble should always be anticipated, and an escape route (e.g., getting to the side, grabbing a tree) should be kept in mind. 43
CHAPTER 2 AVALANCHES
overlying layers and the support provided by specific stability testing performed near the edge of the slope. This is no easy task, and results may be unreliable as a result of the spatial variability of weaknesses on the slope. In addition, most fieldstability tests do not test for deep instabilities in the snowpack. Another method is to try jumping on your skis while standing on a shallow test slope of similar aspect. Collapse is a good indication that comparable snow cover on a steeper slope will produce an avalanche. Often skiers and climbers cause inadvertent collapses while skiing or walking on a depth-hoar– riddled snowpack. The resulting “whumpf” sound is a warning of weak snow below. In recent years, attention to the frequency of faceted snow layers near the surface of the snowpack and their relation to avalanches—particularly in the deeper snow cover of the transitional (intermountain) snow climate—have been well studied. Several mechanisms involved in the evolution of these layers may account for the majority of avalanches in this region, because significant depth hoar-related avalanches are less common. Graupel, which are pellet-like heavily rimed crystals, can act as ball bearings after they are buried in the snowpack; they can be responsible for the layer that is involved in avalanche initiation. Finally, a weak layer can be created within the snow cover when surface melting or rain causes water to percolate into the snow and then fan out on an impermeable layer, thereby lubricating that layer and destroying its shear strength. This phenomenon can be seen during the winter months in the maritime snow climate of the West Coast mountains. Combining the constellation of contributory factors on a dayby-day basis is the avalanche forecaster’s art. Every avalanche must have a weak layer on which to release, so knowledge of snow stratigraphy or layering and what level of applied load will cause a layer to fail form the essence of forecasting.
PART 1 MOUNTAIN MEDICINE
Poor route
Poor route
Good route
Good route
B
A
Gentle slopes d oo
te
rou
G
Poor route Poor route
Steep slopes
Good route
C
D
FIGURE 2-16 Four ski-touring areas showing the safer routes (green dashed lines) and the more hazardous routes (red dashed lines). Arrows indicate areas of wind loading. (From the U.S. Department of Agriculture Forest Service: Avalanche handbook, agricultural handbook 489, Washington DC, 1976, U.S. Government Printing Office, with permission. Courtesy Alexis Kelner.)
STABILITY EVALUATION TESTS People who are traveling on snow-covered slopes should perform hands-on tests of snow strength and instability. Testing the strength of snow helps with the location of weak layers, and checking for instability demonstrates how well the layers are adhering to one another. Several simple but meaningful tests can be performed without digging holes in the snow, although much more information can be learned by digging snow pits. A fast and simple test to find significant weak layers is to push a ski pole into the snow; this should be done handle-end first if the snow is dense. This helps the individual to feel the major layering of the snowpack. For example, the skier may feel the layer of new snow, and stronger or weaker layers in the middle of the pack can be appreciated by the ease of the push. 44
Hard-snow layers and ice lenses may resist penetration altogether, but these can sometimes be felt as resistance by pulling out the pole slowly along the side of the hole. This test reveals only the gross layers within the reach of the pole; thin weak layers, such as buried surface hoar or a poor bond between any two layers, cannot be detected. Thus, although the ski-pole test has limited value, it can provide useful information that must then be correlated with other testing. The simple but very meaningful ski cut test reveals how a similar slope may react to the additional weight of a skier, snowboarder, or snowmobiler. On a small slope that is not too steep (and therefore probably not avalanche prone), the skier can try a ski cut by skiing along a shallow traverse and then setting the ski edges in a hard check. Any cracks or collapse noises indicate instability and that slopes of similar aspect and elevation, if
CHAPTER 2 AVALANCHES
steeper, would have probably avalanched. Ski cuts can be made on steeper suspect slopes by starting a diagonal straight path from an area of safety in a continuous cut to another planned area of safety on the other side of the slope. This can be a dangerous maneuver, but the momentum—even if an avalanche is initiated—increases the chances of escaping off of the starting zone to a safe position. An experienced snowmobiler can perform a similar test by riding his or her machine across the test slope. A much better way to directly observe and test snowpack layers is to dig a hasty snow pit. In a spot as near as possible to a suspected avalanche slope, without putting the traveler at risk, a pit 120 to 150 cm (4 to 5 feet) deep and 90 cm (3 feet) wide should be dug. With the shovel, the uphill wall is shaved until it is smooth and vertical. Now the layers of snow can be observed and felt. The tester can see where the new snow touches the layer beneath, poke the pit wall with a finger to test hardness, and brush the pit wall with a brush to see which layers are soft and fall away and which are hard and stay in place after being brushed. Buried surface hoar, faceted grains, graupel, and crusts are better appreciated; in shallow snowpacks, basal depth hoar can also be easily reached and evaluated. The shovel shear test (ST) is a simple and quick test that is used to locate weak layers (especially very thin layers); however, its small sample size and subjective nature make it less reliable for determining the stability of the snowpack. A column of snow is isolated from the vertical pit wall. Both the sides and the back of the column are cut with a saw (a shovel or a ski will suffice) so that the column is free standing. The dimensions are a shovel’s width on all sides. The tester inserts the shovel blade at the back of the column and gently pulls forward on the handle. A cohesive layer of the column will shear on a weak layer and make a clean break; the poorer the bond, the easier the shear. The following five-point scale is used to rate the shear: (1) “very easy” (STV) if it breaks as the column is being cut or as the shovel is being inserted; (2) “easy” (STE) if a gentle pull on the shovel does the job; (3) “moderate” (STM) if a slightly stronger pry with the shovel is required; (4) “hard” (STH) if a solid tug is required; and (5) “no shear” (STN) if no shear failure is observed. Generally, “very easy” and “easy” shears indicate unconditionally weak snow, “moderate” means conditionally weak, and “hard” and “no shear” mean strong. The value of the ST is that it can find thin weak layers that are undetectable by any other method, even on flat areas. The ST’s major shortcoming is that it is not a true test of stability, because it does not indicate the amount of weight or compression required to cause shear failure. The compression test (CT) is an effective way to find weak layers near the surface (≈1 m [3.3 feet]), and it works well in soft, new snow. The test also gives a good indication of snow stability, because it stresses the weak layer. The CT involves isolating a block similar to that created for the ST on sloping terrain. Using the shovel blade turned upside down and held on the top of the column, successive taps are made on the shovel: 10 from the wrist using the fingertips, 10 from the elbow using the fingertips, and finally 10 from the shoulder using the palm or the fist. The number of taps required to produce a shear is recorded. For example, a shear after 5 taps from the elbow would be recorded as CT15. The interpretation of the stability of the weak layer that is discovered is defined as “easy” (taps 1 through 10), “moderate” (taps 11 through 20), or “hard” (taps 21 through 30). The CT evaluates the ability of weak layers in the upper snowpack to fail in shear and can be performed quickly, thereby allowing for multiple assessments of different aspects and elevations during backcountry travel (Figure 2-17). Most tests, like the ST and the CT, assess fracture initiation (i.e., the additional force or stress needed to start fractures), but they do not assess fracture propagation (i.e., the propensity for fractures to spread through a weak layer in the snowpack). Without assessing for fracture propagation, tests may conceal the real problem layer in a weak snowpack. In a stable snowpack, a fracture may be easy to initiate, but no avalanche may result, because fracture does not propagate across the weak layer. In an unstable snowpack, a fracture may be easy or difficult to initiate; however, after it has been initiated, the fracture can propagate across the weak layer, thereby resulting in an avalanche.
Tapping
30 cm
30 cm k ea r W ye la
Snow pit
FIGURE 2-17 Photo and schematic of a shovel compression test. (With permission from The American Avalanche Association. Top courtesy Doug Richmond.)
To better assess fracture initiation, propagation, and instability, many backcountry travelers and avalanche professionals use the Rutschblock test (RB). This test is calibrated to the skier’s weight and to the stress that he or she would put on the snow. Again, a snow pit is dug with a vertical uphill wall, but the pit must be about 240 cm (8 feet) wide. By cutting into the pit wall, the skier isolates a block of snow that is about 210 cm (7 feet) wide (i.e., a ski length) and that goes back 120 cm (4 feet; i.e., a ski-pole length) into the pit wall. Both the sides and the back are cut with a shovel or a ski so that the block is freestanding. (The test receives a score of RB1 if the snow fails while the individual is isolating the block.) While wearing skis, the skier climbs around and well uphill from the isolated block and carefully approaches it from above. With skis across the fall line, the skier gently steps onto the block—first with the downhill ski and then with the uphill ski—so that he or she is standing on the isolated block of snow. If the slab of snow fails at this time, the score is RB2. Gently flexing the knees applies a little more pressure (RB3). The tester then jumps and lands in the same compacted spot (RB4). The jump is then repeated (RB5). If no failure occurs, the skier moves to about the middle of the block and repeats the flexing and jumping (RB6). If no reasonably smooth failure is produced at this time, the test is considered an RB7. The results are interpreted as “extremely unstable” if the block fails while the skier is cutting it, approaching it from above, or merely standing on it (RB1 or RB2); “unstable” if it fails with a 45
PART 1 MOUNTAIN MEDICINE
knee flex or one gentle jump (RB3 or RB4); “moderately stable” if it fails after repeated jumps (RB5); and “very stable” if it never fails but merely crumbles (RB6 or RB7). These are objective results that help answer the bigger question of whether the snowpack will slide and that help the mountain traveler to decide how much risk to take. The limitations include the time required to isolate the block; the inability to test deep, weak layers; the spatial variability of the results; and the problem of relying on it as a one-step stability evaluation. A new test that was developed during the late 2000s is the extended column test (ECT), which does a remarkable job of effectively discriminating between unstable and stable slopes by extending the size of the column beyond the size of the loading area. Similar to the loading of the CT, stress can be transmitted across the slab. If conditions are unstable, fracture will propagate across the column’s weak layer. To prepare an ECT, a snow pit is dug with a vertical uphill wall and isolates a column that is 90 cm (3 feet) across the slope by 30 cm (1 foot) up the slope. The column is then loaded from one side with the use of the same successive tap technique as is used in the CT. The result reporting emphasizes what happened to the snow column (i.e., whether a fracture propagated across the column or not). The coding is recorded as ECTPV (“very easy”) if the fracture propagates across the entire column during isolation. Like the CT, the number of taps is reported as ECTP## when a fracture initiates and propagates across the entire column. If a fracture initiates on ## tap but does not propagate across the entire column or if more than one additional tap is required after initiation to cause complete propagation, the result is noted as ECTN##. If no fracture occurs, the result is noted as ECTX. Interpreting stability from a single snow pit or stability test is dangerous as a result of spatial variability. The snow cover is not homogenous in its stability; rather it has a patchwork-quilt–like pattern of stronger and weaker snow. Even within a known combination of an unstable slab and a weak layer, there are variations along the slope where one can trigger or not trigger an avalanche (i.e., the false-stable rate). The implications of spatial variability are significant. On a suspected avalanche slope, explosives set in an area of strength will not result in an avalanche. A ski area might then assume incorrectly that the snow is stable and safe only to have a skier hit a weak spot and trigger an avalanche. Likewise, a backcountry skier might dig a snow pit and find strong snow only to trigger an avalanche on the entire slope after skiing a few turns. All tests are prone to misleading results. Research has shown that the CT and RT tests, which are favored by most avalanche professionals, have a relatively high false-stable rate (i.e., a stable test result on an unstable slope) of about 10% to 20%.6,28,38 On paper, being right 80% to 90% of the time may sound encouraging. However, in practice, the false-stable rate is still too high, because the consequences of an error can be fatal. The falsestable rate of 3% with the ETC is more encouraging, but researchers caution that more studies are needed.39 For backcountry travelers and avalanche workers, the falsestable rate should prompt users to dig multiple snow pits and perform multiple stability tests on the same slope. As an exercise in probability, a false-stable rate of 10% implies that digging two snow pits on the same slope decreases the chances from getting a false-stable rate in both pits to 1 in 100. Three pits drop the chances to 1 in 1000. One should always use a variety of tests and combine those results with direct observations of avalanche, snowpack, and weather conditions. More detailed descriptions and guidelines regarding the performance of all presently recommended stability tests can be found in Snow, Weather and Avalanches: Observation Guidelines for Avalanche Programs in the United States (Pagosa Springs, Colorado, 2009, The American Avalanche Association).
AVALANCHE RESCUE EQUIPMENT Shovel The first piece of safety equipment that the skier or climber should own is a shovel, which can be used to dig snow pits for 46
stability evaluation and snow caves for overnight shelter. A shovel is also needed for digging in avalanche debris, because such snow is far too hard for digging with the hands or with skis. The shovel should be sturdy and strong enough to dig in avalanche debris yet light and small enough to fit into a pack. There is no excuse for not carrying a shovel. Collapsible shovels made of aluminum or high-strength plastic are available in mountaineering stores. Probe Several pieces of equipment are designed specifically for finding buried avalanche victims. The first is a collapsible probe pole. Organized rescue teams keep rigid poles in 3- to 4-m (10- to 12-foot) lengths as part of their rescue caches. The recreationist can buy probe poles of tubular aluminum or carbon fiber that come in 45-cm (18-inch) sections that fit together to make a fulllength probe. Ski poles with removable grips and baskets can be screwed together to make an avalanche probe. Survivors of an accident use probes to search for buried victims by either spot probing in likely burial areas or to confirm transceiver location before shoveling. Avalanche Rescue Beacon Avalanche rescue beacons (transceivers) are the best personal rescue devices for quickly finding buried companions. When used properly, they are a fast and effective way to locate buried avalanche victims. In the United States and worldwide, these devices have become standard issue for ski-area patrollers involved in avalanche work and for helicopter skiing guides and clients. They are also commonly used by highway departments, search and rescue organizations, and anyone traveling into avalanche terrain. Since beacons were introduced in the United States, they have saved several lives each winter. All transceivers act as electromagnetic transmitters that emit a signal on a world-standard frequency of 457 kHz. A buried victim’s unit emits this signal, and the rescuers’ units receive the signal. The signal carries 30 to 50 m (100 to 150 feet) and, after it is picked up, it guides searchers specifically to the buried unit. Beacon technology is evolving rapidly, and the transceivers that are on the market are continually improving. Two major categories of transceiver have emerged: (1) analog, which processes the receiving signal in a basic electromagnetic convergence of induction pulses to allow for a stronger (visual and audible) signal as the receiving beacon approaches the sending beacon; and (2) digital, which uses a computer chip to microprocess the receiving analog signal and to then display a digital readout of the distance, strength (audible and visual), and, in some units (i.e., dual and triple antennae), the general direction to the buried unit. The newest transceivers are triple-antennae devices that not only give data about distance, direction, and signal strength but that can also identify multiple burials and their approximate location in relation to each other. The tripleantennae transceivers also reduce false signals, which can often be a confusing issue with single and dual devices, in the final few meters of the search. Transceivers are audio-magnetic-induction devices and not radio devices; the directional arrows point only along a flux line of the sending unit’s magnetic field. Likewise the displayed distance represents the distance along a flux line rather than a direct distance to the sending unit. In this regard, the closer the distance displayed, the closer the flux line from the sending unit. Both analog and digital beacons operate on the same internationally standardized frequency and therefore are compatible with one another. However, slightly different search techniques may be necessary to use each type most efficiently, and special training and practice are required before the user attains proficiency. Experience has shown that digital units have a faster learning curve, and these are routinely used by helicopter skiing services and backcountry guides for clients with limited experience. Merely possessing a beacon does not ensure its lifesaving capability. Experience in the United States and from European studies shows that the chances of surviving a full avalanche burial with a beacon and companion rescue are still less than 50%.12,27
Avalanche Airbag The purpose of the avalanche airbag is not to quicken rescue but to prevent burial. German industrialist Peter Aschauer introduced the backpack-integrated avalanche airbag system (ABS) in 1985 (Figure 2-19). It was designed specifically for guides and ski patrollers, but it rapidly became popular in Europe for use by recreationalists who were venturing into avalanche terrain. Accident data have been compiled since the beginning of its use
by the Swiss Federal Institute for Snow and Avalanche Research in Davos, Switzerland.44 The first documented case of survival with the use of an ABS was in February 1991. Since then (as of 2009), 253 ABS-equipped persons have been caught in avalanches; 226 victims survived with deployed airbags, and there were only three deaths among those victims whose airbag deployed. Two deaths occurred among victims whose airbag deployed and who were buried, even though their airbags were visible on the surface. In a third case of death in a victim whose airbag deployed, the victim and airbag were completely buried by a second avalanche. In another 27 victims the airbags failed to work properly or the user did not or could not deploy the airbag, and among these victims seven deaths occurred. Thus, among 253 avalanche victims wearing an ABS system, there were 10 deaths total. The airbag works as a result of inverse segregation (Figure 2-20). An avalanche in motion is composed of many different-sized
BOX 2-1 Avalanche Transceiver Search Initial Search 1. Safely access the slide path and debris area, and have everyone switch their transceivers to “receive” and turn the volume to “high.” 2. If enough people are available, post a lookout to warn others about possible additional slides. 3. Should a second slide occur, have rescuers immediately switch their transceivers to “transmit.” 4. Have rescuers space themselves no more than 30 m (100 feet) apart and walk abreast along the slope. 5. If a single rescuer is searching within a wide path, he or she should zigzag across the rescue zone and limit the distance between crossings to 30 m (100 feet). 6. For multiple victims, when a signal is picked up, have one or two rescuers continue to focus on that victim while the remainder of the group carries out the search for additional victims. 7. For a single victim, when a signal is picked up, have one or two rescuers continue to locate the victim while the remainder of the group prepares shovels, probes, and medical supplies for the rescue. Locating the Victim With practice, the induction line search is more efficient than the conventional grid search for getting close to the sending beacon, but the conventional grid search is still necessary to fine search for the buried victim. A probe pole can be used to pinpoint the victim’s exact location. The induction line search is very similar to the flux line search that is used by digital transceivers. Users should always study the owner’s manual to learn the best techniques for the specific brand of avalanche rescue beacon that they are using. Induction Line Search (Preferred Method) When an induction line search is used, the rescuer may initially follow a line that leads away from the victim (see Figure 2-18, A and B). Remember to lower the transceiver volume if it is too loud, because the ear detects signal strength variations better at lower volume settings. 1. After picking up a signal during the initial search, hold the transceiver horizontally (parallel with the ground), with the front of the transceiver pointing forward (see Figure 2-18, C). 2. Holding the transceiver in this position, turn until the signal is maximal (maximum volume), then walk five to seven steps (about 5 m [16.4 feet]), stop, and turn again to locate the maximum signal (see Figure 2-18). When locating the maximum signal, do not turn yourself (or the transceiver) more than 90 degrees in either direction. If you rotate more than 90 degrees to locate the maximum signal, you will become turned around and follow the induction line in the reverse direction. 3. Walk another five steps, as just described, and then stop and orient the transceiver toward the maximum signal. Reduce the volume. 4. Continue repeating these steps. You should be walking in a curved path along the induction line toward the victim (see Figure 2-18, B).
5. When the signal is loud at the minimum volume setting, you should be very close to the victim and can begin the grid search. Grid Search 1. When a signal is picked up, stand and rotate the transceiver, which is held horizontally (parallel with the ground) to obtain the maximum signal (loudest volume). Maintain the transceiver in this orientation during the remainder of the search. 2. Turn the volume control down until you can just hear the signal. Walk in a straight line, down the fall line from where the signal was first detected. (If the signal fades immediately, walk up the fall line.) If you are headed in the right direction, the signal will increase; turn the volume control down until the signal fades. Take an extra couple of steps to be sure that the signal truly fades. If the signal increases, continue until it fades. 3. When the signal fades, mark the point, and then turn 180 degrees and walk back toward the starting position. The signal will increase in volume and then fade again; take two additional steps to confirm the fade. Walk back to the middle of the two fade points; this spot may or may not be the point of loudest volume and maximum signal. If you experience two maximum signals, go to the midpoint between the two maximums. 4. At this point, turn 90 degrees in one direction or the other. From that position, reorient the transceiver (held parallel with the ground) to locate the maximum signal. After orienting the transceiver to the maximum signal, reduce the volume, and begin walking forward. If the signal fades, turn around 180 degrees, and begin walking again. 5. As the signal volume increases, repeat steps 3 and 4 until you have reached the lowest volume control setting on the transceiver. (Be sure to always take an extra step or two to confirm the fade point.) This time, when you return to the middle of the fade points, you should be very close to the buried victim and can now begin pinpointing him or her. a. While stationary, orient the transceiver to receive the maximum signal (loudest volume). At this point, turn the volume control all the way down. b. With the transceiver just above the surface of the snow, continue doing the grid search pattern two to four more times. Always sweep the transceiver a couple of feet beyond the fade point to confirm the fade point. c. Find the signal position halfway between the fade points (i.e., at the loudest signal). At this point, you should be very close to the victim’s position, and you can begin to mechanically probe. Speed is essential. With practice, the transceiver will be accurate to less than one-fourth of the burial depth. For example, a 4-foot burial should result in about a 1-foot square at the surface. d. Depending on the brand, pinpointing with a digital transceiver will involve the use of a slight variation or a combination of the induction line and grid techniques. Be sure to study the owner’s manual.
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CHAPTER 2 AVALANCHES
Frequent practice is required to master a transceiver-guided search, which may not be as straightforward as the directions suggest. Skilled practitioners can find a buried unit in less than 5 minutes after they pick up the signal. Because speed is essential in avalanche rescue, beacons can certainly be lifesavers. The best-proved rescue equipment is a transceiver for a quick find, a collapsible probe or pole to confirm and pinpoint the spot, and a shovel for a quick recovery (Box 2-1 and Figure 2-18).
PART 1 MOUNTAIN MEDICINE
min weak
–
–
E
+
+ 5m – –
–
–
max strong
min weak max strong
W
–
A
S
B
C
FIGURE 2-18 Induction (“tangent”) line search method. A, The arrangement of the electromagnetic flux lines (induction lines) emitted from a buried victim. The signal received by the searching transceiver along the transmitted flux line is strongest when it is oriented in parallel, and it is weakest when it is oriented perpendicularly. B, The searcher moves in short (3 to 5 m [9.8 to 16.4 feet]) “tangents” and then orients the transceiver to the strongest signal. In this way, the receiving transceiver follows a flux line toward the victim. The sensitivity (loudness) of the beacon should be adjusted downward as the victim is approached so that the searcher can discern the strongest signal before proceeding in a new direction. C, The “pinpoint” search is performed when the buried subject is within 3 m (9.8 feet); this typically occurs when the transceiver is at its loudest with the sensitivity turned all the way down. It is a “grid” search on a much smaller scale that is carried out close to the snow surface. The loudest signal is found along one axis (E to W) and followed by the perpendicular axis (N to S) to the likely burial position. A probe is then used to confirm the victim’s location and depth. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby, with permission.)
particles of snow. Gravity causes granular flows to segregate, with smaller particles sinking to the lower portion of the flow and larger particles rising to the surface. The process of inverse segregation depends primarily on the relative sizes of the particles in a granular flow. A person who is carried in the flow of an avalanche is not necessarily a large-enough particle to remain on the surface as compared with a particulate slab. However, the airbag (150 L [5.3 feet3] when inflated) apparently makes the user a large enough particle, which allows for a greater separation effect. Buoyancy plays no role in the efficiency of this system. Since 1995, the ABS has undergone continued and significant improvements with regard to device sizes and cartridge weight. The airbag is integrated into a special backpack, and the user deploys it by pulling a ripcord-like handle. This releases a
A
Inverse segregation
B FIGURE 2-19 A, A small-size Avalanche ABS backpack with deployed airbags. The airbags are stowed in the outside pockets of the backpack. B, Integrated into a backpack, the Avalanche ABS is deployed by pulling the white “T” handle. (Courtesy Peter Aschauer, GmbH.)
48
FIGURE 2-20 Inverse segregation. The physical unmixing of flowing particles is based on size, which distributes larger particles in the upper layers and forms the basis for successful functioning of the Avalanche ABS.
AvaLung In 1996, Dr. Thomas Crowley received a patent for an emergency breathing device to extract air from the snow surrounding a buried avalanche victim after testing a homemade prototype on himself. Black Diamond Equipment, Ltd., in Salt Lake City, Utah, performed the research and development on the device and secured distribution rights in 2000 for the original external vest format of the AvaLung. The company redesigned the device in 2002 for easier and more comfortable use when worn outside of the clothing like a bandoleer (Figure 2-21). The most recent version, which is the most popular, is incorporated into varioussized backpacks with a stowable mouthpiece kept in the shoulder strap (Figure 2-22, online). The AvaLung functions mainly by separating inhaled from exhaled air in the surrounding snowpack with a goal of prolonging survival time by slowing the process of asphyxiation. Ambient air is 21% oxygen and has virtually no carbon dioxide. Expired air is 16% oxygen and 5% carbon dioxide. The AvaLung prevents FIGURE 2-21 The AvaLung is a breathing device that is intended to prolong survival during avalanche burial by diverting expired air away from inspired air drawn from the snowpack and that is worn over all other clothing. The white arrows show the flow of inspiratory air, and the red arrows show the flow of expiratory air. The subject breathes in and out through the mouthpiece (A). Inhaled air enters from the snowpack through the one-way inspiratory valve on the side of the housing inside the mesh-protected harness on the chest (B). Expired air leaves the lungs via the mouthpiece and travels down the respiratory tubing to the housing and then passes through an expiratory one-way valve located at the bottom of the housing (B). It then travels via respiratory tubing inside the harness around to the back (C). (A courtesy Jill Rhead; B courtesy Black Diamond Equipment, Ltd.)
rebreathing of expired air, which is one cause of asphyxiation during avalanche burial, by diverting expired air away from inspired air that is drawn from the snowpack23 (see Avalanche Victim Physiology and Medical Treatment after Rescue, later; see Figure 2-22, online). Survival after complete avalanche burial with use of the AvaLung has occurred in a number of cases.34 The AvaLung system has been proved effective in numerous simulated burials by allowing subjects to breathe for 1 hour in tightly packed snow, including dense, wet snow. In addition, several known cases have occurred in which burial time was fairly short. In a dramatic hallmark case, a helicopter skier survived a 120-cm (4-foot) burial of 35 to 45 minutes by breathing with an AvaLung. Two others were buried in the avalanche a few feet apart at about the same depth but were not wearing the device. Rescue times were similar for the three victims, none of which had suffered any trauma. The two skiers that were not wearing the AvaLung died of asphyxiation.15 The ABS and the AvaLung are designed to help avalanche victims, and they are adjuncts to the basic companion rescue equipment which includes a transceiver, probe, and shovel. These devices should never be used to justify the taking of additional risks. Because surviving any avalanche is uncertain, no equipment should ever replace good judgment.
Avalanche Rescue SELF-RESCUE Escaping to the Side The moment that the snow around a person begins to move, there is a split second during which that person can make a decision or make a move. The person should shout to alert companions and then close the mouth and breathe through the nose to prevent inhaling a mouthful of snow. If the individual is wearing an AvaLung, the mouthpiece should be quickly placed in the mouth, which also helps to prevent oropharyngeal snow impaction. If he or she is using an ABS, every effort should be made to activate the ripcord. Whether on foot, skis, or snowmobile, the person should first try to escape to the side of the avalanche or try to grab onto a tree. Staying on one’s feet or snow machine gives the individual some control and keeps his or her head up. Escaping to the side gets the person out altogether or to a place where the forces and speeds are less. Turning the skis or the snow machine downhill in an effort to outrun the avalanche is a bad move: the avalanche invariably overtakes its victims. Swimming For years, the command to swim if caught in an avalanche was dogma. However, during recent years, the effectiveness of
A
B
C d
mon
ck
Bla
Dia
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CHAPTER 2 AVALANCHES
cartridge of nitrogen gas that escapes at high velocity and that draws in outside air through jets that inflate two 75-L (2.6-foot3) airbags in 2 to 3 seconds with the use of the Venturi effect. In an initial study, Brugger and Falk13 found that the ABS reduces the likelihood of avalanche burial from 39% to 16.2% and that it lowers mortality from 23% to 2.5%. In a more recent analysis by Brugger and colleagues,12 use of the ABS reduced mortality in an avalanche to 2.9% as compared with 18.9% without the ABS in complete or partially buried avalanche burial victims. This dramatic reduction in mortality occurs because the ABS device prevents burial, and very few (i.e., ≈4% to 5%) partly buried or unburied victims die in avalanches. Commercial sales of the ABS system in the United States were delayed until recently because of problems with obtaining certification for the nitrogen-gas cartridges; however, the device is now readily available for sale in the United States. Two American companies have started to produce airbags with different configurations. Both use a single 150-L (5.3 feet3) airbag; one airbag is integrated into a backpack, whereas the other is incorporated into a vest and deployed as a balloon in a horseshoe shape around the back of the victim’s head toward the anterior chest. A third airbag device from Switzerland makes use of a continuous balloon that arches over and along the upper side of a backpack to surround the victim’s head. The latter two systems have the theoretic advantage of preventing head trauma, and both may allow for a greater chance of a head-up partial burial. Unlike the ABS, none of these three new systems has been independently tested by the Swiss Federal Institute for Snow and Avalanche Research or has a documented history of use in avalanche accidents. Only the German ABS has been rigorously tested, with extensive experience. The new airbag designs are too recent for the making of any sound recommendations at this time.
PART 1 MOUNTAIN MEDICINE
swimming has been called into question. It is the process of inverse segregation (see Avalanche Airbag, earlier) rather than swimming that keeps the victim on or near the surface. However many survivors claim that “swimming” (i.e., struggling with the arms and legs flailing) kept them on or close to the surface. It is possible that these motions may create a large particle effect and that inverse segregation applies. The most important thing to do when caught and being tumbled violently and unable to swim with the avalanche is to get a hand or both hands in front of the face to create an air pocket. This is especially important, because the avalanche may stop abruptly, at which time no arm movement will be possible. Without an air pocket, very few buried victims survive. Cumbersome or heavy gear and ski poles should already have been discarded, and, with any luck, the avalanche will strip away the skis. Although skiers should try to discard their gear, snowmobile riders should try to stay on their snow machines. Once they are off their machine, riders are twice as likely to be buried as are their machines. Reaching the Surface Anyone who is caught in an avalanche should fight for his or her life. Creating an air pocket is the key to survival, but some victims, sensing themselves to be near the surface, have thrust a hand or a foot toward the surface. Any clue on the surface that gives the rescuers something to see greatly improves an individual’s odds of survival.
COMPANION RESCUE Marking the Last-Seen Area A companion or eyewitness to an accident needs to act quickly and positively. The rescuer’s actions over the next several minutes may mean the difference between life and death for the victim. First, the victim’s last-seen area (LSA) should be fixed and marked with a piece of equipment or clothing, a tree branch, or anything that can be seen from a distance down slope. It is usually safe to enter the bed surface of an avalanche that has recently run. It is dangerous when the fracture line has broken at mid slope, which leaves a large mass of snow still hanging above the fracture. If the victim was seen riding the avalanche before the LSA, a line of trajectory can be visualized that could narrow down likely areas of burial. Persons equipped with transceivers can go to the LSA to begin their search (see Beacon Search, later). Those without transceivers face a very difficult situation.
SEARCHING FOR CLUES The fall line (i.e., the line of trajectory) should be searched below the LSA in the flow line for any clues of the victim. Shallow probes should be made into likely burial spots with an avalanche probe, a ski, a ski pole, or a tree limb (i.e., spot probing). Likely spots are the uphill and downhill sides of trees and rocks and benches or bends in the slope where snow avalanche debris piles up. The toe of the debris should be searched thoroughly; many victims are found in this area. Rescue Beacons If the group was using beacons, all companions must immediately switch their units to receive mode. While making the fast visual search for clues, companions should at the same time search the debris using their transceivers as described in Box 2-1. When a signal is detected, companions must narrow the search area quickly. If they are skilled with a transceiver, companions can pinpoint the burial site in a few minutes and should confirm the location with a probe that is then left in place. Shoveling Techniques Unfortunately, shoveling will take much longer than the transceiver search, and, depending on the number of rescuers and the technique used, this aspect of the rescue could be the difference between life and death. Recent attention regarding efficient shoveling techniques during avalanche rescue has emerged. It is clear that unburying 50
Snow shoveled to side Burial depth
1.5 x burial depth FIGURE 2-23 Strategic shoveling technique for one or two rescuers. (Courtesy Dale Atkins and the National Ski Patrol, Lakewood, Colo.)
an avalanche victim is the most time-consuming component of the rescue, and inefficiencies have been identified. Strategic Shoveling During companion rescue, where typically only one to three shovelers might be available and where the debris is often softer, the strategic shoveling technique16 increases digging efficiency (Figure 2-23). There are several important things to consider when shoveling when only a few diggers are available: avoid standing over the buried victim, begin digging down slope from the probe, lift snow as little as possible by throwing it to the side, and move snow only once. With the probe left in place, the shovelers begin digging down slope about one to oneand-one-half times the burial depth as determined by the probe. Quickly dig a waist-deep starter hole about one wingspan wide (i.e., the distance between the fingertips when the arms are held out to the sides). If two shovelers are digging, they should work in tandem and side by side rather than one digging behind the other. Throw the snow to the sides. Move to the starter hole, and continue digging downward and forward. As depth increases, snow can be cleared to the back rather than lifted and tossed to the sides. When close to the victim, use a scraping action to clear snow. Use the first body part to estimate the location of the head, and then use the hands to clear away snow from the victim’s face and airway, and continue to clear snow off his or her chest. The most important feature of efficient shoveling is to create a ramp or platform in the snow that leads to the probe (and the victim) instead of digging a hole down around the probe. In this way, extrication and resuscitation of the victim are made easier by having a flat surface available, the air pocket is not compromised, there is space to work on the victim, and raising up the victim is not necessary. V-Shaped Conveyor Belt With an organized rescue, the debris is often much harder as a result of age hardening than what is experienced by companion rescuers, but typically more shovelers are available. In this situation, the V-shaped conveyor belt method18 works effectively to clear snow quickly (Figure 2-24). Starting down slope from the probe, rescuers are arranged in a wedge-shape or inverted-“V” pattern. The lead shoveler chops out blocks of snow and scoops the snow down slope. The other shovelers use paddling-like motions to clear out snow through the center of the “V” to create a platform. When getting close to the buried victim, an additional shoveler may join the lead to increase the working space. Shovelers may rotate clockwise every 5 minutes to decrease fatigue. After the victim is reached, locate his or her head and chest, and use the hands to clear the airway. Teaching efficient shoveling techniques should be included in all avalanche rescue courses, and it should be practiced as often as transceiver searches to reduce the total time to extrication. Going for Help A difficult question during rescues is when to seek outside help. If the accident occurs in or near a ski area and there are several
CHAPTER 2 AVALANCHES
80 cm
A
D
B
C
E F
FIGURE 2-24 V-shaped conveyor belt shoveling approach. A, Positioning of rescuers, with a quick measurement of the distance between shovelers. B, Working in sectors on the snow conveyor belt; snow is transported with paddling motions. C, Clockwise rotation is initiated by the front person; job rotation maintains a high level of motivation and minimizes early fatigue. D, The buried victim is first seen. More rescuers are needed at the front, and the snow conveyor belt only needs to be kept partially running. E, Careful work occurs near the buried victim, while some shovelers aggressively cut the side walls to adapt the tip of the V to the real position of the victim. F, Interface to organized rescue. More space is shoveled only after medical treatment of the victim has begun. (Courtesy Manuel Genswein. From Genswein M, Eide R: V-shaped conveyor belt approach to snow transport, The Avalanche Review 20:20, 2008, with permission.)
companions, one person can be sent to notify the ski patrol immediately. If only one or two companions are present, the correct choice is more difficult. The best advice is to search the surface quickly but thoroughly for clues before anyone leaves to notify the patrol. Cell phones have been the most effective and efficient method of calling for help, because contact can be made without losing manpower for continued companion rescue; however, cell phones do not work in all mountain areas. If a voice connection cannot be made, try sending a text message. In the United States, the Next Generation 911 system is being implemented to support text messages, images, and video. If the avalanche occurs in the backcountry far from any organized rescue team, all companions should remain at the site. The guiding principle in backcountry rescues is that companions search until they cannot or should not continue. When deciding when to stop searching, the safety of companions must be weighed against the decreasing survival chances of the buried victim.
ORGANIZED RESCUE Incident Command System In 2003, Presidential Homeland Security Directive 5 required that all emergencies be managed with the Incident Command System (ICS; visit www.fema.gov for more information). To meet this mandate, members of organized rescue teams should have an
awareness of ICS. ICS only changes how incidents are managed; it does not change how avalanche rescuers do their jobs. No matter how an incident is managed, all avalanche search and rescue operations have four key functional components that are often being organized and managed simultaneously. One component is search, the goal of which is quickly finding and extricating any buried victims. The first team dispatched to the avalanche, which is known as the immediate search team, should consist of skilled and swift-traveling rescuers that are competent not only in avalanche rescue but also in route finding and hazard evaluation. Basic search and rescue tools are transceivers, probes, shovels, avalanche rescue dogs, the RECCO system (described later in this chapter), and basic first-aid equipment. The immediate search team performs the initial search and looks for clues with the hope of making a quick find. If they have no luck, the team determines the most likely burial areas. The person who is reporting the avalanche should meet rescuers at the accident site, or the reporting person should be returned to the same vantage point from which the accident was witnessed to best guide rescuers to locate LSAs. Arriving rescuers will meet the site leader and continue the immediate search until sufficient clues can steer rescuers to positioning probe lines. The second component is emergency care to provide medical care for victims who are found. One or two small teams are dispatched with resuscitation, medical, and simple evacuation equipment. Ideally, the medical team should be sent within minutes of fielding the first search teams to ensure that necessary 51
Probing Probing avalanche debris is a simple but slow method of searching for buried victims. For more than 40 years, the traditional probe line (closed course probing) used by rescue teams was composed of about a dozen rescuers standing elbow to elbow with a probe pole that was 3 to 3.5 m (10 to 12 feet) long. The rescuers probe once between their feet, with each probe entering the snow about 75 cm (30 inches) from the neighbors on either side; the line then advances 70 cm (28 inches), and the rescuers probe again. Open course probing involves the rescuers being an arm’s length apart and probing twice (once in front of each foot) before stepping forward. The probability of detection (POD) with these methods was thought to be about 70%. If the probe line missed the victim on the first pass—which tended to happen—then the area was probed again and again. Behind the probe line, shovelers stood ready to check out any possible strike. The line did not stop in such an event but continued to march forward with a methodic “probe down, probe up, step forward” cadence. In 2004, Ballard and colleagues5 developed a computer program that simulated a human body in an avalanche and compared the POD for any probe-grid spacing. The results showed the POD for the traditional probe line to be 59% as opposed to the 70% as previously believed. At a grid spacing of less than 50 cm (20 inches), the search time increased faster than the POD. Thus, a grid spacing of 50 cm by 50 cm (20 inches by 20 inches) was optimal, yielding the best combination of POD and search time. For a three-holes-per-step probe, probers stand with their arms out, wrist to wrist. Probers first probe between their feet, and then they probe 50 cm (20 inches) to the right and 50 cm (20 inches) to the left (Figure 2-25). At a command from the leader, the line advances 50 cm (20 inches [i.e., one step]). This method gives an 88% chance of finding the victim on the first pass, with an estimated time to discovery that is nearly identical to that of traditional spacing. Ski patrols and mountain rescue teams that have adopted the three-holes-per-step style of probe with a 50 cm by 50 cm (20 inches by 20 inches) grid have noted improved efficiency and effectiveness of the probe line. Because these rescuers insert more probes per rescuer, it is possible to have fewer rescuers on a probe line, and short probe lines are easier to manage and work faster than do long probe lines. Five rescuers doing three holes per step at 50-cm intervals form a slightly longer probe line than do nine rescuers using the traditional method. To ensure proper spacing, it is most helpful to use a guidon cord with marked 50-cm intervals. Suspended between two rescuers, the lightweight guidon cord positions rescuers and probes at the correct spots, thereby allowing the
50 cm
PART 1 MOUNTAIN MEDICINE
medical and evacuation equipment reach the site in a timely fashion. The third component is transportation, which includes travel for additional rescuers to and from the accident site and for the evacuation of victims. The transportation effort must begin immediately so that rescuers and equipment can be moved efficiently and quickly. Likewise, coordination of helicopters, snow machines, and rescuers is essential to a fast and safe evacuation. The fourth component is support, which sustains the entire operation, especially when a rescue is prolonged. This support may include additional rescuers to take over for cold and tired searchers, hot food and drinks, tents, warm clothing, and lights for nighttime searching.
50 cm 50 cm
FIGURE 2-25 Three-probe spacing for 50-cm by 50-cm three-holeper-step probe method.
52
TABLE 2-2 Type of Rescue for Buried Avalanche
Victims in Direct Contact With Snow on the Basis of a Sample of 300 Burials in the United States From the Winter of 1999-2000 to the Winter of 2008-2009
Type of Rescue, 1999-2000 to 2008-2009
Found alive Found dead
Self-Rescue
Companions
11 (10%) —
84 (78%) 73 (38%)
Rescue Teams 13 (12%) 119 (62%)
Total 108 192
Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.
line to move smoothly and efficiently without interruption. When a guidon cord is not used, the probe line must be frequently stopped and reassessed to ensure proper spacing. If the victim is missed on the first pass, the second pass increases the POD to 99%. Rescue teams use probe lines to find most avalanche victims who are not equipped with transceivers or RECCO reflectors, or when an avalanche rescue dog fails to locate the victim. However, these search methods should all be used concurrently. Because probe lines are time intensive, few victims are found alive using this technique alone (Tables 2-2 and 2-3). Avalanche Rescue Dogs Trained search dogs, which are traditionally used in Europe early during avalanche rescues, are capable of locating buried victims very quickly. However, in the United States, few live rescues have occurred, because the dogs are often brought to the scene only after extended periods of burial. In the March 1982 avalanche disaster in Alpine Meadows, California, a dog made the first live recovery of an avalanche victim in the United States. Since then, dogs have made additional live recoveries. Unfortunately no live dog rescue has been reported in the last 10 years; since 1950, there have only been six reported live recoveries, with four occurring at ski areas. The number of trained certified search dogs has increased substantially. Search and rescue teams and law-enforcement agencies work closely with search-dog handlers, and trained avalanche dogs are now common fixtures at ski areas in the western United States. A trained avalanche dog moving rapidly over avalanche debris and using its sensitive nose to scan for human scent (i.e., rafts or shed dead skin cells) diffusing upward
TABLE 2-3 Method of Locating (First Contact)
Buried Avalanche Victims on the Basis of a Sample of 274 Avalanche Burials in the United States From the Winter of 1999-2000 to the Winter of 2008-2009
Method Attached object or body part Spot probe Coarse or fine probe Transceiver Avalanche dog Voice Other (e.g., digging, RECCO) Found after a long time span Not found, not recovered Inside vehicle Inside structure Total
Found Alive
Found Dead
Total
38 3 1 39 0 7 2 — — 1 1 92
18 15 40 58 30 0 8 9 3 0 1 182
56 18 41 97 30 7 10 9 3 1 2 274
Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.
CHAPTER 2 AVALANCHES
A
B
FIGURE 2-26 A, The RECCO reflector is a thin circuit card that is covered in soft plastic. It does not need batteries and does not need to be turned on or off. The reflector can be attached to jackets, pants, boots, and helmets. B, The RECCO detector consists of a transmitter and a receiver. It can also be used from a helicopter. (Courtesy RECCO AB, Sweden.)
through the snowpack can search more effectively in 30 minutes than can 20 searchers in 4 hours with the use of course probing. Dogs are not infallible, and their ability to find buried human scent may be affected by several factors, such as the length of burial, weather, snow density, and contamination of the debris field with spit, urine, cigarettes, or gasoline from snowmobiles or generators. Dogs have found bodies buried 10 m (30 feet) deep, but have also passed over persons buried only 2 m (6 feet) deep.
electronic cameras, radios, and even turned-off avalanche rescue beacons, so RECCO should be used by rescue teams together with avalanche rescue dogs, rescue beacons, and probers as part of the first response to any avalanche rescue. A detector operator can search as quickly as if he or she were using an avalanche beacon. In North America, more than 130 ski areas, mountain rescue teams, and National Parks have detectors. Worldwide, more than 600 ski resorts and helicopter rescue teams make use of them.
RECCO RECCO (www.recco.com) is an electronic rescue system that enables organized rescue teams to find victims who are equipped with reflectors (Figure 2-26). The system consists of two parts: a detector that is used by the rescue teams (either on the ground or from helicopters) and the reflector that is worn by the recreationist. About the size and weight of a notebook computer, the detector is easily transported to the accident site. The detector transmits a directional radar signal. When it hits the reflector, the signal’s frequency is doubled and reflected back to the detector, and the rescuer can follow the signal to the buried person. The reflectors are small and passive (i.e., no batteries) electronic transponders that are fitted into outerwear, ski and snowboard boots, and helmets. The system will detect some electronic equipment (with diminished range), such as cell phones,
Avalanche Guard When considering the need for an avalanche guard, if the threat of a second avalanche exists, one person should stand in a safe location to shout out a warning. This gives the searchers a few seconds to flee to the safety of a predefined escape route. Rescues are often carried out under dangerous conditions, and self-preservation should be the primary consideration.
The Avalanche Victim After reaching a 20-year low in the late 1980s, avalanche deaths in the United States soared during the 1990s (Figure 2-27) and spiked in the winter of 2007-2008 with 36 deaths, which was the highest number killed during the modern era (i.e., after 1950). Figure 2-27 also presents the 5-year moving average. After the end
Avalanche deaths (number of persons)
40 U.S. fatalities U.S. 5-year moving average
35 30 25 20 15 10 5 0 1950
1955
1960
1965
1970
1975
1980
1985
1990
1995
2000
2005
Winter season by fall and spring year 1950-1951 to 2008-2009
FIGURE 2-27 Avalanche deaths in the United States in the modern era (i.e., after 1950) by winter, by season, and showing a 5-year moving average. (Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.)
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Snowmobilers Backcountry skiers Climbers Out-of-bounds skiers Backcountry snowboarders Snowshoers Out-of-bounds snowboarders In-area skiers/snowboarders Hikers Hunters Residents Avalanche forecasters Roof shovelers Avalanche course students Highway workers Ski patrolers
Recreation
Nonrecreation
0
20
40
60
80
100
120
Number of fatalities
FIGURE 2-28 U.S. avalanche fatalities by activity, the winter of 1999-2000 to the winter of 2008-2009. (Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.)
of the 1980s, the average number of fatalities per winter rose from 11 to 30, but this number decreased slightly during the mid 2000s. However, in recent years, the 5-year average has begun to edge back upward to 28 deaths per winter. As more people head into the winter backcountry, avalanches continue to be deadly. In the United States, since 1950, avalanches have claimed 854 lives, and 33% (280) of the victims died between 1999 and 2009 in 232 fatal avalanche accidents. During the prior 10 years, avalanches killed 220 people. The mean age for all victims is 33 years (median, 31 years). The average age for men is 33 years, and the average age for women is 36 years. From 1999 to 2009, nearly all avalanche victims (96%) were pursuing some form of recreation at the time of the accident. Figure 2-28 shows the activity groups of the victims. Snowmobilers constitute the largest single group of avalanche victims, primarily because snow machines with powerful engines and better tracks can climb steep avalanche-prone terrain, thereby exposing riders to greater avalanche risk. A snowmobiler can cover a much greater area in a given time than can a skier or snowboarder, which also exposes them to a greater risk of being caught in an avalanche. When the skier and snowboarder categories are combined, these riders are not far behind the snowmobilers (109 vs. 114 deaths). Backcountry and “out of bounds” skiers and snowboarders venture into areas that are not parts of a ski resort and thus not managed for avalanches in any way. The backcountry-skier category includes ski mountaineers, helicopter skiers, and snowcat skiers. Out-of-bounds skiers and snowboarders refer to those who leave the ski area boundary or enter into “closed” areas within the ski area. In-area skiers and boarders are those who are caught and killed on open terrain within the ski area boundary that is managed for avalanches. In-area avalanche fatalities are rare. However, three fatalities occurred in in-area spaces in three different states during a 2-week period of the 2008-2009 season. The slopes had been managed to mitigate avalanches, but the avalanches occurred nonetheless, and they were attributed to an extremely unstable snowpack. Among nonrecreation groups, avalanches strike houses (residents), highways (motorists and plow drivers), and workplaces (ski patrollers, avalanche forecasters, and roof shovelers). Since 1999, 14 states have registered avalanche fatalities (Figure 2-29, online); however, since 1980, avalanche deaths have also occurred in Arizona, Maine, and New Mexico. 54
STATISTICS OF AVALANCHE BURIALS The factors that affect a buried victim’s chances of survival are the length of time buried, depth of burial, clues on the surface, available rescue equipment, competence of the rescuers, presence of injury, body position, snow density, and presence and size of an air pocket. A victim who is uninjured and able to fight on the downhill ride usually has a better chance of being only partly buried, or, if completely buried, a better chance of creating an air pocket for breathing. A victim who is severely injured or rendered unconscious will more likely be rolled, flipped, and twisted during the slide. Being trapped in an avalanche is a lifeand-death struggle. Avalanches kill in two ways. First, traumatic injury may occur as the victim tumbles down the avalanche path. Trees, rocks, cliffs, and the wrenching action of snow in motion can produce blunt or penetrating trauma. Up to one-quarter of all avalanche deaths are caused by trauma, especially to the head and neck. Second, snow burial causes asphyxiation in at least three-quarters of avalanche deaths from either airway obstruction or hypercapnia and hypoxemia as a result of rebreathing expired air. A very small percentage of avalanche victims succumb to hypothermia (see Avalanche Victim Physiology and Medical Treatment After Rescue, later). A victim who is swept down in the churning maelstrom of snow has a difficult time breathing. Inhaled snow clogs the mouth and nose; if the victim is buried with the airway already blocked, asphyxiation will occur more quickly. Snow that was light and airy when a skier carved turns becomes viselike in its new form. Where the snow might have been 80% air to begin with, it might be less than 50% air after an avalanche, and it is much less permeable to airflow, thereby making it harder for the victim to breathe. Snow sets up hard and solid after an avalanche. It is almost impossible for victims to dig themselves out, even if they are buried less than a foot deep. Hard debris also makes recovery very difficult, so a sturdy shovel is essential. The pressure of the snow in a burial of several feet is sometimes so great that the victim is unable to expand the chest to draw a breath.42 Warm exhaled breath freezes on the snow around the face, eventually forming an ice lens that cuts off all airflow. This process usually takes longer to develop than do snow-clogged airways, but the result is still death by asphyxiation.
90
Alive % Dead % Survival %
80 70 60 50 40 30 20 10 0 1
2
3
4
5
6
7
Burial depth (feet) FIGURE 2-30 Percent survival versus depth of burial for U.S. avalanche fatalities and survivors in direct contact with the snow (i.e., not in a structure or vehicle) from the winter of 1999-2000 to the winter of 2008-2009. (Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.)
Statistics regarding survival are derived from a large number of avalanche burials (Figures 2-30 and 2-31). When compiling these figures, only persons who were totally buried in direct contact with the snow were included. Victims who were buried in the wreckage of buildings or in vehicles are not included, because they can be shielded from the snow in situations in which sizable air pockets may be present. Under such favorable circumstances, some victims have been able to live for days. In 1982, Anna Conrad lived for 5 days in Alpine Meadows, California, in the rubble of a demolished building; this is the longest avalanche victim survival on record in the United States. A completely buried victim has a poor chance of survival, which is related to both time and depth of burial, as shown in Figure 2-30. Survival diminishes with increasing burial depth,
Survival probability (%)
100 Swiss data 1981 to 1998 (N = 638)4 Swiss data 1981 to 1991 (N = 422)9
80 60 40 20 0 0
20 40 60 80 100 120 140 160 180 200 220 240 Time buried under avalanche (min)
FIGURE 2-31 The solid blue line indicates data from Switzerland for survival probability for completely buried avalanche victims in open areas from 1981 to 1998 (n = 638) in relation to time (minutes) buried under the snow. The median extrication time was 37 minutes. The dashed red line represents survival probability for completely buried avalanche victims in open areas (n = 422) on the basis of the Swiss data for 1981 to 1991. (Data from Falk M, Brugger H, Adler-Kastner L: Avalanche survival chances, Nature 386:21, 1994. From Brugger H, Durrer B, Adler-Kastner L, et al: Field management of avalanche victims, Resuscitation 51:7, 2001, with permission.)
because it takes longer to uncover a victim who is buried deeper. To date, no one in the United States who has been buried deeper than 3 m (10 feet) has been recovered alive; however, in Europe, two victims survived burials of 6 to 7 m (20 to 23 feet).45 Burial depth is important in avalanche survival, but time is the true enemy of the buried victim. Figure 2-31 shows survival probability function calculated from European data, which have become a classic demonstration of decreasing survival chances with increasing burial time. During the first 15 minutes, most people (≈90%) are found alive. At 30 minutes, an equal number are found dead and alive. After 30 minutes, more are found dead than alive, and the survival rate continues to diminish with longer burial time. Speed is essential to the search. Buried victims can live for several hours beneath the snow under favorable circumstances, and rescuers should therefore never abandon a search prematurely. A miner in Colorado who was buried by an avalanche near a mine portal was able to dig himself free using his hard hat from nearly 1.8 m (6 feet) of debris after approximately 22 hours. In 2003, two snowshoe hikers caught near Washington’s Mt. Baker survived burials of 23 and 24 hours. Such long survival times are a reminder that no rescue should be abandoned prematurely on the assumption that the victim is dead.
RESCUE STATISTICS A buried victim’s chance of survival directly relates not only to the depth and length of time of burial but also to the type of rescue. Table 2-2 shows the statistics for survival as a function of the rescuer. Buried victims rescued by companions or groups nearby have a much better chance of survival than those who are rescued by organized rescue teams. Companions can potentially rescue a victim in minutes, whereas it may take hours to mount an organized rescue. Of people who are found alive, 78% were rescued by companions, and 12% were found by an organized rescue team. Table 2-3 compares the results of rescue by different techniques. Sixty-eight percent of victims (38 of 56) buried with a body part (e.g., a hand) or an attached object (e.g., a ski tip) protruding from the snow were found alive. In most cases, this was simply good luck, but, in some cases, it was the result of actively fighting with the avalanche or of thrusting a hand upward when the avalanche stopped. Either way, this statistic shows the advantages of a shallow burial: less time required to search, shorter digging time, and the possibility of attached objects or body parts being visible on top of the debris. Of the fatalities in this category, many of the individuals were skiing or snowboarding alone with no companion present to identify the hand or ski tip and provide rescue. Organized probe lines have found more victims than any other method, but, because of the time required, most victims (88%) are recovered after they are already dead. During the past 10 years, the avalanche transceiver has been used to find more victims than any other method; it is the best method for finding the completely buried victim if it is carried and used correctly. The bad news is that the mortality rate over the last 10 years was 60% (see Table 2-3). Unfortunately most companions cannot use a transceiver fast enough to save a life. However, even in textbook rescues (i.e., the signal was quickly located and the victim is dug free in a short time), many victims did not survive. Organized probe lines are an effective way to find a buried victim, but, because this method requires many rescuers and much time, most victims (i.e., 98%) are recovered dead. Despite the sound-insulating properties of snow, seven victims who were shallowly buried were able to yell and be heard by rescuers (i.e., voice contact; see Table 2-3). These statistics point out the extreme importance of rescue skills. Organized rescue teams (e.g., ski patrollers, mountain rescuers) must be highly practiced. They must have adequate training, manpower, and equipment to perform a hasty search and probe the likely burial areas in a minimal amount of time. For backcountry rescues, the buried victim’s companions remain the best hope for survival. The need to seek outside rescue units practically ensures a body recovery mission. 55
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TABLE 2-4 Injuries Among Survivors of Avalanche
Accidents (Partial and Total Burials)
Total injuries Major orthopedic injuries Hypothermia requiring hospital treatment Skin and soft-tissue injuries Craniofacial injuries Chest injuries Abdominal injuries
Utah
Europe
9 (total of 91 avalanche accidents) 3 (33%) 2 (22%)
351 (total of 1447 avalanche accidents) 95 (27%) 74 (21%)
1 (11%) — 3 (33%) —
84 83 7 4
(25%) (24%) (2%) (1%)
From Grossman MD, Saffle JR, Thomas F, et al: Avalanche trauma, J Trauma 29:1705, 1989.
Avalanche Victim Physiology and Medical Treatment After Rescue AVALANCHE VICTIM MORBIDITY AND MORTALITY Asphyxiation is the most common cause of death during avalanche burial. More than 75% of avalanche deaths result from asphyxiation; less than 25% result from trauma, and very few result from hypothermia.8,25,30,31,42,45 These statistics vary with geographic location and the terrain over which the avalanche slides. Because asphyxiation is the major cause of death during avalanche burial, time to extrication is a major determinant of survival. Fully buried avalanche victims have a more than 90% chance of survival if they are extricated within 15 minutes, but this chance drops to only 30% after about 35 minutes (see Figure 2-31),11,17 thus emphasizing the need for a swift companion rescue at the avalanche site. Survival beyond 30 minutes of burial requires an air pocket for breathing. If the air pocket is large enough, avalanche victims may survive for hours and develop severe hypothermia. Traumatic injury to avalanche victims depends on the terrain over which the avalanche occurred. If the victim is carried through trees or over rock bands, then trauma is more likely and may result in death. Grossman and colleagues,25 with the use of data that included both partial and complete burials in Utah and Europe, reported that traumatic injuries occurred among 25% of survivors of avalanche accidents. The most common traumatic injuries were major orthopedic, soft-tissue, and craniofacial injuries (Table 2-4). Hohlrieder and colleagues26 reviewed the injuries of 105 avalanche victims in Austria and noted mostly no or only minor injuries (Table 2-5). They also noted a high incidence of
TABLE 2-5 Pattern of Injury Among
105 Avalanche Victims
Trauma Cerebral trauma Chest trauma: all Chest trauma: sternum or rib fracture (n = 16) Chest trauma: pneumothorax or hemothorax (n = 6) Spine fracture: all Spine fracture: cervical (n = 3) Spine fracture: thoracic (n = 1) Spine fracture: lumbar (n = 3) Abdominal trauma Pelvic fracture Extremity trauma: all Extremity trauma: lower-leg fracture (n = 8) Extremity trauma: shoulder dislocation (n = 6) Extremity trauma: femur fracture (n = 4)
Frequency (n) 2 18
7
1 1 20
From Hohlrieder M, Brugger H, Schubert HM, et al: Pattern and severity of injury in avalanche victims, High Alt Med Biol 8:56, 2007.
56
lower-leg fractures and shoulder dislocations, which were thought to be caused by the attached skis and poles causing additional mechanical leverage on the extremities. Spine fractures were found in 7% of the cohort. Johnson and colleagues29 reviewed autopsy reports from 28 avalanche deaths in Utah over a 7-year period. Among 22 avalanche victims who died from asphyxiation, one-half experienced mild or moderate traumatic brain injury, which the authors argued could cause a depressed level of consciousness and contribute to death from asphyxiation. All six of the avalanche deaths that were the result of trauma involved severe traumatic brain injury. In another review of 56 avalanche fatalities in Utah, all three deaths that were due solely to trauma involved evidence of head injury.31 Although these studies demonstrate the role of head injury in avalanches, Hohlrieder and colleagues26 noted that the only two solely traumatic deaths in their series were caused by isolated fracture and dislocation of the cervical spine. This reveals the force that an avalanche applies to the human body and the vulnerability of the cervical spine in an avalanche, because repeated hyperflexion and hyperextension can occur. In addition, it emphasizes the need for proper cervical spine stabilization during the rescue and resuscitation period. Avalanche victims can sustain virtually any trauma type to any body part during their slide. The head and neck are especially vulnerable to the enormous forces, and these areas appear to be the cause of much of the traumatic mortality during avalanche accidents.
RESPIRATORY PHYSIOLOGY OF AVALANCHE BURIAL Asphyxiation occurs during avalanche burial because inhaled snow occludes the upper airway or because expired air is rebreathed. Acute upper airway obstruction that results in asphyxiation is one of the causes of asphyxiation during the first 15 to 30 minutes of avalanche burial. Asphyxiation caused by rebreathing expired air may also occur during this time if there is no air pocket for breathing, or it may be delayed if an air pocket is present. Inspired air contains 21% oxygen and less than 0.03% carbon dioxide; expired air contains about 16% oxygen and 5% carbon dioxide. Rebreathing expired air in an enclosed space results in progressive hypoxia and hypercapnia that eventually causes death from asphyxiation. The larger the air pocket, the greater the surface area for the diffusion of expired air into the snowpack and for the diffusion of ambient air from the snowpack into the air pocket and thus a longer survival time before death occurs as a result of asphyxiation. An ice mask is formed when water in the warm, humid, expired air freezes on the snow surface in front of the face. Because this barrier is impermeable to air, it accelerates asphyxiation by preventing diffusion of expired air away from the air pocket in front of the mouth. The physiology of asphyxiation from breathing with an air pocket in the snow was demonstrated in a study by Brugger and colleagues.14 Subjects sat outside a snow mound and breathed through an air-tight mask connected by respiratory tubing to 1- or 2-L (0.9- or 1.8-quart) air pockets in the snow. The snow had a density similar to that of avalanche debris (i.e., 150 to 600 kg/m3 or 15% to 60% water). The initial fraction of inspired oxygen (FIO2) in the air pocket was 21%, and the initial fraction of inspired carbon dioxide (FICO2) was near 0%. As expired air was rebreathed in the air pocket over about 30 minutes, the FIO2 decreased to about 10% and the FICO2 increased to about 6% (Figure 2-32, online). These changes in the oxygen and carbon dioxide levels in the air pocket resulted in decreased arterial oxygen saturation as measured by a pulse oximeter and increased end-tidal partial pressure of carbon dioxide. Most subjects were not able to complete the entire 30 minutes of the study and had to stop as a result of dyspnea, hypercapnia, and hypoxia. Hypoxemia and hypercapnia occur as expired air is rebreathed. A smaller air pocket or denser snow causes the more rapid development of hypoxia and hypercapnia. Larger air pockets and less-dense snow allow for more mixing of expired air with ambient air in the snowpack and result in longer survival times before hypoxia and hypercapnia become severe enough to cause death from asphyxiation. Brugger and
MEDICAL TREATMENT AND RESUSCITATION OF AVALANCHE BURIAL VICTIMS The key points regarding assessment and treatment of an extricated avalanche burial victim are presented in an algorithm in Figure 2-34. An initial impression of the level of consciousness is made as the head is exposed and cleared of snow. Opening the airway and ensuring adequate breathing are the primary medical interventions. Every effort should be made to clear the airway of snow as soon as possible and to provide assisted ventilation if breathing is absent or ineffective. These measures should be instituted as soon as possible and not be delayed until the entire body is extricated. If traumatic injury to the spinal column is suspected or if there is evidence of head or facial trauma, then the spinal column is immobilized as the airway is opened, adequate breathing ensured, and oxygen provided. When the avalanche burial victim is unconscious, maintaining the airway may be challenging because of space limitations of the opening of the snow leading to the victim. If endotracheal intubation is required for the unconscious apneic patient who is not yet fully extricated from snow burial, then the inverse intubation technique may be required.36 With this technique, the laryngoscope is held in the right hand while straddling the victim’s body and facing the head and face. While facing the victim, insert the laryngoscope blade into the oropharynx with the right hand so that the larynx and cords can be visualized by leaning over and looking into the victim’s mouth; the endotracheal tube is then passed through the vocal cords with the left hand. After an adequate airway and breathing are established and supplemental oxygen is provided, circulation is assessed. The conscious patient is assumed to have a perfusing rhythm, and further treatment is directed at treating mild hypothermia and traumatic injuries. A patient who is found unconscious but with a pulse may have moderate or severe hypothermia and should be handled gently to avoid precipitating ventricular fibrillation. The medical treatment of this patient is focused on ensuring adequate oxygenation and ventilation, either noninvasively with a bag-valve-mask device or by endotracheal intubation if clinically indicated, and on immobilizing the spinal column for transport and treatment of any obvious signs of trauma. Intravenous access may be obtained and warmed isotonic fluids infused. Treatment of hypothermia is described later in this chapter.
Extrication from avalanche burial
CHAPTER 2 AVALANCHES
colleagues11 suggest that equilibrium may occur when FIO2 and FICO2 in an air pocket reach a plateau within a physiologically tolerable range, and the avalanche victim may then survive prolonged burial. This may occur even with small air pockets, which has been observed when extricating avalanche burial survivors of up to 2 hours’ duration. Radwin and colleagues35 demonstrated that there is sufficient ambient air in densely packed snow to permit normal oxygenation and ventilation as long as all expired air is diverted out of the snowpack. They studied subjects who were totally buried in dense snow who inhaled air directly from the snowpack (density, 300 to 680 kg/m3 or 30% to 68% water) through a two-way nonrebreathing valve attached to respiratory tubing that diverted all expired air to the snow surface. Subjects maintained normal oxygenation and ventilation for up to 90 minutes. This study demonstrated that there is sufficient air for breathing in snow with a density similar to that of avalanche debris as long as expired air is not rebreathed. This is the principle behind the AvaLung (see Avalanche Rescue Equipment, earlier), which has been designed to prolong survival during avalanche burial; Figure 2-21 describes its operation. Although the device prevents the formation of an ice mask, the expired air permeates around the buried person’s body and through the snow, and it eventually contaminates inspired air. Grissom and colleagues23 compared breathing with this device while buried in dense snow and breathing without the device but with a 500-cc (0.45-quart) air pocket in the snow. Mean burial time was 58 minutes when breathing with the device and 10 minutes when breathing with a 500-cc air pocket in the snow. Development of hypoxia and hypercapnia was significantly delayed by breathing with the device (Figure 2-33, online). The AvaLung has resulted in survival during actual avalanche burials.34
Yes
Conscious?
Treat for hypothermia I (core temperature >32° C) or hypothermia II (28 to 32° C): clear the airway, provide oxygen, dry warm insulation, hot drink containing sugar if awake, medical transport to closest appropriate facility.
No
Yes
Breathing?
Treat for hypothermia II (core temperature 28 to 32° C) or hypothermia III (24 to 28° C): clear the airway, provide oxygen, assist ventilations, consider intubation and ventilation with heated and humidified oxygen, dry warm insulation, heated IV fluid, medical transport to tertiary care facility.
No
Yes
Obvious fatal injuries?
Cease efforts
No Clear the airway, assist ventilation, provide oxygen, intubate, warm IV fluids, handle gently. Check for pulse after ventilating and oxygenating. If no pulse start CPR. Check ECG.
Rhythm asystole?
No
If rhythm is VF defibrillate once if core temperature <30° C and hold ACLS drugs until rewarmed. Treat for hypothermia III or IV as indicated below.
Yes Burial >1 hour?
No
Yes Core temperature <30° C?
No
Yes Airway patent during burial?
No
Death from asphyxiation likely. Resuscitation per ACLS protocol. Cease efforts when clinically indicated. May continue resuscitation and transport to the nearest appropriate medical facility. A K+ of greater than 12 mEq/L suggests that resuscitation may be futile and death has occurred from asphyxiation.
Yes
Treat for hypothermia III or IV (core temperature <28° C): intubation, assisted ventilation with warmed humidified oxygen, monitor ECG, CPR, warmed IV fluids, dry insulation, medical transport to a facility capable of extracorporeal rewarming. FIGURE 2-34 Assessment and medical care of extricated avalanche burial victims.
If a pulse is not present after opening the airway and ventilating the patient, cardiopulmonary resuscitation (CPR) is begun. However, before CPR is initiated, careful evaluation for the presence of a pulse should occur. Avalanche burial victims are hypothermic, which causes peripheral vasoconstriction and makes pulses difficult to palpate. In addition, moderate to severe hypothermia causes depression of respiration and bradycardia. Before initiating CPR, palpation for a pulse should be done for a period that is long enough to ensure that spontaneous circulation is not present, which may take 30 seconds or more in a wilderness setting. American Heart Association CPR guidelines 57
victims who are extricated from burials of more than 1 hour who have no signs of life but who are severely hypothermic (i.e., who have a core temperature of <30° C [86° F]) and who have a patent airway may be considered for ongoing resuscitation and transport to a medical facility that is capable of extracorporeal rewarming (Figure 2-35). Avalanche burial victims who are extricated in cardiac arrest after more than 1 hour of burial and who have an obstructed airway have most likely died from asphyxiation, and continuing resuscitation efforts until rewarming occurs is unlikely to result in survival. In a study by Locher and Walpoth,30 none of 13 avalanche victims who were found in cardiac arrest after burials of 30 to 165 minutes’ duration survived. These results suggest that cardiac arrest was the result of asphyxiation rather than hypothermia. An air pocket for breathing and a patent airway must be present for an avalanche burial victim to survive long enough to develop severe hypothermia. If an air pocket for breathing is not present or if the airway is obstructed, the avalanche victim who is extricated from snow burial in cardiac arrest has most likely died from trauma or asphyxiation. This is not meant to discourage initial attempts at resuscitation but rather to suggest that prolonged CPR may be a futile exercise. It is always warranted to initially start CPR to see if return of circulation can be achieved in a reasonable time. This is because the rescuer can never know when the avalanche burial victim went into cardiac arrest; it may have been minutes or hours before extrication. The case of an 11-year-old boy in Utah who was extricated in cardiac arrest after 40 minutes of full burial demonstrates why it is important to immediately start CPR. Return of circulation was achieved 5 minutes after the initiation of CPR, and the boy went on to full recovery. When laboratory testing equipment is available, serum potassium level can be measured and used as a prognostic indicator for avalanche burial victims in cardiac arrest.2,7,37 In an adult hypothermic avalanche burial victim in cardiac arrest, a serum potassium level of greater than 10 mmol/L may, in combination with other factors, indicate that resuscitation efforts will not be successful. If the serum potassium is greater than 12 mmol/L in an adult or a child, resuscitation efforts should be terminated.7
38.0 Extrication 37.5 Afterdrop Rewarming Temperature (° C)
PART 1 MOUNTAIN MEDICINE
suggest checking for a pulse for at most 10 seconds,1 which may not be long enough to confirm that there are no signs of life in an extricated avalanche burial victim. CPR initiated on a severely hypothermic patient who actually has a perfusing rhythm may cause ventricular fibrillation. The State of Alaska Cold Injuries Guidelines recommend checking for a pulse for 60 seconds, then providing assisted ventilations, and then checking again for another 60 seconds before starting chest compressions.43 We suggest that a defined timeline for palpating a pulse may not be appropriate for all situations and that the rescuer should take enough time to confirm that there are no signs of life before beginning chest compressions. In a pulseless avalanche burial victim, electrocardiographic monitoring should be used to assess cardiac rhythm, or, alternatively, an automatic external defibrillator may be applied. In the moderate or severely hypothermic patient in ventricular fibrillation with a core body temperature of less than 30° C (86° F), defibrillation should be performed according to published guidelines,1,2 with the caveat that, after multiple unsuccessful defibrillations, further defibrillation may be deferred until rewarming is underway as chest compressions continue. Drugs may be administered as part of advanced cardiac life support in accordance with published guidelines.2 The likelihood of the successful resuscitation of an avalanche burial victim who is in cardiac arrest at the time of extrication depends on whether cardiac arrest occurred from asphyxiation or from hypothermia. Factors that may be used to indicate the likelihood of survival in an extricated avalanche burial victim are the length of time of burial, airway patency, core temperature, and serum potassium level.2,7 For burials of less than 1 hour with a core body temperature of more than 30° C (86° F) where the airway is obstructed, resuscitation is unlikely to be successful, because death has most likely occurred as a result of asphyxiation. If the airway is patent with burial duration of less than 1 hour, there is a greater chance of successful resuscitation. Even if the airway is occluded, resuscitation should always be attempted for a limited time period if feasible for safety reasons. Avalanche
37.0
36.5
36.0
35.5
Esophageal core temperature Rectal core temperature
35.0 –60
–50
–40
–30
–20
–10
0
10
20
30
40
50
60
Time relative to extrication (min) FIGURE 2-35 Esophageal ( ; Tes) and rectal ( ; Tre) core temperatures in ° C ± standard deviation during snow burial and after extrication during passive rewarming. Time zero is relative to extrication from snow burial. At extrication from snow burial, both Tes and Tre show an afterdrop, but the afterdrop of Tes is attenuated and the Tes shows rewarming of the core as insulation is provided to the shivering subject. Tre lags behind Tes during rewarming, which represents temperature gradients from the body core to the body shell as rewarming occurs. These findings suggest that core cooling rates during avalanche burial will cause only mild hypothermia during burials of up to about 1 hour in duration, but significant afterdrop can occur among avalanche burial victims after they are extricated from snow burial. Insulation should be provided as quickly as possible. Avalanche burial victims who are awake and shivering after extrication from snow burial can be rewarmed in the field by spontaneous endogenous rewarming (i.e., providing insulation and allowing shivering to occur to rewarm the avalanche burial survivor). (From Grissom CK, Harmston CH, McAlpine JC, et al: Spontaneous endogenous rewarming of mild hypothermia after snow burial, Wilderness Environ Med 21:229, 2010.)
58
In avalanche burial victims who are extricated alive, hypothermia is the major medical problem that requires treatment.8-10 Clinical definitions of hypothermia severity correlated with core body temperature are shown in Table 2-6. As the patient is extricated from snow burial, warm dry insulation is provided during packaging, and wet clothing is removed as soon as is practical. If the patient is unconscious, moderate or severe hypothermia is suspected, and handling should be gentle to avoid precipitating ventricular fibrillation. When treatment of moderate or severe hypothermia is clinically indicated, intravenous access is obtained, and warmed (42° C [107.6° F]) isotonic fluid is infused. If the patient is unconscious, endotracheal intubation is appropriate to provide adequate oxygenation and ventilation with heated (40° to 45° C [104° to 113° F]) humidified oxygen. The goal of treating moderate to severe hypothermia before reaching the hospital is to limit temperature afterdrop during medical transport to the location at which definitive rewarming can occur. The shivering patient with mild hypothermia can rewarm in the field if dry insulation is provided.19 If the patient is conscious and alert, warm fluids that contain sugar may be given by mouth. If possible, patients with mild hypothermia should remain supine until rewarming has occurred to prevent a greater temperature afterdrop from ambulation. Optimally the severity of hypothermia is determined by a core body temperature measurement in the field, preferably with the use of an esophageal probe, but tympanic membrane sensors or rectal probes may also be used. If core body temperature cannot be measured in the field, the severity of hypothermia may be estimated with the use of Swiss hypothermia stages I through IV as determined by the clinical presentation (see Table 2-6).9 Severity of hypothermia may also be estimated from the time that the victim was buried and the average rate of core temperature cooling during burial. Grissom and colleagues22 measured core temperature cooling rate during snow burial in a controlled experiment. Among subjects who were buried in dense snow for up to 60 minutes wearing a lightweight clothing insulation system while breathing with an artificial device (i.e., the AvaLung), core body temperature cooling rate was about 1.3° C (2.3° F) per hour. Retrospective studies of core temperature on hospital arrival by Locher and Walpoth30 suggest that the average core temperature cooling rate is 3° C (5.4° F) per hour (range, 0.75° to 4.75° C [1.4° F to 8.6° F] per hour in survivors), which is greater than the 1.3° C (2.3° F) per hour that was estimated by Grissom and colleagues.24 The higher rate of cooling reported by Locher and Walpoth is based on a known time of burial and known arrival time at the hospital where core body temperature was recorded, and does not differentiate between core temperature cooling rate during snow burial and cooling rate during medical transport. Burial cooling rates are accelerated by hypercapnia that occurs during snow burial. Grissom and colleagues21 found that cooling
TABLE 2-6 Hypothermia Clinical Prehospital
Evaluation: Swiss Society of Mountain Medicine Definitions
Hypothermia I: Patient alert and shivering (core temperature ≈35-32° C [95-90° F]) Hypothermia II: Patient drowsy and not shivering (core temperature ≈32-28° C [90-82° F]) Hypothermia III: Patient unconscious (core temperature ≈28-24° C [82-75° F]) Hypothermia IV: Patient not breathing (core temperature <24° C [75° F]) Data from Brugger H, Durrer B, Adler-Kastner L: On-site triage of avalanche victims with asystole by the emergency doctor, Resuscitation 31:11, 1996; and Brugger H, Durrer B, Adler-Kastner L, et al: Field management of avalanche victims, Resuscitation 51:7, 2001.
rates measured in hypercapnic as compared with normocapnic buried subjects were 1.28° C and 0.97° C, (34.3° F and 33.7° F) respectively. In addition, minute ventilation, respiratory heat loss, total metabolic rate, and respiratory muscle metabolic rate were greater for the hypercapnic subjects. The same study group also reports that the afterdrop cooling rate increases transiently after extrication from snow burial.20 The afterdrop cooling rate accelerated fourfold for a mean of 12 minutes after extrication in subjects who were buried in snow for 60 minutes. An accelerated cooling rate during and after extrication places avalanche burial victims at greater risk for complications caused by hypothermia. Every effort should be made by rescue personnel to prevent further heat loss in avalanche burial victims starting as soon as possible during extrication from the snow. Core temperature cooling rate during avalanche burial may also be estimated from anecdotal reports of prolonged survival during avalanche burial. In one case, a 25-year-old male snowboarder with a large air pocket in front of his body survived 20 hours of avalanche burial.41 At the time of extrication, he had a tympanic core body temperature of 25.6° C (78.1° F) in snow at 5° C (23° F) and was spontaneously breathing; he had a Glasgow Coma Scale score of 8, heart rate of 35 beats/min, and a palpable pulse. Core body temperature cooling rate in this anecdotal report was about 0.6° C (1.1° F) per hour. The large air pocket probably allowed for adequate diffusion of expired air away from inspired air and prevented asphyxiation. In that same rescue, the survivor’s companion was found dead from asphyxiation after 20 hours of burial with a tympanic core body temperature of 6° C (42.8° F), which is an average core body temperature cooling rate of about 1.5° C (2.7° F) per hour. The highest reported rate of core body temperature cooling in an avalanche burial victim is 9° C per hour, which was reported for a 29-year-old male who was buried for 100 minutes and extricated alive with an epitympanic core temperature of 22° C.33 He was intubated and ventilated, but went into ventricular fibrillation during helicopter transport and was transported with ongoing CPR (except for 15 minutes during the initial helicopter evacuation from the scene to a local hospital). He was in cardiopulmonary arrest for 150 minutes before defibrillation on the fifth attempt resulted in return of spontaneous circulation after cardiopulmonary bypass rewarming. He made a full recovery. These anecdotal reports demonstrate that core body temperature cooling rates during avalanche burial may vary significantly and that survival after a long-duration avalanche burial or after cardiac arrest after extrication from avalanche burial is possible.
Summary Asphyxiation is the major cause of death during avalanche burial, and it is time dependent. Avalanche burial victims who are extricated within 15 minutes have a greater than 90% chance of survival, but this decreases to about a 30% chance of survival if they are extricated after 30 minutes, thus emphasizing the need for companion rescue with use of avalanche transceivers and shovels. Survival beyond 30 minutes of burial depends on the presence of an air pocket for breathing. The larger the size of the air pocket, the longer that survival is possible during the burial; this is because asphyxiation during avalanche burial is caused by rebreathing expired air that contains 16% oxygen and 5% carbon dioxide. A larger air pocket provides more surface area for diffusion of expired air away from an avalanche burial victim, thus allowing more ambient air from the snowpack to diffuse into the air pocket for inspiration. Opening the airway, ensuring adequate ventilation, and providing supplemental oxygen are the primary medical interventions for an extricated avalanche burial victim. If the victim is conscious, mild hypothermia is most likely, and treatment consists of proving warm, dry insulation and warm, sugar-containing liquids. Rewarming will occur through shivering. Avalanche burial victims who are not shivering have progressed to moderate or severe hypothermia and require medical transport to a hospital for definitive rewarming. Unconscious avalanche burial victims who are breathing may require endotracheal intubation for airway control and assisted ventilation, and are most likely moderately to severely hypothermic. Victims who are extricated in asystolic cardiac arrest have 59
CHAPTER 2 AVALANCHES
HYPOTHERMIA IN THE AVALANCHE BURIAL VICTIM
most likely died from asphyxiation; however if the burial time is greater than 1 hour and the core body temperature is less than 30° C (86° F), these individuals may be severely hypothermic and resuscitation efforts may be continued while they are transported to a medical facility that is capable of extracorporeal rewarming. Head and cervical spine trauma should be anticipated, although any injury pattern can occur. Many victims have no traumatic injuries.
Acknowledgments. The authors thank Betsy R. Armstrong, Richard L. Armstrong, and Knox Williams for their contributions to previous editions of this text.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 3
Lightning Injuries MARY ANN COOPER, RONALD L. HOLLE, CHRISTOPHER J. ANDREWS, AND RYAN BLUMENTHAL
Historical Overview* Lightning has caused injuries to humans since humans evolved on Earth. It has played a major part in nearly every ancient religion and culture. Priests, some of whom were the earliest astronomers, also became proficient at weather prediction, interpreting changes in weather as omens of good or bad fortune, sometimes to the advantage of their political mentors. To this day, it continues to engender stories, perceptions, and myths and is a popular topic for the press and science and weather documentaries.114,234 Lightning was often depicted in the art of ancient cultures and religions and has long been feared as an atmospheric flash of supernatural origins. A roll seal from Akkadian times (2200 BC) portrays a goddess holding sheaves of lightning bolts in each hand. Next to her, a weather god drives a chariot and creates lightning bolts by flicking a whip at his horses, while priests offer libations. A relief found on a castle gate in northern Syria (900 BC) depicts the weather god Teshub holding a three-pronged thunderbolt (Figure 3-1, online). Beginning around 700 BC, Greek artists began to incorporate lightning symbols representing Zeus’s tool of warning or favor. Zeus, as the king of the gods, could control the weather. Early Greeks believed that lightning was his weapon and that when lightning struck Earth, it was a direct sign of Zeus’s presence or influence. The ancient Greek poet, Hesiod, called him the “cloudgatherer” and the “thunderer.” Zeus was also concerned with hospitality. If you treated a guest or stranger badly, you could outrage Zeus and not be treated so favorably (Figure 3-2). *References 72, 114, 234, 274.
FIGURE 3-2 Zeus, king of gods who hurls the lightning.
60
Because lightning was a manifestation of the gods, any spot struck by lightning was regarded as sacred. Temples often were erected at these sites, where the gods were worshipped in an attempt to appease them. Roman mythology saw lightning as more ominous than did the Greeks, with Jupiter using thunderbolts as tools of vengeance and condemnation. Romans killed by lightning strikes were considered damned by Jupiter and denied burial rituals. Several Roman emperors wore laurel wreaths or sealskin to ward off lightning strikes. Important matters of state were often decided on observations of lightning and other natural phenomena. Both Seneca and Titus Lucretius discussed lightning in their treatises on natural events, and Plutarch noted that sleeping persons, having no spirit of life, were immune to lightning strikes. The Navajo Indians of North America have a story about the hero Twins who used “the lightning that strikes straight” and “the lightning that strikes crooked” to kill several mythic beasts that were plaguing the People (Navajo) and in the process created the Grand Canyon. Bantu tribesmen in Africa believed that lightning was due to the flashing feathers of a mystic bird whose flapping wings produced the sound of thunder. Umpundulo is the name of the lightning bird-god (Figure 3-3, online). They hold that lightning has great power in their healing rituals. Even today, their medicine men go out in storms and bid lightning to strike far away. Sand paintings show the lightning bolt as a wink in the thunderbird’s eye. Lightning is associated with wind, rain, and crop growth. The art of native Australians incorporates lightning symbols, where the lightning spirit is depicted as having axes, attached to his joints, that beat together to make thunder. Lightning also played a role in Buddhist symbolism. Early statues of Buddha show him carrying a thunderbolt with arrows at each end. Although lightning is most frequently rendered as fire, it has also been represented as stone axes hurled from the heavens. In the pantheistic Hindu religion, Indra (Figure 3-4, online) was the god of heaven, lightning, rain, storms, and thunder. The Maruts used thunderbolts as weapons. The Yakuts of eastern Asia regard rounded stones found in fields hit by lightning as thunder axes and often use the powdered stones in medicines and potions. In Chinese mythology, the goddess of lightning, Tien Mu, used mirrors to direct bolts of lightning. She was one of the deities of the “Ministry of Thunderstorms” of ancient Chinese religion. Scandinavian mythology alludes to Thor (Figure 3-5, online), the thunderer, who was the foe of all demons. Thor tossed lightning bolts at his enemies, and Thursday is named for him. For the Vikings, lightning was produced by Thor as his hammer struck an anvil while riding his chariot across the clouds. Throughout early Europe, church bell ringers would make as much noise as possible, hoping to scare away the storms from
For online-only figures and videos, please go to www.expertconsult.com
Common Modern Myths, Superstitions, and Misconceptions* The Roman author Pliny noted that a man who heard thunder was safe from the lightning stroke. This implies that the person who hears the thunder is far enough away from the lightning strike to survive it, although today we know the person may still be injured. Persons so close that they cannot hear the thunder are much more likely to be injured. Persons who receive ground current are more likely to report both seeing the flash and hearing the stroke, indicating that the main stroke was some distance away. Many myths about lightning, including the notion that lightning strikes are invariably fatal, persist (Box 3-1). According to an American study of cases reported in the lightning literature since 1900, lightning strike carries a mortality rate of 30% and a morbidity rate of 70%.64 A slightly different statistical interpretation of the same data yielded a mortality figure of 20%.18 Because literature reports are usually biased toward severe or interesting cases, case reviews tend to overestimate mortality rate. In reality, mortality rate may be as low as 5% to 10%.54 Most people suspect that the major cause of death is from burns. However, the only cause of immediate death is from cardiac arrest.64 Persons who are stunned or lose consciousness without cardiopulmonary arrest are highly unlikely to die, although they may still have serious and long-term sequelae.67,74,212,232 Delayed causes of death include suicide induced by depression and disability wrought by lightning.67 Most people “have enough sense to come out of the rain” and seek shelter when storm clouds roll overhead. Unfortunately, a large number of injuries occur as the storm is approaching because people misjudge it, do not pay attention to warning signs, or want to finish one more thing before seeking shelter.66,135 Lightning may travel nearly horizontally as far as 10 miles or more in nearly any direction from a thunderstorm and seem to occur “out of a clear blue sky,” or at least when the day is still *References 66, 72, 234, 274.
sunny where the person is located. At least 10% of cloud-toground strikes occur when no rain is occurring at the time and location of the strike. The faster the storm is traveling and the more violent it is, the more likely a fatal strike will occur. Another dangerous time is at the end of a thunderstorm, when people go out to begin activities before the danger has passed. Lightning casualties have decreased dramatically in the last few decades,138,143,217 but people continue to be injured when they could easily be in safe shelters only a few feet away from where they were hit. “When thunder roars, go indoors” is the teaching mantra of the National Weather Service’s (NWS’s) Lightning Awareness Week for individuals and small groups (http://www. lightningsafety.noaa.gov).217 Although one might suppose seeing lightning is a reliable warning, this is not always the case. On the great plains of the United States, lightning may be seen up to one-hundred miles away, but in the woods of Maine, it may not be seen at all before people are in danger. Thus, seeing lightning is too variable to use reliably because it may overestimate or underestimate the risk. Thunder is a much more reliable tool for estimating distance and danger, because it is seldom audible more than 10 miles away. Unfortunately, in special cases, such as in a city, heavy traffic areas, or a noisy sports stadium, it may be less audible. The flash-to-bang method is now used less often than it was a decade ago, because of uncertainty in linking flashes to thunder, as well as confusion in how to calculate the distance. The “30-30 rule,” a modification of the flash-to-bang method, was adopted in the mid-1990s as a catchy teaching tool.27,217 The first 30 stood for counting the seconds from seeing lightning to hearing its thunder at the beginning of a storm. If the count was 30 or less, the person was in danger and should be seeking safer shelter. It soon became apparent that the recommendation should be that the person actually be in safe shelter at that point. This part of the rule was replaced by “When thunder roars, go indoors.”217 The second 30 is still useful and indicates the number of minutes at the end of the storm after seeing the last lightning or hearing the last thunder that one should wait before once again going outside and resuming activity. Although the “30-30 rule” has been abandoned for individuals, it is useful for some larger venues such as industrial sites.216,217 One of the most dangerous and consistent places of injury is standing near a tree or other tall object. Tent poles, regardless of their construction, can be a source of lightning injury. Standing in an isolated flat area (larger than 15 to 30 m [49 to 98 feet] in diameter) is a recipe for disaster. Lighting injuries may occasionally occur indoors, particularly from contact injury or side flashes from plumbing fixtures, computers, hard-wired telephones or electronic game devices, and other appliances.8,95,96 With a hard-wired phone, persons may suffer acoustic damage,17,209 neurocognitive deficits, death, or other lightning-related problems, because the phone system in most houses is not grounded to the house’s electrical system and so acts as a conduit for lightning either to come into the home or to exit from it. Cell phones, on the other hand, offer complete protection from the indoor electrical effects.* Because of the nearly universal use of cell phones, more injuries have been reported to people using them. It has been mistakenly concluded that they “attract” lightning (Figure 3-7, online). However, injury occurs because mobile phones, iPods, and similar devices distract people from paying attention to the weather, as well as other dangers, when they are outside, delaying them from seeking safe shelter, not because the devices have any effect on thunderstorms or lightning.† Although small sheds, such as hikers’ lean-tos, or sun, rain, bus, or golf shelters, may be protected or “hardened” against lightning strike under the National Fire Protection Association (NFPA) lightning codes (NFPA780), this is no guarantee of safety to persons sheltering within them.171,215,216 Personal safety is not guaranteed by structural protection. Grounding of the building is no guarantee of safety. In fact, it is likely that using these *References 3, 14, 104, 126, 127, 206, 217. † References 3, 14, 104, 126, 127, 206, 217.
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CHAPTER 3 Lightning Injuries
holy dwellings whose steeples were struck frequently by lightning. French peasants carry a pierre de tonnerre, or lightning stone, to ward off lightning strikes. Even Santa Claus gets into the act with his reindeer Donner (thunder) and Blitzen (lightning). People in both developed and Third World countries often regard lightning and thunder with a great deal of fear as mys terious, uncontrollable, and unmanageable. Cambodians, for instance, believe that by doing good deeds, they can avoid lightning strikes and that people with moles on their calves are susceptible to lightning strikes, as are people who have broken promises. To resuscitate a victim, Cambodian villagers may drape the person’s body with a white cloth, or jump over it three times, or place the victim in a bed and light a fire under the bed. In South Africa, there is a belief that lightning can be “sent” to steal something, or from a traditional healer to someone else. In the Venda and Tsonga cultures of South Africa, families may petrol bomb the house of an enemy who they believed called down lightning on a relative who was struck. In Africa in the 1990s, when only the members of one soccer team were injured, it was ascribed to witchcraft on the part of the other team. Other African beliefs state that burying a hippopotamus hide 2.4 m (8 feet) under ground will protect their area. Wearing red is believed to be protective, but mirrors are felt to attract lightning, not only in Africa but in other cultures, including the United States. South Africans believe that the Syringa tree (Figure 3-6, online) attracts lightning. So strong is this belief that some farmers will cut down every Syringa tree on their farm. Even in “civilized” Western societies, lightning can take on mystical significance. When lightning struck an English cathedral just before enthronement of a controversial bishop in the late 20th century, some regarded it as an omen. Bullock,35,36 in a modern article, advances a case that the conversion of Saul on the road to Damascus was a result of a lightning strike.
PART 1 MOUNTAIN MEDICINE
BOX 3-1 The Most Common Myths and Facts No Truth • Lightning injuries are always fatal.9,15,18,64 • Lightning is spelled with an E as in “lightening.” • The cause of death from lightning injury is burns.9,15,18,64 • Burns are a major component of lightning injury.9,15,18,64 • Nothing is left of a person after a lightning strike except a pile of ashes.64,65 • Lightning victims have “entry” and “exit” points.18,65 • Lightning victims have internal burns.65 • One can predict the degree of injury from the voltage, amperage, or polarity of the strike. • Metal (on the body or not) attracts lightning. • Lightning does not hit outside the rainstorm.217 • It is safe to wait until the rain arrives to evacuate.217 • It is safe to finish the game if lightning is nearby.135,217 • As soon as the rainstorm passes and rain stops falling, it is safe to resume activity.135,217 • If you can see blue sky, lightning danger is minimal. • Lightning never strikes the same place twice. • It is safe to seek shelter and dryness under a tree.217 • Tall objects provide a 45-degree “cone of protection.” • The majority of persons injured are golfers.135,217 • Lightning injuries cannot occur inside a building. • Rubber tires (shoes, raincoats, sitting on a backpack) protect a person from lightning.217 • Cell phones, iPods, and other electronics attract lightning.* • Golf, picnic, bus, rain, beach, and other shelters are safe.171,217 • Grounding a building or shelter makes it safe for people from lightning injury.171 • Grounding a building makes it safe from structural damage.171,216,234 • Lightning victims remain electrified and dangerous to touch. • Lightning victims are easier to resuscitate than are other cardiac arrest victims.266 • If there are no outward signs of lightning injury, the damage cannot be serious.66,67 • Lightning victims usually require treatments similar to those for high-voltage electrical injuries with aggressive fluid resuscitation, alkalinization, and fasciotomies.65,71 • Lightning survivors have few permanent problems.67,74,212,232
Some Truth • Lightning always hits the highest object. • The “pointier” an object, the more likely it will be hit. True • No place outside is safe near thunderstorms.217 • It is better to be “proactive” rather than “reactive” with lightning injury avoidance.217 • The top activities and places for lightning casualties in the United States are all outdoors:217 • Near trees (or other tall object) • Open fields and elevated locations • Water-related activities (e.g., swimming, boating, fishing) • Safe shelter is a typical house or other fully enclosed and substantially constructed building with properly earthed plumbing and wiring.217 • Another safe shelter is a fully enclosed solid metal-topped vehicle such as a car or bus.217 • Open picnic, bus, golf, and rain shelters, as well as tents and other camping cover, offer absolutely no protection from lightning and may actually increase the risk for injury.171,216,217 • Having and following a lightning safety plan can decrease the number of lightning deaths and injuries.217 • There is nothing that a person can do that will substantially decrease his or her lightning injury risk if “caught” in a thunderstorm. • The lightning crouch does not significantly decrease the chance of injury or death.217,242 • Sitting on a backpack or sleeping pad does nothing to decrease an injury. • Lying flat on the ground increases injury by increasing ground current effect.72 • The primary cause of death is cardiac and respiratory arrest at the time of the injury.64 • Ninety percent of lightning victims survive, but often with disability.67 • Lightning victims are safe to touch and do not retain an electrical charge.216,217 • Automated external defibrillators (AEDs) have been useful in some resuscitations.78,158,218 • Cell phones, iPods, and other small electronic devices do not attract lightning.† • Lightning can strike the same place more than once. • Lightning has no E in it.
*References 3, 14, 104, 126, 127, 206, 217. † References 3, 14, 104, 126, 127, 191, 206, 217.
shelters can actually increase a person’s risk for injury for reasons including side flash and ground current. One should think of these shelters as capacitors with air insulation between the capacitor plates (roof and the floor). It is easy to see why someone standing inside decreases the amount of energy needed to “discharge” the capacitor and send lightning energy through the person. Similarly, sheltering within a shallow cave on a mountainside may protect from rain but may be very dangerous from a lightning standpoint. The “crispy critter” myth is the belief that someone struck by lightning bursts into flames or is reduced to a pile of ashes.59 In reality, lightning often flashes over the outside of a victim, sometimes blowing off the clothes but leaving few external signs of injury and few, if any, burns. Less than one-third of lightning survivors have any signs of burns or marks to their skin. Two other myths held by the public and many physicians are that “If you’re not killed by lightning, you’ll be OK” and “If there are no outward signs of lightning injury, the damage can’t be serious” (Box 3-2).66 Medical literature, because of lack of follow-up or longitudinal reports, implies that there are few permanent sequelae of lightning injury. Several permanent sequelae may 62
occur.* In addition, many lightning victims with significant sequelae have no evidence acutely of burns. Peripheral neuropathy, chronic pain syndromes, and neuropsychological symptoms, including severe short-term memory difficulty, difficulty processing new information, attention deficit, depression, and post-traumatic stress disorder, may be debilitating.221,229-233,235,237 A myth still prevalent is that the lightning victim retains the charge and is dangerous to touch because he or she is still “electrified.” A person does not retain a charge like a battery. This myth has led to unnecessary deaths by delayed resuscitation efforts.66 Medical literature and practice are plagued by myths that grew out of misread, misquoted, or misinterpreted data and continue to be propagated without further investigation. Not the least of these is the tenet that lightning victims who have resuscitation for several hours may still successfully recover. This belief seems to be grounded in the old idea of suspended animation—the concept that lightning is capable of shutting off systemic and cerebral metabolism, allowing rescuers a longer period in which *References 16, 62, 65, 67, 74, 212, 223, 232, 272, 280.
These apply to electrical injury as well as lightning injury. Behavior of Current in the Body • Current seeks Earth. • Current seeks the path of lowest resistance. • Nerve tissue is a good conductor, or alternatively, current is preferentially conducted by nerve tissue. • When a person touches a source of potential, current flows through the skin to other parts of the skin in contact with the same conductor (i.e., current passage is local only). The Severity of Electric Shock Myth: If the following are absent, the shock cannot be severe and no deleterious effect can result: • Being thrown (i.e., if a person is not thrown, the shock is not severe). • Burns (i.e., if burns are not present, the shock is not severe). • If the only surface change is a blister, the shock was not severe. • Entry and exit wounds • Must be present • Demonstrate the current path • If not present, indicate no shock occurred. • Fuses being blown (i.e., if a fuse does not blow, the shock is not severe enough to harm a victim). • Low voltage cannot harm. • Electroconvulsive therapy does not give long-term post– electric-shock symptoms (also false), so any other electric shock cannot be harmful. Investigations • If computed tomography (CT) and magnetic resonance imaging (MRI) scans are normal, there are no injuries. • Negative investigations (e.g., nerve conduction study, electroencephalogram, CT, MRI) mean a victim has not sustained an electric shock. • Neuropsychological testing is objective and easily interpreted. • Burns of electrical origin can be distinguished on histologic examination. Remote Symptoms • Remote symptoms do not exist. • Remote symptoms are proportional to the size of the shock. • Symptoms of the shock that are not present immediately after the shock are not related to it. • A person getting remote symptoms was psychologically vulnerable all the time. Miscellaneous • Litigation increases the potency of the claimed symptoms. Corollary: resolving litigation terminates symptoms. • Medical specialists understand electricity or lightning. • Electrical experts can predict lightning or electrical injury. • A diagnosis of depression, post-traumatic stress disorder, adjustment disorder, and so on, negate an electrical injury causation. • Residual current devices (RCDs) eliminate the possibility of all shocks. Corollary: a shock occurring when an RCD breaks the circuit cannot be severe.
to resuscitate the patient without anoxic injury. This concept, credited to Taussig,266 actually appeared some time before her article. In addition, the case recounted by Taussig that is the basis for this myth, when searched to its source, was a case report by Morikawa and Steichen.210 The case shows a somewhat longer resuscitation period than usual, but not as miraculous as reported in Taussig’s paper or as propagated in subsequent references to her paper. In a study of lightning survivors, Andrews, Colquhoun, and Darveniza13 have shown prolongation of the QT interval, bringing up the theoretic possibility of torsades de pointes as a mechanism
for the suspended animation reports. There is evidence from animal experiments to support the teaching that respiratory arrest may persist longer than does cardiac arrest.9,80,81 One study, in which Australian sheep were hit with simulated lightning strokes, showed histologic evidence of damage to the respiratory centers located beneath the fourth ventricle.9 Prolonged assisted ventilation may in some cases be successful after cardiac activity has returned, but this is obviously difficult to test in any clinical study.69,70,225 Another series of animal experiments with hairless rats has shown that it is possible to obtain the skin changes (keraunographic markings), primary and secondary cardiac arrest with prolonged respiratory arrest, and temporary lower extremity paralysis with simulated lightning strike.80,81 Several booklets listing precautions for personal lightning protection appeared in the late 1700s and early 1800s. One of the superstitions listed was that humans, by their presence, could attract lightning to a nearby object. A book of the times, Catechism of Thunderstorms, illustrated other myths. Lightning was said to follow the draft of warm air behind a horse-drawn cart, so that coachmen were cautioned to walk their horses slowly through a storm. Historically, many remedies for resuscitation of lightning victims have been offered. On July 15, 1889, Alfred West testified in a New York court that he was revived by “drawing out the electricity” when his feet were placed in warm water while his rescuer pulled on Mr. West’s toes with one hand and milked a cow with the other.29 Other early attempts at resuscitation included friction to bare skin, dousing the victim with a bucket of cold water, and chest compression. An early attempt at cardiopulmonary resuscitation was given in 1807 when mouth-to-mouth ventilation was used for lightning victims, and it was proposed that gentle electric shocks from galvanic batteries passed through the chest might be successful in resuscitating a victim of lightning.40 Before that, Benjamin Franklin110 had purposely electrocuted a chicken during a lightning experiment and reported successful, albeit temporary, resuscitation with mouth-to-beak ventilation. A myth in current treatment is that lightning injuries should be treated like other high-voltage electrical injuries. The injuries seen with lightning are very different from high-voltage injuries and should be treated differently if iatrogenic morbidity and mortality are to be avoided.15,65 “Lightning never strikes the same place twice.” In reality, the Empire State Building and the Willis Tower are hit dozens of times a year, as are mountaintops and radio-television towers. If the circumstances facilitating the original lightning strike are still in effect in an area, the laws of nature will encourage further lightning strikes.
OTHER MYTHS* • Victims may have “internal burns.” False. There may be cellular damage and certainly nervous system damage but rarely, if ever, internal burns such as those suffered with high-voltage electrical injuries. However, some physicians use this euphemism with patients to explain their pain and neurologic injuries. • Wearing a raincoat or rubber-soled shoes, sitting on a foam pad or backpack, or the like will protect a person or decrease the severity of the injury. False. If lightning has burned its way a mile or more through the air, which is an excellent insulator, it is foolish to believe that a fraction of an inch of rubber or that a few inches of any material will serve as an adequate insulator. • The rubber tires on an automobile are what protects a person from lightning injury. False. See the preceding myth. Electrical energy travels along the outside of a metal conductor (the car body) and dissipates through the rainwater to the ground or flashes off the axles or bumper of the car (Figure 3-8).
*References 66, 234.
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CHAPTER 3 Lightning Injuries
BOX 3-2 Myths Commonly Cited as Facts in Litigation
PART 1 MOUNTAIN MEDICINE
attract lightning. Tall objects tend to be made of metal, but their height, isolation, and pointiness, not their composition, are factors. • Carrying an umbrella increases the risk. The lightning “crouch” can be used to protect someone “caught” in a thunderstorm. Both false: Compared with the mile or two that lightning has already traveled to reach the person, increasing or decreasing their height by a foot or so has minor effect. • Lightning may occur without thunder. False. Whenever there is lightning, there is thunder, and vice versa. Sometimes it will appear that there is lightning without thunder because thunder is seldom heard more than 16 km (10 miles) from the lightning stroke. It can also be blocked by buildings, mountains, and noisy activities, and from perception because of distraction by mobile phones or other electronic devices. Survivors who are very close to a strike may not hear or remember the thunder.
Incidence of Injury LIGHTNING ACROSS THE UNITED STATES The distribution of lightning across the United States is well known because of the operation of real-time lightning detection networks for the past two decades.86,94 About 25 million cloudto-ground flashes occur each year in the lower 48 states.226 In addition to the strike points of the first return strokes, 45% of flashes have a subsequent return stroke that terminates at a different location on the ground.271 As a result, about 37 million ground terminations are directly impacted by cloud-to-ground lightning over the United States each year. The variability from year to year over the entire country is only a few percent due to the compensating effects of a variety of meteorologic regimes over the course of a year. On a shorter time scale, more than 50,000 flashes per hour sometimes occur on summer afternoons across the United States. Existing technology detects over 90% of all cloud-to-ground flashes within the contiguous United States.86 The most recent 11-year climatology of cloud-to-ground lightning from the National Lightning Detection Network shows that three locations along the east and west coasts of peninsular Florida have the largest density of flashes per area during the entire year (Figure 3-9). Flash density decreases northward and westward from Florida, although there are many variations that depend on the well-identified meteorologic factors of strongly heated land surfaces producing strong upward motions in the atmosphere because of coastal sea breezes during most summer afternoons. This acts on deep moisture in the lower levels of the atmosphere. Similar important features occur along the coast of the Gulf of Mexico. In the mountainous western states, strong upward atmospheric motions are produced during many summer days along with large changes in elevation.194
FIGURE 3-8 Simulated lightning in a high-voltage laboratory travels across the external metal body of the car, escaping through the axle, hubcaps, or other metal closer to ground (arrow). The Faraday cage effect of the metal body of the car protects the person from injury but does not protect the tires or wiring system of the vehicle.
• Lightning always hits the highest object. False. Lightning only “sees” objects about 30 to 50 m (98 to 164 feet) from its tip. In addition, several pictures exist of lightning hitting halfway down a flagpole or striking in a parking lot next to light poles. Someone standing in the middle of a football field will not be protected by the goalposts if lightning is coming down over his or her head. Similarly, there are many photographs of lightning branching to meet the earth in several places. • Metal attracts lightning; wearing metal increases the risk or “attracts” lightning. False. The only factors that affect where lightning will strike are the following: • Height of an object • Isolation of an object from taller objects • “Pointiness” of an object (not a factor for people) Metal objects, such as fences and bleachers, conduct electricity and lightning after they have been hit, but they do not attract lightning. Metal objects worn by the victim may heat and cause secondary injury but do nothing to
FIGURE 3-9 Cloud-to-ground flashes per square kilometer per year in the United States from a network of lightning detection sensors from 1997 to 2007. (Courtesy Vaisala, Inc, Tucson, Ariz.)
N W
E S
64
Avg flash density fl/sq km/year 14 and up 10 to 14 8 to 10 6 to 8 5 to 6 4 to 5
3 to 4 2 to 3 1 to 2 0.5 to 1 0.1 to 0.5 0+ to 0.1
CHAPTER 3 Lightning Injuries
30
–30
–180 Orbits 17,371 Areas 808,854 Flashes 4,345,364 Groups 20,727,622 Events 42,265,608 (Created: 02/15/100)
–90 <10 >10
0
90
180
>25 >50 >100 >150 >200 >300 >400 >500 >750 >1000
Flash scale April 12, 1995 – December 31, 1999
NASA/MSFC
FIGURE 3-10 Total flashes per square kilometer per year for the world from April 12, 1995, to December 31, 1999 from the Optical Transient Detector. (http://thunder.nsstc.nasa.gov/data/OTDsummaries/gifs/mission_world.gif )
LIGHTNING AROUND THE WORLD Over 60 cloud-to-ground lightning detection systems using commercial instrumentation in the very low frequency (VLF) and low frequency (LF) range have been installed in more than 45 countries on every continent except Antarctica.86 Some have operated for longer than two decades. However, the only formally published compilation of flash data from more than one country at a time is for the United States and Canada.226 The ability to detect the full horizontal and sometimes vertical extent of flashes in cloud has been developed in recent years.86,193 These cloud lightning or total lightning flashes are detected in the VHF range over regions as large as metropolitan areas. Total lightning networks detect three to five cloud flashes for every cloud-to-ground flash, although some storms have much higher ratios. The longest detected cloud flash stretched horizontally across 190 km (118 miles) over the Dallas-Fort Worth area and was connected with two cloud-to-ground flashes during its 2-second lifetime.92 Cloud flashes do not directly affect people on the ground. However, their association with cloud-to-ground flashes helps to understand the location and timing of ground strikes. No maps of total lightning have been developed to date, although there is a general view of worldwide total lightning detected by the satellite-borne Optical Transient Detector and Lightning Imaging Sensor that measure both cloud-to-ground and cloud flashes as shown in Figure 3-10.59 The highest rates of all types of lightning occur over tropical and subtropical continents. Maxima have been found in central Africa and northwest South America.2 Lightning frequencies in these areas far exceed those over Florida and the Gulf Coast. The uncertainty concerning the portion of these maxima that are cloud-to-ground flashes is being resolved by the recent deployment of the Global Lightning Dataset GLD360.93
TIME OF U.S. LIGHTNING* During the year, lightning is by far most common during summer months. Two-thirds of U.S. cloud-to-ground flashes occur in June, July, and August (Figure 3-11, online). The maximum during the warmer months of the year, especially in the southeastern states,
*References 141, 191, 194, 277.
is due primarily to daytime heating of the lower and middle levels of the atmosphere. An equally critical ingredient is the large amount of moisture in the lower and middle levels of the atmosphere that provides fuel for the daily thunderstorm cycle. The concentration of U.S. cloud-to-ground lightning in June, July, and August is present over nearly all of the United States.141 During the day, cloud-to-ground lightning is most common in the afternoon (Figure 3-12, online). Nearly one-half of all lightning occurs between noon and 18:00 local standard time (LST). Lightning is at a maximum in the afternoon because updrafts necessary for thunderstorm formation are strongest during the warmest times of the day when surface temperatures are highest, resulting in the greatest vertical instability. Other factors can extend the maximum into the evening hours, especially in the plains and southeastern states, because of outflows and other propagating features that usually originate with the afternoon convection.
U.S. LIGHTNING CASUALTIES Each month, NWS offices compile a list of damaging or notable weather phenomena that occurred in the office’s area of responsibility. These lists are combined into a monthly national report issued by the National Oceanic and Atmospheric Administration (NOAA) titled Storm Data. During the last 20 years, U.S. lightning fatalities have averaged 51 per year. Lightning deaths have equaled or exceeded those from tornadoes in 11 years and equaled or exceeded those from hurricanes in 18 of the 20 years (Figure 3-13). Flood deaths exceeded lightning fatalities during 16 of these 20 years. Males (84%) make up a much higher number of fatalities in the United States than females.87 This male majority has been found in every region of the world over the last two centuries, although some subsets can have less dominance of males than this typical value. The most common situation is for one victim to be involved in a lightning incident. The largest single death total in one U.S. event resulted from a 1963 airliner crash that killed 81, and the largest U.S. injury total was 90 at a Michigan campground. Although single-incident cases dominate the more developed countries’ data sets, very large numbers of deaths and injuries often occur in developing countries.140 Lightning-related casualties and damages are often less spectacular and more dispersed in time and space than are those from other storm phenomena. As a result, lightning deaths, 65
PART 1 MOUNTAIN MEDICINE
+
150 125 100 75 50 25 0 1989
1991
1993
1997
1995
1999
2001
2003
2005
2007 2008
Lightning Tornado Flood Hurricane FIGURE 3-13 U.S. storm-related fatalities from 1989 through 2008 from the National Oceanic and Atmospheric Administration publication Storm Data. The + sign indicates that hurricane Katrina had 1016 fatalities in 2005.
injuries, and damages have been found to be underreported in Storm Data.19,144,196,258 The following factors contribute to this underreporting: most casualties occur to one person or object at a time, Storm Data collection is not entirely consistent among offices, there are some differences in the definitions of lightning versus secondary lightning-related deaths, and there is inconsistency in listing medical diagnoses.1,19,239,258 Nonfatal injuries are underreported to a greater extent than are fatalities. A thorough search of Colorado hospital and emergency department visits found a ratio of 10 injuries to every death.53 Although this ratio of injuries to fatalities is generally applicable, there may be additional injuries that are not reported. Damage reports in Storm Data are an extremely small portion of the estimated total damages, direct or indirect, of several billion dollars per year in the United States.19,144 Despite its underreporting and sometimes incomplete nature, Storm Data has been a consistent national database for lightning impacts since 1959 and is likely the best system in the world for such information. Data drive change. It would be highly desirable for similar data to be collected and made available in many other areas of the world, both to have a baseline of damage and injuries to measure changes and to spur governments and other organizations to address injury prevention.
DISTRIBUTION OF U.S. LIGHTNING DEATHS BY STATE Lightning casualty deaths in the United States by state for the decade from 1999 to 2009 are shown in Figures 3-14 and 3-15. The general pattern is somewhat similar to the distribution of lightning in Figure 3-9. In general, there are more fatalities in the Southeast, but the more populous states also have larger totals. Note that Florida has had more than twice as many deaths as Colorado, the next state in terms of frequency. Fatality information is used for these maps, rather than injuries, because of the greater uncertainty due to injury underreporting, as mentioned previously. The lightning hazard is shown more clearly when population is taken into account in Figure 3-15. There are two maxima with this approach, one in the southeast and the other in the northern Rocky Mountain states. Most populous states, such as Illinois, no longer have high ranks. The only states in the top 10 of both lightning fatality and fatality rates are Florida, Colorado, Alabama, and South Carolina. Similar tabulations were recently made by Ashley and Gilson,19 and earlier maps for single U.S. states are listed by Curran and colleagues.87 Outside the United States, the distributions of fatalities by political boundaries have been developed for Canada,207
FATALITIES 2000-2009 0
0
2
0
7
3
1
3 9
27
8 7
66
9 3
7
27
9
11
14
10
5
10 0
24
17
11
6 11
1
5 4
13
13
4
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3
Source: Storm Data Alaska: 0 Hawaii: 0 American Samoa: 1 D.C.: 0 Guam: 1 Puerto Rico: 3 Virgin Islands: 1
8
4
2 1
2 0
3
20
14
70
Rank 1-10 11-20 21-30 31-52
FIGURE 3-14 Rank and number of lightning fatalities in each state from 2000 to 2009 from Storm Data. (Modified from Curran EB, Holle RL, López RE: Lightning casualties and damages in the United States from 1959 to 1994, J Climate 13:3448, 2000.)
CHAPTER 3 Lightning Injuries
FIGURE 3-15 Rank of population-weighted lightning fatality rate in each state from 2000 to 2009 from Storm Data. (Modified from Curran EB, Holle RL, López RE: Lightning casualties and damages in the United States from 1959 to 1994, J Climate 13:3448, 2000.)
FATALITY RATE 2000-2009
Source: Storm Data Ranks include 50 states, D.C., and Puerto Rico
Singapore,228 Australia,61 and France.116 Many additional studies have included national casualty totals, but not maps, over periods from several to many years.138
time series in the plains and Midwest.87 At night between 18:00 and 06:00, the relatively few fatalities occur mostly in the plains, upper Midwest and some populous eastern states, because of outflows and other propagating features that usually begin with afternoon convection. More than one-half of the deaths after midnight occurred when people were in a house set on fire by lightning,139 whereas some fatalities were campers.
TIME OF U.S. FATALITIES During the course of the year, lightning fatalities are nearly symmetric around the most frequent month of July (Figure 3-16, online). This annual casualty cycle is quite similar to the cloud-toground lightning variation by month in Figure 3-11, online. Because summer dominates the sample size, summer fatality maps are very similar to Figures 3-11 and 3-12, online for the entire year.87 On the West Coast, fatality rates are highest during autumn and winter, and these rates are also higher in the southern states than elsewhere in months other than summer. Outside the United States and away from the tropics, summer also accounts for the largest number of fatalities, such as that shown by the January peak in Australia because of the reversal of seasons from the northern hemisphere.61 In the equatorial location of Singapore, fatality maxima in November and April are similar to the annual maxima in local thunderstorms.228 During the hours of the day, most lightning fatalities occur during the afternoon (Figure 3-17, online). About two-thirds of U.S. fatalities occur between noon and 18:00 LST.87 There is a somewhat faster rise up to the maximum then a slower decrease afterward. This general cycle is very similar to cloud-to-ground lightning in Figure 3-12, online. However, there is a somewhat narrower concentration of fatalities in the afternoon in the Rockies, southeast, and northeast compared with the broader
FIGURE 3-18 Annual reported U.S. lightning fatalities from 1900 to 2007. (Modified from López RE, Holle RL: Changes in the number of lightning deaths in the United States during the twentieth century, J Climate 11:2070, 1998.)
Rank 1-10 11-20 21-30 31-52
TRENDS IN U.S. LIGHTNING FATALITIES During the early years of the 20th century, U.S. lightning deaths were much more frequent than at present (Figure 3-18). Not all states participated in lightning fatality data collection systems in the early years of the period shown in Figure 3-18. However, once all states reported, the peak was reached in 1921, when 459 lightning fatalities were reported.195 Since then, there has been a steady decline in the number of fatalities listed in Storm Data. In recent years, there have been less than 50 fatalities annually. The steady downward trend is made more noticeable by population weighting, shown in Figure 3-19. Although the U.S. population has increased greatly since 1900, the weighted rate has decreased from as high as 6 fatalities per million people per year in the early 20th century to about 0.3 in recent years. Paralleling this decrease is a shift from a mainly rural to a mostly urban population in the United States during the same years (see Figure 3-19). Other significant factors that contribute to this downward trend are improved grounding of home and building electrical and plumbing systems, ready access to fully enclosed metal-topped vehicles, improved medical treatment, and greater
500
300 200 100 0
19 00 19 07 19 14 19 21 19 28 19 35 19 42 19 49 19 56 19 63 19 70 19 77 19 84 19 91 19 98 20 05
Reported fatalities
400
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Deaths per million Percent rural
Deaths per million
6 5
70 60 50
4 3
40
2
30
1
20
0 1900
10 1920
1940
1960
1980
Percent rural to total population
7
2000
meteorologic and lightning awareness and warnings. The potential effects of changing fatality data collection rules and methods are difficult to identify but may account for some variations in all data sets. The net effect of these changes is apparent in a comparison of fatality data from the 1890s to 1990s in Figure 3-20.195 Agricultural cases have decreased from 26% to 10%, while indoor cases went from 40% to 5%. The latter may be due to the introduction of grounding into buildings, often on a farm or ranch, which has greatly reduced the lighting threat in recent years. There has been a large increase in recreational and sports incidents during that century and in the general category of outdoors, often in the yard of a dwelling and other everyday situations.
WORLDWIDE LIGHTNING FATALITIES
Lightning deaths (per million)
The weighted U.S. lightning fatality rate dropped during the 20th century by more than a factor of 10, from 6 deaths per million in some early years to under 0.3 in most recent years, as shown in Figure 3-19. Three apparently dominant factors are reduction in the rural population involved in labor-intensive agriculture, substantial grounding of most buildings where people live and work, and ready availability of fully enclosed metal-topped vehicles. Other more developed countries, such as Australia, Canada, England and Wales, France, Japan, and Sweden, have seen very similar reductions. All show current rates of less than 0.5, although some had rates exceeding 2 a century ago in areas where the lightning frequency is not as high as in the United States.138 Many people continue to participate in labor-intensive agriculture and live in ungrounded buildings in areas of the world where lightning frequency is high.163,164 The rates a century ago in the United States and other more developed countries can be considered for estimating fatalities and injuries in locations where lightning injury statistics are not readily available. Populous regions of Africa, South America, and Southeast Asia have as many as 4 billion people who are vulnerable to the lightning
Australia Canada India Japan
Agriculture
0
FIGURE 3-19 Annual lightning fatalities weighted by population ( ) from 1900 to 2007 for the United States and rural percentage ( ). (Modified from López RE, Holle RL: Changes in the number of lightning deaths in the United States during the twentieth century, J Climate 11:2070, 1998.)
10 9 8 7 6 5 4 3 2 1 0
1890s 0
25%
Indoors
25%
Outdoors
50%
75%
Recreation
100%
Small Sports structures
75%
100%
1990s FIGURE 3-20 Types of U.S. lightning fatalities from 1891 to 1894 compared with 1991 to 1994. (From Holle RL: Lightning-caused recreation deaths and injuries. Preprints, 14th Symposium on Education, January 9-13, San Diego, Cali. Boston, 2005, American Meteorological Society.)
threat, although urbanization makes it difficult to know the number of agriculturally dependent people living in unsafe structures. If the annual rate of 6 fatalities per million is used for 4 billion people, a total of 24,000 lightning deaths per year is obtained. If there are 10 injuries for every death,54 then 240,000 injuries occur per year in these areas. Holle138 lists all known published estimates of the lightning totals and converts them to fatality rates per population. Some of the countries indeed reach the rate of 6 per million per year, whereas other less developed countries have much lower rates (Figure 3-21). There is such a dearth of reliable data in regions such as Africa and Southeast Asia that it is very difficult to know whether these estimates are generally correct. However, a study of lightning casualties in and near dwellings and other buildings showed that large losses of life occur in schools, huts, and agricultural field shelters in these regions.139 Also in these countries, people spend less time inside the safety of fully enclosed metal-topped vehicles while working or traveling between school, work, and home than in more developed regions.137 Better systematic and reliable lightning fatality collection in these regions is needed to determine the validity of the global estimate of 24,000 deaths and 240,000 injuries per year from lightning.
Forensic Investigation An unwitnessed lightning event can be one of the most difficult clinical presentations to diagnose.50,111 The forensic examination of a critical lightning event can be divided into the following five stages:33,197,253,282 1. Case history 2. Scene investigation 3. Physical and/or autopsy examination 4. Special investigations 5. Collation
Singapore S. Africa U.S. Zimbabwe
1900-9 1910-9 1920-9 1930-9 1940-9 1950-9 1960-9 1970-9 1980-9 1990-9
68
50%
FIGURE 3-21 Lightning deaths per million people per year for eight countries outside Europe by decade during the 20th century. Note that the 1990s Zimbabwe value is 17.8. (From Holle RL: Annual rates of lightning fatalities by country. Preprints, International lightning detection conference, April 21-23, 2008, Tucson, Ariz., Vaisala.).
If a witness is available, it is important to ascertain the following: • Was there a storm? • Was there lightning? • Did the witness actually see the lightning strike the victim? • Was death immediate or not? • Where was the deceased at the time of the strike (e.g., under a tree, on an open golf course)? • Was any attempted resuscitation applied? • What was the activity of the deceased before death? • A meticulous description of the lightning event must be given. • How many people were involved? • Were there any survivors? If so, where are they? • What was the medical history of the deceased? Specifically, were there any cardiac problems? • A history of electrical storm activity should be ascertained from the weather service, because lightning network detection and location systems should be able to assist with the exact time and location of the strike.103
SCENE INVESTIGATION Attending a critical lightning incident is a very specialized activity that crosses many disciplines. Insurance investigators, electrical engineers, scene reconstruction experts, and/or investigating officers will be called to review the scene of a lightning strike. Signs of lightning strike on the scene can be subtle or blatant.154 Lightning scene investigation can be divided into the following: • Environmental signs of direct lightning strike • Structural signs of direct lightning strike • Trace evidence signs of direct lightning strike Environmental Signs of Direct Lightning Strike • At the scene there may be damage to nearby trees, such as splitting or removal of bark. • Arc marks may be present on the walls or nearby structures. • The ground may display a fern pattern.
A
CHAPTER 3 Lightning Injuries
CASE HISTORY
FIGURE 3-22 Damage to the roof of a clubhouse from direct lightning strike. The damage was extensive and included structural damage to the clubhouse. (Copyright Ian R. Jandrell.)
• Soil may show fulgurite formation—bore or tube-like structures formed in sand or rock by lightning. • Often a crater will be exposed in the earth, with rock and sand being flung far afield. Craters of up to 2 meters (6.6 feet) in diameter have been reported. • To preserve the case history for scientific purposes, a relevant academic institution or other expert in the field should if possible be advised of the incident, more specifically should there be any suggestion of litigation by a surviving party. Structural Signs of Direct Lightning Strike Jandrell and associates described the effects of direct lightning strike to housing structures in southern Africa.118,203,204 Figure 3-22 shows damage to the roof of a clubhouse from direct lightning strike. The damage was extensive and included structural and internal damage (Figure 3-23). Figure 3-24 shows damage to curtaining material covering the window. Thatched structures have been known to ignite as a result of lightning strike. Thatch is very combustible, so inhabitants are at greater risk for severe injury and burns.118,139
B
FIGURE 3-23 Damage to the ceiling (A) and internal wall (B) of the clubhouse in Figure 3-22 with resultant damage to the electrical and electronic devices connected to the electrical system. (Copyright Ian R. Jandrell.)
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Trace Evidence Signs of Direct Lightning Strike This can be very difficult to prove. Cindering on clothing or arc marks on metallic structures may be seen. In “zincification” and/ or “cuprification” metal with a lower melting point vaporizes, leaving the other metal behind. Magnetization of metallic objects has been mentioned in the literature, although current thinking is that this could possibly be a myth. Reports of metallic chains being magnetized and “sticking” to metallic postmortem trays have yet to be verified.
PHYSICAL AND/OR AUTOPSY EXAMINATION A complete postmortem examination should be performed. • The external examination should include a meticulous description of clothing and any evidence of resuscitation (Figures 3-25 and 3-26; Figure 3-25, online). • Metal objects may have burned underlying skin or may have been marked by the heat of electrical arcing. Figure 3-27 shows damage to clothing and underlying burns. Figure 3-28 shows permanent tattooing from a metal necklace burned into skin in a nonfatal injury.159
FIGURE 3-24 Damage to curtaining material covering a window of the clubhouse in Figure 3-22. (Copyright Ian R. Jandrell.)
A
B
FIGURE 3-26 Damage to the socks of a fatally injured farmer. (Copyright Mary Ann Cooper.)
A
B
FIGURE 3-27 A, Melting of synthetic clothing material from lightning damage. B, Underlying damage to skin from zipper and melted material. (Copyright Ryan Blumenthal.)
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CHAPTER 3 Lightning Injuries
A FIGURE 3-28 Metal necklace burned into skin by lightning with permanent tattooing (nonfatal injury). (Copyright Mary Ann Cooper; courtesy R. Washington.)
• Metal objects may show signs of fusing, zincification, or cuprification. Always check for magnetization. Metallic objects, such as tooth fillings, spectacles, belt, buckles, coins, and pacemakers, should be specifically described. • The type, pattern, and distribution of any cutaneous thermal injuries, including clusters of punctuate burns, blisters, or charred burns, should be noted. Figure 3-29 shows damage to a hiking shoe with underlying damage to the skin of the foot.15 • Determine if there has been rupture of tympanic membranes. Barotrauma has been cited as one of the injuring mechanisms of lightning. Pneumomediastinum has been cited in the literature.124 Burst eardrums and pneumomediastinum are signs suggestive of barotrauma. • Singed or scorched hair should be noted. • Ocular injuries, such as retinal detachment, should be determined. Cataracts may be difficult to demonstrate postmortem. • Unique arborescent or fern-like injuries (Lichtenberg figures) (Figure 3-30) should be noted. • Determine if there are lightning wounds on the bases of the feet—the “tiptoe” sign typically on the base of the foot.213 • The procedure for internal examination is identical to that for any forensic autopsy. • In female victims, ascertain whether or not the victim was pregnant, and if so, carefully examine the fetus macroscopically and microscopically for any injuries.112
SPECIAL PROCEDURES • Diagrams: Where possible, diagrams of the pattern and distribution of the lightning injury to the body should be constructed to provide graphic documentation of the nature and extent of the electrothermal injury patterns. • Photographs: Close-up and distance photographs should be taken to document all injuries. • Radiographs: Radiographic examination may be helpful. Certain fractures, dislocations, and subluxations may be missed at autopsy examination.155 Computed tomography (CT) or magnetic resonance imaging (MRI) might add to the body of knowledge that constitutes postmortem, noninvasive, and virtual analyses. Certain keraunopathologic findings, such as pneumomediastinum, may be missed at autopsy examination.124 • Histologic examination:155,159 The skin burn wounds should always be microscopically examined for signs of electrothermal injury patterns such as vacuolation in the epidermis, eosinophilia, and elongation and streaming of the nuclei of the lower epidermis. Histologic staining of the heart with hematoxylin and eosin may prove useful. The heart should also be carefully examined under the
B FIGURE 3-29 The heat from a lightning strike caused water in the wet boot to instantaneously turn to steam, exploding the boot off the foot (A) and causing burns (B). (Courtesy Sheryl Olson, RN.)
microscope for signs such as “waviness” of the myofibers,155 necrosis, and contraction bands.286 Special staining of the heart with Mallory, Weigert elastic, Movat pentachrome, acid fuchsin orange, and immunohistochemical staining with monoclonal anti–complement C9 antibodies may help in the diagnosis of myofiber breakup—an antemortem change that may be a distinct finding in electrothermal injury cases.105 Any neuropathologic condition should also be specifically investigated and commented on. • Toxicologic studies: Ethanol, recreational drugs, and carbon monoxide levels would be justified as the minimum toxicologic investigations required in such cases. From a mitigating-circumstance point of view, ethanol and recreational drugs are always important to know. Carbon monoxide levels will be valuable, especially if there is a thermal component to the injuries.
FIGURE 3-30 Lichtenberg figures in a teenager who survived. (Courtesy/copyright Mary Ann Cooper.)
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• Collection of evidence: Collect and preserve evidence or specimens, because equivocal cases may require electrical testing of equipment by an electrical expert. Nearby damaged electrical equipment should be sent to an electrical engineer for testing. Unwitnessed lightning cases are typically complex, and unusual situations may arise from time to time. The approach to all these cases should be multidisciplinary. Only by means of a careful forensic investigation, with strict adherence to guidelines, will the truth be revealed. This becomes even more important in determining whether or not a lightning strike was the cause of a later medical condition.
COLLATION If the fresh facts which come to our knowledge all fit themselves into the scheme, then our hypothesis may gradually become a solution. SHERLOCK HOLMES
The Adventures of Wisteria Lodge
Data become information, which becomes knowledge, which becomes scientific opinion. Scientific opinion depends on experience, cognitive ability, and facts. At the end of the investigation, one should collate one’s findings with the known physics and effects of lightning.234
Early Scientific Studies and Invention of the Lightning Rod* The study of electrical phenomena is often traced to the publication of Gilbert’s De Magnete in London in 1600. Experiments in France and Germany and by members of the Royal Society of London led to invention of the Leyden jar in 1745. Benjamin Franklin is generally regarded as the father of electric science and during his lifetime was known as the American Newton. The reason he was accepted into the French and English courts around the time of the American Revolution was not because he was an ambassador from America but because he was considered to be one of the foremost scientists of his time. Franklin was elected to every major scientific society at the time and received medals of honor from France and England for his scientific contributions.60,234 Before his work, it was thought that two distinct types of electric phenomena existed. Franklin’s work111 unified these two aspects and is responsible for renaming them positive and negative. He went on to prove that lightning was an electrical phenomenon and that thunderclouds are electrically charged, as demonstrated by the famous kite and key experiment.110 Because of the damage he saw to buildings, he invented the lightning rod and announced its use in 1753 in Poor Richard’s Almanack: It has pleased God in his Goodness to Mankind, at length to discover to them the Means of securing their Habitation and other Buildings from Mischief by Thunder and Lightning. The Method is this: Provide a small Iron Rod (It may be made of the Rod-iron used by the Nailers) but of such a Length, that one End being three or four Feet in the moist Ground, the other may be six or eight Feet above the highest Part of the Building. To the upper End of the Rod fasten a Foot of brass Wire the Size of a common Knitting-needle, sharpened to a fine Point; the Rod may be secured to the House by a few small Staples. If the House or Barn be long, there may be a Rod and Point at each End, and a middling Wire along the Ridge from one to the other. A House thus furnished will not be damaged by Lightning, it being attracted to the Points, and passing thro the Metal into the Ground without hurting any Thing. Vessels also, having a sharp pointed rod fix’d on the Tops of their Masts, with a Wire from the Foot of the Rod reaching down, round one of *References 60, 110, 111, 234.
72
the Shrouds, to the Water, will not be hurt by Lightning. In the 1750s and 1760s, the use of lightning rods became prevalent in the United States for the protection of buildings and ships. Some scientists in Europe urged installation of lightning rods on government buildings, churches, and other tall buildings. Religious advocates at the time, unfortunately, maintained that it would be blasphemy to install such devices on church steeples, which received “divine protection.” Some groups chose to store munitions in churches, leading on more than one occasion to significant destruction and loss of life when the buildings were struck by lightning. Part of the delay in installing lightning rods in England has been attributed to distrust of scientific theories originating in the upstart, newly independent United States. Years and numerous unsuccessful trials with English designs were required before the Franklin rod became accepted on Her Majesty’s ships and buildings.40 At one time (and still believed by some laymen today), lightning rods were theorized to diffuse electric charge, neutralizing storm clouds and averting lightning. This may have been an outgrowth of the observation of St Elmo’s fire, an aura appearing around the tip of lightning rods, noses of airplanes, and ships’ masts during a thunderstorm, caused by an electron discharge that results from the strong electromagnetic field induced around the glowing object. Properly installed lightning rods and lightning protection systems neither “diffuse” nor “attract” lightning, but rather protect a building by allowing the current from a lightning strike to be harmlessly directed through the system to the ground.34,215,217 Lightning otherwise can travel into or through the building and cause extensive damage (see Figures 3-22 to 3-24) Around the late 1800s and 1900s, it was not uncommon for charlatans to take advantage of the fear of lightning and the danger of lightning-caused fires. They drove from farm to farm, offering to “discharge” the lightning rods on buildings for a fee. The first Lightning Rod Conference was held in London in 1882. Recommendations from this conference were published that year and again in 1905. Several countries developed codes of practice for lightning protection (Germany, 1924; United States, 1929; Britain, 1943; British colonies, 1965).87 In the past decade, NFPA 780 (U.S. National Fire Protection Act) has been accepted worldwide as a reliable standard.215 Building codes and industrial standards may require particular structures to have lightning protection systems.34,215 Including a system in the initial design and construction is always easier and less expensive than modifying a completed building. Other factors to be considered include relative frequency of strikes in an area; height, construction, and design of the building; and degree of protection desired, depending on whether the building is a storage shed, house, school, hospital, or munitions factory. In instances not covered by code, a lightning protection system, despite high exposure to lightning, may not be worth the expense, such as for a mountain cabin that is seldom visited.170,216 Today the most important economic impacts from lightning include electrical utility interruption; interruptions at airports and other outdoor locations; loss or corruption of financial, security, and other databases and control systems; and down time of industrial equipment. Lightning may pose significant danger not just to individuals, but to larger groups, such as when hundreds of miners are trapped deep underground after lightning has made elevators, ventilation systems, and water pumps nonoperational.216 At home the most reliable way to protect electronic equipment is to unplug it from the wall before the arrival of a thunder storm. Surge protectors, which may be effective for minor household electrical surges, are seldom effective with lightning, despite manufacturers’ claims. The best source of information on lightning risk for people is the NWS Lightning Safety website (http://www.lightningsafety.noaa.gov) and for more general risk, the National Lightning Safety Institute (http:// www.lightningsafety.com).132,216,217
CHAPTER 3 Lightning Injuries
High-altitude winds
40,000
30,000
–36
Snow
–16 Snow
25,000 20,000
10,000
18
air
Freezing
W ar m
15,000
–3
32
level
Rain
46
Temperature (° F)
Altitude (feet)
35,000
–60
Ice
63
5000
A
Heavy surface rain
B
Downward leader
Return stroke
Upward streamer
C
D
E
F
FIGURE 3-31 A, Air rises and condenses into a cumulonimbus cloud. B, Typical anvil-shaped thundercloud. C, Water droplets within the cloud accumulate and layer charges. D, Stepped downward leader initiates the lightning strike. E, Positive upward streamer releases from the ground to meet the stepped leader. F, Return stroke travels back up the channel made by the stepped leader.
Physics of Lightning Stroke* LIGHTNING DISCHARGE The study of lightning discharge and formation is complex and has led to development of a separate specialization within physics and meteorology Here we describe the simplified and most common mechanisms of thundercloud formation and lightning strike. Thunderstorms can be formed by a number of methods to produce the necessary vertical updrafts. These ingredients are afternoon heating of warm moist air, large-scale upward motions (Figure 3-31, A), sea and lake breezes, lifting of deep layers of the atmosphere by mountains, and cold fronts.141,269 As warm air rises, turbulence and induced friction cause a complex redistribution of charges within the cloud (Figure 3-31, B). Although the ground temperature may be very warm to hot, thunderstorms are tall enough that their highest parts are colder than freezing. In fact, all lightning comes from clouds that have ice aloft at temperatures colder than freezing. At temperatures colder than freezing, water droplets and ice particles of several types within the cloud acquire and increase their individual charges as they interact and transfer charge. The varying sizes and shapes of the frozen snow and ice crystals, supercooled water droplets, and hail are moving vertically at different speeds because of their different fall speeds. The result is separation of charge into several layers. A large potential difference develops *Reference 230.
between layers as a result of the interaction of charged water and ice particles, updrafts that vary in time and space, and internal and external electric fields within the cloud. Lower layers of the cumulonimbus generally become negatively charged relative to the earth. The earth, which normally is negatively charged relative to the atmosphere, has a strong positive induced charge as the negatively charged thunderstorm passes overhead. The induced positive charge tends to flow as an upward current from trees, tall buildings, poles, people, or sometimes very small objects or flat open ground beneath the overhead thunderstorm cloud and may move up in upwardpropagating leaders.234 Normally the discharge of the potential difference is discouraged by the strong insulating nature of air. However, when the potential difference between charges within the clouds or between the cumulonimbus cloud and the ground becomes too strong, the molecular structure of the intervening air may break down under the influence of the electric field that has developed, and the charge is then dissipated as lightning. A downward stroke begins as a relatively weak and slow downward leader from the cloud (Figure 3-31, C ). Although the tip of the leader may be luminous, the stepped leader itself is barely discernible with the unassisted eye. Recent very high-speed video has shown this bright tip and more faint trailing leader as it travels to the ground.249,251 The leader travels at about one-third the speed of light (1 × 108 m/sec), and the potential difference between the leader’s lower tip and the earth ranges from 10 to 200 million volts. The leader ionizes a pathway that contains superheated ions, both positive and negative, and forms a plasma column of very low resistance. The leader travels in relatively short 73
PART 1 MOUNTAIN MEDICINE
branched steps downward about 50 m (164 feet), and then retreats upward. The next time the leader goes downward toward the ground, it fills the original ionized path but branches at the end to go down another 50 m (164 feet) and then retreats again. This up-and-down multiple-branching process continues until the leader comes to within 30 to 50 m (98 to 164 feet) of the ground. Because lightning follows this ionized path, its lower tip only can sense the existence of nearby objects within a radius of about 30 to 50 m (98 to 164 feet), meaning that lightning will not be affected by the existence of a hill or tower farther away. For human safety, being within 50 m (164 feet) of the lowest tip of a cloud-to-ground lightning flash as it comes to ground is very unsafe.
DIAMETER AND TEMPERATURE OF LIGHTNING* Although many techniques have been used to measure the diameter and temperature of lightning, all measurement techniques have artifact problems. Visual measurements of the lightning stroke using standard photography usually show the diameter of the main body of the stroke to be about 2 to 3 cm (0.8 to 1.2 inches). The diameter of the channel is sometimes measured indirectly, using measurements of holes and strips of damage that lightning produces when it hits aircraft wings, buildings, or trees. Measurements vary from 0.003 to 8 cm (0.001 to 3.15 inches), depending on the material that was destroyed. Hard metallic structures sustain smaller punctures than relatively softer objects such as trees. The ionized sheath around the tip of the bright leader stroke has not been measured but is estimated to have a diameter of 3 to 20 m (9.8 to 6.6 feet). The temperature of the lightning stroke varies with the diameter of the stroke and has been calculated to be about 8000° C (14,400° F). Other estimates of the temperature are as high as 50,000° C (90,000° F). After a few milliseconds the temperature falls to 2000° to 3000° C (3600° to 5400° F), similar to the temperature of a high-voltage electric arc.
FORMS OF LIGHTNING Lightning can be divided into cloud-to-ground and cloud (intracloud) flashes (Figure 3-32). Cloud-to-ground flashes contain one or more return strokes. The flickering often seen in a cloudto-ground flash is due to the return strokes, which average three to four per flash. Cloud-to-ground flashes contact the surface of the earth at one or more locations, because one of the subsequent return strokes often takes a different path to the surface, *Reference 230.
FIGURE 3-32 Cloud-to-ground flash (right) and cloud flash (center). (Copyright Ronald L. Holle.)
74
up to a few kilometers from the first return stroke; the average is 1.47 ground contact points per flash.262 The term total lightning describes the sum of cloud-to-ground and cloud flashes. An extremely small portion (less than 0.01 of 1%) of all lightning travels from ground to cloud, when this is induced by the special circumstances of high towers or mountains. Cloud flashes can travel between clouds, within clouds, from cloud to cloud, and in all combinations of these paths. The same flash can simultaneously strike ground at one or more locations and travel a long distance in cloud (see Figure 3-32). There are several times as many cloud flashes as those that reach the ground. Cloud flashes have been measured to exceed 190 km (118 miles) in horizontal length and last up to 2 seconds.92 From the point of view of a person on the ground, cloud flashes may appear to travel in long streaks across the sky, or the channels may be obscured and visible only by the brightening within clouds along their paths. Such cloud flashes are seen more often in regions with low cloud bases in humid areas. This effect was one of the reasons for the phenomenon to be originally called “lightening.” The most unusual and least understood type of lightning is ball lightning. It is usually described as an orange, blue, or white globe between the size of a softball and a basketball. It has been observed to enter planes, ships, or houses and travel down narrow spaces such as hallways. Ball lightning very infrequently injures people and objects and often exits through a door, chimney, or window.257 It may explode with a loud bang or exhibit other bizarre behavior. Cloud-to-ground lightning flashes usually lower negative charge to the ground.234 The less frequent (5% to 10%) positive cloud-to-ground flashes tend to occur during the winter, at the end of thunderstorms, on the U.S. high plains, and in relatively shallow thunderstorms. Positive flashes usually have one return stroke. It is not known if positive cloud-to-ground flashes cause a different injury profile, although they have a tendency to have long continuing current that may impart more energy to a person than do the usually shorter-pulsing negative cloud-to-ground flashes.
THUNDER Thunder is formed when shock waves result from the almost explosive expansion of air heated and ionized by the lightning channel. Understanding some basic features of thunder is important because of its usefulness in many lightning safety recommendations.114,217 The following are accepted features of thunder: • Cloud-to-ground lightning flashes produce the loudest thunder. • Thunder is seldom heard more than 16 km (10 miles) away, except under extremely quiet conditions. • The time interval between the perception of lightning and the first sound of thunder can be used to estimate the distance from the lightning channel, at a rate of 3 sec/km (5 sec/mile). • Wind, rain, man-made noise such as traffic, and vegetation, as well as intervening buildings, hills, and mountains, reduce the audibility of thunder. • The pitch of thunder deepens as the rumble persists, because only lower frequency sounds remain at greater distances. • Atmospheric turbulence reduces the audibility of thunder. The thunderclap from a close lightning flash is heard as a sharp crack. Distant thunder rumbles as the sound waves are refracted and modified by the thunderstorm’s turbulence.269 Because there is a large difference between the speed of light and the speed of sound, the distance to lightning can be estimated by a person on the ground. The estimation is made by the flash-to-bang method of counting the seconds between seeing a flash and hearing thunder from the same flash, when the two can be matched. The time interval between lightning and thunder is 3 sec/km (5 sec/mile). For example, if the difference is 30 seconds between when a flash is seen until its thunder is heard, the flash is 10 km (6.2 miles) away. This time interval is part of the basis for the 30-30 rule described in Precautions for Avoiding Lightning Injury.
BOX 3-3 Mechanisms of Lightning Injury
CONCEPTS IN ELECTRICAL MECHANISMS— DIFFERENCES BETWEEN LIGHTNING AND INDUSTRIAL ELECTRICITY
Electrothermal Effects 1. Direct strike 2. Contact potential 3. Side flash, sometimes called “splash” (1 to 3 may include surface arcs over the body surface) 4. Step voltage (also termed “Earth potential rise” or “ground current”) a. Transmitted through the ground b. Surface arcing 5. Upward streamer current1,53 (also called “fifth mechanism”)
A voltage can be applied to a body. It can be regarded as the pressure applied to a body to force it to conduct electric current, like water pressure applied at one end of a pipe to cause water flow. It is an external force, and after it is applied, a current (measured in amperes) flows through the conductor (i.e., body), like water in the pipe. The amount of current is inversely proportional to the resistance of the body. That is, for a given applied voltage, the higher the resistance of the body, the smaller the resulting current. For technical or generated electrical injuries, the voltage is externally selected, and the resistance of a body is a given. The current is the result. Resistance is a given property of a body. A piece of metal has a predictable and exact resistance, for our purposes invariable. It might be thought of as analogous to the diameter of the water pipe, or friction within the pipe. It is the property that determines how easy it is to force current through the body. Resistances of various tissues have been measured and characterized as properties. If it is assumed that resistance is predictable, then resistance, voltage, and current can be linearly related, making modeling, and therefore prediction, possible. Voltage, current, and resistance are related by Ohm’s law (Voltage = Resistance × Current). However, tissue resistance is not constant but affected by a number of factors that do not depart from principles of linear analysis. Alterations in tissue resistance are predictable, so analysis can proceed on a “piecewise linear” basis. Unlike generated electricity that is voltage driven, lightning is a “current” phenomenon. If a current is forced to flow through a body of a given resistance, as is the case with lightning, a voltage directly proportional to the resistance of the body can be measured across the body. That is, for a given current forced through a body, the higher its resistance, the higher will be the measured voltage. The relationship is, once again, governed by Ohm’s law. The terms voltage and potential tend to be used interchangeably. In the case of lightning, current and resistance are the external variables. The resulting voltage is derived. The remaining concept is that of an electric field. When a voltage is applied to a distance (for instance, the “gap” between a cloud and the ground), an electric field results. Air generally has a high resistance and is a very good insulator, conducting very little current under normal circumstances. The electric field is defined as the voltage across the gap divided by the width of the gap. If the magnitude of the field is increased, it reaches a size where the intervening insulator will “break down.” Before this point, a degree of current will be conducted under the influence of the field. After this point, entirely new processes come into play, causing the physical structure of the conducting medium to be disrupted, resulting in an avalanche of current—“breakdown.” The actual moment that this event occurs varies with the voltage applied and the width of the gap. The voltage that is necessary to flash over an air gap is about 4000 V/cm (10,000 V/inch), depending on humidity and other factors, and is also referred to as the “dielectric” constant of air. A large noisy flashover (thunder) may be observed if the gap is sufficiently large. By definition, fields operate over a space. The longer or wider the space, the more effect. Because nerves are by far the longest cells in the body, they are preferentially injured by an electric field, explaining why lightning injury is a primarily a neurologic injury rather than a burn injury as one might otherwise expect from the high voltages associated with lightning.
CHAPTER 3 Lightning Injuries
Mechanisms of Injury by Lightning*
Blunt Force Trauma Effects 6. Barotrauma 7. Concussive injury 8. Musculoskeletal injury from muscle contraction, falls
Lightning is dangerous to humans because of the effects caused by electricity, heat, and concussive force. In addition, lightning may injure indirectly via forest fires, house fires, explosions, or falling objects. Only injuries directly caused by lightning are
discussed here. The later discussion on pathophysiology states that when lightning current is injected into an individual, the current is initially transmitted directly through the individual. Then, as internal structures (capacitances) charge, flashover occurs over the surface of the individual, and internal current reduces dramatically.225 Lightning current may initially be inflicted on a person in one of several ways, described in more detail later (Box 3-3 and Figure 3-33). In each of these mechanisms, the following processes can occur:169 1. The internal current phase may be the most causative for development of cardiac and respiratory arrest, particularly if the pathway directly includes the heart. 2. As the body’s electric potential builds up in response to the internal current, it produces an electric field over the surface of the body. At a certain level (about one-half the air breakdown field of 4000 V/cm [10,000 V/inch]), current can emerge or escape the body at various points on the body’s surface. Because of the very fast rise time and high current associated with lightning, this occurs after only a few microseconds. In wood, current travels over the surface of wood or internally to it, but not both.89 The consistency and resistance of wood are much closer to the human body than one would initially expect. Metal pieces inserted into wood enhanced “swapping” from internal to external flow. It is unknown if metal pieces on the body may trigger, enhance, or reroute surface discharges and flashovers. However, there is no evidence that metal “attracts” a lightning attachment, regardless of where it may be on or near the body, including whether one is using a mobile phone or other personal digital device* 3. As the current continues to increase, the surface flashover bridges the strike point and the ground. At this level, most of the lightning current flows as an arc current through the air outside the body (flashover effect). Only a very tiny fraction flows through the body at this point and may be too little to cause cardiac and respiratory arrest. A direct strike occurs when the lightning stroke attaches directly to the victim (see Figure 3-33, A). This is most likely in the open when a person has been unable to find a more safe location and probably occurs no more often than in 3% to 5% of injuries. Even though it seems intuitive that direct strike might be the most likely to cause fatalities, there are no studies on the relative fatality rate for each strike mechanism. This low rate of occurrence is estimated on the basis of the examination of thousands of cases by the authors (Figure 3-34).77 Contact, or touch potential, injury occurs when the person is touching or holding onto an object to which lightning attaches. A voltage gradient is set up on that object from strike point to ground, and the individual in contact with the object is subject
*References 4, 6, 7, 15, 25, 43, 53, 68-73, 77.
*References 3, 14, 104, 126, 127, 206, 217.
MECHANISMS OF INJURY
75
PART 1 MOUNTAIN MEDICINE
Contact voltage
Side flash
A
Direct strike
B
C
Upward streamer Ground current
D2
Step voltage
Step voltage
D1 D3
E
FIGURE 3-33 Illustrations of mechanisms of injury. A, Direct. B, Contact. C, Side splash/flash. D1, Ground current through the earth. D2, Ground arcing. D3, Ground arcing cave. E, Upward streamer.
76
Upward streamer 10–15% Side splash/flash 30–35%
Ground current 50–55%
FIGURE 3-34 This chart shows the frequencies of primary lightning fatality mechanisms. (From Cooper MA, Holle RL: Mechanisms of lightning injury should affect lightning safety messages, 2010, University of Illinois at Chicago.)
to the voltage between his or her contact point and the earth (see Figure 3-33, B). A current therefore flows through them. Contact injury probably occurs in about 3% to 5% of injuries. A more frequent cause of injury, perhaps as much as 30% to 35%, is a side flash, also termed “splash.” Side flashes occur when lightning that has hit an object such as a tree or building travels partly down that object before a portion “jumps” to a nearby victim (see Figure 3-33, C). Standing under or close to trees and other tall objects is a very common way in which people are splashed and is the reason safety instructions stress keeping away from trees or other tall or overhanging objects. Current divides itself between the two paths in inverse proportion to their resistances. The resistance of the “jump” path represents an additional path separate from the path to the earth through the originally stricken object. Side flash may also occur from person to person. Earth potential rise (EPR) occurs because the earth, modeled ideally as a perfect conductor, is not so in reality. When lightning current is injected into the earth, it travels through the earth just as it would in any other conductor. Earth has a finite resistance, and so voltages are set up in the ground, decreasing in size with distance from the strike point. The voltage (or potential) of the earth is raised, hence the term EPR. EPR may account for 50% or more of lightning injuries. There are several consequences of EPR. If a person is standing in an area where EPR is active, that is, near the base of a strike, a voltage will appear between their feet and current will flow via the legs into the lower part of the body. This is more significant between the front and back legs of animals, where the path may involve the heart (see Figure 3-33, Dl and D2). A special case occurs on those relatively rare occasions when a person is injured inside a building as lightning hits nearby and is transmitted through the land line of the telephone, pipes of plumbing and faucet handles, or electrical wiring as one uses a computer or attempts to dispatch an ambulance.8,16,95 This is caused, for example, when the person, along with the environment around the person, is raised in potential via EPR. If the telephone line is not locally earthed (grounded), it is at the same voltage as the environment. The fact that the line is earthed remotely away from the local EPR environment causes the person to be subjected to a shock with current flowing between the local Earth at high potential and the distant unaffected Earth. This highlights that local electrical apparatus, including telephones, should be well grounded locally. The grounds of all local structures (power, telephone, plumbing, structural steel) should have a common grounding point (i.e., be bonded) to eliminate any voltage differences developing between separated ground points for each system. For the special case of indoor or telephone
injury, EPR may account for 80% or more of the injuries. It should be noted that all of these refer to hard-wired phones. Cell phones, not being hard wired or distantly grounded, provide no connection or EPR effect to a person during a lightning strike. Static electrical discharges may occur when a person reaches for a car door or stands close to a metal window or door frame in a thunderstorm, because the surrounding electric field induces static electrical charges. These are not lightning injuries. Although people may be startled when this happens, these discharges are unlikely to be any more dangerous than static discharges experienced in the winter months from shuffling across the carpet and reaching for a door handle. Kitagawa and colleagues169 have identified further subdivisions of the EPR phenomenon. They note that not only can EPR occur as discussed, but it can also occur in a manner similar to the surface flashes over a body, with arcs developing over a ground surface (Figure 3-35). Despite modeling that assumes the contrary for mathematical reasons, the grounding Earth is not homogeneous and provides arc generation points. Ground current effects are possibly more likely to be temporary and less likely to produce fatalities. However, multiple victims and injuries are frequent. Large groups have been injured on baseball fields, at racetracks, while hiking, and during military maneuvers.40,41,188 Shocks via telephones can produce significant long-term problems, and the majority of these are via EPR.16,95,212 Irregularities occur on mountainsides. If the terrain is markedly irregular, spreading lightning current may reach the surface. A surface arc discharge may develop together with flow of the conduction current in the ground. Because arcs carry considerable energy, a person exposed to a surface arc discharge is more likely to have a more severe effect, including thermal injuries, temporary
A
B FIGURE 3-35 A, Lightning injury and ground current effect to a golfing green—photographed a few days after the strike when the grass had died. B, Laboratory lightning onto a pool surface.
77
CHAPTER 3 Lightning Injuries
Contact Direct Blunt injury strike injury 3–5% 3–5% ?
PART 1 MOUNTAIN MEDICINE
FIGURE 3-36 Example of contact injury.
paralysis, or even death. This mechanism of injury makes it particularly dangerous for someone on a mountainside to shelter inside a shallow cave or under a small cliff or outcropping of terrain where surface arcing is much more likely to occur, injuring the person just as they feel some degree of safety has been achieved (see Figure 3-33, D3). All these factors point to the danger of being anywhere outside in the presence of lightning. The danger of upward streamers has been documented.4,41,68 Injury may occur when a victim serves as the conduit for one of the usually multiple upward leaders induced by a downward stepped leader and its field (see Figure 3-33, E). Streamers occur even when there is no attachment between them and the stepped leader. Although one might think that these are weak in energy compared with the full lightning strike, they may carry several hundred amperes of current to be transmitted through the victim. Upward streamer injury is probably a much underestimated mechanism of injury and may account for as much as 10% to 15% of injury cases, but needs substantial additional study and documentation. Finally, persons may suffer from (nonelectrical) blunt injury, either by being close to the concussive force of the shock wave produced as lightning strikes nearby or if ground current or some other mechanism induces an opisthotonic contraction. Victims have been witnessed to have been thrown tens of yards by either mechanism. In addition, some have theorized that a person struck by lightning may suffer from explosive and implosive forces created by the thunderclap, with resulting contusions and pressure injuries, including tympanic membrane rupture (barotrauma—see Lightning Explosive Barotrauma, later). Another mechanism of blunt injury is blast injury resulting from vaporization of water on the body surface from a surface flashover spark. Lightning blast injury to the skull, brain, and viscera has been elegantly demonstrated in animals.224 Many cases of multiple injuries are likely a combination of many of these effects, with the majority of them from EPR and upward streamers, sometimes complicated by side flashes if people or animals are standing too close together (Figures 3-36 and 3-37).
medical literature. Figure 3-38 shows 20 kV applied to a 1.8-m (6-foot) man, causing current to ground. This produces an internal electric field strength of approximately 10 kV/m. When a child chews on an electric cord and suffers a lip burn, the field strength is approximately the same: 110 V applied to 1 cm of a child’s lip generates a field strength of 11 kV/m. Even though no one would classify the child’s injury as “high” voltage, it is a high electric field strength and produces the same tissue destruction in a small localized area, much as would a high-voltage injury. Electric fields operate over a space. The longer or wider the space, the more effect. Because nerves are by far the longest cells in the body, they are preferentially injured, explaining why lightning injury is a primarily a neurologic injury. Although Lee184 has discussed the importance of internal electric field calculations in describing electroporation damage, this has not been studied for lightning injury. A similar inconsistency involves the breakdown strength of air (the force needed to cause a spark of electricity to cross a gap), which is roughly 4000 V/cm, or 10,000 V/inch. Most people are familiar with the shock experienced from walking across a carpet in the winter, although few appreciate this phenomenon would be classified as “high-voltage” injury by the 500- to 1000-V criterion used in medical literature. Thus terms used in the medical literature to categorize electrical injuries, such as high versus low voltage and exit versus entry in alternating current injuries, as well as the simplistic application of Kouwenhoven’s six factors, do not reflect either medical or engineering reality and are poor predictors of injury.
LIGHTNING INJURY PHYSICS It is necessary to distinguish between lightning and generatorproduced high-voltage electrical injuries, in that there are significant differences between the mechanisms of injuries and their treatment.65 Although lightning is an electrical phenomenon and is governed by the laws of physics, it accounts for a unique spectrum of induced signs and symptoms that are best understood relative to specific physical properties of lightning.
FREQUENCY, VOLTAGE, AMPERAGE, AND RESISTANCE Lightning is neither a direct nor an alternating current. At best description, lightning is a unidirectional massive current impulse. The cloud-to-ground impulse results from breakdown of a large electric field between cloud and ground, measured in millions of volts. Once connection is made with the ground, the voltage difference between cloud and ground disappears and a large current flows impulsively in a very short time. The study of massive electrical discharges of such short duration, particularly
Pathophysiology of Lightning Injury* ELECTRICAL INJURY PHYSICS REVISITED Kouwenhoven determined six factors that affect the type and severity of injury encountered with electrical accidents: frequency, duration of exposure, voltage, amperage, resistance of the tissues, and pathway of the current. However, several inconsistencies appear when these are applied too literally. Electric field strength, not listed as one of the factors, is a more useful and accurate concept in explaining and predicting injuries from technical or man-made electricity than are the classic Kouwenhoven factors that have traditionally been cited in the
*References 15, 64, 72, 153.
78
FIGURE 3-37 Example of side flash or “splash.”
Energy ( heat ) = Current 2 × Resistance × Time
20 kV
6 feet
= Electric field approx. 10 kV/m 20 kV 2m
A
= 10 kV/m
PATHWAY, DURATION OF CURRENT, FLASHOVER EFFECT, AND TIME
110 V
1 cm
1 cm = 11 kV/m
B
where a current flows through a resistance for a time T. As resistance goes up, so does the heat generated by passage of the same current. In humans, when low energy levels are encountered, much of the electric energy may be dissipated by the skin, so that superficial burns are often not accompanied by internal injuries. Although lightning occasionally creates what appear to be discrete entry and exit wounds, these are rare. Lightning more commonly causes only superficial streaking burns. Burns are discussed later and are a most important distinction between lightning and technical electric shocks. The exception to this is when there occurs long continuing current. This is a prolonged stroke lasting up to 0.5 second that delivers a tremendous amount of energy, capable of exploding trees and setting fires. Other poorly understood factors may contribute to the formation of deep burns, although deep burns similar to those of high-voltage electrical injuries generally are quite rare with lightning.
110 v/1 cm = 11 kV/m
C FIGURE 3-38 A, If 20 kV is applied to a 1.8-m (6-foot) man source to ground, an electric field strength of approximately 10 kV/m is produced. B, When a child chews on the end of an extension cord, the applied voltage of 110 V across 1 cm produces an electric field strength of 11 kV/m—higher than the classic “high-voltage” injury. C, This explains the deep full-thickness burns the child receives, which one would not predict given the “low-voltage” source.
It takes a finite amount of time for the skin to break down when exposed to heat or energy. Generally lightning is not present long enough to cause this skin breakdown. Probably a large portion travels along the outside of the skin as “flashover.” There is some experimental evidence that a portion of the current may enter the cranial orifices—the eyes, ears, nose, and mouth.10 This pathway would help explain the myriad eye and ear symptoms that have been reported with lightning injury. Andrews further examined the functional consequences of lightning on cardiorespiratory function and concluded that entry of current into cranial orifices leads to passage of current directly to the brainstem. In a sheep study, he was able to demonstrate specific damage to neurons at the floor of the fourth ventricle in the location of the medullary respiratory control centers. It is postulated that current travels via cerebrospinal fluid (CSF) and blood vessel pathways to impinge directly on the myocardium. Andrews also showed histologic damage to the myocardium, consistent with a number of autopsy reports of inferior myocardial necrosis.9,17 An alternative hypothesis can be tested with mathematical modeling.15 Certain assumptions are made in any model, usually based on principles accepted in the literature.31 Figure 3-39, A shows a model for skin resistance, and its connection to the internal body milieu is shown in Figure 3-39, B. Note that the internal body structures are regarded as purely resistive, whereas the skin contains significant elements of capacitance.31 In the model, the sequence of events during the strike starts with the postulate that the stroke attached initially to the head of the victim. From our knowledge now that “direct strike” occurs in probably only 3% to 5% of lightning injuries, it seems that this is an uncommon point of attachment, but the model is still useful in illustrating lightning energy flow. For a small fraction of time, current flows internally as the skin capacitance elements become charged. At a voltage taken as 5 kV, the skin was assumed to break down. (A lightning stroke is modeled as a current wave, building to a maximum value in around 8 msec, although this may be “modulated lightning,” that is, lightning that has passed through other structures, such as wiring. Others have measured the rise time of direct lightning as 1.2 to 1.5 msec.) Once the internal current increased, the voltage across the body to the earth built up, and external flashover across the body occurred when the field reached the breakdown strength of air. 79
CHAPTER 3 Lightning Injuries
their effects on the human body, is not well advanced. Lightning is said to be a “current” phenomenon rather than a “voltage” phenomenon. Examining the particular voltage in these equations becomes difficult because the voltage between cloud and ground disappears after lightning attachment, and equations such as Ohm’s law (V = I × R) and power calculation (P = V × I) cannot be accurately applied. Thus we must resort to alternative formulations of the equations. The energy dissipated in a given tissue is determined by the current flowing through the tissue and its resistance by:
PART 1 MOUNTAIN MEDICINE
10 k
0.25 µ 10 k
10 kΩ
200 0.25 µF
200 0.25 µ
Key
A
300
300
10 k
0.25 µ
300
10 k
0.25 µ
B FIGURE 3-39 A, Electrical model for human skin impedance. B, Model of human body for the purpose of examining current flow during lightning strike.
The results of mathematical modeling of these events are shown in Figure 3-40, and the relative magnitudes of the various voltage components can be seen with their time scale. On this time scale, the times to breakdown are short and most events occur early in the course of the stroke. In summary, in this model, lightning applies a current to the human body. This current initially is transmitted internally, following which skin breaks down. Ultimately, external flashover occurs. Andrews9 draws support for this model from measurements made in the experimental application of lightning impulses to sheep. Further modeling of step voltage injury verified that, for the erect human, this mechanism is less dangerous than is a direct strike, although this has not been corroborated in clinical studies.169 Experimental evidence suggests that “a fast flashover appreciably diminishes the energy dissipation within the body and results in survival.”225 In addition, Ishikawa obtained experimental results with rabbits similar to the human data found by Cooper’s study.64,153 Cooper has carried her studies to animals in developing a model of lightning injury and has successfully shown primary cardiac arrhythmias, prolonged ventilatory arrest, secondary cardiac arrest, keraunographic skin changes, and temporary lower extremity paralysis.80-82 As current flashes over the outside of the body, it may vaporize moisture on the skin and blast apart clothes and shoes, leaving the victim nearly naked, as noted by Hegner128 in 1917: The clothing may not be affected in any way. It may be stripped or burned in part or entirely shredded to ribbons. Either warp or woof may be destroyed leaving the outer garments and the skin intact.… Metallic objects in or on the clothing are bent, broken, more or less fused or not affected. The shoes most constantly show the effects of the current. People are usually standing when struck, the current then enters or leaves the body through the feet. The shoes, especially when dry or only partially damp, interpose a substance of increased resistance. One or both shoes may be affected. They may be gently removed, or violently thrown many feet, be punctured or have a large hole torn in any part, shredded, split, reduced to lint or disappear entirely. 80
The soles may disappear with or without the heels. Any of the foregoing may occur and the person not injured or only slightly shocked. The amount of damage to clothing or the surface of the body is not an index to the severity of injuries sustained within a human. Either may be disproportionately great or small. However, in unwitnessed situations, Cooper and others have found that forensic evidence of damage to shoes and clothing may be the most important and reliable indicator in determining whether lightning caused a person’s death, in addition to ruptured tympanic membrane when no other cause is apparent.32,162,279 The factor that seems most important in separating the effects of lightning from high-voltage electrical injuries is the duration of exposure to the current, both because lightning is not present long enough to cause tissue breakdown in the classic burn sense and because of the results of the mathematical modeling describing the path of the energy and how long it is in contact with the body.
ESTIMATES OF STREAMER CURRENTS A fifth mechanism of current impingement on an individual has been described.4-6,68 This mechanism recognizes that as a stepped leader steps toward the earth from a cloud, an upward leader will emanate from several objects that are possible points of attachment. Of these, a return stroke will evolve perhaps from only one. Alternatively stated, there will be several upward leaders that dissipate without attachment. The current needed to establish and maintain any upward leader nonetheless must be supplied from the earth, and if a person is the source of an upward leader, then current must flow through the person as a first approximation. Becerra and Cooray25 have studied the amount of current to which a victim of upward leader current may be exposed. They identify two processes that are important to model. First, current flows through a victim to establish the upward streamer and the space charge around the victim’s head, under the influence of the electric field resulting from the stepped leader’s downward
Response
No flashover 5 MV
G4
VAC VAB
4 MV
CHAPTER 3 Lightning Injuries
A
5 kV
F
5 kA VAF VEB,DB
IFH
1.11.7
50
G1 500 kV
Time (µsec)
H
5 kA peak 8/20 µsec wave
With flashover E
D VAB
500 kV
IFH
800A
G2
5 kV
150
VDB 340 nsec
B
Physical Earth
<<5 kV
VAF
G3
5 kV
True Earth
C
Time
FIGURE 3-40 Model of human body adapted for the circumstance of direct lightning strike. Responses of the body model are shown for cases of direct strike with and without subsequent flashover.
path. Second, once a leader other than the leader affecting the person makes connection with the stepped leader, then the electric field collapses rapidly. In that case, the charge in the unattached upward leader rapidly returns to the earth. The first process is relatively prolonged and regular, and the second is rapid and impulsive. In an analysis using a human model and a 30-kA lightning strike grounding just beyond the striking distance, current rises to approximately 20 A over 150 µsec. At the very start of this rise, there is an extremely short pulse of about 5 A. This represents a body charging component before the propagation current for the actual streamer. This is a significant current; however, the duration is extremely short. In fact, the flow of any substantial current internally occurs for less than 10 µsec before the current escapes externally and flashover occurs. The fatal effect of this current, conducted internally within a victim for such a short time, theoretically depends on its timing to the vulnerable period of the cardiac cycle. For an 80-kA return stroke, the peak current is approximately 80 A, again significant. Once the aborted leader collapses, there is a current pulse of opposite polarity. This is exquisitely short. Little is known about the collapse of an aborted leader, and assumptions are made regarding the time constant of the collapse. This ranges from 0.1 to 1 µsec. Cases are examined for a 30-kA and an 80-kA return stroke. The peak current can be large, depending on the size of the stroke and the time constant. The least is computed at about -600 kA, with the least energy deposited being .22 kJ. Again, these are highly significant currents that are large enough to produce significant injury and death.
BEHAVIOR OF ELECTRIC CURRENT IN TISSUE High- or low-voltage electric current may be carried through tissue in a direct conduction fashion, obeying simple linear equations such as Ohm’s law. The result is heating of tissues under Joule’s law, with thermally induced cellular death and dysfunction. Simple passage of current may interfere with neural and muscular function.184
Earlier in the previous century, electrical injury was thought to occur not only because of thermal effects but also because of some mysterious cellular effects.29,157 Unfortunately, the technology was not available to investigate these effects, and this idea was largely forgotten until the past few decades. Cell wall integrity, enzyme reactions, protein shape and structure, and cell membrane “gates” and pumps all operate by changes on the order of microvolts. It is not beyond the realm of imagination that passage of an electric current too small to produce significant thermal damage may cause irreversible changes in these functions, leading to cell death or dysfunction.184 Induction of electric charges by external electromagnetic fields has been shown to force water molecules into cell walls (electroporation), causing fatal “pores.” Cells can die from exhausting their energy and resources attempting to maintain intracellular integrity. Although electroporation has been demonstrated in the laboratory for electrical injuries, it has never been documented for lightning injury with lightning’s very different properties and effects on the body.184
MAGNETIC FIELD EFFECTS* It has been stated that some effects of lightning might be magnetically mediated. A case cited in support of this contention was of a golfer under a tree in the company of three other persons. It was stated that death occurred without evidence of current entering or leaving the index case. On the other hand, one accompanying golfer showed evidence of current traversal but survived. It is stated that three methods of shock may have existed—direct strike, side flash, and ground potential—but no evidence of any was seen. It was considered that contact potential was not relevant. In this case, with persons under a tree, it would seem possible to explain deleterious effects without resorting to a magnetic hypothesis, but the hypothesis bears examination if only because it is a recurrent question. *References 7, 53.
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PART 1 MOUNTAIN MEDICINE
In the case under consideration, the stroke was considered as a line current 1 m (3.3 feet) distant from the victim, and calculation of peak fields and their effects were given. In considering the contention, it is useful to consider the stroke as a single line current as referenced; however, one must also gain a feeling for how far from a victim such a stroke will act. If the stroke is close to a victim, then attachment to the victim takes place and electrical effects apply as described earlier. If further away, the magnetic field is operative without attachment and magnetic effects need to be examined. Ground potential also exists at this 1-m (3.3-foot) distance. It is necessary to find the minimum distance away from a victim that a stroke can reach ground without attachment to the victim. This gives the worst case distance from a victim (the worst case being the closest) at which a pure magnetic field acts without attachment. The standard striking distance formula gives such a distance.91 The formula is as follows: d s = 10 I 0.65 where ds (m) is the striking distance and I is the stroke current in kiloamperes. This represents the distance at the last turn of the downward stepped leader, such that if an object lies inside this distance, attachment of the leader to the object will take place. For illustrative purposes, let a stroke have a peak current of 18,000A (the 50th percentile) so that ds is 65.5 m. Pure magnetic effects are applicable at this distance and beyond. Inside this distance, the victim will be subject to electrical current effects. By comparison, the ground potential between two points 1 m (3.3 feet) apart at 60 m (197 feet) from a stroke of 18 kA is about 60 V, assuming Earth resistivity of 100 ohm-meters. In examining the magnetic fields involved at this distance, assume an 18-kA stroke at a distance of 65 m (213 feet) from an individual. The peak magnetic B field (the “magnetic induction” formally quantifying the force on a moving charge in its influence) is: µ0 I peak B peak = 2π d s At 65 m (213 feet), the peak B field is 88 µT. For comparison, the earth’s magnetic field is about 1 µT, and the magnetic fields causing concern for power-line fields are in the 1 to 100 µT range. The magnetic fields used in MRI scanning are around 2,000,000 to 5,000,000 times these levels. As with other exposures, effects from chronic exposures may be quite a bit different from acute or momentary exposures. Power-line fields, for instance, are arguably dangerous only if chronic. If one is concerned about a lightning stroke magnetic field, it would be wise to be concerned about MRI fields as well, where, to this date, no effect has been found in practice. Certainly, the time-varying nature of any B field is important, both in terms of the rate of change of the field and of movement of a conductor within this field. If one assumes that the above B field is generated in about 2 µsec, then the time rate of change for the B field is about 22 T/sec. Andrews applied this field to a model heart and found an entirely noninjurious current resulting. It is concluded that magnetic field danger in normal circumstances does not seem to exist.7 Certainly special circumstances might exist, such as the presence of a pacemaker or the presence of an arrhythmic pathway, but in normal terms, magnetic effects would not seem to be clinically significant during occurrences of lightning strike.
BOX 3-4 Lightning Injuries Immediate • Cardiac arrest and cardiac injuries • Pulmonary injuries • Neurologic signs • Seizures • Deafness • Confusion, amnesia • Blindness • Dizziness • Contusion from shock wave • Chest pain, muscle aches • Tympanic membrane rupture • Headache, nausea, postconcussion syndrome Delayed • Neurologic symptoms and signs • Neuropsychological changes • Memory deficits • Attention deficit • Coding and retrieval problems • Distractibility • Personality changes • Irritability • Chronic pain • Seizures
INITIAL PRESENTATION MODEL* Minor Injury These victims are awake and may report symptoms such as dysesthesia in an extremity, a feeling of having been hit on the head or having been in an explosion. They may or may not have perceived lightning or thunder. They often suffer confusion, amnesia, temporary deafness or blindness, or temporary unconsciousness at the scene.65 They seldom demonstrate cutaneous burns or paralysis but may complain of confusion and amnesia lasting from hours to days. Paresthesias, muscle pain, and headaches may last for days to months. Victims may suffer tympanic membrane rupture from the explosive force of the lightning shock wave. Vital signs are usually stable, although occasionally, victims demonstrate transient mild hypertension. They may experience soreness for a few days, but recovery is usually gradual and may or may not be complete. Permanent neurocognitive damage may occur. Some victims may suffer post-traumatic stress disorder and other psychological sequelae.
There have been at least two useful categorizations of lightning injuries by severity of injury: one starts from initial presentation and one is based on neurologic outcome (Box 3-4).
Moderate Injury Moderately injured victims may be disoriented, combative, or comatose. They often exhibit keraunoparalysis: motor paralysis, particularly of the lower extremities, with mottled skin and diminished or absent pulses. Nonpalpable peripheral pulses may indicate arterial spasm and sympathetic instability, which should be differentiated from hypotension. If true hypotension occurs and persists, the victim should be scrutinized for fractures and other signs of blunt injury. Spinal shock from cervical or other spinal fractures, although rare with lightning, may also account for hypotension. Occasionally victims have suffered temporary cardiopulmonary standstill, although it is seldom documented. Spontaneous recovery of the pulse is attributed to the heart’s inherent automaticity. However, respiratory arrest that often occurs with lightning injury may be prolonged and lead to secondary cardiac arrest from hypoxia or some other yet-to-be-elucidated cause. Seizures may also occur.
*References 15, 46, 65, 72.
*Reference 15, 72.
Injuries from Lightning*
82
Severe Injury Victims with severe injury may be in cardiac arrest with either ventricular standstill or fibrillation when first examined. Cardiac resuscitation may not be successful if the victim has suffered a prolonged period of cardiac and central nervous system (CNS) ischemia. Direct brain damage may occur from the lightning strike or blast effect. Tympanic membrane rupture with hemotympanum and CSF otorrhea is more common in this group. The prognosis is usually poor in the severely injured group, complicated by any delay in initiating cardiopulmonary resuscitation with resultant anoxic injury to the brain and other organ systems. There are anecdotal reports of successful resuscitation of these victims with automated external defibrillators (AEDs).218
NEUROLOGIC OUTCOME MODEL* Cherington proposed the classification, focusing on neurologic complications consisting of four groups based on time of onset, duration of symptoms, and severity of the clinical situation. Immediate and Transient Symptoms These may include loss of consciousness, amnesia, confusion, headache, paresthesia, and weakness. Many patients experience a temporary paralysis of their limbs called keraunoparalysis, a term introduced by the French neurologist Charcot. Keraunoparalysis is a brief paralytic state with loss of sensation that affects lower limbs more than upper limbs. Muscle strength and sensation usually return to normal within one to a few hours. The paralysis is accompanied by pallor, severe vasoconstriction, and hypertension. Some have suggested that this peculiar state is caused by transient outpouring of catecholamines.
TABLE 3-1 Lightning Injuries Compared With
High-Voltage Electrical Injuries
Factor
Lightning
High Voltage
Energy level Time of exposure Pathway Burns Renal
30 million volts, 50,000 Å Brief, instantaneous
Usually much lower* Seconds
Fasciotomy
Flashover, orifice Superficial, minor Rare myoglobinuria or hemoglobinuria Rarely if ever necessary
Blunt injury
Explosive thunder effect
Deep, internal Deep, major injury Myoglobinuric renal failure common Common, early, and extensive Falls, being thrown
*Range is 500 V up to millions of volts in transmission lines.
DIFFERENCES BETWEEN INJURIES FROM HIGH-VOLTAGE ELECTRICITY AND LIGHTNING* There are marked differences in injuries caused by high-voltage electrical accidents and lightning (Table 3-1). Exposure to highvoltage generated electricity tends to be more prolonged, particularly if the victim “freezes” to the circuit. In this context, “long” may mean only a few to several seconds of contact. With skin breakdown, electrical energy surges through the tissues with little resistance to flow, causing massive internal thermal injuries that sometimes necessitate major amputations. Myoglobin release may be pronounced, and renal failure may occur. In addition, compartment syndromes requiring fasciotomy may occur. Burns may be severe. Lightning contact with the body is almost instantaneous, often leading to flashover with very little energy going through the body, if at all, particularly because the vast majority of lightning injuries are indirect, as with side flash and ground current. Burns and deep injury are uncommon. Fluid restriction and expectant care are usually the rule. Lighting injury is primarily a neurologic injury, not a burn injury.
CARDIOPULMONARY ARREST AND CARDIAC INJURIES†
Lightning-Linked Secondary Trauma From Falls or Blast Lightning can cause trauma secondarily when the patient is thrown or falls. Injuries include epidural, subdural, and subarachnoid hemorrhages. Blunt and blast effects can damage the brain and other organs and cause tympanic membrane rupture, the most common blast effect seen in patients with lightning strike.
Cardiac Arrest The most common cause of death in a lightning victim is cardiopulmonary arrest. In fact, a victim is highly unlikely (P <.0001) to die unless cardiopulmonary arrest is suffered as an immediate effect of the strike.64 In the past, nearly 75% of persons who suffered cardiopulmonary arrest from lightning injuries died, many because cardiopulmonary resuscitation was not attempted. Primary and secondary cardiac arrests had previously been hypothesized and confirmed with animal studies.9,80-82,266 Injury first occurs with immediate asystolic cardiac arrest and respiratory standstill. Because of the heart’s automaticity, contractions generally resume within a short time. Unfortunately, respiratory arrest caused by unknown factors may last far longer than cardiac arrest. Unless the victim receives immediate ventilatory assistance, attendant hypoxia may induce arrhythmias and secondary cardiac arrest. Alternatively, the respiratory arrest and secondary cardiac arrest may be from more severe injury and not cause and effect. The course has been verified experimentally in sheep, with initial asystole followed by resumption of a short run of bradycardia, then tachycardia, followed by atrioventricular block or bradycardia, and finally with second asystolic arrest.9 Prolonged respiratory arrest has also been confirmed in hairless rats.82,174 It is unknown whether cardiac arrest and arrhythmias induced by lightning are a result of damage to central cardiac and res piratory centers in the brain, to the carotid body and other pacemakers along the cardiac control paths, to feedback control
*References 45, 46, 58.
*References 15, 65. † References 23, 64, 71, 78, 79, 85, 173, 286.
Immediate and Prolonged or Permanent Patients have structural lesions that may be seen on imaging studies or on postmortem examination. The great majority of these neurologic complications involve the CNS, including posthypoxic ischemic encephalopathy, intracranial hemorrhage, cerebral infarction, cerebellar syndromes, and spinal cord injuries. Possible Delayed Neurologic Syndromes Delayed neurologic disorders attributed to lightning include motor neuron disease and movement disorders. These sequelae have followed lightning strikes by days to years, although the cause-and-effect relationship between lightning and all subsequent delayed neurologic complications is open to question.
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CHAPTER 3 Lightning Injuries
Burns are uncommon in lightning victims. First- and seconddegree burns not prominent on admission may evolve over the first several hours. Rarely, third-degree burns may occur. Tympanic membrane rupture should be anticipated and, along with hemotympanum, may indicate a basilar skull fracture. Whereas the clinical condition often improves within the first few hours, victims are prone to have permanent sequelae, such as sleep disorders, irritability, difficulty with fine psychomotor function and attention, chronic pain and dysesthesia, generalized weakness or easy fatigability, sympathetic nervous system dysfunction, chronic headaches, and sometimes post-traumatic stress syndrome. A few cases of atrophic spinal paralysis have been reported.
PART 1 MOUNTAIN MEDICINE
mechanisms within the autonomic nervous system, to the heart, or to a combination of these.70,82 Certainly, clinical evidence of general damage to autonomic nervous system regulation has been well documented and confirmed in the animal laboratory.82 Asystole and ventricular fibrillation has each been reported with lightning strike.10,113 As noted in the animal studies, asystole seems to be both the first and last responses to the strike, as the secondary agonal arrest rhythm of ventricular fibrillation deteriorates. Other Cardiac Injuries An immediate prolongation of the QT interval has been shown with consequent predisposition to arrhythmias.13 An associated enzyme rise has been noted in some.108 The QT interval changes may have implications for the cessation of metabolism hypothesis if torsades de pointes is involved.13 The electrocardiogram (ECG) pattern after initial shock may show tachycardia or bradycardia and may show the pattern of myocardial infarction. In the long term, arrhythmias—tachycardia, bradycardia, premature contractions, and atrial fibrillation—have all been reported.79,99,187,259 Postural tachycardia also has been reported, implicating the autonomic nervous system.122 Although the initial ECG may be unreliable for reasons given below, it is not uncommon to find ECG ST changes consistent with ischemia and damage in subepicardial, posterior, inferior, or anterior patterns.18,187 Creatine phosphokinase MB-isoenzyme elevation has been reported. The first report of troponin level elevations and cellular damage in a lightning survivor was published by a high-altitude pulmonary physiologist who suffered injury while climbing in the Alps, using himself as a control.24 Saglam and co-workers250 present a typical case of infarct changes with normal coronary angiography. They summarize the widespread cardiac consequences of lightning strike: “the victim may develop hypertension, tachycardia, nonspecific electrocardiographic changes (including prolongation of the QT interval and transient T-wave inversion), and myocardial necrosis with the release of creatine phosphokinase–myocardial band fraction.” Unfortunately, their case of a “13-year-old boy with myocardial infarction secondary to an indirect lightning strike” resulted in early death, so the progress of the changes was not able to be reported. Others tend to show resolution of infarct changes.117,248 All that is stated in the articles is that the ECG pattern resolves; no indication is given if there is permanent scarring associated with an infarct. ECG changes may not occur until the second day, making the initial ECG a poor screening tool for ischemia. Several clinicians stress that cardiac symptoms may not be apparent on initial presentation. Premature ventricular contractions were reported in one patient nearly 1 week after presentation. Whereas most ECG changes resolve within a few days, some may persist for months. Several reports of cardiomyopathy have appeared. Rivera and associates241 refer to “stunned myocardium” and document a 42-year-old victim with severe cardiogenic shock and left ventricular dysfunction. This was demonstrated clinically with ECG changes and scan changes. The victim recovered fully with no long-term disability. They concluded that “the exact mechanism of abnormal contractility in the absence of direct electrofulguration is unknown but may be explained by release of oxygen-free radicals, proteolysis of the contractile apparatus, and cytosolic overload of intracellular calcium, followed by reduced myofilament sensitivity to calcium.” Takotsubo-shaped hypokinesis with aneurysmal dilation (transient left ventricular apical ballooning syndrome) has been described with associated cardiomyopathy.125 This is noted in the setting of ECG changes mimicking myocardial infarction, but with minimal enzyme release.100,117 Recovery from dramatic dysfunction is complete over days to weeks. Some clinicians have theorized that vascular spasm is a cause of cardiac damage not dissimilar to keraunoparalysis.228 However, ECG changes are not always consistent with cardiac vascular supply patterns. Areas of focal cardiac necrosis have been reported in autopsies, and histologic changes have been shown in sheep hearts.10 84
PULMONARY INJURIES Pulmonary edema may accompany severe cardiac damage. Pulmonary contusion, with hemoptysis and pulmonary hemorrhage, may result from blunt injury or direct lung damage.260 Blunt thoracic trauma may also cause pneumomediastinum.124
NEUROLOGIC INJURIES* Although cardiac arrest may be the only immediate cause of death, lightning injury is primarily a neurologic injury with damage possible to central, peripheral, and sympathetic nervous systems. Injury to the nervous system far and away causes the greatest number of long-term problems to survivors. Tools commonly used in evaluation and treatment include functional scans, such as single photon emission computed tomography (often positive); positron emission tomography; anatomic scans, such as CT and MRI (usually negative); neuropsychological assessment; cognitive retraining; pharmacotherapy; and psychotherapy. Electroencephalography is often mentioned in the literature but is seldom helpful.17,65 Central Nervous System Injury† Gross structural changes to the brain, such as coagulation of brain substance, formation of epidural and subdural hematomas, paralysis of the respiratory center, and intraventricular hemorrhage, have been reported but are all rare and may be more from blunt trauma than from electrical injury. Autopsy findings include meningeal and parenchymal blood extravasation, petechiae, dural tears, scalp hematomas, and skull fractures.269 Although MRI or CT may show diffuse edema, intracranial hemorrhage, or other injuries, they are more commonly normal.57,58 There have been reports of hemorrhage on MRI findings in a few acutely injured victims.57,227,275 In animals, direct cellular damage to the respiratory center beneath the fourth ventricle, as well as to the anterior surface of the brainstem, has been shown.9 Lightning energy has been theorized to enter through the orifices of the head, pass through the pituitary and hypothalamus and also through the CSF into the retropharyngeal area, so that signs and symptoms of endocrine dysfunction, respiratory or cardiac arrest, and sleep disturbances could be reasonably expected to occur. Seizures may accompany initial cardiorespiratory arrest as a result of hypoxia or intracranial damage. Electroencephalographs may show epileptogenic foci in the acute phase. These patterns may be focal or diffuse, varying with the site and type of injury. However, most patients do not experience seizures during hospitalization. Some victims, however, including children, develop delayed seizures, some of which manifest as “absence spells,” memory losses, or blackouts that are often diagnosed as “pseudoseizures.” Obviously the victim of prolonged cardiopulmonary arrest may have anoxic brain injury that is not specific to lightning injury. Whether by this mechanism or others, cell loss and/or infarction of various areas (e.g., cerebellum,21 cerebrum) has been reported. In Cooper’s study64 of severely injured victims, nearly twothirds had some degree of lower extremity paralysis (keraunoparalysis), usually demarcating around the waist or pelvis, and about one-third of victims had upper extremity paralysis. The affected extremities appear cold, clammy, mottled, insensate, and pulseless.15 This is probably the result of sympathetic instability and intense vascular spasm, similar in appearance to Raynaud’s phenomenon. It usually clears after several hours.15,65 Fasciotomies are seldom indicated for lightning injuries, because signs of compartment syndrome or distal ischemia usually clear with patient observation. Pulses can sometimes be elicited with Doppler examination. Atrophic spinal paralysis has been reported, as have persistent paresis, paresthesias, incoordination, delayed and acute cerebellar ataxia, hemiplegia, aphasia, quadriplegia
*References 21, 46-49, 55, 57, 67, 161, 168. † References 21, 46-49, 55-58, 67, 168.
Peripheral Nerve Injury‡ The peripheral nervous system may be affected. Pain and paresthesias are prominent features of the injury, particularly in the line of presumed current passage, although this is difficult to ascertain from external burns or other injury. Symptoms may be delayed by weeks to months. Almost any peripheral nerve can be involved. Autonomic Dystrophy§ Chronic pain syndromes may occur. Autonomic dystrophy, also called sympathetic dystrophy or sympathetically mediated pain syndrome, may occur. Such chronic pain syndromes are now subsumed under the classification of the complex regional pain syndromes, which are of type 1 (reflex sympathetic dystrophy) or 2 (previously causalgia). The complex regional pain syndromes are long-term neurologic sequelae that may be caused by even minor injuries to nerves and are characterized by pain, edema, autonomic dysfunction, trophic changes (including atrophy secondary to disuse from pain), and movement disorder. Post-Traumatic Headache¶ Many victims of lightning injury exhibit severe, unrelenting headaches for the first several months after lightning injury, along with other symptoms, including gastrointestinal distress, that resemble postconcussion symptoms. Acupuncture may be effective. Many victims complain of nausea and unexpected, frequent vomiting spells early in their recovery period. Dizziness and tinnitus from eighth cranial nerve injury are also common complaints, especially with telephone-transmitted lightning strikes.16,67,72,278,281
*References 45-48, 129, 227, 229-232, 237, 254, 263, 267, 272, 281. † References 62, 130, 161, 233, 254, 255. ‡ Reference 276. § References 62, 129, 130, 161, 233, 254, 255. ¶ References 71, 270.
BURNS* Most people assume that because of the tremendous energy discharge involved, a lightning victim will be flash-cooked.40,66 Fortunately, the physics of lightning flashover, as well as the fact that the vast majority of injuries are from indirect strikes, saves most victims from suffering more than minor burns. Less than one-third of lightning survivors have any signs of burns or skin marks. Although extensive third- and fourth-degree burns may occur in combination with skeletal disruption, these are quite rare. The incredibly short period of exposure may explain the lack of significant burn injury in most cases. As shown in mathematical models, a portion of the lightning current may travel through the tissues.9 If the electric field in the tissue becomes too large, electrons can be freed from their atoms. Referred to as dielectric breakdown, this can cause a large increase in the flow of current and become manifest as an electric arc. This may occur internal or external to the body, the latter when the breakdown strength of air (2 × 106 V/m) is exceeded. Arc-like burns can result. This happens more often with high-voltage electrical injury but may occasionally occur with lightning. Discrete entry and exit points are uncommon with lightning. The burns most commonly seen may be divided into five categories: linear burns; punctate, full-thickness burns; feathering or flowers; thermal burns from ignited clothing or heated metal; and combinations. Linear burns (Figure 3-41) often begin at the victim’s head and progress down the chest, where they split and continue down both legs. The burns generally are 1 to 4 cm (0.5 to 1.5 inches) wide and tend to follow areas of heavy sweat concentration, such as beneath breasts, down the midchest, and in the midaxillary line.65 Linear burns are usually first- and seconddegree burns that may be present initially or develop as late as several hours after the lightning strike. They are not primary lightning injuries but more likely steam burns secondary to vaporization of sweat or rainwater on the victim’s skin as flashover and current flow occurs around the body. In patients wearing thin or cotton clothing, the steam tends to escape through the clothing with less damage than in areas where the clothing is bunched (axilla, antecubital fossa [see Figure 3-41, C], groin) or under nonporous material, such as leather jackets or belts (Figure 3-42). Punctate burns (Figure 3-43) are discrete circular burns that individually range from a few millimeters to a centimeter (0.5 inch) in diameter and may be multiple and closely spaced. They may be full thickness and resemble cigarette or cinder burns and are usually too small to require grafting. Particularly useful for forensic investigation is explosion of clothing, such as occurs with vapor explosion of wet socks in shoes. This may blast shoes off with subsequent contusion and avulsion injuries to parts of the foot (see Figure 3-41, H). Examination of clothing may show singeing of fibers at the edge of the damage (see Figures 3-26 and 3-43, B) and absence of the very fine fibers on material, such as cotton, because they were vaporized and/or burned away. With a handheld 10× magnifier, plasticized or polyester materials may show frank melting. Even in cotton clothing with no apparent damage to the material, examination of the threads used in joining pieces together at the seams will often show a tiny droplet of plastic, because thread contains a polyester or nylon core for strength and durability. Feathering burns (Figure 3-44; see Figure 3-30) are pathognomonic of lightning and are known by such names as Lichtenberg’s flowers, filigree burns, arborescent burns, ferning, and keraunographic markings.† These markings are not true burns but usually appear as transient pink to brownish, sometimes lightly palpable, arborescent marks that follow neither the vascular pattern nor nerve pathways. The pattern found is similar to that on a photographic plate exposed to a strong electric field and has been compared with fractals.131 Sometimes the most superficial skin over the areas will slough or flake off after a few *References 22, 63, 71, 72, 131, 152, 202, 213, 214, 257, 261, 273. † References 51, 52, 63, 98, 149, 179, 198, 238, 273.
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CHAPTER 3 Lightning Injuries
(immediate or delayed), and one report of progressive muscle atrophy of the upper extremities. Nearly 72% of victims in Cooper’s study64 suffered loss of consciousness. Nearly three-fourths of these also suffered cardiopulmonary arrest.64 Those with cranial burns were two to three times more likely to suffer immediate cardiopulmonary arrest and had a three to four times greater probability of death.64 Persons who are stunned or lose consciousness without cardiopulmonary arrest are highly unlikely to die, although they may still suffer serious sequelae.64 Whether or not victims have suffered loss of consciousness, they almost universally demonstrate anterograde amnesia and confusion, which may last for several days. Retrograde amnesia is less common. Although the victim may carry on a conversation and remember his or her actions before the strike, he or she is often unable to assimilate new experiences for several days, even when there is no external evidence of lightning burns on the head or neck. Survivors may have persistent sleep disturbances, difficulty with fine mental and motor functions, dysesthesias, headaches, mood abnormalities, emotional lability, storm phobias, decreased exercise tolerance, and post-traumatic stress disorder.67 Early on, their symptoms resemble postconcussion syndrome. The basal ganglia and cerebellum may be affected.45-48,57,58,221,227 This agrees with older reports of localization. CNS damage may also eventually manifest as parkinsonism, extrapyramidal syndrome, or other involuntary movement disorders or signs of intracranial hematomata and hemorrhage; infarction; hypoxia; edema; cerebellar signs of infarction, dysfunction, and atrophy; and centrally derived pain and psychological syndromes.* Spinal cord injury developing over months following the injury has been reported.182,183 Paresthesias are frequently seen, often mirroring the area of keraunoparalysis. There is also evidence of autonomic neuropathy.†
PART 1 MOUNTAIN MEDICINE
A
C
B
D
E
G
H
F
I
J
FIGURE 3-41 Linear burns from a fatal 1977 lightning injury to 22-year-old baseball player. Most of these marks did not appear until a few hours to a few days (those with small eschar) after the injury. A, The mark that matured on the back of the head by the third day. B, The linear marks continuing down the side of the neck. C and D, Continuing marks down the anterior and lateral torso. Note that these are the normal “sweat lines” that a baseball player in July would develop. Also note the burn to the antecubital fossa where sweat would accumulate under the baseball jersey as the player stood crouched and ready to catch near second base. Note that all of these burns are partial thickness with sparse blistering. E, More extensive burns where a metal belt buckle or athletic supporter may have been causing secondary thermal burns or electrical discharge to the skin from the metal. F to H, Damage to the right leg and foot. Note the parallel marks on the foreleg, which would correspond to sweat accumulation or wetness in the ribbing of the athletic socks. Note also the mark on the heel, which may have been from the metal heel cup in the shoe or contusion from the shoe being ripped off by the vapor explosion of the flashover. The socks were destroyed or exploded off below the ankles, and the shoes were never found. Blunt injury from the explosion caused nonburned ripping of the fifth toe web as well (H). I and J, Damage to the left lower leg and foot. (Copyright Mary Ann Cooper.)
A
B
FIGURE 3-42 Steam burns on a motorcyclist who was wearing a leather jacket, belt, and pants. This man was injured 3 weeks after and only a few miles away from the man in Figure 3-41. A, Note the more extensive burn to the back where the steam was held against the skin longer by the leather jacket than would occur with more porous clothing. B, More linear burns where the jacket was not as close to the skin. Note that the burns take a right angle under the belt at the waist before splitting at the groin and continuing laterally down the leg. Old scarring on the right knee was from a previous airplane crash and not part of the lightning injury. (Copyright Mary Ann Cooper.)
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BLUNT, CONCUSSIVE, AND EXPLOSIVE INJURIES
B FIGURE 3-43 A, Punctate burns to the shoulder and arm of a 12-yearold girl who was at a campfire with friends. B, Note singeing of the cotton T-shirt that she was wearing at the time over the area of the right arm burn. (Copyright Mary Ann Cooper.)
The recipient of a lightning strike may be injured directly from the explosive force of lightning or from a fall (as from a horse or mountain ledge, out of a vehicle, or being hurled by endogenous opisthotonic force). Back and spinal injuries unrelated to the electrical effects of lightning injury may occur from these mechanisms. A variety of fractures, including skull, ribs, extremities, and spine, have been reported in lightning victims.165,190 Unfortunately, these are often missed, particularly in the workups of persons with chronic pain. Rarely a burst-like injury of soft tissue occurs and discloses extensive underlying injuries, especially in the feet, where boots or socks may explode as a result of vapor expansion (see Figures 3-29 and 3-41, H). Tympanic membrane rupture is common. Abdominal injuries due to blasts are well described and include gastrointestinal perforation and an abdominal compartment syndrome.20,166 Hemoglobinuria and myoglobinuria are seldom reported. When they occur, they are usually transient. Myoglobinuric renal failure has not been reported in the literature, although one case has been verbally relayed to the first author. Persistent hypotension should alert the physician to blunt injuries to the chest, spine, lungs, heart, and intestines that may lead to complications of prolonged coma, pulmonary contusions,260 heart failure, and ischemic bowel. Several victims have complained of jaw pain. A number have suffered loss of teeth or fillings or necrosis of the jaw and teeth, and many describe a metallic taste in the mouth for months after the acute injury. At least one was found to have a styloid process fracture. Many recovering victims believe that premature arthritis may be a result of their injury.
EYE INJURIES*
A
Ocular injuries may be due to direct thermal or electrical damage, intense light, contusion from the shock wave, or combinations of these factors. Although cataracts most commonly develop within the first few days, they may occur late and are often bilateral.† Whereas the cataracts may be the typical anterior midperipheral type, posterior subcapsular opacities and vacuolization seem to occur more often with lightning injuries.38 Corneal lesions, hyphema, uveitis, macular holes, iridocyclitis, vitreous hemorrhage, choroidal rupture, chorioretinitis, retinal detachment, macular degeneration, optic atrophy, diplopia, loss of accommodation, and decreased color sense have also been reported. Autonomic disturbances of the eye, including mydriasis, Horner’s syndrome, anisocoria, and loss of light reflexes, may be transient or permanent. Transient bilateral blindness of unknown etiology is not uncommon. Intense photophobia may be present as the victim recovers. An interesting paper conjectures that the
B FIGURE 3-44 A, Feathering marks. B, Ferning developed after the victim received a side flash lightning strike. (A courtesy Mary Ann Cooper; B courtesy Sheryl Olson, RN.)
*References 38, 42, 95-97, 102, 121, 123, 151, 160, 172, 208, 219, 220, 240, 261, 285. † References 38, 95-97, 102, 121, 123, 172, 208, 240, 261.
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CHAPTER 3 Lightning Injuries
A
days. Although many pictures exist of these marks, they have never been described histologically. The most current theory is that they represent blood cells forcefully extravasated into the superficial layers of the skin from contracting capillaries, much like a superficial bruise, which is consistent with their rapid resolution and pattern of color changes. Experimentally, they follow the flashover current lines seen in Cooper’s animal model.80,81 Burns may be caused by metal worn close to the skin.72,159 Figure 3-41, E shows a burn resulting from a metal belt buckle or athletic supporter worn by a young man who was struck while playing softball. Figure 3-28 shows a necklace burned into the skin with permanent tattooing. Another theory for these burns involves discharge of current from metal to underlying skin. On rare occasions, clothing is ignited by lightning, causing severe thermal burns.15,65 Victims of lightning may exhibit various combinations of burns, as demonstrated in Figure 3-41.
PART 1 MOUNTAIN MEDICINE
conversion of St Paul on the Damascus Road and his subsequent blindness were due to lightning.35,36 Dilated or unreactive pupils should never be used as a prognostic sign or as a criterion for brain death in a lightning victim until all anatomic and functional lesions have been excluded.44
EAR INJURIES* Between 30% and 50% of more severely injured lightning victims may have rupture of one or both tympanic membranes from the shock-wave effect, concomitant basilar skull fracture, or direct burn damage because of current flow into this orifice.18,64 Otorrhea of CSF or hemotympanum rarely occur. Disruption of the ossicles and mastoid has been reported. Many cases of permanent deafness are noted in older literature but are seldom found today. Facial palsies, both acute and delayed, may occur from direct nerve damage by lightning. Balance problems and tinnitus are common, probably from eighth cranial nerve injury, and nystagmus and ataxia may occur. Temporary deafness is not uncommon.161 It has been postulated that the intense noise and shock wave accompanying thunder may be responsible for sensorineural hearing loss. Otologic injury from hard-wired telephone–transmitted lightning strikes is common but probably occurs less often now with the advent of mobile phones.8,16,17
FETAL SURVIVAL† The fetus of a pregnant woman struck by lightning has an unpredictable prognosis. Of 11 cases reported, nearly one-half of the pregnancies ended in full-term live births, with no recognizable abnormality in the child. Approximately one-fourth resulted in live births with subsequent neonatal death; the remainder were stillbirths or deaths in utero. There has been one report of ruptured uterus after lightning strike.
HEMATOLOGIC ABNORMALITIES Several unusual hematologic complications have been attributed to lightning injuries in isolated case reports. These include disseminated intravascular coagulation, transiently positive Coombs’ test, and Di Guglielmo’s syndrome, a type of erythroleukemia characterized by erythroblastosis, thrombocytopenia, and hepatosplenomegaly. Although there have been anecdotal reports of increased hypersensitivity, development of allergies, and increased risk for cancer in lightning victims, perhaps indicating an immunologic component to lightning injury, these have not been studied or validated with controlled longitudinal studies.
ENDOCRINE AND SEXUAL DYSFUNCTION Decreased libido for both men and women and impotence for men are common complaints. Sexual dysfunction may be due to neural, spinal cord, endocrine, autonomic, or neuropsychological injury, side effects of therapeutic drugs, and possibly other causes and should not be discounted. A report of male hypersexuality after a lightning strike has not been authenticated but can also be explained from a specific brain injury mechanism. Some victims have reported amenorrhea or menstrual irregularities lasting up to 2 years.
PSYCHOLOGICAL AND NEUROCOGNITIVE DYSFUNCTION‡ It is not uncommon for a person hit by lightning to rest at home for a few days, assuming that he or she is supposed to feel “bad” after being hit by lightning. The victim may not see a physician until family members insist or symptoms worsen or do not abate. Neurocognitive deficits may not become apparent until a victim attempts skilled mental functions. Often the person will attempt *References 26, 28, 39, 113, 115, 120, 160, 178, 209, 222, 223, 236, 265, 278. † References 64, 106, 112. ‡ References 47, 48, 72, 229-232, 235, 272, 283, 284.
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to return to work after the injury, but because of decreased work tolerance, short-term memory problems, easy fatigability, and difficulty assimilating new information, he or she will be unable to continue in the prestrike occupation. Chronic pain syndromes are cited as commonly overlooked diagnoses in psychiatric and functional terms.129,130 Although some medical clinicians have been historically suspicious of victims’ complaints of psychological and neurocognitive dysfunction, evaluation of many such patients appears to have confirmed a vast commonality of psychological symptoms. This should begin to reverse a regrettable tendency, both medically and legally, to discount complaints as evidence of malingering, excessive reaction, conversion reaction, personality problems, or manifestations of “weak” coping strategies. The syndrome is described first from a clinical viewpoint and then discussed in light of the extant literature. Functional Issues • Memory disturbance: Individuals show marked diminution of short-term memory ability. They require shopping lists and reminder lists. Memory for recent names and places is diminished to the point of disability. Individuals tend to selfisolate, stop mixing socially, and avoid going into new circumstances.67 • Concentration disturbance (adult attention deficit disorder): Individuals show deficits in their working memory, are unable to focus attention for more than a short period, and are easily distracted. In particular, reading and understanding are poor. Job training is detrimentally affected. This is worsened by sleep disturbance. • Cognitive function: Individuals report diminished mental agility. The keeping of accounts is a noteworthy example. Calculation and estimation become erratic and affect work performance. Ability at mental manipulation and problem solving is markedly decreased. • Higher executive functioning: Individuals are neither able to coordinate multiple tasks simultaneously nor able to follow orders for complex tasks they used to perform easily before the injury. One victim described it as if “the office manager of my brain had quit.” Behavioral Issues • Emotional lability and aggression: Individuals find that they are more aggressive than before. They are easily frustrated and are liable to have outbursts of temper. The strains on a partnership are significant, and marital and relationship dysfunction is common. An increased state of arousal and anxiety may further complicate distractibility as well as proper recognition and assimilation of new learning. • Sleep disturbance: Easy fatigability, sleep disturbance, or hypersomnolence (usually early on) is common and may last for years. Flashbacks and nightmares may be experienced. • Phobic behavior: Avoidance of the precipitant circumstances is demonstrated, in some cases to phobic proportion tantamount to post-traumatic stress disorder. • Depression: Depression is almost always present in classic biologic form and should be anticipated. Although the aforementioned symptoms can certainly arise secondary to a depressive state, it would also be reasonable for a victim to react with depression to the decrements in work power and lifestyle engendered by chronic pain, sleep deprivation, or decreased personal performance. A third reasonable possibility is concurrent neuropsychological syndrome and biologic endogenous depression. Antidepressant medication may be useful. Formal neuropsychological testing may be used to attempt to validate the injury, quantify a functional baseline, and design cognitive therapy. Very few studies have formally examined the syndrome.232,272 Primeau and co-workers point to research difficulties, including sample bias and heterogeneity, methodology (cross-sectional rather than longitudinal or prospective), and the essential difficulties of determining premorbid status or current independent psychiatric status. It is also noted that the magnitude of insult does not correlate with psychological disability.67 Duration, type, and severity of the syndrome are therefore unpredictable.
Recognition and Treatment of Lightning Injuries* DIAGNOSIS Diagnosis of lightning injury may be difficult. History of a thunderstorm, witnesses who can report having seen the strike, and typical physical findings in the victim make diagnosis easier but are not always present. Lightning can strike on a relatively sunny day, thunder may not be appreciated, and sometimes the victim is alone when injured. A diligent historical effort and careful physical examination at the earliest opportunity may help determine the true cause. Any person found with linear burns, mental status changes, *References 65, 67.
ruptured tympanic membrane, and clothes exploded off should be treated as a victim of lightning strike. Diagnosis is made doubly difficult because burns, which most people expect to accompany lightning injuries, are often absent. Feathering marks, also called Lichtenberg’s flowers, are pathognomonic of lightning strike but are rare.* Another sign and/or symptom complex includes linear or punctate burns, tympanic membrane rupture, confusion, and outdoor location. Because there have been several cases of side flash or contact injury from indoor plumbing and telephones, the physician should suspect lightning strike in persons found confused and unconscious indoors after or during a thunderstorm.8,15,16,65 Documentation of lightning activity to support legal or insurance claims is available from commercial sources.
INITIAL FIRST AID AND TRIAGE OF VICTIMS† Ensuring scene safety is paramount. Rescuers are at risk if thunderstorms are in the area.268 As in any other emergency, the first steps are the CAB: compression (circulation), airway, and breathing. If the victim has suffered a cardiac arrest, cardiopulmonary resuscitation should be started immediately and a rescue vehicle called for transportation. AEDs have been helpful in some cases.218 If the strike occurs far from civilization and evacuation is improbable, the victim will probably die unless pulse and respirations resume spontaneously in a short period of time. The heart may resume activity but may slip into secondary arrest. It is unknown whether the secondary cardiac arrest is due to primary brain damage, hypoxia from prolonged respiratory arrest, primary cardiac damage, autonomic nervous system damage, or a number of other mechanisms that could be hypothesized. If no pulse is obtained within 20 to 30 minutes of starting resuscitation, it is reasonable to stop further resuscitation efforts. If a pulse is obtained, ventilation should be continued until spontaneous adequate respirations resume, the victim is pronounced dead, continued resuscitation is deemed unfeasible because of rescuers’ exhaustion, or there is danger to rescuers’ survival. When lightning strike involves multiple victims, resources and rescuers may not meet the demand and triage must be instituted. Normally, the rules of triage in multiple-casualty situations dictate bypassing dead persons for those who are moderately or severely injured and can benefit from resuscitation efforts. However, “resuscitate the dead” is the rule in lightning incidents, because victims who show some return of consciousness or who have spontaneous breathing are already on the way to recovery. The most vigorous attempts at cardiopulmonary resuscitation should be directed to the victims who appear to be dead because they may ultimately recover if properly resuscitated. Survivors should be routinely stabilized and transported to the hospital for more thorough evaluation. The probability that lightning victims can recover after prolonged cardiopulmonary resuscitation is low. There is no evidence to suggest that survival after a longer period than normal without resuscitation is possible in the setting of lightning injury. Often in a remote setting, the rescuer is emotionally tied to the victim by age and friendship and may tend to continue resuscitation past the point of futility. In pronouncing a victim dead, the rescuer must ensure that other problems such as hypothermia are not contributing to the victim’s response to resuscitation efforts. Other stabilization procedures, including splinting of fractures, airway control or intubation, spinal precautions, and institution of intravenous fluids and oxygen, should be accomplished whenever indicated and feasible before transport.
HISTORY AND PHYSICAL EXAMINATION An eyewitness report is helpful because victims are often confused and amnestic.64,65 History that includes a description of the event and the victim’s behavior following the strike may be helpful. *References 51, 52, 63, 98, 238, 273. † References 15, 65, 78, 79.
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Disturbances of verbal memory, attention, concentration, and new learning are very frequently identified.232 This commonality among victims is noteworthy. Primeau and co-workers also draw attention to the similarity of some facets of the disorder and those of other etiologies. They generally find the head injury model a useful one that can guide treatment. Other syndromes to which the lightning and electrical injury syndrome show similarities include post-traumatic stress disorder, depression, anxiety, and obsessional and adjustment disorders. Features of these are seen to be present, although the syndrome is not simply an example of these dysfunctions per se. The authors have considered somatoform disorders as a cause, noting the tendency to be preoccupied with the injury and to overattribute subsequent symptoms to the lightning injury. This may be due in part to physicians’ general lack of knowledge of the problems and the lack of longitudinal controlled studies, so that victims do not know what to expect in the future. Conversion reaction may also be considered, although it cannot account for the symptomatology of lightning and electrical disability.67 Good neuropsychological testing can detect this facet. One difficulty with neurocognitive testing is use and interpretation of the Minnesota Multiphasic Personality Inventory (MMPI). Although it was not developed to characterize patients with chronic problems, particularly those with chronic pain, the MMPI has been applied to them, often resulting in erroneous conclusion of conversion reaction or preoccupation with physical complaints. It should surprise no one that anyone suffering from chronic pain and neurologic injury that hampers their normal preinjury activities will rank higher on the “preoccupation with physical complaints” and “conversion” scales than will uninjured normal individuals. Andrews and Darveniza16 recognized three postinjury syndromes and correlated these with the postinjury periods of 1 week, 1 week to 3 months, and 3 months to 3 years. Primeau and co-workers add a fourth, which is persons experiencing longer and perhaps lifetime dysfunction.120,232 Cherington46,58 has further classified lightning injury by its permanent sequelae. The first 12 months after injury are crucial to recovery. It is during this period that the most recovery is seen, with possible mild improvement up to 3 years after injury. Beyond this time, chronic dysfunction may be assumed, although it is also at this time that the survivor may decide to move on with life, accept limitations, and even sometimes be able to successfully pursue a new career. Van Zomeren and co-workers272 provide one of the few thorough examinations of the syndrome in lightning-injured patients. Fatigue and energy loss were the main complaints; poor concentration, irritability, and emotional lability were other common themes confirmed. Impairment of memory, attention, and visual reaction times were documented. Depression and “convincing signs of post-traumatic stress disorder” were seen. The syndrome was highly differentiable from normal (P <.001), and no parallel model was available for comparison. They stated that the lasting complaints and mild cognitive impairments could not be explained on the basis of anxiety reactions or depression. They summarized their findings under the heading of “vegetative dystonia.”
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After scene safety as been secured, the victim should be undressed to search for hidden signs of injury. Special note should be taken of vital signs, temperature, and level of consciousness. Because many victims are struck during a thunderstorm, they may be wet and cold. Hypothermia should be anticipated and treated appropriately (see Chapter 5). The awake patient should be assessed for orientation and short-term memory. A cursory mental status examination of the lightning victim may reveal good ability to carry on a “social conversation” that easily hides deficits in fine neurocognitive skills. It is easier to detect deficits when the victim cannot assimilate information, perseverates, or asks repetitive questions. Continuing confusion or a deteriorating level of consciousness mandates CT or MRI of the brain to rule out intracranial injury. Examination of the victim’s eyes should be done to establish pupillary reactivity and ocular injury. Lack of pupillary reaction or pupillary dilation should not be taken as a sole indicator of death. Tympanic membrane rupture is an important indicator of lightning strike. Ossicular disruption may be one explanation for a victim’s lack of appropriate response to verbal stimuli. Although the pulmonary system may be affected by cardiac arrest, pulmonary edema, or adult respiratory distress syndrome, it is uncommon to witness these initially. The cardiovascular examination should include distal pulses in all extremities, appreciation of arrhythmias, and evaluation of cardiac damage, including ECG changes. Cardiac enzyme elevations have rarely been reported with lightning injury. The victim’s abdominal examination occasionally demonstrates absent bowel sounds, which suggests ileus or indicates acute traumatic injury, such as contusion of the liver, bowel, or spleen. The examiner should document any skin changes. The victim’s skin may show mottling, especially below the waist. Burns are not universally present or may take a period of hours to evolve. Notation of pulses, color, and movement and sensory examination of the victim’s extremities are important. Keraunoparalysis is common but usually improves in a few hours. The physical findings and mental state of minimally and moderately injured victims tend to change considerably over the first few hours; careful observation and documentation delineate the course so that therapy can be modified. The minimally injured victim can almost always be discharged to a responsible person or requires only overnight observation, whereas the severely injured person may require intensive care with mechanical ventilation, antiarrhythmic medications, and invasive interventions and monitoring techniques.
LABORATORY TESTS AND RADIOGRAPHIC EXAMINATION Minimum laboratory examination includes urinalysis (including a dipstick for myoglobin on fresh urine). The more severely injured victim may require tests such as complete blood count, electrolytes, blood urea nitrogen, and creatinine and testing for cardiac damage. If the victim is to be placed on a ventilator, measurement of arterial blood gas levels will be necessary; if intracranial pressure monitoring is used, determination of serum osmolality may be required. An ECG is desirable for most lightning victims. Although several types of acute arrhythmias have been reported, they are uncommon. QT prolongation is an abnormality sometimes associated with lightning injury. Radiographs and other imaging studies may be obtained, depending on the presentation and history. Cervical spine imaging should be performed if there is evidence of cranial burns, contusions, loss of consciousness, or change in mentation that would make the physical examination unreliable, or if there is any suspicion of a fall or being thrown. The victim who is unconscious, confused, or has a deteriorating level of consciousness requires a CT or MRI scan of the brain to identify trauma or ischemic injury. Other studies to rule out fractures, dislocations, and other bony injuries may be obtained as clinically indicated. 90
TREATMENT* Fluid Therapy Intravenous access is required for the victim who shows unstable vital signs, unconsciousness, or disorientation. If the victim is hypotensive, fluid resuscitation with normal saline or Ringer’s lactate solution may be indicated but with the caution that cerebral edema may develop. Fluid restriction in normotensive or hypertensive victims is recommended because of this risk. In seriously injured or unstable patients, intensive care unit types of monitoring, including arterial or central venous pressure, may be indicated. Careful intake and output measurements are necessary in the severely injured patient and require placement of an indwelling urinary catheter. Myoglobinuria, unless caused by blunt injury or other mechanism, is rarely attributed to lightning injury alone. When it occurs, it is usually transient, so that mannitol-induced diuresis, alkalinization, and aggressive fluid loading used with high-voltage electrical injuries are rarely necessary. However, if burns are severe and extensive, which is rarely the case, fluid resuscitation may be required. Fasciotomy Not Needed Intense vascular spasm with lightning is usually transient and caused by sympathetic instability. The presence of keraunoparalysis, paralyzed and pulseless extremities seen with lightning injuries, should not be treated like similar-appearing traumatized extremities caused by high-voltage electrical injury.15,65,202 Steady improvement in the mottled, cool extremity, with return of pulses in a few hours, is the rule rather than the exception. Fasciotomies are rarely indicated unless the extremity shows no signs of recovery and raised intracompartmental tissue pressures are documented. Antibiotics and Tetanus Prophylaxis Prophylactic antibiotics are not indicated. Antibiotic therapy should only follow culture and identification of pathogens except in obvious cases involving open fractures or cranial fractures that violate the dura. Appropriate tetanus prophylaxis should be given if burns or lacerations are present. Cardiovascular Therapy† Management of cardiac arrest is standard, including the use of an AED if available. In the victim who is not in cardiac arrest, vasospasm may make peripheral pulses difficult to palpate. Usually femoral, brachial, or carotid pulses may be appreciated. Doppler examination may help to locate peripheral pulses and record blood pressure. If a victim remains hypotensive, fluid resuscitation may be necessary to establish adequate blood pressure and tissue perfusion. Causes of hypotension include major fractures, blood loss from abdominal or chest injuries, spinal shock, cardiogenic shock, and occasionally deep burns similar to high-voltage electrical burns. As soon as an adequate central blood pressure is obtained, fluids should probably be restricted because of the incidence of cranial injuries, cerebral edema, and postarrest anoxic brain injury. Mechanical ventilation is required for the victim who is without spontaneous or adequate respirations until the person resumes adequate ventilation, brain death is declared, or the physician and family decide to cease efforts. Cardiac monitoring and serial isoenzyme and troponin measurements are indicated if there is any sign of cardiac ischemia or arrhythmia or if the victim complains of chest pain. Injury patterns, as well as arrhythmias, have been reported.65 The indications for antiarrhythmic drugs and pressor agents are the same as those for a suspected myocardial infarction.65 Transient hypertension may be so short-lived as to require no acute therapy. However, several cases of hypertension have occurred 12 to 72 hours after lightning strike and seemed to respond well to antihypertensive medications. No systematic *Reference 64. † References 78, 79, 106, 173, 187.
Central Nervous System Injury* Every lightning victim should have a screening neurologic examination. If there is a history of loss of consciousness or if the victim exhibits confusion, hospital admission is warranted. The victim with tympanic membrane rupture, cranial burns, or loss of consciousness, or who shows decreasing level of consciousness, should undergo cervical spine imaging, brain CT, and possibly brain MRI. Cerebral edema may be managed with mannitol, furosemide, fluid restriction, cerebral pressure monitoring, and other standard therapies. Although hypothermia was reported to contribute to complete recovery in one victim with prolonged cardiac arrest before resuscitation efforts, there is no evidence that this would benefit all victims.167 Early seizures are probably due to anoxia. If there is evidence of CNS damage or if seizures continue after adequate oxygenation and perfusion have been restored, standard pharmacologic intervention with diazepam, fosphenytoin, phenobarbital, and/or other anticonvulsants should be considered. The response to specific drugs has not been studied. If paralysis does not improve, causes other than lightning, including blunt injury from a fall, may be responsible. Spinal artery syndrome has been reported, perhaps caused by arterial spasm or undiagnosed fractures. A physical therapy program should be initiated before discharge. Unfortunately, neuropathy and autonomic pain syndromes may develop in many survivors. These may respond to chronic pain management therapies, such as combinations of nonsteroidal antiinflammatory drugs, antiepileptic agents, antidepressants, and ganglionic blocks.15,16,129,130,232 Acupuncture may be helpful for resistant post-traumatic headaches that often accompany lightning injury. In recent years, neuropsychological deficits from lightning have become better appreciated.12,172,229-232,272 Heightened anxiety states, hyperirritability, memory deficits, attention deficit, aphasia, sleep disturbance, post-traumatic stress disorder, and other evidence of brain damage should be assessed.16 Some of these deficits are much like those suffered by victims of blunt head trauma. A rehabilitation program should be instituted early for these patients to return them to as functional a state as possible.47,231,284,285 Often, the victim’s family and co-workers have difficulty understanding the change in personality that affects many of these victims. Neuropsychological testing to define the injury, establish a baseline, and plan appropriate cognitive therapy may be helpful. It is unknown if certain personality types may predispose victims to more pronounced neuropsychological symptoms. In some cases, the feeling of isolation and change that victims sometimes experience can lead to depression, substance abuse, and suicidal ideation. Because of unfamiliarity with lightning injuries and their sequelae, many physicians are ill equipped to manage long-term care of lightning victims or may be so skeptical that the victim and family become frustrated and angry with their care. Burns† Lightning burns may be apparent at the time of admission but more commonly develop within the first few hours. They occur in less than one-half of lightning survivors and are generally superficial, unlike high-voltage electrical burns, and seldom cause massive muscle destruction. Myoglobinuria is infrequently seen, so vigorous fluid therapy and mannitol diuresis are not usually indicated. In the rare instance of myoglobinuria, intravenous mannitol and urine alkalinization with bicarbonate may be used. Overzealous hydration with resultant cerebral edema from the presumption of similarity to high-voltage injuries has probably harmed more lightning victims than has myoglobinuric renal failure.
*References 15, 45, 46, 49, 55, 57, 58, 66, 67, 283, 284. † References 22, 63, 71, 72, 98, 131, 152, 202, 213, 214, 256, 257, 261, 273.
Lightning burns are generally so superficial that they do not require treatment with topical agents. In the unusual instance of deep injury, topical therapy is standard. The findings that lightning burns are superficial and do not require active surgical intervention is reinforced by Matthews and Fahey.202 Their paper provides a useful guide to the remote need for surgical intervention in lightning injury. Eye Injuries* Eye injuries are myriad. Visual acuity should be measured and the victim’s eyes thoroughly examined. Cataracts may develop in the first few weeks or months. Eye injuries should be treated in standard fashion and may require referral to an ophthalmologist. Case reports of successful treatment of optic neuritis with highdose corticosteroids similar to those used with spinal cord injury have been reported, but because there were no controls, it is not known if recovery would have occurred without their use. Ear Injuries† Loss of hearing mandates otologic evaluation. Blast as well as direct injury may occur. Simple tympanic membrane rupture is usually handled conservatively with observation until the victim’s tissues heal. Sensorineural damage to the auditory nerve, resulting in hearing changes, dizziness, and permanent tinnitus and facial nerve palsies, is not uncommon. Ossicular disruption or more severe damage may necessitate surgical repair. Otorrhea and hemotympanum suggest basilar skull fracture. Complaints of pain around the angle of the victim’s jaw may indicate occult fracture of the styloid process and other musculoskeletal damage. Pregnant Victims‡ If a pregnant woman is struck, fetal viability should be assessed, including fetal heart tones, ultrasonography to observe fetal activity, and other standard methods. Other Considerations Gastric irritation is sometimes seen.109 A nasogastric tube is appropriate if ileus or hematemesis occurs. An abdominal CT scan may be indicated in comatose patients who remain hypotensive, because intestinal contusions and hemorrhage have been reported. It is common for survivors to report continuing nausea for several weeks to months. Endocrine dysfunction, perhaps as a result of pituitary or hypothalamic damage, including amenorrhea, impotence, and decreased libido, has occurred in some victims. Spinal cord or sympathetic nervous system injury or postinjury depression, as well as side effects of medications, may also cause impotence, decreased libido, and sexual dysfunction after lightning injury. Pronouncing the Victim Dead§ Dilated pupils should not be taken as a sole sign of brain death in the lightning victim. It is always necessary to exclude other causes of dysfunction and eliminate them before death is declared. Hypothermia with lightning injury may cloud end-of-life decisions. If the victim has not regained a pulse after 20 to 30 minutes of resuscitation, it is reasonable to cease cardiopulmonary resuscitation. Long-Term Care¶ In the long run, there is no specific treatment for lightning injury. It should be remembered that lightning is a nervous system injury that can involve chronic pain, neuropathy, and brain injury, sometimes complicated by initially unrecognized musculoskeletal injury. Most symptoms can be treated in standard fashion, including cognitive therapy, pain management, job retraining, and counseling as indicated by the survivor’s signs and symptoms. *References 38, 42, 95-97, 102, 121, 123, 151, 160, 172, 208, 219, 220, 240, 261, 285. † References 10, 26, 28, 39, 113, 115, 120, 160, 178, 209, 222, 223, 236, 265, 278. ‡ References 106, 112. § References 37, 44, 72, 78, 79. ¶ References 47, 83, 84, 183, 231, 256, 283, 284.
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study of antihypertensive agents has been undertaken for lightning survivors.
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As with any serious illness, the caregiver and family may be the unsung heroes and need support, recognition, and counseling. Referral to Support Groups and Other Information Sources Lightning Strike and Electric Shock Survivors International (LSESSI), a support group founded in the late-1980s, has numerous materials for survivors and their families. LSESSI is located at PO Box 1156, Jacksonville, NC 28541-1156 (Tel: 910-346-4708, http://www.lightning-strike.org).83,84,189 Other useful websites are http://www.uic.edu/labs/lightninginjury and http://www. lightningsafety.noaa.gov.
Precautions for Avoiding Lightning Injury LIGHTNING SAFETY GUIDELINES* Most lightning casualties in the United States involve only one person at a time. The possibility for multiple injuries exists where large crowds gather for fireworks, holiday beach outings, sporting events, concerts, and other similar situations. Lightning injury prevention behavior should be proactive, rather than reactive, after the threat becomes imminent. Clearly defined education is important to help make proper decisions at the critical times when lightning threatens. Prevention is more important than cure, as is apparent from the impacts of lightning injuries described in the medical discussions of this chapter. There are about 25 million cloud-to-ground lightning flashes in the United States every year, and one-half of them have a subsequent return stroke coming to ground at a different location up to a few kilometers from the first stroke.262 As a result, it is impractical for the NWS to warn of every potentially dangerous lightning flash, so the key to safety is individual education and responsibility.† Only one-quarter of U.S. lightning fatalities are associated with tornado or severe thunderstorm warnings issued by the NWS.19 As a result of this situation, a broad collection of lightning safety guidelines for minimizing the lightning risk is available from a multiagency group coordinated by the NWS at http:// www.lightningsafety.noaa.gov. Cloud-to-ground lightning data from the National Lightning Detection Network have shown that lightning deaths and injuries occur in generally equal portions before, during, and after the strongest lightning activity in a thunderstorm.147,185 Weak thunderstorms are as likely to result in casualties as are moderate or strong storms.146,185 A detailed study by Lengyel and associates185 found that nearly one-half of lightning victims had enough warning to reach safety from nearby lightning before they became a lightning casualty, so that anticipation would have been beneficial. A multidisciplinary group of lightning safety experts met in 1998 to develop guidelines that had not been adjusted in any meaningful way for several decades.147,288 Development of national lightning detection networks and availability of other meteorologic data sets had caused major rethinking of existing guidelines. Since then, most of the 1998 guidelines have been supported, others have been evaluated, and some have been adjusted further or placed into a more limited context. At this point, most pre-1998 recommendations are recognized as based on false assumptions and have become obsolete. The following sections describe the stages of a lightning safety approach and how the plan varies according to the circumstance and size of the group.
LIGHTNING SAFETY PLAN‡ For a person who is watching the sky and has prepared by being aware of the forecast, lightning rarely appears so suddenly that precautions could not have been taken to minimize the risk. *References 27, 72, 74, 88, 101, 142, 147, 186, 217, 244-247, 276, 288. † References 61, 74, 147, 185, 186, 276, 288. ‡ References 27, 74, 88, 101, 147, 217, 244-246, 276, 288.
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Thunderstorms take tens of minutes to develop or move into an area, so the only surprise is because it was not anticipated correctly. The surprise is avoided by a series of steps in a lightning safety plan. The plan includes knowing the safest place to reach, how long it takes to reach it, how far in advance action should be taken, who makes the decision, and backup plans when the people or situations change. The National Collegiate Athletic Association (NCAA) website has a succinct version at http:// www.ncaapublications.com/productdownloads/MD10.pdf.27 Before working in the open or going on a recreational trip, be aware of weather forecasts and conditions. If thunderstorms are forecast later in the day, pay attention to updated forecasts by using NOAA weather radio, cell phone alerts, websites, and tailored information from private weather providers. Because access is available for much of the United States via mobile methods, there should be fewer surprises with regard to storms that are growing or moving into an area. Users, however, should be aware that many sources of lightning data, particularly free sources, may be delayed by several minutes or more. Unless users ensure that lightning data are real time, they may be lulled into a false sense of security and not take timely safety precautions. Thunderstorm and tornado warnings issued by the NWS indicate that thunderstorms are almost certain to occur in the area, and most likely in surrounding counties. However, most lightning does not occur within a warning area, but in less intense yet frequent nonsevere thunderstorms that also contain the lightning danger.19 Most lightning occurs in the summer months of June, July, and August, as shown in Figure 3-16, online.141 Further, most lightning occurs between noon and 6 PM, as shown in Figure 3-2. These general figures make it much more apparent when to avoid long, risky exposure to lightning. Storms start before noon on some days, such as over the high mountains of Colorado, where a few flashes are not uncommon by 10 AM on active days. In such a location, starting hikes very early in the morning helps to eliminate the lightning threat, but beginning in late morning on active thunderstorm days, there is increased vulnerability to lightning.136,287 Similarly, lightning may linger into the summer evening in almost all regions of the country, when sports and recreation users are more likely to be outdoors on every day of the week.27
APPROACHING THUNDERSTORM Pay more attention to lightning than rain. About 10% of all cloudto-ground lightning strikes occur without rain at the location of the lightning ground strike, so waiting for rain to arrive does not provide absolute protection from lightning as a thunderstorm approaches. Thunder can be heard up to about 10 miles away in quiet conditions, but not nearly that far in the presence of wind, traffic, and when inside a structure. A simple rule at the start of a storm is, “When thunder roars, go indoors.”132,216,244-247 This rule removes any doubt about whether it is time to take action and is effective as a thunderstorm approaches. Although there is some overwarning because of distant lightning that may not reach a location, it is an effective and easy way to manage the lightning threat. For a more objective approach, use the 30-30 rule developed at the 1998 lightning safety meeting.* The first 30 refers to the time in seconds between seeing lightning and hearing thunder from that flash (the second 30 refers to the wait time; see next section). If the time interval from flash to bang is 30 seconds or less, people are in danger from lightning and should actively seek a designated safe place. This count of 30 seconds indicates that lightning is no more than 10 km (6.2 miles) away, using the speed of the sound of thunder of 5 sec/mile. Ten kilometers (6.2 miles) includes about 80% of all subsequent cloud-to-ground lightning flashes in a storm.148 Variations of the 30-second rule are widely used at military and civilian airports for radii between 8 and 16 km (5 and 10 miles), where validated and accurate cloud-to-ground lightning detection systems are used. In such *References 27, 74, 101, 145, 147, 199, 276, 288.
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situations, too many warnings from a large radius around a point result in a lack of trust in the method, whereas too small a radius misses too many storms and leads to more injuries. Comparison of the two methods indicates that “When thunder roars, go indoors” is a useful approach for everyday use. The first 30 of the 30-30 rule corresponds to a 10-km (6.2-mile) radius and is more objective than the previous phrase. It may be adjusted based on local preferences to balance down time with operational efficiency at a facility such as an airport or mine. With either approach, when the rule indicates that lightning is a threat, attention should focus on the lightning rather than the rain. Outdoor activity should be stopped with immediate evacuation to a designated safe place.
END OF THUNDERSTORM Do not underestimate the danger of lightning at the end of a thunderstorm. As many people are killed or injured by lightning at the end as at the start or during the middle of a storm.148,185 A number of people are killed every year when going outside into the backyard of a home too soon because of impatience or crossing a field or parking lot before the storm is finished.137,139 The second 30 of the 30-30 rule says to wait 30 minutes after the last lightning is seen or thunder is heard before resuming outdoor activities.27,74,101,147,288 At night, flashes may be visible low on the horizon inside tall thunderstorms up to 80 km (50 miles) away, but these are not of much concern unless the lightning channel itself is visible to the ground. Since the 1998 meeting, it has become apparent that 30 minutes is longer than is needed in most situations because the lightning threat is minimal after 15 minutes.148 But in a large group situation where a long evacuation time is needed, the full 30 minutes is needed to avoid returning people to a field or stadium too soon, then sending them to safety again a few minutes later when the lightning threat returns. In one’s own backyard, a person can wait 15 minutes after lightning and thunder and be quite safe, although a lingering flash can cause a return to a dwelling in a matter of a few seconds if necessary. In practice, most airports and other industrial situations use a wait time of 15 minutes, although local high levels of safety concerns may make 30 minutes more desirable. Less than a 10-minute wait time is not desirable. There are exceptions to all rules when a large overhead thunderstorm lingers for hours over a location.156 In such a situation, the policy is difficult to balance between efficiency and safety of outside workers.
SAFE PLACES INSIDE There are two reliable places to be safe from lightning. One safe place is inside a large substantial building and the other is inside a fully enclosed metal-topped vehicle. Buildings Large substantial buildings where people live and work are very safe from lightning in more developed countries. Although such structures are often hit directly by lightning, fatalities inside them are extremely rare, considering the amount of time spent by people inside them. In a study of U.S. dwellings and buildings, the only lightning-caused fatalities among many hundreds of cases were to older adults, very young persons, or persons with physical or intellectual disabilities who were unable to leave the dwelling when a fire broke out, usually at night.139 There were no fatalities inside offices, schools, or other large buildings. As a result, adequate safety is attained by directing people to go inside a large substantial building, including a dwelling, rather than staying outside.216 The protection in modern buildings is provided by grounded wiring and plumbing, as well as metal structural members inside the buildings that carry the charge of a strike to the structure around people and into the ground. Contact with conducting paths of wiring, plumbing, corded telephones, and large openings such as garages and doors can result in injuries. Such contact needs to be avoided during the presence of lightning to avoid potentially serious injury, but these are not known to lead to fatalities in well-constructed and grounded buildings.
FIGURE 3-45 Lightning-unsafe picnic shelter in Tucson, Arizona. Note warning sign on roof, which states: “WARNING: This structure is unsafe for shelter during lightning storms. Seek suitable shelter elsewhere.”
Unsafe indoor locations are small structures such as those used as golf, beach, sun, rain, school, agricultural, or bus shelters (Figure 3-45). All of them are to be considered unsafe and must be abandoned for a larger safe building. It is possible to make such small structures safe, but their protection must be designed and installed by a knowledgeable lightning protection specialist.171 Also on this list of unsafe structures are all tents that provide rain protection but are invisible to lightning.135 Pads on the ground inside a tent are of no value in lightning protection, and the composition of the tent structure and poles provides no protection. In less developed countries, these dwellings and workplaces may be thatched-roofed huts that provide no protection from lightning because they are often ungrounded and made with nonconducting material.139 Note that it is possible to provide low-cost lightning protection for such unsafe structures by using simple towers and natural local materials for grounding; however, these must be designed and installed by knowledgeable lightning protection specialists to be sure of their efficacy.180 Vehicles* Fully enclosed metal-topped vehicles are safe from lightning and should be used as a safe place when no large substantial building is available. In a study of hundreds of vehicle incidents, there were injuries to vehicle occupants in less than one-half of the cases; the majority said the experience was frightening but they were amazed to be unscathed. There have been no documented “electrical” injuries to occupants, with the exception of those involving direct wiring, such as the older handheld police radios.137 The only unambiguous fatality was due to an older adult who was startled or incapacitated by a nearby flash and drove into oncoming traffic. Damage to the vehicles ranged from minor, such as antennas vaporizing, to a few cases of major engine failure and electrical fires; nevertheless, all passengers escaped such vehicles. Unsafe vehicles are those without the safety of fully enclosed metal surroundings that act in a manner consistent with a Faraday cage.76 Safety is provided from a direct vehicle strike by the lightning energy traveling across the outside shell of the metal vehicle and around anyone inside, with subsequent arcing to the ground through bumpers or axles. This path may account for the mistaken impression that tires are the safety feature; they are sometimes blown apart by current passing through the vehicle’s metal frame (nearest to the ground) through the tires. Unsafe vehicles have cloth tops (convertibles) or fiberglass or plastic bodies. Others include golf carts and four-wheelers with open sides. Strikes to such vehicles have no defined path to ground, *References 137, 156, 216, 288.
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and it is not safe for people to be inside them. Although it is possible to design lightning protection for unsafe golf carts and other open-sided vehicles, there is no such commercially available product; such an approach requires an exacting configuration and correct behavior of people inside them.90 Another very serious cause of injury is the step voltage when people are on the ground while working on a vehicle during a thunderstorm. Any place outside such a vehicle is as unsafe as anywhere else outside.137 Particularly dangerous is step voltage, when a person is in contact with both the vehicle and the ground. This situation occurs when stepping into or out from a vehicle when lightning strikes the vehicle, because the step potential between the energized vehicle and the ground is very large. Conversely, a nearby ground strike will travel to a person with one foot on the ground and the other in contact with an unaffected vehicle. Other situations outside a vehicle include frequent cases on parking lots, waiting for buses, and law enforcement and other people near but not inside disabled vehicles. Finally, a fully enclosed metal-topped vehicle can be used as a safe place at a school or sports event. If flashes are going to strike the ground at such a venue, it is an easy choice to be inside such a vehicle rather than outside at the same location.
ALWAYS UNSAFE OUTSIDE* There are no reliable places outside to be safe from lightning. Earlier recommendations had not sufficiently emphasized the nearly complete safety of being inside a large safe building or fully enclosed metal-topped vehicle, as described in the previous two sections. Some recommendations continue to emphasize the speculative safety approaches outside, at the expense of pointing out the reliable safety that is often present in more developed countries in nearby substantial buildings and fully enclosed metal-topped vehicles. One of the most important misconceptions of such outdoor safety advice is the expectation that the direct strike is the most common mechanism of lightning injury and that avoiding such a direct strike resolves the danger. As described elsewhere in this chapter, it is estimated that only about 3% to 5% of lightning injuries and deaths are due to direct strikes. The result of this mistaken direct-strike approach is the recommendation that lowering one’s height is sufficient, rather than recognizing the other more likely mechanisms and having reliable safety plans and evacuation. The reliable lightning safety approach is to recognize the lightning threat early and go to the known safe places of buildings and vehicles described above. The sooner a person reaches the safety of one of these locations, the sooner the lightning threat is ameliorated. As a result, the everyday lightning situation encountered by an individual is to anticipate the lightning threat, know where the safe building or vehicle is located, how long it will take to reach that location, and complete the plan by reaching it before lightning arrives. Lightning is not predictable in its path to ground, and what it strikes is not predictable to any certainty. Case reports have indicated that the prior advice of seeking a small tree among larger ones is unreliable. Recent very high-speed video shows lightning traveling toward ground in multiple branches. The first branch that contacts the surface of the earth is the only important one, whereas the rest dissipate in the air. Which branch reaches the surface appears to be random within the flash.251 Roeder242 examined the relative values of common outdoor lightning avoidance advice according to the five mechanisms of lightning injury described elsewhere in this chapter. It was found that if every precaution were followed, and some are quite difficult, only a 50% reduction in risk is achieved. The other 50% of the time results in an injury or fatality, which is unacceptable. As mentioned, one of the least effective approaches is to stress the direct strike by lowering one’s height, because the directstrike situation is scarce. More implications of this analysis will be described in the next section. The recommendation is *Reference 212.
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reinforced that reliable safety is achieved by reaching the safe building or vehicle in a timely manner. The Difficulty of Wilderness Situations No action will achieve certain safety from lightning in the wilderness away from a substantial building or fully enclosed metaltopped vehicle. The two approaches to lightning safety in the wilderness are to avoid the risk in the first place and to accept that a lightning risk exists. The amount of time spent by hikers and climbers in multiday situations is quite small. The more common situation is a hike or climb lasting 1 day or less, often during a weekend day.135 For this common situation, the first approach of avoiding the risk is most manageable, because a vehicle or sometimes a large building is available at the trailhead. Pay close attention to the forecast for the day, and avoid the daytime period when lightning is most prevalent. Over high mountains of the West, for example, storms start as early as 1000 or 1100 LST, so hikers should be off the higher parts of the mountain by that time. Otherwise, postpone the hike to another day. Such an approach does not preclude hiking on most days, because a study over Colorado’s Rocky Mountains203 showed that no location had lightning on more than one-third of summer days, and almost none during spring and fall months.141,194 The choice exists, then, to manage the risk by choosing the time and place of a day hike. Once the hike is under way, pay attention to building clouds that indicate future lightning, stop the hike or climb, and return to safety when the situation arises (see Approaching Thunderstorm and End of Thunderstorm). The pressure of a schedule or other factors may be such that a wilderness activity will take place in spite of the possibility of a very real lightning threat. Then a hiker or climber has accepted the personal risk in the same manner as risks from dangerous animals, falls, or other natural hazards. A portable device has been developed for lightning safety involving a triangle of tall rods, but it has not been made commercially available.90 Roeder242 analyzed the relative risk when no acceptable buildings or vehicles are nearby. The five mechanisms of lightning injury were considered to identify actions that are to be taken, such as crouching (minimal value) and staying away from tall objects. The results of the Roeder analysis show a reduction in risk to about one-half of the full lightning exposure. In other words, following all precautions does not prevent half of the lightning risk. Because the steps must be performed correctly, remembered under duress, and reduce the risk for death or injury by only half, they are not to be considered when lightning safety can be attained at a safe building or vehicle.
LARGE GROUP SAFETY An individual can respond to the lightning threat quickly by going inside a large substantial building or fully enclosed metaltopped vehicle. In less than a minute in the backyard of a dwelling, for example, quick action places the person in safety. When the threat is over, using a rule such as 15 minutes for the cessation of lightning and thunder, an individual can return to the backyard. If the lightning threat returns, a person can quickly go back into the dwelling or a safe vehicle until the threat is over. For larger crowds, all of these steps are more difficult. Steps include accepting that the lightning threat is important, knowing how to identify the lightning threat, where the safe locations are located, how long it will take to reach them, when the threat is over, and who makes these decisions.27,74,88,147,199,216,276 In the case of a neighborhood youth soccer game, for example, safety can be reached in minutes in nearby fully enclosed metaltopped vehicles. When game officials or others make the decision to go to safety, players and spectators need to go immediately to the cars, vans, or buses. Note that small venues may have rest rooms or concession stands that are likely to be unsafe from lightning, and people in those locations need to be informed to abandon them for the safety of vehicles in parking lots around the field (see Buildings section of Safe Places Inside). At a somewhat larger school sporting event, including practices, there are likely to be nearby lightning-safe large buildings. Sports and custodial staff need to be informed to leave doors unlocked or
the all-clear signal is appropriate. Nothing is more ineffective and reduces confidence more in the evacuation process than sending people back to their seats, making them return to a safe place again a short time afterward, only to return once again to their seats. For a large stadium or golf tournament, for example, at least 30 minutes should be used for the wait time, and still longer times may be needed to avoid the back-and-forth crowd movement. At a fireworks show, people may be unwilling to leave a favored spot on a field, so crowd control and security specialists may be needed to address the situation. However, in many cases after the first suspension of a concert, for example, some of the crowd does not return, so the problem may be somewhat reduced. Instead of moving a large group from one place to another, it is possible, and usually much less expensive than managers might expect, to provide safety in place. The approach is to place large, properly grounded poles and overhead wires that divert the flash from striking a crowd by using these down-conducting paths into the ground.11 The principles are the same as those routinely applied in lightning protection of buildings, towers, utility poles and lines, and many other aspects of modern infrastructure. This approach has long been used for the space shuttles and other critical government activities and structures. There are large benefits to installing such a system, such as no evacuation, no need for safe places to be identified, and no uncertainty in the process and its execution. However, people must stay at the correct locations within the protection provided by such a system and trust that it will work as intended. Flags or banners at the top of the protection poles can make the installation as unobtrusive as possible for the crowd and media at such an installation (Figure 3-46).
A
B
C FIGURE 3-46 A, Natural protection zone of a stand. B, The effect of flagpoles implementing Franklin rods. C, The added effect of a catenary added to a stand. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)
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be available to open doors when players and spectators need to go inside. When the crowd is large at a sporting or other outdoor event, the situation becomes more complex. Advance planning is essential. The first step is convincing a venue owner or manager in advance of the potential lightning risk. Many lightning threats are accompanied by rain, strong winds, hail, and other significant weather, so that placing lightning into the context of the thunderstorm threat may be more acceptable. In the United States, the lightning threat at collegiate football games was examined by Gratz and Noble,119 who found that a single game’s threat is not large but the large number of games per year makes a lightning incident at a football game inevitable over a period of years. A case study of an individual game’s response to the lightning threat is presented by Holle and Krider.142 Edwards and Lemon101 emphasized the potential for major storm-related disruptions at auto, dog, and horse races; professional and collegiate sporting events; and outdoor concerts but have often been met with silence or limited positive responses. Among the situations examined by Edwards and Lemon101 are recent close calls of tornadoes passing near large crowds. Fortunately there has been a positive lightning recommendation by the NCAA for NCAA schools.27 Although not all institutions follow the recommendations, it has become common for all types of U.S. collegiate sporting events to be delayed or suspended because of this policy, as well as many more games at the high school and other levels. In fact, there have been almost no lightning casualties in the last few years in the United States at organized sports events. It is a useful tactic in convincing venue operators that they should follow the lead of the NCAA in accepting the lightning risk. This recommendation applies equally to practices and rehearsals. Once there is acceptance of the lightning threat, a method of identifying the existence of lightning is needed. For a large crowd, the sound of thunder is probably not applicable. Reliable, proved, and accurate cloudto-ground lightning data are now available on cell phones, websites, and other portable devices that are objective measures of lightning. Any purchaser or monitor of these, however, should make sure that lightning data are real time. Currently, many sources of lightning data, particularly free sources, may be delayed by several minutes or more, depending on the supplier. Rules need to be established for how close is close enough at a particular stadium or event site. Stadium managers need to know how long a lead time is needed to evacuate people to safety. Once that time is decided, it determines the distance to lightning for action to be taken as it approaches. The rule needs to be followed objectively on days when the threat exists. When an announcement is made of a lightning threat, the plan goes into action. At a football game, for example, players and coaches may try to stay on the field, which gives the impression that the situation is not really important. In every case, the game or performance area needs to be empty and nothing shown on video screens except the current safety announcement, so that the event no longer provides an attraction to the crowd. In many stadiums, there is adequate room beneath the stands.142 At other locations, a nearby gymnasium or warehouse may be the best alternative, so plans need to include permission to enter those buildings. In the case of a golf tournament, the first concern of organizers is for player and sponsor safety; they can be sent quickly to a safe building or vehicle. However, spectators need a much longer time to reach the safety of their vehicles and may need to walk several miles. While at the safe location, information needs to be given to the audience and participants concerning the status of warnings. This can be difficult in many situations, and warning horns or message boards may be the best approach. Informing people waiting in diverse locations involves complete and active planning in advance on the part of the venue operator. The safe location also needs to be comfortable enough for the crowd to accept a long wait. Appropriate signage or inclusion of lightning safety information in event programs may also be useful in communicating safety information. The all-clear at the end of the lightning threat needs to be identified as objectively as is the beginning (see End of Thunderstorm). As crowds become larger, a very long wait time until
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Covered stand
FIGURE 3-47 Protected zones on a pathway from light poles of varying height. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)
Protection in Situ* The Franklin rod is often the basis of lightning protection schemes. Many existing structures can be turned into such rods with ease without detracting from appearances. Examples are given below. It is emphasized that these are illustrative only, and proper design is needed when these are being implemented. Figure 3-47 shows a pathway with light poles of a given height. Spacing of these poles may be selected to protect the pathway, depending on the height of the poles and width of the path. Figure 3-46, A shows the “natural” protected zone around a temporary stand that might form an evacuation region if other risks are accepted. Franklin rods (see Figure 3-46, B) added along the back of the stand extend this zone and also add some in situ
FIGURE 3-49 Effect of existing covered stands and lighting stanchions. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)
protection. Useful Franklin rods are formed by flagpoles that have the required “look.” A horizontal wire at a given height above a stand also provides in situ protection (see Figure 3-46, C ). These can be made all but invisible, especially to media cameras. Alternatively, they can carry banners, lights, or media cameras. Figure 3-48 shows horizontal wires providing protection to a group of stands. The width of the protective corridor depends on the height of the catenary, and the position of the corridor can be altered as a design parameter for effectiveness. Figure 3-49 shows a stadium for a field game like baseball, where an existing stand provides some protection, as do lighting pylons. The addition of overhead wires can complete the coverage. Figure 3-50 shows the main stadium stylistically and shows how open stands at either end of the stadium can be protected by fine wires, which are all but invisible.
Controversies in Lightning Injury* Much remains to be learned about lighting injury, and knowledge at present remains partial.
Covered stand Open stand
Open stand
Open field—overhead is a network of cables along which cameras travel—providing adequate protection.
Covered stand
FIGURE 3-48 Use of catenaries to protect several stands. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)
FIGURE 3-50 Open field—a properly installed network of overhead cables that can double for moveable cameras can also provide adequate protection. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)
*Reference 10.
*References 69, 70.
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This is especially evident when expert and legal assessments are made of victims. For example, the area of the psychological effects of lightning injuries is under active research and still needs clarification. The effects are well documented in the literature. Nonetheless, psychiatric and psychological standards (e.g., the Diagnostic and Statistical Manual of Mental Disorders and other standard teaching and textbooks) have not yet incorporated the syndrome into their formularies. This highlights the fact that victims represent a numerically small group in routine practice, and most practitioners are rarely aware of the literature on the subject. Consequently, we see established practitioners struggling for a diagnosis and trying to fit the “new” syndrome into existing categories.
RESEARCH METHODOLOGY PROBLEMS Cooper69,70 draws attention to further features of what is not yet known in lightning injury and documents methodology difficulties. She states that without knowledge of the basic physiology, only general symptomatic aftercare can be rendered. It may be more desirable to have specific treatments or even early interventions that might stop or change the course of the injury cascade that is precipitated by the initial injury. Research on lightning injuries is difficult (Box 3-5). There are no public health regulations that require reporting of lightning injuries, so cases are difficult to collect and survivors are difficult to locate in any systematic fashion.54,143,205 Although it may be convenient to use select populations, such as the membership of LSESSI, as a study group, people who join support groups differ from those who do not. They represent only a subset of survivors and may have systematic biases developed from the services and materials that LSESSI supplies to its members.69,70,189 In addition, limited research can be done with them because of ethical limitations on human research, national dispersion, and lack of funding for the research, among other difficulties. To sort out lightning electrical effect from other etiologies, it is necessary to obtain relatively recently injured patients (no more than 6 to 12 months) with a “clean” history. There must be no *References 69, 75. BOX 3-5 Research Problems Human Research • Recruitment of cases • Study biases • Dispersion of subjects • Cases must be free from • Diabetes and other neuropathic illnesses • Drug history • Psychiatric history • Blunt head trauma Animal Research • Expensive—both animals and equipment • Large number of animals for some studies • Difficult signal processing problems • Monitoring equipment design • Shock timing control considerations • Definition of dose • Standardization of dose • Flashover effect Molecular Biology • Cell culture, blood levels of indicators of injury, and so on • Requires specialized techniques • Bioengineering, collaboration • Expensive
past history of alcohol or drug abuse, head injury, psychiatric problems, or concurrent medical problems that cause neuropathic pain or psychiatric symptoms and no blast effect during the injury that would confound investigation of the electrical effects of lightning. Unfortunately, this further narrows the available pool. Difficulties therefore compel selection of other models, raising problems of applicability. Because it is difficult to recruit volunteers to stand in a thunderstorm, animal work is a reasonable alternative. Kitagawa, Ishikawa, Ohashi, and Andrews have all done credible research using animals.9,10,153,169,225 Cooper and colleagues80-82 have built a reasonable rat model, inducing most of the clinical signs that are seen in humans. Unfortunately, such research is expensive, time consuming, and sometimes requires large numbers of animals to show significant differences. Most problematic is the delivery of a “standardized dose” that can reliably reproduce a specific pattern of injury. Many hurdles must be overcome in research equipment design, anesthetic choice, and animal care, as well as shock timing and delivery, given instrumentation requirements. Monitoring equipment must be electrically isolated from the animal and shocking platform, or the connections may preferentially transmit the lightning shock to the equipment, not the animal, clouding the experiment and destroying the equipment. Some anesthetics are neuroprotective, whereas others affect cardiac function. Temperature control in anesthetized rats is a significant issue. Animals that are studied for neurocognitive injury using water maze and other behavioral models need a standardized quiet environment, which is not always possible in the cramped quarters of most animal facilities. In survival or cardiac studies, timing of the shock to either target or avoid the “vulnerable period” must be done on a statistically predictive basis, because direct sensing of the specific targeted cardiac cycle would again result in damage to the equipment.
AREAS OF SPECIFIC CONTROVERSY Survival Statistics Box 3-6 lists factors concerning the unknown issues as to why the vast majority of casualties survive.54 It is possible that characteristics of a lightning strike or possibly the mechanism by which the current impinges on the individual may be different for lightning fatalities. It is possible that timing of the lightning strike may be the important factor, particularly if it hits during a more vulnerable portion of the cardiac cycle. Although it is possible, it is unlikely that the physical characteristics of people differ sufficiently to cause a difference in mortality. Remote and Psychological Symptoms A further area of active research is the etiologic origin of symptoms not directly in the line of passage of current. This is as much for electrical injuries as for lightning injuries.211 Even when there is no indication of current near the brain or evidence of blast/blunt injury, neuropsychological testing consistently suggests an organic origin to the deficits. Imaging, imperfect as it is, suggests unspecified organic impairment. The exact nature of the impairment, its relation to functional pathologic conditions, and its origin remain obscure. BOX 3-6 Why Do 70% to 90% of Victims Survive? • Lightning characteristics (possible factor) • “Type” of lightning • “Dose” of lightning delivered • Timing of hit during cardiac cycle or other factors • Pathway of lightning • Other meteorologic conditions (possible factor) • Physical characteristics of those “hit” (possible factor) • Comorbidities • Rescue/resuscitation efforts • Where people were/what they were doing (possible factor)
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PROBLEMS WITH EXPERT REPORTING*
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BOX 3-7 Possible Injuring Forces • Blunt trauma—explosive injury • Structural changes—direct damage • Pathway of the injury • Orifice entry • Flashover—how much goes through versus around • Neurochemical changes • Autonomic nervous system effects • Electrical effects • Electroporation • Cellular level mechanical effects • Cellular level enzymatic effects • Subcellular organelle damage
Increasing awareness of the role of the spinal cord in nociception and existence of proximally directed neural pathways may provide a fruitful connection. Release of humoral transmitters may play a role. The importance of premorbid personality predisposition is unknown. It has been noted by some that the neuropsychological constellation bears resemblance to the psychological effects of other syndromes, like head injury and the response to autoimmune disorders. It is possible the symptom complex that is seen represents a “final common pathway” of brain injury due to many etiologies. Psychiatric insights, for example the effect of cortisol on hippocampal changes in depression, may offer insight into depression following lightning and electrical injury. There is a tantalizing observation allied to this of hippocampal neuron loss in electrical injury, regardless of cranial or peripheral application of current.181 Box 3-7 lists other possible factors yet to be verified. Technical Matters The degree of lightning injury, or “dose,” may vary considerably with the mechanisms of injury (e.g., direct, splash, contact), few of which have been modeled or quantified. Other technical factors regarding interaction of a lightning stroke with the body, such as the effect of multiple return strokes, are poorly known. Although flashover is known to occur, the course of energy going through the victims versus around them and the duration of energy flow initially or with return strokes is unknown. Although these factors have been calculated based on engineering assumptions, actual measurements have never been done on research subjects or simulated subjects to test the assumptions. Medical Resources Because common imaging techniques like CT and MRI are anatomic tests, results are limited by resolution achieved by the equipment. As anatomic tests, they do not show functional deficits in how the brain, heart, nerves, or other structures behave when injured. Although it has been hypothesized that deficits are at a cellular, subcellular, synapse, or enzymatic level, this has not been actually investigated or measured, either clinically or in an experimental model. Lee has corroborated electroporation of muscle cell walls with high-voltage electrical injury, but the physics of such injury are quite different from lightning physics, and certain important symptoms are also different.65,69,184 Electroporation has not been investigated in the lightning model or investigated in nerve or brain cells that are more affected clinically than is muscle tissue. Our knowledge of very short (submillisecond) impulses and their effects on the body is poor, and it is not a priori obvious that results attributed to longer durations of exposure (electrical) are immediately transferable to short (lightning) durations.
SAFETY CONTROVERSIES Predictability of Lightning Atmospheric physicists, electrical engineers, meteorologists, and other lightning experts have spent their careers working to 98
describe the characteristics of lightning, how it forms, and how it acts. However, one must always remember that, however learned and mathematical, these are descriptions and not “rules” that lightning must follow. Lightning, at best, is capricious in its behavior. We do not have complete knowledge of why lightning acts the way it does. At best, we can describe the conditions under which lightning is likely to form. The common thunderstorm cell is much smaller than expected and arises, moves on, and resolves over a period less than an hour. That is why when a huge downpour occurs with lots of lightning, all one need do is seek shelter for 20 to 30 minutes as the cell passes by, the rain decreases, and perhaps sunlight even shows. When conditions are right, multiple smaller cells of varying intensity can stack and follow each other so closely that the storm seems continuous. Sometimes, very intense storms, including huge tornadoes, can arise. The NWS is charged with providing severe weather warnings to minimize property and personal injury. Life is a calculated risk. There are always tradeoffs between absolute safety, convenience, and getting on with your life and work. The weather, like life, is somewhat unpredictable. One of the controversies is the compromise between absolute safety that results from issuing many warnings that later turn out to be “false” and lesser guarantees of safety with fewer but more reliable warnings. People learn not to pay attention when too many warnings turn out to be false. An additional complication is that because of the small areas in which thunderstorm cells arise, it is impossible for regional forecasts to cover all of them. Individuals should be aware of the general weather forecasts and incorporate their own knowledge of local weather patterns, along with an eye to the sky, when fast-changing weather is predicted, to notice quick development of nearby storms that may contain dangerous lightning. Preplanning, alertness, and knowing the lightning safety rules, primarily “When thunder roars, go indoors,” can save lives.216 Lightning Exposure Prudent outdoors people educate themselves and plan for foreseeable risks, whether they be grizzly bears, mosquitoes, hypothermia, falls, or weather problems such as flash floods, unexpected early or late snows, or lightning. In leaving civilization behind, they realize that they are giving up 5-minute response times for emergency medical services, easy food sources, warm showers, and other benefits. Unfortunately, some risks have no halfway measures that will significantly improve safety. Lightning is one of those. At the current time there is an outcry for advice on improving lightning safety for wilderness situations. However, NO place outdoors is safe when thunderstorms are in the area. Avoidance of the risk is the only prudent recourse. One must look at the risk–benefit ratio in considering any other response. During the vast majority of their lives, most people are within a very short distance of safety from lightning. Many routine outdoor adventures are on frequently hiked paths, common ascents of mountains, and gatherings at tent-only campgrounds and scenic overlooks. Planning to avoid being in these areas during times of high risk (afternoons) can minimize but not entirely exclude the chance of injury. In addition to avoidance of risk, the other part of the “When thunder roars, go indoors” rule is seeking safe shelter. Modified metal shipping (Figure 3-51) containers are used in many countries in industrial, heavy construction, and mining sites and are moved as needed by truck or heavy lift helicopter. These could be used in many wilderness situations to provide lightning-safe shelters within easy hiking distance of common paths, particularly in areas such as summer camps and parks. Development of inexpensive shelters that could be backpacked in by a scout group and set up as a summer project is potentially possible but fraught with design, testing, maintenance, and liability issues, particularly in the United States. Other considerations would be location, accessibility, expense, signage, ownership, vandalism, and permits, not to mention resistance from some at altering the environment for what may not be perceived as major risk.
Research LIGHTNING SAFETY RESEARCH There is a variety of unresolved issues relating to improving lightning safety recommendations. The topic includes a mixture of scientific, social, economic, and demographic variables that are often very difficult to identify. Although the phenomenon of lightning has become better understood in the last decade or two, many features of how lightning results in fatalities and injuries remain elusive. The mechanisms of lightning injury have been categorized more completely than before, as described in this chapter, and identifying this mixture of mechanisms has made a difference in lightning safety advice. Most importantly, the commonly held perception of a direct strike is now thought to represent only 5% or less of lightning injury. However, the estimates in Cooper70 and related publications are based on subjective experience of researchers studying large numbers of cases, showing the need to better identify the ratio of mechanisms causing lightning injury. The issue of the upward leader with regard to human injury is in need of more study. Roeder243 provides a set of questions and comments on research needed to improve lightning safety. The requirements can be divided into several main groups from Table 3-1:243 safety of buildings and vehicles, determining the range to be safe from lightning, and demographics. Building and Vehicle Safety Lightning safety recommendations now state that safety is reached inside large well-constructed buildings or fully enclosed metaltopped vehicles.* Although fatalities in these locations are rare in more developed countries, injuries continue to occur, and their circumstances are not well understood or identified. Smaller structures are always problematic, so recommendations stress staying away from them, although it is possible to make them safe in certain situations.171 A related issue is how much time people spend outdoors in more developed countries. People may now spend more of their time inside safe buildings and vehicles than in the past. Although these social data are extremely difficult to quantify, knowing this information may explain a portion of the steady decrease in lightning fatality rates in all of the more developed countries studied in recent years.138,143 In less developed regions, safe buildings and vehicles are not available to many people much of the time. Lack of such a safe place nearby is an unknown, but likely, contributor to the higher lightning fatally rate in such regions compared with more developed countries.138 Safe Distance to Lightning Real-time cloud-to-ground lightning data have been available across the United States since 1989, and monthly maps have been *References 27, 74, 88, 139, 147, 199, 216, 276.
Demographics Lightning fatality and injury rates are quite well known in more developed countries, as described earlier in this chapter. The global impact of lightning, however, is not well specified. Lightning casualty data are beginning to be collected systematically in some very populous countries, but data collection methods are in early stages and will need to be established over longer periods.239 Global lightning impacts were first estimated in Holle and López143 to be 24,000 deaths and 240,000 injuries per year around the world. This estimate is based on minimal or no data from Africa, Southeast Asia, and India, where lightning casualty rates appear to be quite high and flash densities are coincidentally often large. Availability of safe or unsafe buildings and vehicles is important in understanding the data that may be collected in less developed areas of the world. It is important that related casualty data be collected concerning activity, location, gender, age, nearby structures, and other issues related to fatality and injury data, in order to separate the influences that have been outlined here and in Roeder’s work.243 Such information can then be used to develop relevant safety recommendations and strategies.
Lightning Detection and Data Applications DETECTION Cloud-to-ground lightning over the United States has been detected and located in real time since the late 1970s. Pulses from lightning in the VLF and LF range that propagate along the earth are used to detect and locate return strokes in cloud-toground flashes. Such sensors can also locate distant lightning in the VLF because signals propagate thousands of kilometers between the earth and ionosphere.86 The U.S. National Lightning Detection Network (NLDN) has gone through several stages of improvements to combine direction finding and time-of-arrival location methods. Networks with some or most of the NLDN capabilities operate in real time in more than 40 countries; most are owned and operated by national meteorologic services or electric utilities. The NLDN has been operating continuously since 1989 and has become the benchmark for cloud-to-ground lightning detection; it has typical 99
CHAPTER 3 Lightning Injuries
FIGURE 3-51 Metal shipping container modified for use as a safe shelter in mining areas of New Guinea, Tanzania, and Peru. (Courtesy Richard Kithil, National Lightning Safety Institute.)
compiled.85,141 Similar regional or national lightning detection network data are also available to a varying extent in many other regions of the world, and a global lightning data set is becoming accessible everywhere.93 These data sets have been considered in some situations for determining the distance between flashes and the time of day and year when flashes occur.148 The linkage to specific applications is less developed than these and other major advances in detection.156 How long a lead time is needed for the general public, for airports, for sports events, and other applications? The lead time includes identifying the safe places that are nearby and a plan to reach them. What amount of risk is acceptable for each application? For example, a munitions depot has no tolerance for any direct lightning strike, whereas other situations accept more lightning exposure in exchange for economic efficiency. The role of cloud lightning in the warning process is also less well understood. Does an overhead flash without a cloud-toground flash demand the same response? What are the safe distances to anvil lightning? With the development of total lightning detection, it is becoming possible to address these questions in a more systematic way than could be accomplished earlier.94 Thunder distancing is often recommended for safety when lightning detection network data are not available. Few if any studies of thunder have been made in the last few decades, so the audibility of thunder is not well understood from the practical point of view of lightning safety. The issues involved are the normal distance that thunder can be heard, the effect of nearby noise on that distance, the role of cloud lightning in producing thunder to its use in warnings, and the relationship of hearing thunder to the actual lightning threat.243
PART 1 MOUNTAIN MEDICINE
distances between sensors of 300 to 350 km. The NLDN has been calibrated by rocket-triggered lightning, tower strikes, and camera studies to determine location accuracy over the contiguous United States of 300 to 500 m and flash detection efficiency exceeding 90%.30,86,107 The NLDN also provides polarity and peak current and measures the quality of each flash location. Approximately 70% of the multiple-return strokes within a cloudto-ground flash are also located by the NLDN, and a small fraction of cloud flashes contain pulses that are strong enough to be detected and located.86 Direction finding and time-of-arrival methods have been recently combined into an advanced method that allows global coverage to detect lightning over extremely long distances.93 The new global data set, known as the Global Lightning Dataset GLD360, achieves 70% cloud-to-ground flash detection efficiency with a horizontal location accuracy of 5 to 10 km (3.1 to 6.2 miles). Several lightning detection satellites have made twice-daily or regional passes for a few years at a time; the new GOES-R lightning sensor scheduled for launch in 2015 will cover much of the western hemisphere at an expected 8-km (5-mile) resolution. In addition to cloud-to-ground lightning detection networks, detailed cloud lightning can be detected by regional VHF networks that use direction finding and/or time-of-arrival techniques over line-of-sight distances.92,134,175-177,192,264 These networks track the horizontal branching associated with cloud-to-ground flashes, and some provide vertical resolution. Such cloud lightning networks have closer spacing between sensors than the NLDN, because they use line-of-sight detection in the VHF frequency range. Growth of both larger global and smaller regional networks has occurred beyond the medium-area coverage of wide-area VLF/LF networks. These technologies indicate the need for different techniques or frequency ranges to meet differing demands for lightning information.86
APPLICATIONS The first operational U.S. lightning detection network was developed for early recognition of lightning-caused fires. Eventually, large networks were established to detect cloud-to-ground lightning across the western United States, Canada, and Alaska. Cloud-to-ground lightning is the largest cause of transients, faults, and outages in electric power transmission and distribution systems in lightning-prone areas. As a result, this was the other early application of such wide-area networks.86 In these situations, each flash or stroke is carefully identified as the cause, for example, of a power-line fault on a transmission or distribution line. It should be noted that the initial motivation leading to development of real-time lightning detection was concern about lightning during ground activities and launches at Kennedy Space Center in the 1970s.86 A very broad array of applications of lightning detection data has developed over the last three decades. There are more than 2200 published papers on the applications and operations of real-time lightning detection networks in the United States and elsewhere. The applications can be separated into four categories, those of the direct threat from lightning and lightning as an indicator, substitute, or covariate. Direct Threat The direct threats to forest and utility concerns are described in the previous section. In addition, archived and real-time lightning data are used in many forensic and insurance applications. Other direct threats include munitions, ground safety in aviation and defense operations, recreational and workplace safety, spacecraft launches, and many other situations. However, the linkage of lightning network data with human casualties has not often been made, and more research is needed.133,148,156,185 Indicator Climatologies of lightning have been developed over a variety of regions and time periods.141 Such annual, monthly, or hourly maps can also be divided according to the type of meteorologic regime at the time to provide information about where thunderstorms and associated impacts are most likely. Lightning 100
climatologies have been found to be easier to compile than are many other data sets, such as radar reflectivity, because VLF and LF lightning detection is unaffected by terrain. In remote regions where conventional radar and surface observations are not available, tracking of thunderstorms and assessing topical and nontropical cyclone status are important challenges in weather prediction for civilian and defense purposes. Thunderstorms over the ocean represent a threat to aircraft routing and ocean shipping and are usually beyond the range of ground-based meteorologic radars. Current research with longrange lightning data has indicated the presence of sporadic cloud-to-ground lightning in the inner cores of tropical cyclones that may be useful for assessing their intensity changes. There are many other ways that meteorologists use lightning data to indicate the state of the atmosphere. These include identifying the difference between showers and thunderstorms; deciding when convection has become strong enough to produce the first flash in a developing thunderstorm; identifying storm orientation, size, and shape; the location of frontal boundaries; and when excessively high lightning rates are occurring in a thunderstorm that may indicate significant weather of many types. Isolated versus organized thunderstorms can sometimes be assessed better with lightning data than with radar and/or satellite information. Lightning data can also be used to indicate the location and timing of a developing low over the oceans, as well as the presence of very cold air aloft. In addition, some winter storms have distinct bands of ice and snow that include lightning where the heaviest precipitation may be falling. Substitute In many situations, such as over oceans and less developed countries, the desired meteorologic data are not available to identify the situation that may lead to significant or severe weather. For example, over the oceans beyond radar range of about 300 km (186 miles), aircraft can use lightning as a radar substitute to identify turbulence for air traffic management. Similarly, meteorologic radar information is lacking in mountainous areas of the United States below mountain tops due to blockage of the radar beam, so lightning can identify thunderstorms in rugged terrain. Rainfall can also be estimated to some extent with lightning information in regions, times, or areas when radar, rain gauge, or other information is missing during flash floods, tropical cyclones, and other severe weather. National meteorologic agencies also use lightning data along borders of neighboring countries without accessible radar data. Lightning data have proved valuable in geophysical research concerning the natural versus man-made production of nitrogen oxides. Covariate When radar, satellite, and surface data are available, real-time lightning detection data can be used to identify trends that occur simultaneously or earlier or later than other data, as well as spatially displaced from other information. Examples include lightning jumps combined with radar in severe weather situations, and hurricane eyewall outbreaks as the storm changes intensity. More complex methods are also being actively pursued with respect to the assimilation of lightning network information into numeric weather prediction models to help initialize them by better locating convection. There is also promise that lightning can be combined with radar or satellite data to more accurately locate heavy and excessive rainfall, because VLF and LF lightning network data do not suffer from terrain effects. Changes of cloudto-ground lightning polarity and rate changes, as well as ratios of cloud to cloud-to-ground lightning, are areas that require large, accurate, and complex data sets and statistical analyses over multiple regions but hold promise for many applications.
Lightning Explosive Barotrauma Lightning is a multiphysics phenomenon requiring a multidisciplinary approach. Current lightning injury models suggest that lightning injury is chiefly electrical and/or thermal in nature. Although electrothermal phenomena explain the vast majority of injuries observed in lightning strike victims, including cardiac and at least some of the neurologic injuries, review of the lightning
The return stroke heats the channel created by the preceding stepped or dart leader from nearly 10,000 K to near 30,000 K or more in several microseconds or less. Such a channel overpressure will result in an expansion of the luminous channel and the formation of a shock wave that propagates outward and eventually beyond the luminous channel, which attains pressure equilibrium with the surrounding atmosphere within tens of microseconds. The shock wave differs from the acoustic wave (thunder) in that it compresses and heats the air and, as a result, propagates at supersonic speeds. The initial propagation speed of the shock wave is probably about 10 times the speed of sound. After the bulk (probably 99%) of the energy delivered to the shock wave has been expended in performing thermodynamic work on the surrounding atmosphere, the shock wave is transformed, within a few meters or less from the lightning channel, into an acoustic wave that propagates at the velocity of sound. Thus, the heated-channel thundergeneration mechanism involves the production and evolution of the shock wave, which is typically characterized by its pressure as a function or radial coordinate at different instants of time. A further review of the lightning literature reports that thunder consists of a roughly cylindric initial pressure shock wave in excess of 10 atm at the lightning channel. The shock wave rapidly decays to a sound wave within meters. The pressure wave—shock propagation—sometimes may cause exterior
and interior damage to structures. There have been anecdotal reports of popping of nail-supported drywall away from horizontal and vertical wooden studs inside houses and broken glass windows. It is not uncommon for a lightning flash to enter an unprotected building through a water pipe or wiring. The sometimes explosive effect may rip a hole in the wall where the flash passed through a ventilator, splinter the ceiling, or blow off roof tiles. A case is on record where a lightning flash entered a small double-storied house and caused complete collapse of one of the walls.200 There are multiple well-documented reports of trees being split asunder, blast holes in the ground, and flying masonry.5 Physics of Lightning by D.J. Malan,200 under the heading Explosive Effect, notes: Should the heavy current of a lightning flash pass through a confined space, the heated air is not free to expand and will exert a pressure on the walls of the cavity. The larger the cavity, the smaller the excess pressure, since only part of the air in a large cavity will be heated. When a lightning flash is incident on rocky soil the electric current tends to follow the interstices between the rocks or cracks, which are filled with moist soil. Rocks may be split asunder or thrown aside with explosive violence. Muller Hillebrand carried out detailed studies of the effects produced by lightning on the rocky soils of Sweden. On one occasion investigated, lightning struck a pine tree and from there plowed branching furrows in the ground. The total length of the furrows was 250 m (820 feet), and in one spot there was a craterlike hole 2 m (6.6 feet) in diameter and 75 cm (29.6 inches) deep. Rocks of up to one-half a ton in weight were dislodged, and trees were uprooted. The total volume of stones and Earth cast aside amounted to 25 m3 or the equivalent of 70 tons. He estimated that about 200 kg (441 lb) of high-explosive trinitrotoluene (TNT) would have been required to produce the same effect as a lightning flash. Luckily, few lightning strikes are sufficiently forceful to produce such devastating effects.200 Review of the otorhinologic medical literature sometimes describes the tympanic membrane following lightning strike as “a large tympanic membrane perforation with ossicular chain disruption.”* Proposed mechanisms of injury have included concussive “blast” effect on the ear, “direct” effect of electrical conduction, “splash” effect, “cylindric shock wave of electrons,” and/ or direct “thermal burn.”236 More research is needed to investigate if there is significant concussive blast effect or lightning explosive barotrauma immediately surrounding a lightning channel that could add to our understanding of some of these curious lightning injury patterns that have not been explained in the past. *References 26, 28, 113, 115, 160, 222, 236, 265, 279.
VIDEO RESOURCES Video 3-1: A slow-motion montage of cloud-to-cloud lightning. (Aquavision TV Productions, used with permission. http://www.aquavision.co.za.)
REFERENCES *References 5, 26, 28, 113, 115, 124, 160, 165, 190, 237, 278, 281.
Complete references used in this text are available online at www.expertconsult.com.
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CHAPTER 3 Lightning Injuries
literature shows an interesting injury phenomenon that is difficult to explain with the current electrical and thermal injury models and that has become a topic of controversy.32,279 The phenomenon includes torn and tattered clothing, fractures, rupture of shoes, traumatic perforation of tympanic membranes, lung contusion and hemorrhage, and even pneumomediastinum.* These findings are similar to injuries seen in individuals who have been exposed to a bomb explosion and suggest explosive barotrauma as a mechanism of injury.165,203 To be injured by a blast, one has to be in the immediate vicinity (about a meter or so) of the explosion. About 690 kPa (100 psi) is the minimum threshold for serious damage to humans.252 Blast lung, bowel contusion, and tympanic membrane rupture, all of which may be found in some cases of lightning injury, are typically found in cases of direct transmission of a detonation shock wave.201 It is customary to use Marshall’s triad when considering the pathology of trauma of bomb explosions. The triad includes punctate bruises, abrasions, and small punctate lacerations, all of which are typically found in an explosive bomb blast. Although many similarities exist between injury patterns seen in lightning and concussive injuries, Marshall’s triad findings are not typically found in lightning strike injuries. A blast consists of a wave of compression passing through the air. The velocity of the shock wave depends on the distance from the epicenter, being many times the speed of sound at the start, but rapidly decreasing as it spreads out. The magnitude of the blast varies with the energy released and also the distance from the epicenter, the intensity obeying the inverse square law. Rakov and Uman234 describe something similar in their book, Lightning: Physics and Effects, explaining little-appreciated forces that can occur with lightning:
CHAPTER 4
Thermoregulation LARRY I. CRAWSHAW, KEI NAGASHIMA, TAMAE YODA, MAYUMI NAKAMURA, KEN TOKIZAWA, AND YUKI UCHIDA
A warm body has long been recognized as one of the primary conditions of life. Although humans have physiologic, intellectual, and cultural capabilities that equip them to maintain viable body temperatures under many climatic conditions, thermal extremes, heavy exercise, and injury can rapidly lead to dangerous internal temperatures. For a physician who is operating in primitive circumstances, maintaining or restoring a patient’s body temperature can require quick action and ingenuity, both of which are aided by an understanding of the physiology of temperature regulation. Because the thermal environment can be extremely complicated and the thermoregulatory system of humans is complex, making decisions about body temperature maintenance in the field can be difficult. This chapter is designed to aid in the decision process by providing a basic understanding of the relationships among the ambient thermal environment, the thermal characteristics of the body, and the thermoregulatory system. First, some overall concepts of temperature regulation as well as a way to conceptualize the system will be reviewed. Second, the range of normal body temperatures will be covered, along with the consequences of higher and lower body temperatures. Third, methods and potential pitfalls of monitoring body temperature will be outlined, after which the physical factors that affect heat flow will be covered. Fourth, the neuronal systems involved in processing thermal information (i.e., sensation, integration, and output) will be reviewed, followed by a detailed description of the effector organ responses involved in the maintenance of thermal homeostasis. Last, modifications of thermoregulatory responses, induced alterations of the regulated temperature, and changes in the responsiveness as well as in the capabilities of the thermoregulatory system will be noted. Note that, when values are given for “a person,” they refer to a 70-kg (154-lb) man.
Conceptualizing the Thermoregulatory System Humans are homeotherms and as such are capable of maintaining a relatively constant body temperature across a wide range of ambient temperatures. Such constancy is attained through the use of behavioral processes that involve maintaining or searching for a preferable environment and autonomic processes such as vasodilation of the skin blood vessels and sweating in the heat and shivering in the cold. These processes are controlled via a negative feedback system with a primary feed-forward input from skin sensors that monitor ambient temperature (Figure 4-1).89 The feed-forward input from the skin allows for the elicitation of thermoregulatory responses without a change in core body temperature. Thus, the primary regulated variable, core temperature, can remain relatively constant under widely varying environmental conditions. Without the feed-forward element, if a hot or cold stress were encountered, large amounts of heat would be gained or lost before deep body sensors were sufficiently affected to elicit restorative responses. In addition, when greater thermal stresses were encountered, greater deviations in core temperature would be necessary to elicit sufficient restorative responses. Figure 4-2 illustrates some of the concepts that relate to the thermoregulatory system and that will be discussed in this chapter. Under normal conditions, body temperature is relatively constant under a range of ambient temperatures, as is depicted by trace “a.” The breadth of this range of ambient temperature is called the range of normothermia. The midpoint of this range can be conveniently called the regulated temperature, which is 104
shown by the dot in trace “a.” Toward the upper and lower ends of trace “a,” the core temperature inflects up and down. These inflections represent ambient temperature extremes at which the regulation begins to fail. Altered core temperatures can also accrue when there are alterations in the regulated temperature. Such alterations could be caused by the presence of bacterial toxins (e.g., fever) or starvation, which would cause increases (trace “b”) or decreases (trace “c”) in the regulated temperature. In addition, under various conditions, the effector responses can become compromised, which leads to decreases in the ability to defend against low temperatures (dashed line at “d”), which could indicate a problem with metabolic stores, or high temperatures (dashed line at “e”), which may indicate dehydration. Of course, various combinations of regulatory changes and altered effector responsiveness occur in conjunction with many threatening situations.
Basics of Core Temperature Typical measurements of core temperature provide a good estimate of the temperature of critical internal organs and are quite stable across individuals. In a study that involved 700 observations of 148 healthy individuals,113 90% of the early-morning oral core-temperature measurements were between 36.0° C (96.9° F) and 37.1° C (98.9° F). Core temperature is vigorously defended by the body. At low temperatures, regional heterothermy that results from peripheral vasoconstriction forms an important aspect of this defense. The lowered skin temperature decreases the thermal gradient from the skin to the environment and thus decreases heat loss. At cooler temperatures, there can be a large amount of peripheral tissue that is well below core temperature, which leads to a major decrease in the overall heat content of the body. A nude human resting at 35° C (95° F) or 20° C (68° F) exhibits similar temperatures at various locations within the core. However, because of decreased temperatures in the outer shell, a person resting at 20° C will have a total heat content that is about 200 kcal lower than when resting at 35° C.168 If the peripheral vessels were suddenly dilated, an immediate drop in core temperature of about 3.5° C (6.3° F) would result. In a hypothermic individual, the discrepancy between core and shell temperatures could be considerably greater and could result in a dangerous postdilation drop in core temperature. A method for making a rough estimate of the potential drop in core temperature after peripheral vessel dilation is given in Estimating Mean Body Temperature, later. A different type of heterothermy may be present in hyperthermic humans. As the brain temperature reaches high levels, blood flow that normally moves outward from the intracranium to the face via the ophthalmic vein is redirected and flows from the face inward.75 This results in the brain being cooled by blood that has passed through areas that have been cooled by facial sweating and leads to a brain temperature that is lower than that of the remainder of the core. Although brain cooling is clearly documented and accepted in many mammals,5 there has been some controversy about its importance in humans.15,24 Nevertheless, there is unanimous agreement that the head is an extremely important area for heat loss.15,25 Thus, for hyperthermic patients, it is important to optimize the heat loss from that region and, when necessary, to augment cranial heat dissipation by fanning and moistening. A variety of conditions can lead to an abnormal core temperature. Under some circumstances, the regulator may be defending an altered core temperature for reasons that will be described
For online-only figures, please go to www.expertconsult.com
Sensor Feed-forward signal
(Effectors)
Feedback signal
Regulated variable (Tcore)
Controlled system
Controller
(Body mass) Sensor
FIGURE 4-1 A negative feedback system with feed-forward input from the main disturbance (ambient temperature), which decreases variation of the main regulated variable (core temperature). (From Kanosue K, Crawshaw LI, Nagashima K, et al: Concepts to utilize in describing thermoregulation and neurophysiological evidence for how the system works, Eur J Appl Physiol 109:5, 2010.)
later in this chapter. Alternatively, the thermal load posed by the environment or by heavy exercise may be too great for the capacity of the effectors. Finally, the regulator could be deranged as a result of substance abuse, extreme temperatures, side effects of prescription drugs, or other factors. When interpreting a particular core temperature, it is important to evaluate all of these alternatives. Accidents in the wilderness often involve the compromise of many aspects of thermal balance, and an altered body temperature is very likely.
Consequences of Altered Core Temperature When tissue temperatures change, there are immediate and important effects on metabolism as well as on other physiologic mechanisms. With a 10° C (18° F) increase in temperature, the metabolism of typical human tissue increases by a factor (Q10) of about 2.7. The metabolic rate of the entire organism—apart from thermoregulatory responses—responds similarly. For temperature differences other than 10° C (18° F), these effects can be calculated with the following equation:168
Core temperature
°C °F 39 (102)
37 (98)
b
36 (96)
a e
d
Monitoring the Temperature of the Core and Other Sites The overall status of the thermoregulatory system is determined by measuring the core temperature. This can be done at a number of sites with several types of instruments (i.e., thermometers). In the following paragraphs, the relative merits of locations and instruments are discussed.
MONITORING THE CORE TEMPERATURE
R 2 = R 1 × Q10 ([ T2 − T1 ] /10 )
38 (100)
where R2 and R1 are the two rates of physiologic response; T2 and T1 are the two temperatures; and Q10 is the increase in rate caused by a 10° C (18° F) increase in temperature. Within the normal range of body temperatures, higher temperatures favor speed at the expense of tissue resources, whereas lower temperatures conserve resources. Although both high and low temperature extremes pose a threat to humans, increased temperatures greatly accelerate the development of serious complications and pose a much more immediate danger. A deviation of about 2° C (3.6° F) above or below normal core temperature is well tolerated by the various regulatory systems of the body, but a discrepancy of 3° C (5.4° F) begins to disrupt these systems, including those involved in temperature regulation. At this level of deviation, if there is no intervention, physiologic problems compound very rapidly. A core temperature of 34° to 36° C (93.2° to 96.9° F) disrupts many important physiologic functions, which, taken together, may significantly affect patient outcome. Such mild hypothermia impairs recovery from surgical procedures as a result of such things as impaired peripheral blood flow and oxygen availability, increased possibility of cardiovascular complications, decreased antibody and cellular immune defenses, impaired coagulation, and increased metabolic expenditure for heat production.47,57,103,107 In most situations, it is very important to maintain the patient at normothermic levels. Traumatic brain injury can be present in wilderness accidents, and it may be accompanied by hyperthermia. Heightened temperatures can exacerbate cerebral inflammation and lead to increased neuronal damage.185 There is current interest in invoking mild hypothermia to minimize damage to the central nervous system after neurologic injury.139 However, when this approach is used, care must be taken to deal with the side effects mentioned previously.148
c
35 (95)
A history of clinical thermometry is available111 as are good overviews of the assessment of core temperature.10,32,201 Sites for taking the temperature, in order of increasing invasiveness, include the forehead, axilla, oral cavity, tympanum, rectum, esophagus, bladder, and pulmonary artery. There is no clear-cut choice regarding the best site to monitor; particular situations demand different techniques. Thermometers that have been employed clinically include mercury-in-glass thermometers (which are now obsolete), electronic thermometers, tympanic radiation thermometers, and liquid crystal thermometers. Whatever instrument is used should have an accuracy of ±0.1° C (0.2° F). The handheld electronic thermometer is a good choice for field emergencies.
MEASURING INSTRUMENTS Ambient temperature FIGURE 4-2 A stylized diagram that represents body temperature at different ambient temperatures. The relatively flat portions of the three traces a, b, and c represent the range of normothermia. Trace a represents regulation under normal conditions; traces b and c represent increased and decreased levels of regulation, respectively. Inflections at the trace extremes depict the ambient temperatures at which the effector responses are unable to compensate for the increased ambient thermal stress. The dashed traces d and e correspond with situations in which the effectors for cold defense and heat loss are compromised. (Modified from Kanosue K, Crawshaw LI, Nagashima K, et al: Concepts to utilize in describing thermoregulation and neurophysiological evidence for how the system works, Eur J Appl Physiol 109:5, 2010.)
The handheld electronic thermometer has replaced the mercuryin-glass thermometer, and it has been widely used for many years. Electronic thermometers can make use of either thermistors or thermocouples as sensors; they have the requisite degree of accuracy, and they are very flexible in application. Although an equilibration time of 1 minute is specified for the typical probe, this is largely because of the need for a stiff casing for ease of insertion; smaller probes are available that can equilibrate in seconds. The digital display of these instruments reduces errors, and the probes can be left in place for continuous monitoring. A quality instrument with a wide range of interchangeable probes is important. Even then, these devices are subject to the usual problems inherent with electronic instruments and rarely 105
CHAPTER 4 Thermoregulation
Disturbance (Ta)
PART 2 COLD AND HEAT
have a range low enough to monitor skin temperature in cold environments. A second electronic thermometer with a wide temperature range is important for measuring skin temperature and as a backup for the standard clinical thermometer. Alternate probes and spare batteries for both instruments are essential. Tympanic infrared radiometers are often used in hospital settings. However, even in this relatively predictable environment, some controversy exists regarding their ability to accurately assess core temperature. These instruments monitor the electromagnetic radiation that emanates from the ear canal; various manufacturers make use of different and complicated electronic circuitry to produce a temperature display. An advantage is that the reading takes only a few seconds,32 but questions remain regarding the overall accuracy of the measurement displayed. In a laboratory situation in which the auditory canal is plugged with a sponge and the probe measures only radiation that emanates from the tympanum, infrared tympanic thermometry provides an excellent estimate of the core temperature.174 In clinical settings, the results are less consistent. In one study, infrared tympanic thermometry produced core temperatures that were much more variable than rectal temperatures. Even after correcting for the higher rectal values (0.5° C [0.9° F]), tympanic measurements still inaccurately displayed one-third of the temperatures that were more than 37.7° C (99° F). An extended training program did not significantly alter the accuracy of the readings.147 In one instance, a child who arrived at an emergency department presented with tachycardia and skin vasoconstriction. Separate tympanic infrared thermometers gave core temperatures of 36.4° and 37.6° C (97.5° and 99.7° F); the rectal temperature was determined to be 42.2° C (108° F).158 Alternatively, in a hospital setting with a trained operator and immobile patients, two brands of infrared tympanic thermometers produced readings that were closer to pulmonary artery readings than those obtained from the axilla or the rectum.155 The potential benefits of a continuous and easily applied core temperature monitor have led to repeated attempts to validate liquid-crystal thermometers, which are typically placed on the head or neck surface. Unfortunately, the temperature readings produced by this method are not reliable.10,111 Because these measurements are compromised by the thermoregulatory vascular changes associated with heat conservation and heat dissipation and by changes in ambient temperature,80 they are particularly unsuited for field emergency measurements.
MEASUREMENT SITES Although the deep internal temperatures of normothermic humans are reasonably similar, no specific anatomic site represents the “official” core temperature. The temperature at each location is a consequence of a combination of the local metabolic rate, local perfusion rate, proximity to the outer shell, and proximity to other locations that have differing rates of meta bolism and perfusion. Nevertheless, because of the generally high overall rates of tissue perfusion in mammals, deep core temperatures rarely differ by more than 0.5° C (0.9° F). The temperature of the pulmonary artery is a good reference temperature for the overall status of the thermal core. At steady state, accepted sites for assessing core temperature differ with regard to varying amounts from this temperature. Esophageal and tympanic temperatures are essentially the same as the temperature of the pulmonary artery,155,166 whereas rectal temperature averages about 0.4° C (0.7° F) higher, and axillary and oral tem peratures are about 0.2° C (0.4° F) and 0.4° C (0.7° F) lower, respectively.10,110,155 Although esophageal temperature is somewhat difficult to obtain, this is the site that is most likely to accurately reflect the temperature of the pulmonary artery. Measurement at this location accurately follows changes in core temperature and is reasonably noninvasive. For placement, the probe is lubricated, and a small amount of local anesthetic is applied. It is then passed via a nasal passage into the distal portion of the esophagus to the level of the heart. The probe can be moved up and down slightly to obtain the highest temperature. Although this procedure is routinely used in physiology experiments, it is somewhat 106
unpleasant for conscious patients. Esophageal temperature is affected by swallowing for about 30 seconds. Tympanic temperature as an estimation of core temperature has long been controversial. Because the tympanic membrane is highly vascular and supplied by branches of the external and internal carotid arteries, it should be an ideal site. Nevertheless, over the years many studies have indicated that tympanic temperature is affected by ambient temperature and local facial cooling.166 Conditions under which these complications can be avoided have now been clarified: (1) if the ear canal is insulated; (2) if the thermocouple is made of fine wire and insulated except at the active junction; and (3) if the thermocouple is in direct contact with the tympanum (which causes the patient to “hear” a continuous and low-pitched sound), then alterations in core temperature are detected more rapidly than by an esophageal probe, are not affected by facial skin temperature, and are otherwise identical to esophageal temperature.166 In fact, if these conditions are adhered to during facial fanning, tympanic temperature provides a better estimate of brain temperature than do measurements made in the esophagus or the rectum.115 Accurate results were also obtained when an insulated probe was used in conjunction with an optical sensor to detect infrared radiation from the tympanum.174 Whether the conditions met in these carefully controlled studies can be duplicated in the field is unknown. In steady-state conditions, rectal temperature is a good index of core temperature, and it can also be used to estimate brain temperature.204 However, when the heat content of the body or of the internal thermal compartments is in flux, rectal temperature changes more slowly than temperatures measured in other commonly used sites.155 There is a thermal gradient along the rectum, so all measurements should be made at a standard depth; 4 cm is recommended.10 The higher temperatures recorded in this region may be caused by a combination of low perfusion rates, digestive reactions, and bacterial activity, but there is not clear evidence of this.111 For assessing core temperature during outdoor exercise in the heat, the National Athletic Trainers’ Association recommends that only rectal temperature be used.29 Oral temperature is an excellent index of core temperature, provided that the mouth is kept closed. The sublingual pocket is well perfused by blood flow, and responds quite rapidly to alterations in core temperature. Mastication, smoking, fluid intake, and mouth breathing can affect sublingual temperature; these should be avoided during the period that immediately precedes the measurement.10,110,111 The use of an electronic thermometer with a rapidly responding sensor makes this measurement considerably more accurate and rapid than when it is performed with a mercury-in-glass thermometer. Although axillary temperature does reflect core temperature, it has a number of negative characteristics and should be used only as a last resort. The axillary temperature is affected by local blood flow as well as by thermal and nonthermal sweating.10 Changes in core temperature are slow to affect the axillary temperature, and there is high interpatient variability.155 However, this measurement has proved to be particularly useful for assessing core temperature in infants.10,111
ESTIMATING MEAN BODY TEMPERATURE Mean body temperature (MBT) provides a mass-weighted average of body tissue temperature and thus can be related to the heat content of the entire body. For a severely hypothermic patient, MBT provides a way to gauge the potential fall in core temperature (afterdrop) after vessel dilation caused by rapid surface warming. Traditionally, estimates of MBT have been made with the use of a formula that combines mean skin temperature and core temperature. Recently, the validity of such estimates was evaluated for patients undergoing various procedures, including cardiac surgery during extracorporeal circulation; these studies included core temperatures as low as 18.5° C (65.3° F).106 “Peripheral compartment temperatures were estimated using fourth-order regression and integration over volume from 18 intramuscular needle thermocouples, 9 skin temperatures, and ‘deep’ hand and foot temperatures.”106 The authors concluded
TABLE 4-1 Thermal Characteristics of Select
Substances
MBT = 0.64 ( Core temperature ) + 0.36 ( Mean skin temperature ) Ramanathan151 found that a rough but reasonably accurate estimate of mean skin temperature could be provided by the temperature of the medial thigh, and that a very accurate estimate of mean skin temperature could be made by measuring and weighting the temperature of four skin sites as follows: 0.3 Chest + 0.3 Arm + 0.2 Thigh + 0.2 Leg
Physical Factors That Govern Heat Exchange: The Heat Balance Equation The physical laws that govern heat transfer determine the net energy flux into or out of the body.* The heat balance equation is a convenient method for partitioning and quantifying the flow of energy between the environment and the body. A high rate of metabolic heat production is critical for maintaining a constant body temperature in mammals. This is represented by total heat production (Htot) on the left side of the following equation. For a person whose body is at thermal equilibrium, the equation is balanced and given as follows: H tot = ± H d ± H c ± H r ± H e where Htot is the total metabolic heat production; Hd is the conductive heat exchange; Hc is the convective heat exchange; Hr is the radiative heat exchange; and He is the evaporative heat exchange. Htot is always positive. The various modes of heat exchange from the right side of the equation can be positive or negative, depending on the situation. Positive values refer to net heat loss from the body. If the equation does not balance, the body either loses or gains heat. When the sum of the net heat exchange through the various channels exceeds Htot, heat content of the body will decrease, and mean body temperature will fall. Alternatively, if Htot is greater than the net heat exchange, heat content of the body will increase, and mean body temperature will rise.
CONDUCTIVE HEAT EXCHANGE Heat transfer between objects that are in direct contact is called conduction (Hd). The direction of heat flow is always from the higher to the lower temperature. Because conduction involves a direct interaction (i.e., contact) between molecules, this type of heat transfer is minimal except under certain circumstances, such as when sitting on a cold rock with a little insulation. Under such conditions, the heat lost to the rock would be similar to that lost from the remainder of the body surface by radiation and convection. Adequate insulation should be placed under patients who are in contact with hot or cold substrates.125 The equation that governs heat exchange by conduction is kA ( Tsk − Ta ) Hd = L where k is thermal conductivity; A is the area of contact; Tsk is the skin temperature; Ta is the ambient temperature; and L is the distance between the two surfaces. The thermal conductivity of a number of substances is given in Table 4-1. Note that water has 25 times the conductivity of air but only one fifth that of granite. Muscle tissue has about twice the conductivity of fat tissue. The conduction of heat through a tissue is called thermal diffusivity. This expression is obtained by dividing the thermal conductivity by the product of the density and the specific heat. The specific heats of various substances are also given in Table 4-1. Water and muscle tissue, which consists mostly of water, have particularly high values. However, specific heats can be misleading, so the volumetric heat *References 37, 69, 124, 133, 168.
Substance Air Water Granite Muscle tissue Fat tissue
Conductivity (cal • s−1 • cm−1 • ° C−1)
Specific Heat (cal • g−1 • ° C−1)
Volumetric Heat Capacity (cal • L−1 • ° C−1)
0.000057 0.0014 0.007 0.0011 0.00051
0.24 1.0 0.2 0.8 0.5
0.29 1000 540 850 460
Data from Schmidt-Nielsen K: Animal physiology: Adaptation and environment, ed 4, Cambridge, 1990, Cambridge University Press; Cossins AR, Bowler K: Temperature biology of animals, New York, 1987, Chapman & Hall; and Hodgman CD, editor: Handbook of chemistry and physics: A ready-reference book of chemical and physical data, ed 43, Cleveland, 1962, Chemical Rubber.
capacities are also listed in Table 4-1. Although the specific heat of water is four times that of air, it takes about 3500 times as much heat to raise the temperature of a given volume of water by 1° C (1.8° F) as it does to accomplish the same feat with a similar volume of air. For someone in the water, the consequence of these properties is that skin temperature is within 1° C (1.8° F) of water temperature, and heat transfer to or from the environment is greatly facilitated. In cool water during rest, skin blood flow is minimized as a result of peripheral vasoconstriction. Heat loss is importantly determined by the subcutaneous fat layer; an average-size fat person with 36% body fat by weight begins shivering at a water temperature of about 27° C (81° F), whereas a lean person with less than 10% body fat starts shivering at about 33° C (91° F).135
CONVECTIVE HEAT EXCHANGE Convection (Hc) can be seen as the facilitation of conduction caused by the movement of molecules in a gas or liquid. This movement decreases the functional value of L, which is the denominator in the conduction equation. Convection can be either forced or natural (free). Forced convection results from gas or liquid movement caused by the application of an external force, such as the movement of a fan or the pumping of a heart. Natural convection results from density changes that are produced by heating or cooling molecules adjacent to the body. These density changes cause the molecules to move with respect to the body surface. For humans, natural convection predominates at air speeds of less than 0.2 m/sec (0.7 ft/sec), whereas forced convection is more important at greater air speeds.124 The relationships that define heat exchange as a result of convection can be complicated. They depend on surface temperature profiles, surface shape, flow dynamics, density, conductivity, and specific heat. Any factor that impedes the movement of the boundary layer (i.e., the molecules immediately adjacent to the body) greatly retards convective heat transfer. Brengelmann and Brown16 have noted that, under relatively neutral conditions (Ta = 29° C [84.2° F], wind velocity = 0.9 m/sec [3 ft/sec]), about 40% of heat loss from a nude human is mediated by convection. Increases in air or fluid velocity greatly increase convective heat transfer. Fanning a minimally clothed patient will greatly augment heat loss in a cool environment.
RADIATIVE HEAT EXCHANGE All objects at temperatures of more than absolute zero emit electromagnetic radiation. This energy transfer occurs through space and does not require an intervening medium. In any given situation, the object is both transmitting and receiving infrared thermal radiation. In some cases, the object also receives solar radiation. The net heat transfer depends on the absolute temperatures, nature of the surfaces involved, and solar input. Surfaces that are effective absorbers of radiation are also effective emitters of radiation. The idealized “black body” illustrates this property; such bodies absorb all and reflect none of the incident radiation. Conversely, poor absorbers (e.g., a polished silver surface) are also poor emitters. Heat transfer that results from 107
CHAPTER 4 Thermoregulation
that the estimation of MBT from Burton’s original formula23 “is generally accurate and precise.”106 That formula is as follows:
PART 2 COLD AND HEAT
infrared (first-term) and solar (second-term) radiation is given by the following equation: H r = σe sk e a ( Tsk 4 − Ta 4 ) + a(1 + r )s where Hr is the radiative heat exchange; s is the Stefan-Boltzmann proportionality constant; esk is the emissivity of the skin; ea is the emissivity of the environment; Tsk is the skin temperature (given in K); Ta is the ambient temperature (given in K); a is the absorptance; r is the reflectance; and s is the solar radiation. For temperatures in the physiologic range and where (Tsk − Ta) is less than 20° C (68.0° F), several authors have noted that infrared radiation heat exchange is roughly proportional to Tsk − Ta.14,168 Also of note is that the spectrum of emitted radiation depends on the temperature of the object. At physiologic temperatures, the predominant wavelengths of emitted radiation are longer (infrared), whereas, at higher temperatures (e.g., like that of the sun’s surface), the predominant wavelengths are shorter (visible radiation) and can be detected by the human eye. This difference leads to some important consequences. The middle infrared radiation that is emitted by mammals is maximal, regardless of skin pigmentation or the color of clothing. However, solar radiation peaks in the visible portion of the spectrum and is differentially absorbed. In other words, dark clothes absorb more heat from solar radiation than do light clothes, but both types emit similar amounts of radiation energy. Incident radiation can vary drastically under different environmental conditions and may severely tax the body’s ability to respond. Heat input from solar radiation on a cloudless day may exceed by several times the heat produced by basal metabolism; on a cloudless night, there is a significant net loss of radiation to the sky. Under the relatively thermoneutral conditions noted earlier by Brengelmann and Brown,16 radiant heat loss accounts for about 45% of the total.
Evaporative Heat Exchange When water changes state, a large amount of energy is either absorbed or given off. Evaporation of 1 g (0.035 oz) of water at 35° C (95.0° F), which is the usual skin temperature of a person who is sweating,168 requires the input of 0.58 kcal of thermal energy. In the field, the preferred cooling measure is to splash water on the patient, and this is coupled with air fanning.66 Heat absorbed by the evaporation of 100 cc of water will lower body temperature by about 1° C (1.8° F). In a neutral thermal environment, sweating does not occur, and evaporation accounts for only 15% of the total heat loss. Of this, slightly more than onehalf is the result of evaporation from the respiratory tract, with the remainder coming from water that passively diffuses through the skin and evaporates.16 Although it is unusual, the evaporation term (He) of the heat balance equation can become negative, which means that heat is being introduced into the body. This occurs during airway rewarming, when water-saturated oxygen is introduced into the respiratory system at about 43° C (109.4° F). Because the victim’s body is considerably colder than 43° C, water condenses in the airways. For every gram of liquid water that is formed, the body heat content increases by 0.58 kcal.
Thermoregulatory Network A regulatory system requires sensing the controlled variable, comparing it with an ideal value, and producing an appropriate output signal. In the following sections, the role of the nervous system in maintenance of a stable body temperature is outlined.
PERIPHERAL THERMAL SENSORS The entire outer surface of the body is well supplied with sensitive thermoreceptive structures. Because one destination of the output of these transducers is the sensory cortex, many properties of the receptors can be gleaned from direct experience. Afferent thermal information produces both hot and cold sensations, and it is particularly rate sensitive. In addition to cortical input that arrives via the medial lemniscus and the ventrobasal thalamus, the brain receives a large amount of thermal information from 108
pathways that synapse in the reticular area.20 Although cortical thermal input is part of the sensory information that is used to reconstruct the external thermal environment, reticular inputs are more important to the behavioral and autonomic regulation of body temperature.43 This distinction was pointed out by Cabanac,26 who found that internal body temperature determined whether a particular surface temperature was perceived as pleasant or unpleasant. However, altered body temperature did not affect the discriminative (cortically mediated) aspects of the thermal stimulus; subjects had no problem correctly identifying the actual peripheral temperature. This study also confirms the intimate relationship between the thermoregulatory network and the pleasure–pain system.142 The structure, location, and properties of peripheral thermoreceptors are well documented. Thermal sensors are free nerve endings, and they are categorized as either warm or cold. Cold receptors are found immediately beneath the epidermis, whereas warm receptors are located slightly deeper in the dermis. The hallmark of both types of receptors is their extremely high rate sensitivity (Figure 4-3, online). Although the static firing rate of cold receptors is usually less than 10 impulses per second, under conditions of rapid temperature change, firing rates are often higher by an order of magnitude. Cold receptors are excited by cooling and inhibited by warming, and they have static maxima at about 25° C (77.0° F); these receptors are active from about 10° C (50.0° F) to 40° C (104.0° F). Warm receptors are excited by warming and inhibited by cooling, and they have static maxima at more than 40° C; they are active from about 30° C (86.0° F) to 45° C (113.0° F). At both ends of the spectrum, more extreme temperatures activate neuronal responses that are phenomenologically reported as “cold pain” and “warm pain.”72 Recent work with the use of cloning and ion-channel characterization has elucidated peripheral temperature transduction mechanisms. A family of related temperature-activated transient receptor potential (TRP) ion channels is highly sensitive to temperature. The cloned receptors TRPV3 and TRPV4 respond over a range similar to that of the warm receptors just described, whereas TRPM8 responds similarly to the cool receptors. TRPM8 also responds to menthol, eucalyptol, and icillin.117,146 TRPV1, TRPV2, and TRPA1 respond similarly to the heat-pain–sensitive and cold-pain–sensitive neurons. The heat-pain channels (vanilloid receptor 1 [VR1]) also respond to low pH, ethanol, and capsaicin, which is the active ingredient in chili peppers.144 Alternatively, TRPM2, TRPM4, and TRPM5 respond to warm temperatures and involve insulin secretion187 and taste.183 However, they are not regarded as warm receptors for thermal sensation, because sensory neurons have none of those receptors. In addition to TRP channels, TREK-1 and TRAAK channels may also be related to control of warm and cold perception.137 Psychophysical and physiologic studies indicate that thermal receptors are not uniformly distributed across the body surface and that there are far more cold receptors.72 Cold receptors are abundant in the face and trunk areas, especially in the lips; however, they are less numerous in the feet and lower legs. The face and fingers have a greater number of warm spots.153,181 Threshold temperature for the perception of thermal sensation follows the anatomic distribution and is not uniform across the body. The face, particularly near the mouth, is exquisitely sensitive, whereas the extremities, by comparison, have poor sensitivity. Other regions of the body are intermediate in sensitivity.179 Because peripheral thermal input is intimately involved in regulation of body temperature, heating and cooling different body sites can differentially affect the magnitude of the restorative physiologic response produced. In one study, cooling the forehead was found to be more than three times as effective (per unit area) for decreasing ongoing sweating as was cooling the lower leg.41 A separate study evaluated regional trunk and appendage sensitivity to cooling by assessing the magnitude of the gasping response that occurs at the onset of immersion. In this case, exposing various parts of the body to water at 15° C (59.0° F) indicated that the upper torso had the greatest cold receptor density or sensitivity (or both). The lower torso was somewhat less sensitive, with the arms and legs exhibiting similar but considerably lower sensitivity.22
Many sites within the body are capable of eliciting generalized thermoregulatory responses. Such areas include the abdominal viscera, spinal cord, hypothalamus, and lower portions of the brainstem.12,69 The genesis of input to the regulator that results from heating or cooling these areas is poorly understood. Some of the effects may result from modulation of synaptic connections rather than from stimulation of specific thermodetectors per se. Input from central detectors is not rate sensitive; rather, it is a direct reflection of the absolute temperature. The area with the highest thermal sensitivity and that has received the greatest amount of experimental attention is the preoptic area/anterior hypothalamus (POAH). Heating or cooling this portion of the brainstem elicits the entire array of autonomic and behavioral heat loss and heat gain responses, respectively.68 Neurons in this portion of the brain exhibit both warm sensitivity and cold sensitivity.12 Recent work on hypothalamic slice preparations with the use of synaptic blockers has indicated that warm sensitivity may be an inherent property of some of the POAH neurons, whereas cold sensitivity in this area of the brain requires synaptic input.12,45 Figure 4-4, online illustrates the effects of temperature on the firing rates of three representative types of hypothalamic neurons. The high level of temperature sensitivity shown by one of the cells (labeled “C”) results from the temperature-dependent characteristic of the prepotential. Voltage-clamp experiments indicate that the altered rate of depolarization is most likely the result of an effect on hyperpolarizing (K+) conductances.64 Work involving the use of hypothalamic slices has also established that about one-half of the thermosensitive neurons also respond to nonthermal stimuli such as osmotic pressure, glucose concentration, and steroid hormone concentration. Such neurons could form the basis for the interactions between the homeostatic systems that are described later in this chapter. Figure 4-5, online illustrates the response of a warm-sensitive POAH neuron in a slice preparation. This cell is excited by increased temperature, low glucose, or increased osmotic pressure.13 TRPV protein expression has been detected in the POAH; thus, it was proposed that the TRPV channels may underlie the thermosensitivity found in POAH neurons144 and that both TRPV1 and TRPV2 channels may be active within the physiologic range of temperature.93,149 However, a large body of evidence is at odds with the proposal of TRPV1 as a thermosensor.157 Furthermore, TRPV channels respond to warming with persistent inward cationic currents, and this would produce a change in the resting membrane potential. In the POAH, both warm-sensitive neurons and temperature-insensitive neurons show identical membrane potential responses to temperature change.203 In addition, several in vivo studies have shown that TRPV1, TRPV3, and TRPV4—all of which are expressed in the hypothalamus—are not likely to be involved in thermoregulation in either the heat or the cold.31,107,118 It is more likely that POAH warm sensitivity is caused by brief ionic currents that determine the rate of change in depolarizing the prepotentials that occur between two successive action potentials.64
REGULATOR As mentioned previously, the brain is capable of accurately regulating body temperature under a wide range of conditions. Although almost all portions of the central nervous system can potentially be involved, the most critical neuroanatomic structures for thermoregulation include the spinal cord, brainstem, hypothalamus, and septum. The preoptic area and anterior hypothalamus are particularly important for both integration and sensing of internal temperature.68,70 Recent advances in neurophysiologic and neuroanatomic techniques have been used to extend our understanding of the systems involved in regulation of body temperature; a number of excellent sources document this progress.11,122,200 Notable advances include demonstration of the relative independence of populations of neurons that control separate effector systems91,202 and elucidation of a pathway that conveys cold-sensitive afferent (feed-forward) information to the hypothalamus.131
A schematic model for regulation of body temperature is presented in Figure 4-6. Credit for much of the information and organization in the figure comes from the authors listed in the figure legend as well as from many others in the field. For ease of understanding, many aspects of the system’s complexity have been simplified or modified. Among the many inputs to this system that are not shown include those mentioned in the section about central thermoreceptors (e.g., glucose concentration, osmotic pressure) as well as factors that are covered later in this chapter (e.g., time of day, hormone levels, pyrogen titer, oxygen concentration of the blood). In addition, central thermoreceptors from many locations in the body provide input to this system. The key sensing elements of Figure 4-6 involve the peripheral warm and cold receptors and the central thermodetectors, the latter of which are depicted by solid cell bodies and bold axons. Peripheral input originates in the skin and enters the central nervous system via the spinal or trigeminal dorsal horns; this information ascends to both the midbrain and the thalamus. The thalamic neurons that receive thermal information project to the sensory cortex and subserve sensory integration and localization of peripheral thermal information. They are also likely involved to some degree in learned behavioral thermoregulatory responses. Thermal afferent pathways reaching the midbrain are involved in the feed-forward aspect of regulation.131 Axons of the cell bodies in the midbrain synapse on cells in the midline subregion of the preoptic area. These preoptic cells receive excitatory input from peripheral warm and cold sensors, but they inhibit the cells upon which they synapse. The systems that subserve heat loss and cold defense act as if they reciprocally inhibit each other and receive output from a unitary integrating system. However, as mentioned previously, the systems are actually functionally separate to a large degree. In the schema of Figure 4-6, both systems depend on inherently warm-sensitive cells that have a high spontaneous firing rate at normal body temperatures. These cells inhibit the succeeding neurons, but the connections are such that, in a cold environment or when the body temperature is below normal, cold defense responses are disinhibited and heat loss responses are further suppressed. The opposite would occur in a warm environment or when the body becomes excessively hot. The output of these systems under different conditions is illustrated in the panels below the neuroanatomic diagram of Figure 4-6. The middle panel illustrates the situation for a person with a body temperature of 37° C (98.6° F) in a thermoneutral environment. At 37° C (98.6° F), both systems are inhibited, and there is no effector response. If the body cools or becomes warmer, the inherently temperature-sensitive neurons disinhibit either the cold defense or the heat-loss system. The panel on the left illustrates the action of the feed-forward cold neurons in a cold environment. Although the inherently thermosensitive neurons do not change their firing rate as a result of a local temperature that stays constant, input from the peripheral cold-sensitive pathway disinhibits the cold defense system. A similar situation—but in reverse—occurs when a person encounters a warm environment; that situation is depicted in the right panel. The error signal or output driving force is shown as the difference between the horizontal dashed line and the effector output at a given body temperature. The system is extremely accurate, and the error signal created by peripheral feed-forward input is usually just sufficient to counteract the sensed disturbance and to maintain body temperature at a constant level. In addition to autonomic responses that are organized and transmitted from the brainstem (e.g., sweating, shivering), various complex whole-animal responses are also activated by the thermoregulatory system. Postural reflexes (e.g., huddling, sprawling) and complex learned behavioral thermoregulatory responses are initiated by cold and warm error signals. Although the mechanism is not understood, appropriate behavior reduces the error signal and activates the reward system, which likely culminates in the release of dopamine in the nucleus accumbens of the septum via cell bodies located in the ventral midbrain.81 109
CHAPTER 4 Thermoregulation
CENTRAL THERMAL SENSORS
Preoptic area/ anterior hypothalamus
GABA
ac
G L U G A B A
+
+
−
Thalamocortical relay
− − − oc
Midbrain Lateral parabrachial nucleus
+
Reward system activated when thermal deficit decreased
+
GLU
Rostral ventro– medial medulla Rostral raphé pallidus
G L U
+
Postural reflexes Sprawl Huddle
− G A B A
Learned behavioral responses— integrate cortical, limbic, and brainstem information
+
To final autonomic organization and output
Collateral fibers ascending to midbrain Dorsal horn– spinal column Input from cutaneous temperature receptors
FIGURE 4-6 A simplified schematic diagram of the basic parts of the nervous system responsible for regulating internal body temperature. Details of how this system functions are given in the text. ac, Anterior commissure; GLU, glutaminergic synapse; GABA, GABAergic synapse; oc, optic chiasm. (Anatomic, neurophysiologic, and conceptual concepts represented in this image are from Boulant JA: Neuronal basis of Hammel’s model for set-point thermoregulation, J Appl Physiol 100:1347, 2006; Hammel HT: Regulation of internal body temperature, Annu Rev Physiol 30:641, 1968; and Morrison SF, Nakamura K, Madden CJ: Central control of thermogenesis in mammals, Exp Physiol 93:773, 2008. These articles should be consulted for a more rigorous explanation of the details of the thermoregulatory system.)
Sweat Vasodilation
+
Cold skin
Increase metabolic heat production Vasoconstriction
To thalamus
+
Heat loss Cold defense
Warm skin
+ Effector output
PART 2 COLD AND HEAT
Cerebral cortex Sensory integration and localization of peripheral thermal information
Dorsomedial hypothalamus
0
0 35
37
39
Cold environment
0 35
37
39
Core temperature (° C) Neutral environment
35
39
Warm environment
Effector Responses VASCULAR ADJUSTMENTS Excellent overviews of the role of the vasculature in coping with thermal stresses are available.16,33 One function of the circulatory system is to maintain a relatively homogeneous internal body temperature. Heat from metabolically active organs is convectively distributed to portions of the body where less heat is produced. More commonly appreciated are alterations of blood flow patterns that increase or decrease the overall thermal conductivity of the body during exposure to hot or cold environments, respectively. Some of these alterations in conductivity result from the preferential shunting of peripheral blood flow superficial or deep relative to the subcutaneous fat layer. Indeed, fat has about one-half the tissue conductivity of muscle. Nevertheless, shunting blood away from major portions of the body is at least as important for determining overall conductivity as is the conductive property of the tissue itself. For example, during immersion in cold water, muscle accounts for about 90% of the total tissue insulation of the forearm.48 Thus directing blood away from poorly insulated (and more highly conductive) regions reduces heat loss and preserves core temperature. In addition to capillaries, microcirculatory units contain arterioles, metarterioles, and arteriovenous anastomoses. Flow through all of these vessels is under the control of smooth muscle. The smooth muscle of precapillary sphincters is largely 110
37
influenced by local factors such as the partial pressures of oxygen and carbon dioxide, whereas the other vessels are well supplied with receptors that respond to both neuronal and endocrine inputs. Glabrous skin (i.e., the palms, lips, and soles) contains numerous arteriovenous anastomoses and is innervated only by sympathetic vasoconstrictor fibers. Nonglabrous (i.e., hairy) skin is innervated by sympathetic vasoconstrictor and vasodilator fibers and contains few arteriovenous anastomoses. The vasoconstrictor system acts primarily through α-1 and α-2 adreno ceptors. By contrast, the active vasodilator system makes use of acetylcholine. This was verified by experiments that involved intradermal injection of botulinum toxin, which blocks the release of acetylcholine.96 However, in the same experiments, involvement of an unidentified cotransmitter was also suggested. Vasoactive intestinal polypeptide is a likely candidate, because nitric oxide is an important end product for inducing active vasodilation.6 About 90% of the elevation in skin blood flow during heat stress is a result of input from the active vasodilator system, and, of this, about 30% is the result of nitric oxide.6 Thermoregulatory skin blood flow can reach up to 8 L/min and involve 60% of the cardiac output.33 Operation of the vasomotor effector system is affected by excessive exposure to ultraviolet B radiation. Moderate sunburn impairs the vasoconstrictor response to cold; an associated uncontrolled increase in thermal conduction is still present 1 week after exposure, although the original erythema will have disappeared.140
Vascular changes are bioenergetically the least costly thermoregulatory autonomic effector response. Because of the high sensitivity of the vasomotor system, ambient temperatures between the thresholds for sweating and shivering are often referred to as being in the zone of vasomotor regulation. If a particular vascular bed is kept at a relatively constant temperature, output from the central nervous regulator can be assessed. Under these conditions in dogs, manipulations of hypothalamic temperature confirm a high level of vasomotor activity between the thresholds for the activation of panting and shivering.71 In humans, forearm blood flow increases rapidly as core temperature rises; a sixfold increase in blood flow can occur with a core temperature that has risen to only 38° C (100° F).191 Within the vasomotor zone (i.e., skin temperatures of 33° to 35° C [91.5° to 95.1° F]), core and skin temperatures linearly combine to control skin blood flow. Skin blood flow responds accurately and rapidly to changes in skin temperature, which leads to a very stable core temperature.17 Although most peripheral arterioles are well supplied with adrenergic receptors, output from the thermoregulatory centers is not homogeneously distributed. Extensive nervous inputs from the thermoregulator occur only in the lips, ears, and distal extremities; thus immersing the feet in cold water leads to marked vasoconstriction in the hands and forearms but not in the abdomen or upper arms.63
LOCAL MODULATION Local temperature has a great effect on the vasomotor status of the peripheral vessels, and, in some cases, may be largely responsible for the observed thermal conductivities. Local heating produces a biphasic response. Initial dilation occurs in a few minutes and depends on release of various factors from the nerve ending. The VR1 receptors mentioned previously are involved in this response. The longer-lasting second phase of dilation is not dependent on local nerve endings, and involves nitric oxide. Local cooling can decrease superficial cutaneous blood flow to almost zero.33 Although vascular beds on the skin surface constrict in response to cooling, other vascular beds dilate when cooled.51 The specific response to cold shown by cutaneous vessels follows from the observed distribution and properties of the α-adrenergic vascular receptors. Although in most of the vasculature α1-receptors predominate, in the superficial cutaneous areas, α2-receptors constitute a clear majority. The usual predominance of α1-receptors is found in the deeper blood vessels. Local temperature affects the α2- and α1-receptors in a reciprocal manner. Although cooling augments the response of the α2-receptors, it either inhibits or does not affect the response of the α1-receptors. Thus cooling the skin not only constricts the superficial vessels but also concomitantly dilates many underlying vessels. The ensuing flow pattern increases tissue insulation and augments countercurrent exchange between incoming cool blood and outgoing warm blood.51,53 Although initial work was done on canine vessels, subsequent studies that involved α-adrenergic agonists and antagonists have demonstrated that a similar mechanism exists in human fingers.49,52 The responsiveness of cutaneous blood vessels is diminished in people with type 2 diabetes mellitus. The increased incidence of this disorder among the general population presages a greater number of patients exhibiting severe hyperthermia.33
Evaporative Responses At high workloads and at environmental temperatures approaching 37° C (98.6° F), the only way to maintain thermal balance is to augment evaporative cooling by mobilizing the eccrine sweat glands. This sympathetic and cholinergically innervated organ system is spread over the entire body surface, but it is more profuse in some areas than in others. A person who is acclimatized to heat can produce several liters of sweat per hour.76 High rates of sweating occur on the forehead, neck, anterior and posterior portions of the trunk, and dorsal surfaces of the hands and forearms. Low rates occur on the medial femoral regions, lateral trunk areas, and
palms and soles.133 Sweat is secreted in these latter two areas in response to emotional rather than thermal inputs.16 Sweating is cholinergically mediated, and can be completely abolished by atropine. Sweat gland activity interacts with the regional vasculature; metabolic products of active sweat glands increase blood flow in areas of active sweating. In well-hydrated individuals, the degree of anhidrosis is correlated with the severity of generalized autonomic failure.63,109 Several reviews discuss the many aspects of sweating disorders.34,109
CENTRAL SIGNAL By controlling the local milieu at different skin sites, it has been possible to separate the central thermoregulatory drive to sweat glands from local effects on the glands themselves. The central thermoregulatory system provides a proportional output that is influenced by both internal and whole-body skin temperatures. Per degree increase above thermoneutral values, internal temperature is about 10 times as important as is mean skin temperature for eliciting an output to the sweat glands.126,128
LOCAL MODULATION Local effects are also important for determining the output of sweat glands. Temperature exerts a multiplicative effect on sweat secretion; the Q10 for this augmentation is about 3.70. In addition, skin wetness has an important local effect on sweat glands. The wetter the skin, the greater the suppression of sweating.127 Moderate sunburn disrupts evaporative cooling. This effect is locally mediated and involves decreases in both responsiveness and capacity of the sweat glands.141
Metabolic Responses Heat is an inevitable by-product of the inefficiencies of the body’s metabolic reactions. When oxidizing foodstuffs to carbon dioxide and water during adenosine triphosphate (ATP) production and transferring the ATP produced to the functional systems of the cells, about 75% of the original chemical potential energy appears as heat. With the exception of excreted or that used to perform physical work, the remaining 25% of the original energy is also converted to heat when ATP is used in the numerous metabolic reactions of the body.169 Mammals—as compared with poikilotherms such as reptiles or fish—use much more ATP to maintain ionic and electrochemical balances of the cells178 and for many other functions. This leads to greatly increased metabolic heat production, which forms the basis for homeothermy. It also creates the need to maintain a substantial thermal gradient between the body and the environment to dissipate the high levels of heat that are produced. An increased rate of metabolism above basal levels is critical for maintenance of body temperature in cold environments. The elevated heat production is derived from shivering and non shivering responses. Shivering consists of simultaneous rhythmic excitation of agonistic and antagonistic skeletal muscles. Under normal circumstances, carbohydrate oxidation provides the major substrate for shivering. In glycogen-depleted individuals, shivering levels are maintained by the greatly increased oxidation of lipid and protein reserves.67 Nonshivering heat production is associated with the presence of uncoupling protein 1 in brown adipose tissue. Uncoupling protein 1 is a transmembrane protein that is located in the mitochondrial inner membrane, which, on activation by the sympathetic nervous system, allows for protons to reenter the mitochondrial matrix without passing through ATP synthase. Because the energy released during substrate oxidation is not conserved as ATP, heat is generated. Although brown adipose tissue was believed to be of little importance in adult humans, recent research has indicated the presence of potentially significant amounts of active brown adipose tissue in adults.44,162 There is evidence that both epinephrine and thyroid hormones are released in humans after cold exposure.56 Because these hormones augment overall tissue metabolism, they are components of the response to cold environments. In the absence of thyroid hormone, metabolic heat production is reduced by 111
CHAPTER 4 Thermoregulation
CENTRAL SIGNAL
PART 2 COLD AND HEAT
30% or more. Thyroid hormone acts by both accelerating ATP turnover and reducing efficiency of ATP synthesis.175 Basal metabolic rate, when calculated on a weight-specific basis, decreases with body size. This relationship holds within as well as across species. Because drug potency as determined by the rate of inactivation is most closely related to metabolic rate, when drug dosing is extrapolated to persons of different sizes, it should not be done on a per-kilogram or per-pound basis unless the weights are similar. Basal metabolic rate relates to size according to the following equation:168 2 = ( 0.676 )M b 0.75 VO 2 is oxygen consumption in L/hr and Mb is body mass where VO in kg.
CENTRAL SIGNAL Of the various thermoregulatory outputs, metabolism is the easiest to evaluate quantitatively; the most complete documentation is available for this response, and most models of the thermoregulatory system are based on this information. Experiments on medium-size mammals have allowed for separate thermal manipulation of various parts of the brain, body core, and skin. This work has made it clear that the thermoregulatory centers act as a proportional controller and that skin temperature provides a feed-forward input to the system.68,84 Thus greater decreases in either core or skin temperature or both below neutral values elicit proportionally larger compensatory increases in metabolism. In addition to an impaired ability to generate metabolic heat, hypothyroidism is also associated with a decrease in regulated core temperature of about 1° C (1.8° F).196 Evidence indicates that humans have a control system similar to that of medium-sized mammals. In a summary of their data and of that collected previously, Hong and Nadel77 noted that central output for shivering is augmented by increased rate of skin cooling. They also concluded that a given decrease in core temperature elicits 10 to 20 times the metabolic response of an equivalent decrease in mean skin temperature. Exercise is not incompatible with shivering, but increased levels of exercise exert increasing degrees of suppression on the shivering response, possibly as a consequence of an increased arousal response.77
LOCAL MODULATION Although the central and local effects of decreased core temperature on shivering have not been directly partitioned, both inputs are important. Slight decreases in core temperature create large compensatory responses, as delineated previously. However, even moderate hypothermia decreases the metabolic response to cold, and, at about 30° C (86.0° F), the shivering response is lost.16 This decrement must involve nervous system malfunction, because the muscles themselves are quite responsive below this temperature. For example, limb muscles and diaphragm muscles develop peak tensions that are not greatly affected by temperatures down to 25° C (77.1° F), and fatigue resistance is considerably increased at 25° C (77.1° F).150,170 Likewise, altering the skin and superficial muscle temperature of the anterior thigh through a range of temperatures between 12° and 40° C (between 53.6° and 104.0° F) for 30 minutes had little effect on subsequent isometric peak torque production during isometric knee extensions to exhaustion. Time to fatigue was longer at the coolest temperature.186
Behavioral Responses In most wilderness situations, a variety of ambient temperatures is available, and external insulation is easily adjusted. Under these conditions, the choice of thermal microenvironment and clothing provides a far higher gain than any of the autonomic effector systems discussed previously. Whole-body adjustments are achieved by all motile animals, and are particularly well developed in vertebrates.40 In addition to moving the body, the somatic effectors are important for optimizing autonomic responses to thermal stress. Thus spreading out the arms and legs during heat stress increases the surface area available for the 112
autonomic augmentation of conductive, convective, evaporative, and radiative heat losses. Cabanac26 found that internal body temperature determined whether a particular surface temperature was perceived as pleasant or unpleasant. When subjects were hypothermic, a warm stimulus applied to the hand was experienced as pleasant and a cold stimulus as unpleasant. The opposite responses were observed in hyperthermic subjects. An overall sensation of thermal pleasantness is obtained when environmental conditions are appropriate for maintaining a normal body temperature with no fluid or energy expenditure. However, altered body temperature did not affect the discriminative (cortically mediated) aspects of the thermal stimuli; subjects had no problem correctly identifying the actual peripheral temperature. This study also confirmed the intimate relationship between the thermoregulatory network and the pleasure–pain system.142
CENTRAL SIGNAL As compared with the knowledge about autonomic thermoregulation, we know little about the neural mechanisms that underlie behavioral thermoregulation. As noted in previous sections, the preoptic area plays a key role in autonomic thermoregulation. Animals with lesions of the POAH are severely compromised with regard to their ability to use autonomic thermoregulatory effectors; however, their ability to behaviorally thermoregulate is relatively intact.28,164 These results indicate that the preoptic area is not as crucial for behavioral thermoregulatory processes as it is for autonomic processes.27,163 Alternatively, lesions of the lateral hypothalamus, which is involved in various reward systems, result in the loss of behavioral thermoregulation.165 Recent studies involving the use of positron emission tomography and functional magnetic resonance imaging have demonstrated that temperature signals from the body surface reach the insular cortex.38,79,138 However, insular activation correlates with the discrimination between hot and cold rather than with thermal pleasure, so this system is likely minimally involved with behavioral thermoregulatory processes. Alternatively, thermal pleasantness is clearly important for behavioral thermoregulation. In studies involving functional magnetic resonance imaging, it has been shown that activation of the amygdala, mid-orbitofrontal and pregenual cingulate cortices, and striatum is correlated with thermally related pleasant and unpleasant feelings.91,156 Because behavioral processes are usually activated before body core temperature changes via the feed-forward system, signals from the skin are important. However, severe deviations in core temperature disrupt this system. When this occurs, the person no longer feels too hot or too cold, and the desire to take corrective action is lost. Regional differences in the contribution of the body surface to thermal comfort are present.132 Facial cooling produces the most pleasant experiences during mild heat exposure, whereas during cold exposure, local warming of the chest and abdomen leads to the most pleasant sensations. This would induce us to preferentially cool the head in the heat and to huddle or add clothing to warm the torso in the cold.
LOCAL MODULATION As with shivering, most problems that involve behavioral temperature regulation probably emanate from disruption of centrally generated output. The muscles used to move the body are fairly resistant to thermal incapacitation, as described previously; however, if this occurs, a major disruption of the body’s thermal defense ensues.
Important Modifications of Thermoregulatory Responses In addition to establishing the status of the body temperature when the regulatory system is functioning normally, monitoring body temperature provides a significant diagnostic indicator for many pathologic conditions. Whether the goal is to stabilize or monitor the body temperature, it is necessary to understand the
NORMAL VARIATIONS IN THE REGULATED TEMPERATURE AND IN THE ABILITY TO MAINTAIN BODY TEMPERATURE The same body temperature can represent a different state of affairs even under regularly encountered circumstances. Some of these conditions are noted here. Level of Activity Activity normally leads to increases in body temperature. However, the level of activity does not appear to provide direct input to the regulator of body temperature, unlike the feedforward input that is received from the peripheral temperature. Thus, the magnitude of the error signal for increased heat dissipation is determined simply by the increase in body temperature.180 Someone who is exercising heavily (or who has just exercised) in a neutral environment will have an unusually high body temperature, whereas someone who is sleeping or resting quietly will have a relatively low body temperature. At a given level of exercise, core temperature will plateau 30 to 40 minutes after the exercise is initiated; higher levels of exercise result in higher plateau levels of the core temperature. For someone who is working at 50% of their maximal aerobic capacity, the increase in core temperature is about 1° C (1.8° F).135 Circadian Changes Body temperature shows cyclic changes throughout the day. Some of this variation is the result of the daily cycle of activity, as described previously. However, there also exists a circadian rhythm for the regulated body temperature. This sinusoidal rhythm accounts for much of the observed variations in body temperature. In a study that involved 700 observations of 148 healthy individuals, the daily mean oral reading was 36.8° C (98.2° F). However, this was only a midpoint; the mean earlymorning low was 36.4° C (97.6° F), and the mean late-afternoon high was 36.9° C (98.4° F).135 These diurnal changes definitely reflect alterations in the controller, because the body temperature thresholds for eliciting sweating and peripheral vasodilation are significantly lower in the early morning than in the afternoon or evening, whereas the sensitivities and maximal response levels remain unchanged.2,3 The body’s biologic clock may directly modulate the body temperature rhythm. The suprachiasmatic nucleus in the hypothalamus is the main pacemaker for the circadian system of the body. The core molecular mechanisms of the circadian clock, which consist of autoregulatory transcription and translation loops by the clock genes, show a periodicity of approximately 24 hours. Removing the circadian clock abolishes the body temperature rhythm as well as the circadian influences on thermoregulatory responses.130,188 Thermoregulatory responses to exercise are affected by the circadian time. At the daily low (5:00 AM), the perceived exertion for a standardized task is the greatest, and thermoregulation is less effective than at the time of maximum temperature (5:00 PM). At the time when the body temperature is rising at the fastest rate (11:00 AM), heat loss mechanisms are less responsive; alternatively, at 11:00 PM, when the body temperature is falling at the fastest rate, heat loss mechanisms are much more responsive.190 An excellent overview of body temperature cycles is available.154 Interindividual Differences Most oral temperature measurements are between 36.0° C (96.9° F) and 37.1° C (98.9° F) in the early morning. Corresponding values for the late afternoon are 36.3° C (97.4° F) and 37.4° C (99.4° F). On the basis of interindividual differences and diurnal changes, it has been suggested that the upper limit for a normal oral temperature should be 37.2° C (98.9° F) in early morning, which then increases gradually to 37.8° C (99.9° F) by early afternoon and remains at that level until early evening.110 These values delineate the 99th percentile for body temperature observed during the respective time periods.
Alternatively, it is important to be aware that the normal body temperature of some individuals falls outside of population norms. The authors encountered one person whose core temperature was consistently 35.5° to 36° C (95.9° to 96.8° F). This person mentioned that on one occasion he had felt chills and malaise, but he was told by his physician that his temperature of 37° C (98.6° F) was normal. However, for this person, it was not; his core temperature of 37° C (98.6° F) in fact represented a febrile state. Many individuals with atypical body temperatures are aware of their condition, and it is prudent to ask about this possibility. Age The circadian rhythm of body temperature develops soon after birth. Although newborns display small-amplitude rhythms, the patterns are not circadian. Circadian rhythmicity begins to develop during the second and third weeks of life, and, after a progressive increase in amplitude, the typical adult temperature rhythms are reached by the age of 2 years.154 Under thermoneutral conditions, rectal temperatures of older adults are similar to those of younger people, whereas oral and axillary temperatures are slightly lower.88 Of the major regulatory systems, temperature regulation is unique in the extent to which the effector organs are “borrowed” from other systems. This makes developmental assessments difficult, because functional changes may be secondary to changes in primary systems such as the skeletal muscles or the blood vessels. Other difficulties, which have been detailed by Cooper,36 include inconsistencies between chronologic age and physiologic viability and the increased incidence of interfering disease states and cerebral microinfarcts as aging progresses. Thermoregulatory capacities of the young show a progressive increase, but they are not fully developed until after puberty. Effectors that are more important to infants than to adults include certain behavioral responses (e.g., calling for help) and the ability to activate thermogenic brown adipose tissue. Shivering is not present in infants; it develops fully only after several years of nervous system maturation. Metabolism in infants is increased to some degree by the increase in motor activity that accompanies cold stress.97 Sweating is present and effective in children, but the typical high capacity for evaporative heat loss that is present in adults is attained only during the changes that occur with puberty.50 Factors that affect loss of body heat during cold stress throughout the adult years have been investigated with a multiple regression analysis to evaluate fitness, fatness, and age from the 20s to the early 50s. Fitness has no effect, but fatness retards heat loss. Aging during this period is correlated with progressive weakening of the vasoconstrictor response to cold.21 Individuals in their late 60s and beyond have a definite decrease in thermoregulatory capacity. Sweating is lessened in response to passive heating,82 vascular responses to heating and cooling are significantly reduced,94,97 and a distinct shivering tremor is rarely observed.97 In older adults, thermoregulatory sympathetic nerve impulses to the skin are reduced by 60%,62 and there is lower resting metabolic rate.192 Young children and older adults are, without a doubt, particularly vulnerable to thermal extremes and should be given treatment priority when possible. Both groups are susceptible to climatic heat injury, and, when their core temperatures exceed 40° C (104° F) and are accompanied by altered mental status, treatment should be immediate, even at the risk of misdiagnosing a febrile condition. As for all such cases, most clothing should be removed; ice, if it is available, should be placed around the groin, in the axillae, and around the neck. Cool water should be sprayed on the skin, and then the individual should be fanned. Blood gas and electrolyte status should be determined and any appropriate treatment measures taken.25,30 Gender Women have a number of physiologic and morphologic characteristics that produce subtle differences in the regulation of body temperature. Such attributes include smaller blood volume, lower hemoglobin concentration, smaller heart, smaller lean body mass, greater percentage of subcutaneous and total body fat, greater surface area–to–mass ratio, higher threshold core temperature for 113
CHAPTER 4 Thermoregulation
many conditions that affect both the regulated temperature and the effectiveness of the thermoregulatory system. In the following sections, these circumstances are elucidated.
PART 2 COLD AND HEAT
cutaneous vasodilation and sweating, greater resting vasoconstriction in the hands and feet, geometrically thinner extremities, and cyclic changes in sex hormone levels.120 Some reports have shown that when age, thermal accli mation, body size, maximal aerobic capacity, cardiovascular responses during exercise, and relative workload are matched, thermoregulatory gender differences are relatively negligible.58 Nevertheless, in situations such as those encountered in the U.S. Navy, men and women do not tend to be matched for such nonthermoregulatory factors, and different thermal exposure standards may be required for different genders.65 The menstrual cycle, menopause, and pregnancy are all associated with important effects on the thermoregulatory system. Relative to the early follicular phase of the menstrual cycle, core temperature is typically 0.3° C (0.5° F) higher during the late follicular phase and 0.7° C (1.3° F) higher during the luteal phase.102 Postmenopausal hot flashes are experienced by most women and involve increases in sweating, vasodilation, and heart rate. Heat and exercise may be particularly stressful during and after these episodes. The proximate mechanism appears to involve estrogen activating the central noradrenergic system53 as well as circulating serotonin levels.116 In addition, hot flashes may be associated with activation of the insular cortex.54 Some information about hormonal effects has been gained by studying postmenopausal women who are undergoing hormone replacement therapy. Administered estrogen acts to lower the core temperature at which heat loss effector mechanisms are activated and results in lowered core temperature. The addition of exogenous progestins blocks these effects.18 By contrast, animal studies have shown that estrogen acts to augment heat production78 and to maintain core temperature in the cold.189 Epidemiologic studies have indicated that lower testosterone concentration may be associated with the sensation of cold.60 Pregnancy is of special concern to the physician in the wilderness. This concern does not apply to well-hydrated women who are exercising at submaximal levels, because the thermoregulatory system makes adaptive adjustments as pregnancy proceeds. In the course of a pregnancy, basal body temperature shows a continuous decline, and heat-loss responses are elicited at progressively lower levels so that, near term, the steady-state temperature during exercise is about 1° C (1.8° F) lower than it was before conception. This reduces thermal stress on the fetus, which is typically 0.5° C (0.9° F) warmer than the mother.35,177 However, concern is warranted if hyperthermia develops in pregnant women. Animal experiments and epidemiologic analysis both indicate that, during pregnancy, it is dangerous for body temperature to exceed 39° C (102.2° F). During the first half of pregnancy, excessive body temperature is likely to produce birth defects; during the latter half, birth weight is more likely to be affected. The fifth week after conception, which is the period of neural tube closure, is a particularly vulnerable time for the fetus.108 Because women in the early stages of pregnancy may be unaware of their condition, it is critical that heat stress be promptly treated in women of childbearing age. When exercising, it is important that pregnant or potentially pregnant women acclimatize gradually to extreme thermal environments, remain well hydrated, wear loose-fitting clothing, exercise at a comfortable pace, and avoid swimming in warm water or immersing themselves in hot tubs.177 A program of water aerobics for pregnant women was reported to decrease requests for analgesia when these women gave birth, and was not found to be detrimental to the health of the mother or the child.4
Induced Alterations of the Regulated Temperature The optimal body temperature is not always the same. In certain conditions of stress or vulnerability, the regulated temperature of the body may be altered; this is often an adaptive response to a particular physiologic crisis. Some of these situations are delineated in the following sections of this chapter. In such circumstances, altered body temperature may be beneficial and should not necessarily be manipulated until the underlying condition is improved. 114
FEVER Increased body temperatures have been associated with illnesses for thousands of years. On the basis of the population data presented previously, febrile body temperatures for resting young adults include morning temperatures that are equal to or that exceed 37.3° C (99.2° F), which increase gradually to 37.8° C (100.0° F) for early afternoon and evening. Such elevated temperature needs to reflect a regulated increase to be considered a true fever. Pathogens and cancers are the usual causes of such increases in the regulated temperature, but they are not directly responsible for the increased body temperature; rather they interact with components of the immune system such as macrophages, T cells, monocytes, and Kupffer cells as well as with glial, epithelial, and many other types of cells. This interaction stimulates the cells to produce pyrogenic cyotokines,113 including interleukin-1, interleukin-6, and macrophage inflammatory protein-1. Cytokines act on cells in the vicinity of the anterior hypothalamus and induce them to release prostaglandin E2, which leads to an increase in the regulated temperature.100 Important avenues by which cytokine-mediated pyrogenic signals reach the brain include peripheral inputs from the abdominal vagus nerve160 and central inputs via the subfornical organs.182 Aspirin and related drugs block fever by inhibiting prostaglandin synthesis.100 Interleukin-1 and other cytokines have many effects in addition to causing fever; these include decreased appetite, hypoferremia, activation of B and T lymphocytes, and increased slow-wave sleep.99 The increase in body temperature during fever helps with many immune functions; neutrophil migration, release of reactive oxygen intermediates and nitric oxide by neutrophils, and interferon production are all augmented. It has been suggested that the most important aspect of fever is to greatly increase the temperatures of the peripheral tissues via selection of a warmer microclimate, addition of insulation, and postural changes. As peripheral temperatures increase from typical levels (i.e., 29° to 33° C [84.2° to 91.4° F]) to those that approximate core temperature, activation, proliferation, and effector production in peripheral cells involved in cell-mediated and humoral immunity are greatly increased and show temperature coefficients (Q10) of 100 to 1000. By contrast, the Q10 for the effectiveness of the newly created effectors themselves, as well as for antigen-nonspecific defense systems, are much lower at about 1.5 to 5.36.100,101,161 The presence and beneficial effects of fever have been documented in a variety of cold- and warm-blooded vertebrates and even in some invertebrates. Under most conditions, it is probably not advisable to alleviate a fever. Exceptions include malignant hyperthermia and particularly high fevers during pregnancy.100,101 In addition, for patients with limited fluid, oxygen transport, or cardiopulmonary reserves, a febrile response should be treated with antipyretics.94 Consequences of the decreased immune response can be treated after the emergency.
ALCOHOL, ANESTHETICS, AND TOXINS Increases in the blood concentrations of ethanol, anesthetics, and a number of toxic substances lead to substantial decreases in body temperature.42,172 In many cases, this fall is caused by a decrease in the regulated temperature. In the case of high concentrations of alcohol and certain toxins, the reduction appears to be an adaptive adjustment that promotes survival. These chemicals disrupt protein structures within the cell membrane, and this effect is counteracted by a lower temperature.42 Indeed, mouse studies have shown that lowered body temperature counteracts ethanol toxicity.114 In humans as well, decrease in the regulated temperature is caused by increases in blood ethanol concentration. After ingestion of ethanol (3.0 mL/kg body weight) at 33° C (91.4° F), sweat rate increased and body temperature fell. Although skin temperature did not increase, subjects reported a warm sensation that paralleled the increase in sweat rate.199 At 18° C (64.4° F), body temperature decreased continuously before and after the drinking of alcohol, with no facilitation of metabolic heat production. During this period, the thermal discomfort sensation became more intense, although the discrimination of cold per se was impaired after the
SEVERE HYPOXIA AND ENDOTOXIN SHOCK When inspired oxygen concentration falls to 10% to 12%, a substantial decrease in the regulated temperature occurs. This reaction has been documented with the use of behavioral responses in fish, amphibians, reptiles, and mammals.59,193 For humans who are exercising in 28° C (82.4° F) water under eucapnic conditions, decreasing inspired oxygen to 12% lowers the core temperature thresholds for vasoconstriction and shivering and increases the rate of core cooling by 33%.87 The value of the resultant lowered body temperature is clear: the affinity of hemoglobin for oxygen is increased, and overall metabolic rate is decreased. The mechanism underlying the change in the regulated temperature may involve differential sensitivities of central neurons; hypoxia specifically increases activity of warm-sensitive neurons in the POAH.184 A somewhat similar regulated hypothermic response occurs when an animal is exposed to very high levels of pyrogens; the same response occurs under less extreme conditions in weak or malnourished animals. The lowered body temperature may serve to decrease the energy costs of maintaining a high body temperature for a severely compromised animal.159
ALTERED SYSTEM RESPONSIVENESS AND CAPACITIES A number of situations alter responsiveness of the thermoregulatory system. Awareness of these conditions is important when assessing the thermoregulatory capabilities of a particular person and when determining possible causes for hyperthermia or hypothermia.
THERMAL ACCLIMATION Thermoregulation is affected by chronic exposure to very cold or hot environments as well as by chronic exercise in cool or warm ambient temperatures. Such exercise in a cool environment greatly increases responsiveness of the sweat glands; if exercise is in the heat, the central temperature at which sweating is initiated is also lowered. The net consequence of these adjustments is that a heat- and exercise-acclimated individual can workout at a given level with far less increase in core temperature.129 Exercise in humid heat appears to decrease resting core temperature in acclimated individuals.145 Increases in both core and skin temperatures contribute to various changes involved in heat acclimation.152 Physical training also increases skin blood flow at any given increase in core temperature.85 Although acclimation to
warm conditions produces many changes in the cardiovascular system, the basic baroreflex responses are not altered.195 Heat acclimation may result in protective cellular adaptations. Intracellular heat shock protein 72 is likely involved in the maintenance of cellular protein conformation and homeostasis during hyperthermia, inflammation, and injury.123 A 10-day heat- and exercise-acclimation test increased heat shock protein 72 levels in peripheral blood mononuclear cells.194 Chronic cold exposure alters many thermoregulatory systems and involves long-term evolutionary changes and thermal acclimation. In many cases, resting metabolic rate is increased after repeated cold exposure;20,204 however, repeated exposure to very cold environments may produce the opposite effect. For example, eighty 30-minute sessions at 5° C (41° F) decreased the metabolic response to a standard cold-air test and often led to lower internal temperatures in these cold-acclimated individuals.74 When the extremities are initially exposed to cold, strong vasoconstriction is seen. At some point, however, cold-induced removal of the superficial α-receptor inhibition leads to vasodilation of the fingers, which warms the extremities and protects against frostbite. This response has a genetic component; for individuals who are not cold acclimated, this response is very strong among Inuit Eskimos, moderate among whites, and minimal among Chinese from Hong Kong. Individual differences in the vasodilation response to cold determine the relative likelihood of the development of frostbite. An environmental influence in this response is also likely; fishermen in northeastern Canada did not exhibit vasoconstriction of the fingers when exposed to cold.63
COMPETITION WITH OTHER HOMEOSTATIC SYSTEMS In addition to a constant core temperature, the body has many other requirements. When fluid balance or energy requirements are not met, thermoregulatory responses can be compromised. For heat production and heat conservation, an adequate energy supply, patent nervous system, and functional effector organs are critical. Thus, hypoglycemia decreases the core temperature at which shivering is initiated while leaving the thresholds for sweating and vasodilation unaffected.143 During exercise, heat is generated by activity of the muscles. About 80% of the energy consumption is converted into heat, with only about 20% going to the actual work produced by contraction of the muscles. High muscle temperature increases efficiency of muscle contraction.7,8 However, an excessive rise in body temperature impairs endurance performance. It is well appreciated that 40° C (104° F) is very near the upper limit of core body temperature when trying to maintain prolonged exercise. The time to exhaustion during heavy exercise is affected by the initial body temperature.61,134,136 In a heat-acclimation study, 2 subjects exercised until exhaustion at 60% of their maximum VO for 9 to 12 consecutive days at 40° C (104° F).136 The time to exhaustion became progressively longer with acclimation, but core temperature at the time of exhaustion remained at about 40° C (104° F). When body temperature was altered by water immersion before bicycle ergometer exercise at 40° C (104° F), time to exhaustion became progressively longer as initial body temperature was progressively lowered. Again, body temperature at exhaustion remained at about 40° C (104° F).61 For the maintenance of exercise performance and body temperature in a warm environment, body water status is critical.121,167 It is common for a person who is working in the heat to lose 1 L of water per hour. Even when fluids are readily available, maintaining a euhydrated state may be difficult. For hypohydration during continued activity, each percent decrease in body weight leads to a core temperature increase of about 0.15° C (0.27° F). This decreased heat dissipation is mediated by two mechanisms. At a given core temperature, hypertonicity decreases the sweating response, and hypovolemia reduces skin blood flow.167 Hyperhydration has no effect on thermoregulation during compensable exercise heat stress.104 During uncom pensable exercise heat stress, hyperhydration slightly increases the time to exhaustion but only by delaying hypohydration; 115
CHAPTER 4 Thermoregulation
ingestion of ethanol.197,198 However, lower blood ethanol levels associated with moderate consumption in humans have minimal and inconsistent effects on thermal balance of the whole body.46,86 Excellent overviews of the effects of general anesthetics on perioperative thermoregulation are available.171,173 Many of these substances (e.g., halothane, fentanyl and nitrous oxide, enflurane, isoflurane) in anesthetic doses act in a similar manner. Heat-loss thresholds are increased by about 1° C (1.8° F), and heat-maintenance thresholds are lowered by approximately 2.5° C (4.5° F). Interestingly, in the typical clinical dose range, the gain (sensitivity) of the effector responses is nearly normal. In the conditions under which general anesthetics are normally administered, body temperature decreases significantly. An initial rapid drop is caused by redistribution of heat; cool blood from the periphery lowers central core temperature. A second and slower decrease results from a fall in body heat content. Finally, a plateau is reached, either because heat production and heat loss are passively balanced or because heat maintenance thresholds are reached. During postanesthetic recovery, there is vigorous shivering. Anesthetic-induced hypothermia is reduced in patients with higher preoperative systolic blood pressures. This difference is associated with higher preoperative plasma norepinephrine levels, which may intensify the vasoconstriction response.92 Cutaneous warming before and during anesthesia prevents the development of hypothermia and decreases the incidence of infectious complications.103,171
thermoregulation is not affected.105 It is important to be alert to the possibility of dehydration in many atypical situations. For example, swimmers training in an outdoor pool with a water temperature of 26° C (78.8° F) lost sufficient fluid (i.e., 2.5% of their body weight) in 3 hours to compromise thermoregulatory responses.176 Hypoxia can undermine thermoregulatory vascular responses because of demands that compete or operate at cross-purposes. Thus, in a hot environment, hypoxia reduces skin blood flow at a given sweat rate. In the cold, hypoxia enhances core cooling by delaying the onset of vasoconstriction and cooling.119
doses of these substances impair or abolish both autonomic and behavioral aspects of thermoregulation. Body temperature then changes passively, depending on the thermal environment. This can be particularly dangerous when elevated levels of alcohol or similar substances are combined with heat stress. Impaired ability to dissipate heat is then combined with the enhanced toxicity of increased tissue temperature. Drugs that increase metabolic heat production (e.g., amphetamines, ecstasy [3,4-methylenedioxymethamphetamine], cocaine) are also particularly dangerous to use in the heat. In addition, cocaine interferes with heat dissipation mechanisms and with the perception of warmth.19,39
ALCOHOL, DRUGS, ANESTHETICS, AND TOXINS
REFERENCES
Although moderate doses of anesthetics and toxins may elicit adaptive changes in a regulated body temperature, elevated
Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 5
Accidental Hypothermia DANIEL F. DANZL
Although used for medical purposes for millennia, cold modalities were not scientifically evaluated until the 18th century. The hemostatic, analgesic, and therapeutic effects of cold on various conditions were well known. Biblical references cite truncal rewarming of King David by a damsel; various remedies were mentioned by Hippocrates, Aristotle, and Galen.270 Folklore from Maine still recounts the buggy ride of “Frozen Charlotte.” The effects of cold on human performance are perhaps best documented in military history.62,247 Frosty conditions have decided many battles.137 Numerous casualties occur even in training, such as four students of the U.S. Army Ranger School in 1995. Most cold injuries encountered today affect the urban destitute and wilderness and sports enthusiasts, such as skiers, hunters, sailors, climbers, and swimmers.6,164,298 The popularity of Arctic and mountain expeditions has increased the number of persons at risk.2,156 Among those challenging the environment are climbers of Mt Everest, Mt Hood, and Mt McKinley.127,233,257
Epidemiology In most countries, primary hypothermia deaths are considered violent and are classified as accidental, homicidal, or suicidal.39 Deaths from secondary hypothermia are usually considered natural complications of systemic disorders, including trauma, carcinoma, and sepsis. The true incidence of secondary hypothermia throughout the world is unknown because hypothermic persons found indoors usually have other serious and diverting medical illnesses. In addition, delays are common between hospital admission and death, so secondary hypothermia is significantly underreported. In contrast, death certificate data more accurately quantify primary hypothermia.80 Hypothermia occurs in various locations and in all seasons.244,315,363 In a multicenter North American survey of 428 cases of civilian accidental hypothermia, 69 occurred in Florida.59,342 Urban settings account for the majority of cases in most industrialized countries.59,168,331 There is an annual average of over 600 deaths attributed to primary hypothermia in the United States. Around one-half of these fatalities are in patients over age 65 years.40,151,152 The reason for any year-to-year decline in fatalities is unknown. Of note, the incidence of secondary hypothermia fatalities is far greater, but there are no reliable histologic criteria to confirm that hypothermia is the cause of death.279 116
CLASSIFICATIONS Accidental hypothermia is best defined as the unintentional decrease of around 2° C (3.6° F) in the “normal” core temperature of 37.2° to 37.7° C (99.0° to 99.9° F) without disease in the preoptic and anterior hypothalamic nuclei (Table 5-1). Classically, hypothermia is defined as a core temperature below 35° C (95° F). Hypothermia is both a symptom and a clinical disease entity. When sufficient heat cannot be generated to maintain homeostasis and core temperature drops below 30° C (86° F), the patient becomes poikilothermic and cools to the ambient temperature.204,306 Among clinical classifications, the most practical division includes healthy patients with simple environmental exposure (primary), those with specific diseases that produce hypothermia (secondary), and those with predisposing conditions. Other divisions that reflect the etiology of hypothermia include immersion versus nonimmersion, and acute versus chronic heat loss.225,249 Various physiologic stressors and other factors can impair thermoregulation.307 Age extremes, state of health and nutrition, type of exposure, and a multitude of intoxicants or medications can jeopardize thermostability by decreasing heat production or increasing heat loss. Physiologic stressors also include dehydration, sleep deprivation, and fatigue. These challenges increase heat loss via evaporation, radiation, conduction, and convection, and compensatory responses often fail.225 The resulting mortality rates range to well over 50% in many clinical series, depending largely on the severity of risk factors and on patient selection criteria.59,244,289,363 For safety, experimental investigations of induced hypothermia in human volunteers usually terminate cooling at about 35° C (95° F). Naturally, this precludes analysis of some of the more significant pathophysiologic features of moderate or severe hypothermia. Design limitations also occur in studies of anesthetized animals, because the results of these experiments require varying degrees of extrapolation to humans. For example, large differences exist both in the cardiovascular responses to interventions and in the amounts of peripheral musculature that are present, particularly in nonporcine animal models. As a result, clinical treatment recommendations must be predicated on the degree and duration of hypothermia and on the predisposing factors that are subsequently identified.125
For online-only figures, please go to www.expertconsult.com
Fahrenheit†
Celsius*
Fahrenheit†
Celsius*
95 94 93 92 91 90 89 88 87 86 85 84 83 82 81 80 79 78 77 76 75 74 73 72 71 70 69 68 67 66 65 64
35.00 34.44 33.89 33.33 32.78 32.22 31.67 31.11 30.56 30.00 29.44 28.89 28.33 27.78 27.22 26.67 26.11 25.56 25.00 24.44 23.89 23.33 22.78 22.22 21.67 21.11 20.56 20.00 19.44 18.89 18.33 17.78
63 62 61 60 59 58 57 56 55 54 53 52 51 50 49 48 47 46 45 44 43 42 41 40 39 38 37 36 35 34 33 32
17.22 16.67 16.11 15.56 15.00 14.44 13.89 13.33 12.78 12.22 11.67 11.11 10.56 10.00 9.44 8.89 8.33 7.78 7.22 6.67 6.11 5.56 5.00 4.44 3.89 3.33 2.78 2.22 1.67 1.11 0.56 0.00
Pathophysiology NERVOUS SYSTEM
*C = (F − 32) × 5/9 † F = 9/5 C + 32
Normal Physiology of Temperature Regulation Warm-blooded animals maintain a precariously dynamic equilibrium between heat production and heat loss.166,167 The normal diurnal variation in humans is only 1° C (1.8° F). Because physiologic changes occurring in humans are modified by predisposing or contributory factors, the normal responses to severe temperature depression require significant extrapolation.229,258
Numbing cold depresses the central nervous system, producing impaired memory and judgment, slurred speech, and decreased consciousness. During cold-weather expeditions, leaders are prone to risk-taking behavior and its attendant trauma. Temperature-dependent enzyme systems in the brain do not function properly at cold temperatures that are well tolerated by the kidneys. As a result, most patients are comatose below 30° C (86° F), although some remain amazingly alert.147 Neurons are initially stimulated by a 1° C (1.8° F) drop in temperature, but the brain does not always cool uniformly during accidental hypothermia. After the initial increase, there is a linear decrease in cerebral metabolism by 6% to 10% per degree Celsius from 35° C (95° F) to 25° C (77° F). Hypothermia can afford cerebral protection because of the diminished cerebral metabolic requirements for oxygen.108 The electroencephalogram is abnormal below 33.5° C (92.3° F) and becomes silent at 19° to 20° C (66.2° to 68° F). The triphasic waves commonly noted in hypothermia are also observed in various metabolic, toxic, and diffuse encephalopathies. Visual evoked potentials, another objective measure of cerebral function, become smaller as the mercury drops. After cerebral cortical function becomes impaired, lower brainstem functions are also deranged. Cerebrovascular autoregulation is protectively intact until the temperature drops below 25° C (77° F). Although vascular resistance is increased, blood flow is disproportionately redistributed to the brain. In canine studies, blood flow in the brain, muscle, kidneys, and myocardium recovers quickly to control levels after rewarming. Flow deficits persist in the pulmonary, digestive, and endocrine systems for up to 2 hours after rewarming. Chilling the peripheral nervous system increases muscle tension and preshivering tone, eventually leading to shivering. Shivering, which is also centrally controlled, is a much more efficient heat producer than are voluntary muscle contractions of the extremities.
Cold exposure
Thermosensitive end-organs (cutaneous and others)
Blood temperature
Lateral spinothalamic tract
Direct reflex vasoconstriction
Relevant hypothalamic nuclei (preoptic and anterior)
Involuntary muscle contraction (shivering)
Endocrinologic
Autonomic nervous system
Extrapyramidal stimulation of voluntary skeletal muscles
Adaptive behavioral responses
FIGURE 5-1 Physiology of cold exposure.
117
CHAPTER 5 Accidental Hypothermia
Basal heat production usually averages 40 to 60 kcal/m2 of body surface area per hour, which approximates the heat from a 100-watt incandescent bulb. This increases with shivering thermogenesis,243 food ingestion, fever, activity, and cold stress. Normal thermoregulation in vertebrates involves transmitting cold sensation to hypothalamic neurons via the lateral spinothalamic tracts and the thalamus (Figure 5-1). The physiologic characteristics of the four zones of hypothermia appear in Table 5-2. A complete discussion of the physiology of thermoregulation and cold exposure is presented in Chapters 4 and 6.
TABLE 5-1 Fahrenheit-to-Celsius Conversion Scale
PART 2 COLD AND HEAT
TABLE 5-2 Characteristics of the Four Zones of Hypothermia Core Temperature Stage Mild
Moderate
Severe
Profound
°C
°F
37.6 37.0 36.0 35.0 34.0
99.7 ± 1 98.6 ± 1 96.8 95.0 93.2
33.30
91.4
32.0 31.0 30.0
89.6 87.8 86.0
29.0 28.0 27.0 26.0 25.0
84.2 82.4 80.6 78.8 77.0
24.0 23.0 22.0 20.0 19.0 18.0 13.7 15.0 10.0 9.0
75.2 73.4 71.6 68.0 66.2 64.4 56.7 59.0 50.0 48.2
Characteristics Normal rectal temperature Normal oral temperature Increases in metabolic rate, blood pressure, and preshivering muscle tone Urine temperature 34.8° C (94.6° F); maximal shivering thermogenesis Development of amnesia, dysarthria, and poor judgment; maladaptive behavior; normal blood pressure; maximal respiratory stimulation; tachycardia, then progressive bradycardia Development of ataxia and apathy; linear depression of cerebral metabolism; tachypnea, then progressive decrease in respiratory minute volume; cold diuresis Stupor; 25% decrease in oxygen consumption Extinguished shivering thermogenesis Development of atrial fibrillation and other arrhythmias; poikilothermia; pupils and cardiac output two-thirds of normal; insulin ineffective Progressive decrease in level of consciousness, pulse, and respiration; pupils dilated; paradoxical undressing Decreased ventricular fibrillation threshold; 50% decrease in oxygen consumption and pulse; hypoventilation Loss of reflexes and voluntary motion Major acid–base disturbances; no reflexes or response to pain Cerebral blood flow one-third of normal; loss of cerebrovascular autoregulation; cardiac output 45% of normal; pulmonary edema may develop Significant hypotension and bradycardia No corneal or oculocephalic reflexes; areflexia Maximal risk of ventricular fibrillation; 75% decrease in oxygen consumption Lowest resumption of cardiac electromechanical activity; pulse 20% of normal Electroencephalographic silencing Asystole Lowest adult accidental hypothermia survival106 Lowest infant accidental hypothermia survival264 92% decrease in oxygen consumption Lowest therapeutic hypothermia survival258
CARDIOVASCULAR SYSTEM Many cardiovascular responses caused by or associated with hypothermia are well described.206,207 Cold stress increases consumption of myocardial oxygen. Autonomic nervous system stimulation causes tachycardia and peripheral vasoconstriction, both of which increase systemic blood pressure and cardiac afterload. As core temperature drops, there is a fairly linear decrease in pulse rate. After premonitory tachycardia, decremental bradycardia produces a 50% decrease in heart rate at 28° C (82.4° F). Because this bradycardia is caused by decreased spontaneous depolarization of pacemaker cells, it is refractory to atropinization. If there is a “relative” tachycardia not consistent with the degree of hypothermia, the clinician should be concerned. Associated conditions include occult trauma with hypovolemia, drug ingestion, and hypoglycemia. During hypothermic bradycardia, unlike normothermia, systole is prolonged longer than diastole. In addition, the conduction system is much more sensitive to cold than is the myocardium, so the cardiac cycle is lengthened. Cold-induced changes in pH, oxygen, electrolytes, and nutrients also alter electrical conduction.224 Hypothermia progressively decreases mean arterial pressure and cardiac index. Cardiac output drops to about 45% of normal at 25° C (77° F). Systemic arterial resistance, determined by invasive hemodynamic monitoring, is increased. Even after rewarming, cardiovascular function may remain temporarily depressed, with impaired myocardial contractility, metabolism, and peripheral vascular function.341 Mild, steady hypothermia in patients with poikilothermic thermoregulatory disorders causes electrocardiographic (ECG) alterations and conduction abnormalities.68 First the PR, then the QRS, and most characteristically the QTc intervals are prolonged. Clinically invisible increased preshivering muscle tone can obscure the P waves; ST-segment and T-wave abnormalities are inconsistent.9,347 Of note, ordinary surface ECG electrodes, when attached to dry skin, will accurately reflect cardiac electrical activity. Needle electrodes are not necessary to detect weak ECG signals.187 118
The J wave (Osborn wave or hypothermic hump; (Figure 5-2), first described by Tomaszewski in 1938, occurs at the junction of the QRS complex and the ST segment. It is not prognostic but is potentially diagnostic.112,197 J waves occur at any temperature below 32.2° C (90° F) and are most frequently seen in leads II and V6. When core temperature falls below 25° C (77° F), J waves are found in the precordial leads (especially V3 or V4). The size of the J waves also increases with temperature depression, but is unrelated to arterial pH.373 J waves are usually upright in aVL, aVF, and the left precordial leads.3,175,262 J waves may represent hypothermia-induced ion fluxes, resulting in delayed depolarization or early repolarization of the left ventricle, or there may be an unidentified hypothalamic or neurogenic factor. J waves are not pathognomonic of hypothermia but occur also with central nervous system lesions, focal cardiac ischemia, and sepsis. They may also be present in young, healthy persons. When pronounced, J waveform abnormalities can simulate myocardial infarction. Computer software is not widely available that can successfully recognize and suggest the diagnosis of hypothermia.202,235,255 The prehospital capability to differentiate between J waves and injury current is important in rural and wilderness settings.57 Thrombolysis is unstudied in hypothermia but would be expected to exacerbate coagulopathies.110 Below 32.2° C (90° F), all types of atrial and ventricular arrhythmias are encountered.75 The His-Purkinje system is more sensitive to cold than is the myocardium. As a result, conduction velocity decreases and electrical signals can disperse. Because conduction time is prolonged more than the absolute refractory period, reentry currents can produce circus rhythms that initiate ventricular fibrillation (VF). In addition to causing bradycardia, widening the QRS complex, and prolonging the QT interval, hypothermia increases the duration of action potentials (Figure 5-3, online).21,22 During rewarming, nonuniform myocardial temperatures can disperse conduction and further increase the action potential duration, another mechanism to develop the unidirectional blocks that facilitate reentrant arrhythmias. At temperatures between 25° and 20° C (77° and 68° F), myocardial conduction time is prolonged further than the
CHAPTER 5 Accidental Hypothermia
FIGURE 5-2 The J or Osborn wave of hypothermia. Note that the obvious J waves were not properly interpreted by the computer.
absolute refractory period. Another arrhythmogenic mechanism is development of independent electrical foci that precipitate arrhythmias. Various electrolyte abnormalities can further complicate the situation during hypothermic conditions, because they exacerbate the effects of prolonged action potentials. Most conspicuously, hypothermia-induced cellular calcium loading mimics digitalis toxicity and may predispose to a forme fruste of torsades de pointes. Hypothermia-induced VF and asystole often occur spontaneously below 25° C (77° F). The VF threshold and transmembrane resting potential are decreased. Because the heart is cold, the conduction delay is facilitated by the large dispersion of repolarization, and the action potential is prolonged. The increased temporal dispersion of the recovery of excitability is linked to VF. Nature’s model of resistance to VF is the heart of hibernating animals during rewarming.163 Animals with this capacity seem to be protected by a shortened QT duration and a calcium channel handling system that prevents intracellular calcium overload. Asystole and VF may both result from hypovolemia, tissue hypoxia, therapeutic manipulations, acid–base fluxes, autonomic dysfunction, and coronary vasoconstriction coupled with increased blood viscosity. Other causes may include rough handling or jostling, sudden vertical positioning, and acute metabolic stress from exertion or very rapid rewarming.
CORE TEMPERATURE AFTERDROP Core temperature afterdrop refers to the continued decline in a hypothermic patient’s temperature after removal from the cold (see also Chapter 6). Contributing to afterdrop is the simple temperature equilibration between the warmer core and cooler periphery. Circulatory changes account for another set of observations. The countercurrent cooling of blood that perfuses cold extremities results in core temperature decline until the existing
temperature gradient is eliminated. In cold-water immersion, post-rescue collapse may also result from abrupt hypotension after loss of hydrostatic squeeze contributed by the water. The incidence and magnitude of core temperature afterdrop vary widely in clinical experiments and in surgically induced hypothermia.103,104,125 Hayward128 measured his own esophageal, rectal, tympanic, and cardiac temperatures (via flotation tip catheter) during rewarming after being cooled in 10° C (50° F) water. On three different days, rewarming was achieved via shivering thermogenesis, heated humidified inhalation, and warm bath immersion. Coincident with a 0.3° C (0.5° F) afterdrop during warm bath immersion, his mean arterial pressure fell 30% and his peripheral vascular resistance fell 50%. Therefore the circulatory mechanism is another major contributor to afterdrop. A human study of peripheral blood flow during rewarming from mild hypothermia suggests that minimal skin blood flow changes can also lead to afterdrop (Figure 5-4). The largest core temperature afterdrops occur when subjects are rewarmed with plumbed garments and heating pads. In summary, core temperature afterdrop appears to become most clinically relevant when a large temperature gradient exists between the periphery and the core, particularly in dehydrated, chronically cold patients. Both conductive and convective mechanisms are responsible for afterdrop.104 Stimulating peripheral blood flow can increase afterdrop. Major afterdrops are also observed when frostbitten extremities are thawed before crystalloid volume resuscitation and thermal stabilization of the core temperature.
RESPIRATORY SYSTEM Any exposure to a big chill initially stimulates respiratory drive, which is followed by progressive depression of respiratory minute volume as cellular metabolism is depressed. The respiratory rate often falls to 5 to 10 breaths/min below 30° C (86° F), and ultimately brainstem neurocontrol of ventilation fails. An 119
PART 2 COLD AND HEAT
The etiology of the cold diuresis is multifactorial.114,115 Some of the suggested mechanisms include inhibition of antidiuretic hormone (ADH) release and decreased renal tubular function. Neither hydration nor ADH infusions seem to influence the diuretic response, which appears to be an attempt to compensate for initial relative central hypervolemia caused by vasoconstrictive overload of capacitance vessels. The diuresis may also be pressure related, caused by impaired autoregulation in the kidneys. Cold diuresis has circadian rhythmicity and correlates with periods of shivering. Cold water immersion increases urinary output 3.5 times, and the presence of ethanol impressively doubles that diuresis.
A
B
FIGURE 5-4 Infrared scan of the palmar hand surface. Blue, 43° C (109.4° F); red, 68° C (154.4° F). A, At room temperature. B, After 5 minutes in a cold room, with evidence of vasoconstriction. (Courtesy Naval Health Research Center, San Diego, Calif.)
important physiologic observation is that carbon dioxide production drops 50% for each 8° C (14° F) fall in temperature. In severe hypothermia, carbon dioxide retention and respiratory acidosis reflect the aberrant responses to normothermic respiratory stimuli.99 Other pathophysiologic factors contributing to ventilation– perfusion mismatch include decreased ciliary motility, increased quantity and viscosity of secretions, hypothermic acute respiratory distress syndrome, and noncardiogenic pulmonary edema.332 The thorax loses elasticity, and pulmonary compliance drops. The respiratory “bellows” stiffen and fail because contractile efficiency of the intercostal muscles and diaphragm declines. Pertinent potentially protective or detrimental factors that affect tissue oxygenation in endothermic humans are listed in Box 5-1.
RENAL SYSTEM The kidneys respond briskly to hypothermia-induced changes in the vascular tree’s capacitance. Peripheral vasoconstriction can result initially in a relative central hypervolemia, producing diuresis, even with mild dehydration. In addition, renal blood flow is depressed by 50% at 27° to 30° C (80.6° to 86° F), which decreases glomerular filtration rate. Nevertheless, there is an initial large diuresis of this dilute glomerular filtrate, which does not efficiently clear nitrogenous wastes.
BOX 5-1 Oxygenation Considerations
During Hypothermia
Detrimental Factors • Oxygen consumption increases with rise in temperature; use caution if rewarming is rapid; shivering also increases demand • Decreased temperature shifts oxyhemoglobin dissociation curve to the left • Ventilation–perfusion mismatch; atelectasis; decreased respiratory minute volume; bronchorrhea; decreased protective airway reflexes • Decreased tissue perfusion from vasoconstriction; increased viscosity • “Functional hemoglobin” concept: capability of hemoglobin to unload oxygen is lowered • Decreased thoracic elasticity and pulmonary compliance Protective Factors • Reduction of oxygen consumption by 50% at 28° C (82.4° F), 75% at 22° C (71.6° F), and 92% at 10° C (50° F) • Increased oxygen solubility in plasma • Decreased pH and increased PaCO2 shift oxyhemoglobin dissociation curve to right
120
COAGULATION Coagulopathies often develop in hypothermic patients because the enzymatic nature of the activated clotting factors is depressed by cold.88 In vivo, prolonged clotting is proportional to the number of steps in the cascade. For example, at 29° C (84.2° F), a 50% to 60% increase in the partial thromboplastin time (PTT) would be expected. Kinetic tests of coagulation, however, are performed in the laboratory at 37° C (98.6° F). As the blood warms in the machine, the enzymes between the factors in the cascade are activated. The sample of warmed in vitro blood then clots normally.77 The reversible hemostatic defect created by hypothermia may not be reflected by the “normal” prothrombin time (PT), PTT,292 or international normalized ratio (INR). This coagulopathy is basically independent of clotting factor levels and cannot be confirmed by laboratory studies performed at 37° C (98.6° F). Treatment is rewarming and not simply administration of clotting factors.288 When rapid rewarming is difficult, concentrations of 0.01 to 1 nM of desmopressin may partially reverse hypothermiainduced coagulopathy in vitro.376 Thrombocytopenia as a cause of bleeding becomes progressively significant in severe hypothermia. Proposed mechanisms include direct bone marrow suppression and splenic or hepatic sequestration. Thromboxane B2 production by platelets is also temperature dependent, so cooling skin temperature produces reversible platelet dysfunction. Thrombocytopenia is a common but poorly recognized corollary of hypothermia in older adults and neonates. Coagulopathy in trauma patients is attributed to enzyme inhibition, platelet alteration, and fibrinolysis.320 The critical temperature at which enzyme activity slows significantly is 34° C (93.2° F).358 In addition, clot strength weakens as a result of platelet malfunction. Fibrinolysis is not significantly affected at any temperature in the range measured (33° to 37° C [91.4° to 98.6° F]) (see Trauma, later). Physiologic hypercoagulability also develops during hypothermia, with a sequence similar to that seen in disseminated intravascular coagulation (DIC). This produces a higher incidence of thromboembolism during hypothermia. Causes include thromboplastin release from cold tissue, simple circulatory collapse, and release of catecholamines and steroids. Because fibrin splitproduct levels can be normal, bleeding is not always considered a hematologic manifestation of DIC.282 Whole blood viscosity increases with the hemoconcentration seen after diuresis and the shift of fluid out of vascular compartments. Red blood cells (RBCs) simply stiffen and have diminished cellular deformity when chilled.276 The elevated viscosity of hypothermia is also exacerbated by cryoglobulinemia. Cryofibrinogen is a cold-precipitated fibrinogen occasionally seen with carcinoma, sepsis, and collagen vascular diseases. Blood viscosity is also increased by the transient increases in platelet and RBC counts seen with mild surface cooling. This could explain the increased mortality from coronary and cerebral thromboses that occur in winter.225
Predisposing Factors The factors that predispose to hypothermia can be separated into those that decrease heat production, those that increase heat loss, and those that impair thermoregulation.225 There is significant overlap between these groups (Box 5-2).
Decreased Heat Production Endocrinologic Failure • Hypopituitarism • Hypoadrenalism • Hypothyroidism • Lactic acidosis • Diabetic and alcoholic ketoacidosis Insufficient Fuel • Hypoglycemia • Malnutrition • Marasmus • Kwashiorkor • Extreme physical exertion Neuromuscular Physical Exertion • Age extremes • Impaired shivering • Inactivity • Lack of adaptation Impaired Thermoregulation Peripheral Failure • Neuropathies • Acute spinal cord transection • Diabetes Central or Neurologic Failure • Cardiovascular accident
• Central nervous system trauma • Toxicologic effects • Metabolic failure • Subarachnoid hemorrhage • Pharmacologic effects • Hypothalamic dysfunction • Parkinson disease • Anorexia nervosa • Cerebellar lesion • Neoplasm • Congenital intracranial anomalies • Multiple sclerosis • Hyperkalemic periodic paralysis Increased Heat Loss Environmental • Immersion • Nonimmersion Induced Vasodilation • Pharmacologic effects • Toxicologic effects Erythrodermas • Burns • Psoriasis • Ichthyosis • Exfoliative dermatitis
DECREASED HEAT PRODUCTION Thermogenesis is decreased at both extremes of age. In older adults, neuromuscular inefficiency and decreased physical activity impair shivering. Aging progressively diminishes homeostatic and cold adaptive capabilities. Although most older adults have normal thermoregulation, they tend to develop conditions that impair heat conservation.283,286 Older adults are physiologically less adept at increasing heat production and the respiratory quotient (the ratio of the volume of carbon dioxide produced to the volume of oxygen consumed per unit of time). Impaired thermal perception, possibly caused by decreased resting peripheral blood flow, leads to poor adaptive behavior. Metabolic studies also demonstrate that in severely hypothermic older adults, lipolysis occurs in preference to glucose consumption.256,271 Neonates have a large surface area–to–mass ratio, relatively deficient subcutaneous tissue layer, and virtually no behavioral defense mechanisms. Newborn “unadapted” infants attempt to thermoregulate with initial vasoconstriction and acceleration of metabolic rate. In contrast, “adapted” infants who are older than 5 days can increase lipolysis immediately and burn oxidative brown adipose tissue. No cause-and-effect relationship has been found between hypothermia and the mortality rate of premature infants.129,301 Although the smaller infants in a neonatal intensive care unit are at the greatest risk for hypothermia, mortality is related to hypothermia only in larger neonates. Emergency deliveries and resuscitations are responsible for most acute neonatal hypothermia. Other common risk factors are prematurity, low birth weight, inexperienced mother, perinatal morbidity, and low socioeconomic status. In babies with more chronically induced subacute hypothermia, lethargy, a weak cry, and failure to thrive are common.335 Many cold infants have “paradoxical rosy cheeks,” looking surprisingly healthy. After the first few days of life, hypothermia frequently indicates septicemia and carries a high mortality rate. Low weight and malnutrition are common. Hypothermia in a low-birth-weight neonate should suggest the possibility of
CHAPTER 5 Accidental Hypothermia
BOX 5-2 Factors Predisposing to Hypothermia Iatrogenic • Emergency childbirth • Cold infusions • Heatstroke treatment Miscellaneous Associated Clinical States • Multisystem trauma • Recurrent hypothermia • Episodic hypothermia • Shapiro syndrome • Infections: bacterial, viral, parasitic • Pancreatitis • Carcinomatosis • Cardiopulmonary disease • Vascular insufficiency • Uremia • Paget disease • Giant cell arteritis • Sarcoidosis • Shaken baby syndrome • Systemic lupus erythematosus • Wernicke-Korsakoff syndrome • Hodgkin’s disease • Shock • Sickle cell anemia • Sudden infant death syndrome
intracranial hemorrhage; hypothermia is also observed in shaken baby syndrome. Endocrinologic failure, including hypopituitarism, hypoadrenalism, and myxedema, commonly decreases heat production. Interestingly, congenital adrenal hyperplasia with mineralocorticoid insufficiency is more common in cold climates, possibly an adaptive response to prolonged exposure to cold temperatures, because “normal” cold diuresis is reduced in these patients. Hypothyroidism is often occult, with no history of cold intolerance, dry skin, lassitude, or arthralgias. The physician should check for a thyroid scar or any history of thyroid hormone replacement. The degree of temperature depression correlates fairly directly with mortality. Eighty percent of patients in myxedema coma, which is several times more common in female patients, are hypothermic. The effects of insufficient nutrition extend from hypoglycemia to marasmus to kwashiorkor. Kwashiorkor is less often associated with hypothermia than is marasmus, because of the insulating effect of hypoproteinemic edema. Central neuroglycopenia distorts hypothalamic function. Many alcoholic patients with hypothermia are hypoglycemic. Malnutrition decreases insulative subcutaneous fat and directly alters thermoregulation. Poor nutrition predisposes to hypothermia and its attendant clumsiness in older adult women with femoral neck fractures. Partly because of fuel depletion, hypothermia is as great a threat as hyperthermia in marathon races run in cool climates. Runners slowing from fatigue or injury late in a race are at serious risk of hypothermia.170
INCREASED HEAT LOSS Poorly acclimated and insulated individuals often have high diaphoretic, convective, and evaporative heat losses during exposure to cold. Because the skin functions as a radiator, any dermatologic malfunction increases heat loss. Such erythrodermas include psoriasis, exfoliative dermatitis, and toxic epidermal necrolysis. Hypothermia with hypernatremic dehydration is also seen in congenital lamellar ichthyosis. 121
PART 2 COLD AND HEAT
Burns and inappropriate burn treatment cause excessive heat loss, as do other iatrogenic factors, including massive cold intravenous (IV) infusions and overcooling heatstroke victims.188 When carbon dioxide is used for abdominal insufflation before laparoscopy, warming the gas before administration helps prevent hypothermia. Environmental immersion exposure is discussed in detail in Chapter 6.102 Many pharmacologic and toxicologic agents both increase heat loss and impair thermoregulation.165-167,343 The most common is ethanol, which interacts with every putative thermoregulatory neurotransmitter. Although ingestion of ethanol produces a feeling of warmth and perhaps visible flushing, it is the major cause of urban hypothermia.59,244 In fatal cases of accidental hypothermia, many victims are under the influence of ethanol. In children with ethanol intoxication, hypothermia is common. Ethanol is also a poikilothermia-producing agent that directly impairs thermoregulation at high or low temperatures.165 Body temperature is lowered both from cutaneous vasodilation with radiative heat loss and from impaired shivering thermogenesis. Chronic ethanol ingestion damages the mamillary bodies and posterior hypothalamus, which modulates shivering thermogenesis.277 Ethanol also increases the risk for being exposed to the environment, by modifying protective adaptive behavior. The ultimate example is paradoxical undressing, or removal of clothing in response to a cold stress. As an organic solvent, ethanol confers a few theoretically redeeming qualities in freezing cold injuries by lowering the cellular freezing point.114,115 The neurophysiologic effects of ethanol are modified by duration and intensity of exercise, food consumption, and applied cold stress.94 Aging increases sensitivity to the hypothermic actions of ethanol in some primate experiments. Chronic ingestion yields tolerance to its hypothermic effects, and rebound hyperthermia may be seen during withdrawal. Conditions associated with ethanol ingestion that adversely affect heat balance include immobility and hypoglycemia.368 Inhibited hepatic gluconeogenesis coexists with malnutrition. Hypothermic alcoholic ketoacidosis is reported.363 Intravenous thiamine is diagnostic and therapeutic for Wernicke’s encephalopathy, another cause of reversible hypothermia. The acute triad of global confusion, ophthalmoplegia, and truncal ataxia is often masked by hypothermia, and temperature depression may persist for weeks.
IMPAIRED THERMOREGULATION Various conditions that impair thermoregulation can be considered as having central, peripheral, metabolic, and pharmacologic or toxicologic effects. Central Central conditions may directly affect hypothalamic function and mediate vasodilation. Traumatic lesions include skull fractures, especially basilar, and intracerebral hemorrhages, most commonly chronic subdural hematomas. Pathologic lesions include neoplasms, congenital anomalies, and Parkinson disease. Patients with Parkinson disease or Alzheimer’s disease, because of global neurologic impairment, are particularly at behavioral risk. Finally, cerebellar lesions also impede heat production because of inefficient choreiform shivering. Hypothermia can occur with Reye’s syndrome. In Hodgkin’s disease, hypothermia is seen only in previously febrile patients with advanced disease, independent of cell type. This seems to be a disease-associated functional disorder of thermoregulation, similar to that seen in anorexia nervosa. Centrally induced hypothermia is completely antagonized with thyrotropin-releasing hormone. Peripheral Peripheral thermoregulation fails after acute spinal cord transection. Victims are functionally poikilothermic as soon as peripheral vasoconstriction is extinguished.242 Other peripheral impediments to thermostability include neuropathies and diabetes mellitus. Hypothermia is more common in older adult diabetics than in the general population, even after excluding patients with diabetic metabolic emergencies. The common denominator in 122
metabolic derangements may be abnormal plasma osmolality that interferes with hypothalamic function. Similar causes of hypothermia include hypoglycemia, diabetic ketoacidosis, and uremia. Remarkably, the pH was 6.67 in one hypothermic survivor with lactic acidosis, and 6.41 in another.253 Pharmacologic or Toxicologic Numerous medications and toxins in therapeutic or toxic doses impair centrally mediated thermoregulation and vasoconstriction.172,272,377 The usual offenders are barbiturates, benzodiazepines, phenothiazines, and the cyclic antidepressants. Reduced core temperature may be a prodrome of lithium poisoning. Organophosphates, narcotics, glutethimide, bromocriptine, erythromycin, clonidine, fluphenazine, bethanechol, atropine, acetaminophen, and carbon monoxide all cause hypothermia. In experimental studies, hypothermia after acute carbon monoxide poisoning is associated with increased mortality.
RECURRENT HYPOTHERMIA Recurrent and episodic hypothermias are widely reported. The recurrent variety is more common and is usually secondary to ethanol abuse, with one person having survived 12 episodes.56 Severe, recurrent presentations are also caused by self-poisoning and anorexia nervosa. Persons with episodic hypothermia can be divided into two groups, albeit with significant overlap, as follows: Group 1: Diaphoretic episodes precede the temperature decline, which lasts several hours. This group includes those with hypothalamic lesions and agenesis of the corpus callosum (Shapiro syndrome) and persons with spontaneous periodic hyperthermia. Resultant hyperhidrosis and hypothermia are successfully treated with clonidine, a centrally acting α-adrenergic agonist. The hypothermia of corpus callosum agenesis is also seen with hypercalcemia and status epilepticus. Because no hypothermia results from experimental sectioning of the corpus callosum, associated lesions, including lipomas, probably cause thermoinstability. Spontaneous periodic hypothermia may reflect a diencephalic autonomic seizure disorder and can accompany paroxysmal hypertension. Vasomotor and thermoregulatory mechanisms are successfully treated with anticonvulsants. Florid psychiatric symptoms often mask these intermittent hypothermic episodes. Group 2: The second group consists of persons who remain cold for days to weeks, rather than hours. These people have more seizure disorders, and the central hypothalamic thermostat is set abnormally low. Patients with intermittent hypothermia usually show some characteristics of both groups.225 Circadian rhythm disturbances are also seen in persons with neurologic disorders who have chronic hypothermia.
PREDISPOSING INFECTIONS OR CONDITIONS Among the infestations and infections that may elevate or depress core temperature are septicemia, pneumonia, peritonitis, meningitis, encephalitis, bacterial endocarditis, typhoid, miliary tuberculosis, syphilis, brucellosis, and trypanosomiasis.214 Other diseases, in addition to cerebrovascular and cardiopulmonary disorders, that produce secondary hypothermia include systemic lupus erythematosus, carcinomatosis, pancreatitis, and multiple sclerosis. Hypothalamic demyelination may explain episodic hypothermia observed in some patients with multiple sclerosis. Hypothermia can also result from low cardiac output after a major myocardial infarction, which can be reversed by intra-aortic balloon counterpulsation. Finally, causes include vascular insufficiency, giant cell arteritis, uremia, sickle cell anemia, Paget disease, sarcoidosis, and sudden infant death syndrome. Magnesium sulfate infusion during preterm labor can produce hypothermia with fetal and maternal bradycardia, and hypothyroidism can be manifested as hypothermia after preeclampsia (see Box 5-2).
TRAUMA Hypothermia protects the brain from ischemia but can result in arrhythmias, acidosis, and coagulopathies, and it can extract a
Presentation The patient’s history may suggest hypothermia.33 Diagnosis becomes fairly simple when exposure is obvious, as with avalanche victims. Subtle presentations, however, predominate in urban settings. Victims often complain only of vague symptoms, including hunger, nausea, fatigue, and dizziness. Predisposing underlying illness or ethanol ingestion is also common, as are major trauma, immersion, overdose, cerebrovascular accidents, and psychiatric emergencies (Box 5-3).
During the head, eye, ear, nose, and throat examination, abnormal findings can include decreased corneal reflexes, mydriasis, strabismus, flushing, erythropsia, facial edema, rhinorrhea, and epistaxis. Mild hypothermia usually does not depress pupillary light reflexes. Cardiovascular findings after initial tachycardia include bradyarrhythmias and hypotension. Heart sounds may be muffled and distant. Tachypnea, an early respiratory finding, is usually followed by progressive hypoventilation with bronchorrhea and adventitious sounds. Because the gastrointestinal tract is depressed, abdominal distention or rigidity, ileus, obstipation, and poor rectal tone are often present. Gastric dilation is common in neonates and myxedematous adults. Urinary output ranges from initial polyuria resulting from cold diuresis to anuria. The incidence of testicular torsion increases because of cremasteric contractions. Diffuse neurologic abnormalities vary widely. Some persons can still converse at 32° C (89.6° F) and are normoreflexic. The level of consciousness generally declines proportionate to the degree of hypothermia. The presence of ataxia and dysarthria may mimic a cerebrovascular accident. Speed of reasoning and memory registration are also impaired. Amnesia, antinociception, anesthesia, or hypesthesia can develop. Cranial nerve abnormalities are present after bulbar damage from central pontine myelinolysis. These extraocular muscle movement abnormalities, like extensor plantar responses, do not directly correlate with the degree of hypothermia. Hyperreflexia predominates from 35° to 32.2° C (95° to 90° F) and is followed by hyporeflexia. The plantar response remains flexor until 26° C (78.8° F), when areflexia develops. The knee jerk is usually the last reflex to disappear and the first to reappear during rewarming. From 30° to 26° C (86° to 78.8° F), both contraction and relaxation phases of reflexes are prolonged equally. In myxedema, however, the relaxation phase of the ankle reflex is more prolonged than the contraction phase.225 Spinal cord and other central nervous system lesions may be obscured by depressive neurologic changes that normally accompany hypothermia. Psychiatric presentations and suicide attempts associated with hypothermia are commonly misdiagnosed initially. Preexisting psychiatric disorders can blossom in the cold, even if they were stabilized in temperate climates.30 Mental status alterations include anxiety, impaired judgment, perseveration, neurosis, and psychosis.156 Leaders of expeditions can become moody, apathetic, uncooperative, and risk taking. Older adult patients often withdraw in confusion, become silent, and display lassitude and poor judgment. A peculiar flat affect is common, and psychomotor impairment can resemble organic brain syndrome. Early in hypothermia, simply losing effective use of the hands can be devastating. Appropriate behavior adapted to the cold, such as seeking a heat source, is often lacking. An extreme example is paradoxical undressing.183 The clothing is removed in a preterminal effort to address impending thermoregulatory collapse, and many persons are mistakenly identified as sexual assault victims. This phenomenon is also seen in hypothermic children. Undressing may also occur as a result of Alzheimer’s disease before wandering in the cold.182 Musculoskeletal posturing can extend to pseudo–rigor mortis. Preshivering muscle tone is increased before core temperature drops to 35° C (95° F), and muscular rigidity, paravertebral spasm, and even opisthotonos may occur. Extremity compartment syndromes often develop because of associated conditions causing prolonged compression and immobility, in addition to compartment hypertension seen during reperfusion of frostbitten extremities. Dermatologic presentations of hypothermia include erythema, pallor, edema, and scleral edema. Cold urticaria, frostnip, frostbite, and gangrene should also cause the clinician to consider this diagnosis. Pernio is also observed with chronic myelomonocytic leukemia.
Laboratory Evaluation ACID–BASE BALANCE The strategy for achieving and maintaining acid–base balance in hypothermia differs from that of normothermia.65,126,153,180 After 123
CHAPTER 5 Accidental Hypothermia
high metabolic cost during rewarming.97 Hypothermia hinders protective physiologic responses to acute trauma and affects pharmacologic and therapeutic maneuvers necessary to treat injuries.18,27 An inverse relationship usually exists between the Injury Severity Score (ISS) and core temperature of traumatized patients on arrival in the emergency department (ED). This observation does not settle whether hypothermia is just another risk factor for increased mortality or reflects the fact that the most severely injured patients are in hemorrhagic shock.132 One study assessed the impact of hypothermia as an independent variable during resuscitation from major trauma.97 Patients not aggressively rewarmed with continuous arteriovenous rewarming (CAVR) had increased fluid requirements, increased lactate levels, and increased acute mortality. Of the clinical entities associated with hypothermia, traumatic conditions causing hypotension and hypovolemia most dramatically jeopardize thermostability. Hypothermia is often obscured by obvious hemorrhaging and injuries. Liberalized indications for Focused Assessment With Sonography for Trauma (FAST) ultrasound examinations can minimize unnecessary computed tomography (CT) imaging. On the other hand, traumatic neurologic deficits, including paresis and areflexia, can be misattributed to hypothermia. In trauma patients requiring surgery, the mean temperature loss was greater in the ED than in the operating room.117 Thermal insults are often added during a trauma resuscitation. The patient is completely exposed for examination, and resuscitative procedures cause further heat loss.308 In a study stratifying subjects with the anatomic ISS, hypothermic patients had a higher mortality rate than did similarly injured patients who remained normothermic.171 Another study did not corroborate this finding,322 but those investigators stratified using trauma revised injury severity score (TRISS) methodology, which is probably less valid during hypothermia because its physiologic components overestimate injury severity. To illustrate this point, some component of hypotension is normal for a given degree of hypothermia. Various adverse physiologic events accompany hypothermia with trauma. Decreased skin and core temperatures without compensatory shivering thermogenesis are reported in patients with major trauma as defined by the ISS. Hypothermia directly causes coagulopathies in trauma patients through at least three avenues (see Coagulation, earlier).33 The cascade of enzymatic reactions is impaired, and plasma fibrinolytic activity is enhanced, producing a clinical presentation similar to that of DIC. Also, platelets are poorly functional and become sequestered. Hypothermia is protective only when induced before shock occurs. This reduces adenosine triphosphate (ATP) utilization while ATP stores are still normal, as during elective surgery. ATP stores in traumatized patients are already depleted. Hypothermia worsens the effects of endotoxins on clotting time in vitro and may synergistically exacerbate the coagulopathy seen in trauma.88 The average temperature of 123 initially normothermic trauma patients in whom lethal coagulopathies developed was 31.2° C (88.2° F). In another study, postinjury life-threatening coagulop athy in the seriously injured who require massive transfusion was predicted by persistent hypothermia and progressive metabolic acidosis.50,89 The appropriate target core temperature for a hypothermic patient with an isolated severe head injury may be 32° to 33° C (89.6° to 91.4° F). This target temperature balances neuroprotection against the adverse hematologic and physiologic consequences of hypothermia19,231,232 (see Cerebral Resuscitation, later.)
Head, Eye, Ear, Nose, Throat • Mydriasis • Decreased corneal reflexes • Extraocular muscle abnormalities • Erythropsia • Flushing • Facial edema • Epistaxis • Rhinorrhea • Strabismus Cardiovascular • Initial tachycardia • Subsequent tachycardia • Arrhythmias • Decreased heart tones • Hepatojugular reflux • Jugular venous distention • Hypotension • Peripheral vasoconstriction Respiratory • Initial tachypnea • Adventitious sounds • Bronchorrhea • Progressive hypoventilation • Apnea Gastrointestinal • Ileus • Constipation • Abdominal distention or rigidity • Poor rectal tone
• Gastric dilation in neonates or in adults with myxedema • Vomiting Genitourinary • Anuria • Polyuria • Oliguria • Testicular torsion
124
Dermatologic • Erythema • Pallor • Cyanosis • Icterus • Scleral edema • Ecchymosis • Edema • Pernio • Frostnip • Frostbite • Panniculitis • Cold urticaria • Necrosis • Gangrene
Psychiatric • Impaired judgment • Perseveration • Mood changes • Peculiar “flat” affect • Altered mental status • Paradoxical undressing • Neuroses • Psychoses
initial respiratory alkalosis from hyperventilation when a person first becomes chilled, a common underlying disturbance is mixed acidosis. The respiratory component of the acidosis is caused mainly by direct respiratory depression. In addition, as body temperature decreases, solubility of carbon dioxide in blood increases. Further contributors to the metabolic component of this acidosis include impaired hepatic metabolism and acid excretion, lactate generation from shivering, and decreased tissue perfusion.134 Nevertheless, reliable clinical prediction of the acid– base status in accidental hypothermia is not possible. In one series of 135 cases, 30% were acidotic and 25% alkalotic.244 Circulatory changes also prevent adequate mobilization and delivery of organic acids to buffer systems. As in normothermia, mixed venous blood may best reflect acid–base status during resuscitation.328 Despite flow changes in a canine model of moderate hypothermia, a significant correlation persists between arterial and mixed venous pH. The arteriovenous change in pH is 0.03 to 0.04 pH unit. The buffering capacity of cold blood is also markedly impaired. In normothermia, when the arterial partial pressure of carbon dioxide (PaCO2) increases 10 mm Hg, a decrease in pH of 0.08 unit occurs. At 28° C (82.4° F), the decrease in pH doubles to 0.16 unit. The accepted earlier assumption was that 7.42 was the ideal “corrected” patient pH at all temperatures and that therapy should be directed at maintenance of the corrected arterial pH at 7.42.362 A better intracellular pH reference is electrochemical neutrality, at which pH equals pOH. Because the neutral point of water at 37° C (98.6° F) is pH 6.8, Rahn281 hypothesizes that this normal 0.6 unit pH offset in body fluids should be maintained at all temperatures. Because the neutral pH rises with cooling, so should blood pH (Figure 5-5).287 Relative alkalinity of tissues makes physiologic sense. Intracellular electrochemical neutrality ensures optimal function of enzyme systems and transport proteins at all temperatures
• Suicide • Organic brain syndrome • Anorexia nervosa • Depression • Apathy • Irritability Musculoskeletal • Increased muscle tone • Shivering • Rigidity or pseudo–rigor mortis • Paravertebral spasm • Opisthotonos • Compartment syndrome
Neurologic • Depressed level of consciousness • Ataxia • Dysarthria • Amnesia • Anesthesia • Areflexia • Poor suck reflex • Hypoesthesia • Antinociception • Initial hyperreflexia • Hyporeflexia • Central pontine myelinolysis
and allows excretion of the neutral intracellular waste product urea.13 Depressed metabolism and carbon dioxide generation are physiologic responses to temperature depression, because each temperature has its associated metabolic rate. Ventilation is intrinsically adjusted to maintain a net charge on the defended parameter, the peptide-linked histidine imidazole buffering system.
8.0
ted
ec corr
d
bloo
” un rmic e h t to “Ec “Endothermic” corrected blood
7.7
pH
PART 2 COLD AND HEAT
BOX 5-3 Signs of Hypothermia
7.4 7.1
ter
l wa
tra Neu
6.8 0 40 37
30
20
10
0
Temperature (° C) FIGURE 5-5 Neutrality is the pH of water at any given temperature. At 25° C (77° F), the neutral pH of water is 7.0; at 37° C (98.6° F), it is 6.8. An ectotherm’s physiologic 0.6 pH offset from neutral water progressively diminishes if the arterial blood gases are temperature corrected. After the in vitro sample is warmed in the analyzer to 37° C (98.6° F), do not mathematically correct the reported values to reflect the in vivo temperature.
HEMATOLOGIC EVALUATION Severity of blood loss is easily underestimated. Hematocrit value increases because of a decline in plasma volume that leads to a 2% increase per 1° C (1.8° F) fall in temperature. In addition, total RBC mass might already be low because of preexisting anemia, malnutrition, leukemia, uremia, or neoplasm. The white blood cell count is frequently normal or low, even if sepsis is present. As a result, systemic leukopenia does not imply absence of infection, especially if the patient is at either age extreme, is debilitated, intoxicated, myxedematous, or has secondary hypothermia.214 The leukocyte count also drops during hypothermia because of direct bone marrow depression and hepatic, splenic, and splanchnic sequestration. Serum electrolyte levels must be continuously monitored and rechecked during warming. There are no safe predictors of electrolyte values.125 Serum electrolytes fluctuate with temperature, duration of exposure, and rewarming technique selected. Both membrane permeability and sodium–potassium pump efficiency also change with temperature. Isolated temperature depression per se has no consistent effect on sodium and chloride levels until well below 25° C (77° F). Plasma electrolyte levels are also affected by ongoing fluid shifts, prehydration, rehydration, and endocrine or gastrointestinal dysfunction. The plasma potassium level is independent of temperature. Empirical potassium supplementation during hypothermia often results in normothermic toxicity. From a clinical perspective, hypokalemia occurs as potassium moves into the musculature and not simply out of the body through kaliuresis. The physiologically illogical discrepancy of decreasing potassium level with decreasing pH results from greater intracellular than extracellular pH changes. Hypokalemia is much more common in prolonged or chronically induced hypothermia. Systemic potassium deficiencies can also be exacerbated by prior diuretic therapy, alcoholism, diabetic ketoacidosis, hypopituitarism, and inappropriate antidiuretic hormone secretion. Hypokalemic digitalis sensitivity can be masked by hypothermia, and gradual correction of persistent and severe hypokalemia during rewarming is necessary for optimal cardiac and gastrointestinal function. When hyperkalemia is identified, the physician should search for other causes of metabolic acidosis, crush injury or rhabdomyolysis, renal failure, postsubmersion hemolysis, or hypoaldosteronism. Temperature depression can increase hyperkalemic cardiac toxicity. An important caveat is that the well-known diagnostic ECG changes are often obscured by hypothermia, and VF can occur with serum potassium levels of less than 7 mEq/L. *References 16, 66, 180, 200, 287, 328.
Hypothermia has no consistent effect on magnesium or calcium levels. Severe hypophosphatemia can occur during treatment of profound hypothermia. Although increases in serum enzyme levels are not seen in mild experimental hypothermia, numerous serum enzymes are elevated when diffuse intracellular structural damage occurs in severe accidental hypothermia. Creatine kinase (CK) levels over 200,000 international units are observed, and rhabdomyolysis is often present.56 Inhibition of cellular membrane transport decreases glucose utilization. In addition, insulin release and activity are markedly reduced below 30° C (86° F). Because target cells are insulin resistant, hyperglycemia is commonly seen initially. Markedly elevated glucose levels often correlate with hyperamylasemia and increased cortisol secretion.363 Acute hypothermia initially elevates the serum glucose level through catecholamine-induced glycogenolysis. Chronic exposure after exhaustion and glycogen depletion leads to hypoglycemia. The symptoms often resemble those of hypothermia. Cold-induced renal glycosuria is common and does not imply normoglycemia or hyperglycemia. When hypoglycemia and central neuroglycopenia are present, correction improves the level of consciousness only to that expected for the current core temperature. Cholesterol and triglyceride levels are also often below normal. Hyperglycemia that persists during and after rewarming should suggest diabetic ketoacidosis or hemorrhagic pancreatitis. Insulin is ineffective until the core temperature is well above 30° to 32° C (86° to 89.6° F) and therefore should be withheld to avoid iatrogenic hypoglycemia after rewarming. Although prior renal disease should be a consideration, blood urea nitrogen (BUN) and creatinine concentrations are often elevated because of decreased nitrogenous waste clearance by the cold diuresis. Because of ongoing fluid shifts, BUN poorly reflects circulatory volume status.100 The relationship between primary accidental hypothermia and hyperamylasemia appears to correlate with the severity of temperature depression, but preexisting or hypothermia-induced pancreatitis is present in up to 50% of patients in some urban series. Because the abdominal examination is frequently unreliable, amylase and lipase levels should be measured, except in minor cases.47 Ischemic pancreatitis is attributable to microcirculatory collapse in hypothermia. Decreased pancreatic blood flow activates many proteolytic enzymes. The extent of hyperamylasemia can correlate with mortality rates. Hypothermia with hypothalamic astrocytoma and pancreatitis also occurs.
Treatment Four decisive factors should be considered when assessing nonperfusing, severely hypothermic victims at the site. Rescuers should reconsider the decision to resuscitate if there is evidence of asphyxia or lethal injuries. A rigid thorax precludes closedchest cardiopulmonary resuscitation (CPR), and a probable field core temperature below 10° to 12° C (50° to 53.6° F) is ominous. Pulses are difficult to palpate in vasoconstricted and extremely bradycardic patients. If possible, check for an organized rhythm on a cardiac monitor. Doppler ultrasound is an ideal tool to assess cardiac activity.29,250 The combination of cold and exhaustion is a common cause of hypothermia in the field.154,245 The individual’s cold tolerance depends on temperature, wind, clothing worn, and wetness. It does not take an extremely cold temperature to produce hypothermia after energy depletion. As mental function decreases, the victim cannot respond to the rising threat. Judgment is impaired, and the victim seldom takes necessary precautions to prevent further disaster.25 Field presentation of victims who are awake covers a wide spectrum. Some persons are obtunded but conscious. Victims may or may not be shivering and often have a distant gaze and slurred speech.101 The type of power available in the transport vehicle determines the options for active rewarming. These include forced-air warming devices, heated IV fluids, and resistive and combustive heat.103,104,111 125
CHAPTER 5 Accidental Hypothermia
One homeostatic approach to maintain a steady pH is to keep the bicarbonate content constant. This is achievable only if total blood carbon dioxide content does not change. Because carbon dioxide solubility increases with temperature depression, alveolar ventilation must increase to compensate by lowering the PaCO2. Active ectotherms exhibit this respiratory adaptation and do not depress their respiratory minute volume when cold. This response, termed the ectothermic, or alpha-stat, strategy, allows them to maintain total bicarbonate and carbon dioxide content while increasing pH.269 Hibernating mammals are far more acidic because of respiratory acidosis and use an acid–base strategy that suppresses metabolism, termed the endothermic, or pH-stat, strategy. The ideal acid–base strategy continues to be debated.138,180,293 Some of the surgical literature about induced hypothermia, which clearly differs from accidental hypothermia, suggests that the alpha-stat approach improves neurologic outcome and also cellular and myocardial function.* On the other hand, various animal models suggest that the pH-stat strategy may be better.74 In summary, it seems that accidental hypothermia in a human should not be considered a protective form of hibernation. The ectothermic (alpha-stat) approach appears to ensure adequate alveolar ventilation and acid–base balance at any temperature when the uncorrected pH is 7.42 and the uncorrected PaCO2 is 40 mm Hg.
PART 2 COLD AND HEAT
FIGURE 5-6 In this patient, ventricular fibrillation developed during a code 3 transport by emergency medical services to the emergency department. Note the pronounced J waves after the QRS complexes.
Comatose victims require careful handling because they are extremely likely to develop VF and asystole with rough handling (Figure 5-6). Gurneys should be carried or rolled slowly to avoid jostling, and “code 3, full lights and sirens” transport should be avoided if victims are perfusing adequately. It is often impossible for rescuers to separate primary from secondary hypothermia when an unwitnessed cardiac arrest victim is found in a frigid environment. Because patients with cold, stiff, and cyanotic primary hypothermia and fixed and dilated pupils have been “reanimated,” the treatment dictum for prehospital personnel remains, “No one is dead until warm and dead.”10 A succinct summary of prehospital care of the hypothermic patient is rescue, examine, insulate, and transport. The initial rescuer and first responder often encounter obstacles to preventing further heat loss.246,357 In certain imposing geographic settings, treatment protocols are helpful to standardize treatment while tacitly acknowledging that available health care facilities may offer limited expertise and equipment. All treatment recommendations must be adapted to local rescue systems and facilities.76,295 Aeromedical transport is often ideal in these circumstances.370 In difficult environments, proper protocols with rehearsal and critique of mass casualty plans in the cold are far more important than similar adjuncts in flat and consistently sunny terrain. The history obtained at the scene helps determine optimal treatment. The pertinent past medical history regarding prior cardiopulmonary, endocrinologic, and neurologic conditions is particularly helpful. The circumstances of discovery, duration of exposure, associated injuries or frostbite, and obvious predisposing conditions should be recorded, as should the Glasgow Coma Scale score, although none of these is predictive. No prognostic neurologic scale during hypothermia is valid, but trends are often useful. Accurate field measurement of core temperature is difficult. The International Commission for Mountain Emergency Medicine recommends tympanic or esophageal field measurements, although they have significant limitations. Never insert an esophageal probe unless the patient is already tracheally intubated.295 Prolonged field treatment should be avoided whenever possible, although the rescuer must attempt to prevent further heat loss (Box 5-4). The rescuer should anticipate the presence of an irritable myocardium, hypovolemia, and a large temperature gradient between the periphery and the core. The crux of the prehospital quandary surrounds the safety of providing prehospital heat. On the one hand, the original “metabolic icebox” concept245,246 implies that the risk of inducing a nonperfusing rhythm in a hostile environment justifies simple stabilization of the core temperature. On the other hand, the warmer the heart, the better. Core temperature can decrease beyond reversal. Operant factors impacting the decision whether or not to provide prehospital heat include core temperature, fluid status, predisposing factors, extent of frostbite, length and type of exposure, available expertise and position of transport, and type of active rewarming available. The rescuer should stabilize injuries, protect the spine, splint fractures, and cover open wounds. Rescuer safety factors commonly include unstable snow or ice and falling rocks. Passive external rewarming with dry insulating materials minimizes conductive, convective, evaporative, and radiant heat losses. Remove any wet clothing from awake victims, and insulate them with sleeping bags, insulated pads, bubble wrap, metallized or regular blankets, or even newspaper. One device, the 126
Hypothermic Stabilizer Bag, has a nylon shell and a polyester-pile liner to wick moisture. In a survey of common field rewarming methods used by mountain rescue teams, the most common techniques include chemical pads, sleeping bags, body-to-body contact, and hot water bottles.123 If extrication will be delayed, give mildly hypothermic patients warm, sweet drinks, warm gelatin (Jell-O), Tang, juice, tea, or cocoa, because carbohydrates fuel shivering. Avoid heavily caffeinated drinks. Because a significant diuresis is usually associated with the cooling process, the victim’s fluid balance must be assessed. Once mildly hypothermic victims are well hydrated, they can be walked out to safety. Handle severely hypothermic victims gently, immobilizing them to prevent exertion. Although exercise can rewarm a person more rapidly than can shivering, it also markedly increases afterdrop.100,104 Because of autonomic dysfunction, victims should be kept in a horizontal position whenever possible to minimize orthostatic hypotension. Vigorously massaging cold extremities is also contraindicated, because skin rubbing, like ethanol, suppresses shivering thermogenesis and increases cutaneous vasodilation. Field management of the comatose victim first involves ventilation to raise oxygen saturation. Rescue breathing may be difficult because of chest stiffness and significant resistance to diaphragmatic motion. Forced ventilation increases oxygenation, which helps stabilize the heart electrically. The single greatest factor in maintaining perfusion is oxygenation provided during severe hypothermia.101 During a storm, prolonged field rewarming may be the only viable option until meteorologic conditions become more favorable for land or, preferably, aeromedical evacuation.370 Many prehospital medications freeze in solution. If this occurs, their pharmacologic activity after thawing is indeterminate (see Appendix at the end of this book).
BOX 5-4 Preparing Hypothermic Patients for Transport 1. The patient must be dry. Gently remove or cut off wet clothing, and replace it with dry clothing or a dry insulation system. Keep the patient horizontal, and do not allow exertion or massage of the extremities. 2. Stabilize injuries (i.e., the spine; place fractures in the correct anatomic position). Open wounds should be covered before packaging. 3. Initiate heated intravenous infusions (IVs) if feasible; bags can be placed under the patient’s buttocks or in a compressor system. Administer a fluid challenge. 4. Active rewarming should be limited to heated inhalation and truncal heat. Insulate hot water bottles in stockings or mittens, and then place them in the patient’s axillae and groin. 5. The patient should be wrapped. Begin building the wrap by placing a large plastic sheet on the available surface (floor, ground), and on it place an insulated sleeping pad. A layer of blankets, a sleeping bag, or bubble wrap insulating material is laid over the sleeping pad. The patient is then placed on the insulation. Heating bottles are put in place along with IVs, and the entire package is wrapped layer over layer, with the plastic as the final closure. The patient’s face should be partially covered, but a tunnel should be created to allow access for breathing and monitoring.
inhalation rewarming devices in volunteers, however, which suggests the importance of proper instruction for the rescuer.324 Under certain conditions, the impact of inhalation therapy on the rate of rewarming may not be significant.111 In shivering, mildly cold patients, the thermal advantage is minimal.71,72,241 One rewarming device weighs 3 kg, including oxygen tank, and consists of an oxygen cylinder, demand valve, 2-L reservoir bag, soda lime, and pediatric water canister. An in-line thermometer measures mean air temperature at the face mask. In the field, heat and moisture exchangers are practical, light, and inexpensive. They are, however, less efficient than are active humidifiers.217,219 The Res-Q-Air model HT1000 is a lightweight, portable, noninvasive core-rewarming system that delivers heated humidified air or oxygen at 42° to 44° C (107.6° to 111.2° F). It operates from any 12-volt DC power source. This system consists of a heating chamber connected via a corrugated hose to a one-way flow valve and an oronasal mask. The temperature is controlled by a transducer in the one-way flow valve that provides feedback to the electronic control circuits. Although surface rewarming suppresses shivering, it may be the only option when the victim is isolated from medical care. Active external rewarming options include radiant heat, warmed objects placed on the patient, and body-to-body contact. Care must be exercised not to burn victims with hot objects, including commercially produced hot packs. Total body contact rewarming may carry some risk,125 but logistical impediments limit the use of this method unless extrication will be significantly delayed. In a prospective prehospital rewarming study, hot pack rewarming was the only technique that increased body temperature during transport.357 A hydraulic sarong or vest, in which heated water is circulated via a hand pump, is also used occasionally.123 Immersion rewarming is dangerous in the field because monitoring and resuscitation capabilities are limited. The Norwegian HeatPac Personal Heater can deliver 100 watts for 8 hours. The charcoal “vest” burns a briquette and has a favorable heat-to-weight ratio, unlike most rewarming devices.48 Battery polarity is critical to prevent carbon monoxide exposure.324 This device uses a single D battery that must be inserted correctly to avoid a CO exhaust hazard. It is durable, lightweight (1 kg), efficient, and effective. It circulates hot air within a blanket or sleeping bag and provides a comfortable, warm, and dry environment for transporting victims. Allow the unit to heat up for 5 minutes before use. Another option under development is a modified forced-air warming system for field use.71,100,105 The Portable Rigid ForcedAir Cover is heated with a Bair Hugger 505 Heater/Blower. It covers the patient’s trunk and thighs and can adapt to various transport vehicle power sources. Experimentally, convective warming is more efficient than is resistive heating.158
PREHOSPITAL LIFE SUPPORT A patent airway and the presence of respirations must be established (Figure 5-7). The victim may appear apneic if respiratory minute ventilation is significantly depressed. A common error in tracheally intubated patients is overzealous assistance of ventilation, which can induce hypocapnic ventricular irritability. The indications for prehospital endotracheal intubation are identical to those under normothermic conditions. Appropriate ventilation with 100% oxygen may protect the heart during extrication and transport. Avoid overinflation of the tracheal cuff with frigid ambient air. As the victim warms, air in the cuff can expand and kink the tube. Careful protection and fixation of the tubing of the cuff port during extremely cold conditions are necessary to prevent breakage and cuff leak. Palpation of peripheral pulses is often difficult in vasoconstricted and bradycardic patients. Apparent cardiovascular collapse may actually reflect cardiac output that is depressed just enough to meet minimal metabolic demands. The rescuer should auscultate and palpate for at least 1 minute to find pulses if a cardiac monitor or ultrasound is unavailable. Iatrogenic VF can easily result from chest compressions that were not indicated. If a cardiac monitor is available, use maximal amplification to search for QRS complexes. If the victim is in VF, the rescuer 127
CHAPTER 5 Accidental Hypothermia
The rescuer should administer an IV fluid challenge with 250 to 500 mL heated (37° to 41° C [98.6° to 105.8° F]) 5% dextrose in normal saline solution. Empiric 50% dextrose is indicated only in select cases. The safety of several reversal agents, such as naloxone or flumazenil, used in the field is unknown. Concerns regarding these agents before warming include precipitation of acute withdrawal, seizures, and markedly increased oxygen utilization. Most patients are volume depleted. Nevertheless, iatrogenic volume overload should be avoided, because myocardial contractility is impaired. Improvisation during transport is often helpful. For example, a plastic IV container can be placed under the patient’s back, shoulders, or buttocks to add warmth and infusion pressure. Taping heat-producing packets to IV bags is another option. These heating agents may be chemical packets or phase-change crystals, which produce heat for up to several hours. A variety of “hot pack” hypothermia devices are commercially available, including the Wilderness IV Warmer and the Ultimate Hot Pack. Another commercially available device is the Wilderness Oxygen Warmer. IV fluid compressors are bulb-inflating cuffs that surround IV pouches to maintain flow. The Israeli army has a spring steel compressor system for IV bags. Portable IV fluid heaters are commercially available. The devices fit in-line and are DC powered. Commercial heaters are available that are powered by a PhysioControl battery or from a DC converter plugged into an AC outlet. The Hot Sack IV Warmer runs on 12 volts from any vehicle or portable battery. The current drain is 4 amperes, and the insulation case loses only 0.5° C (0.9° F) over 10 minutes. In a study comparing IV warming techniques, meals ready to eat (MRE) heat packs or a camp stove outperformed standard chemical heat packs.275 Another option is an in-line battery-powered, disposable, lightweight fluid-warming device (Thermal AngelTex). Peripheral vessels may be difficult to locate, and IV lines are hard to maintain during transport. Ideally, IV fluids should be warmed to body temperature or slightly higher, but total body warming is not accomplished with IV fluids in the field. Using intraosseous infusions may provide a reasonable pathway for fluid replacement in the field when peripheral vessels have collapsed and cannot be entered. The methods selected to stabilize core temperature should be tailored to the severity of hypothermia and the field circumstances. Gently removing or cutting off wet clothing while the patient remains prone may be the best option to limit heat loss and prevent orthostasis. Passive external rewarming with waterproof insulation suffices for mild chronic hypothermia. In their series of patients requiring cardiopulmonary bypass (CPB), Walpoth and colleagues354,355 “maintained” hypothermia during transport. Whether supplemental active field rewarming should be initiated en route to the ED, and in which subsets of patients, is not definitively established. Intentionally maintaining hypothermia during transport seems wise only for patients with an isolated closed-head injury. For long helicopter or ambulance transports, the ideal ambient temperature in the vehicle is unclear. Rescue personnel comfort is important to maximize performance, and it is unlikely that heating the interior above 25° C will accelerate the rate of rewarming or induce vasodilation. “Field rewarming” is a misnomer, because adding much heat to a hypothermic patient in the field is difficult.81 Warmed IV solutions, heated sarongs, or heated humidified oxygen can provide only a small amount of heat input. Hot water bottles or heat packs can be placed in the axillae, in the groin, and around the neck. Casualty evacuation bags are available in many models and designs. Some have more insulation than others, and some have specialized zippers and openings that allow access to the victim during transport. Most bags are windproof and waterproof. Experimentally, convective air warming is more effective than resistive heating158 and might be a viable option in some transport situations. Inhalation therapy is safe for active rewarming of victims with profound hypothermia in the field.125 It helps prevent respiratory heat loss, which represents an important percentage of heat production when the core temperature is below 32° C (89.6° F). Technical difficulties have been experienced while using
PART 2 COLD AND HEAT
Rescue/examine Responsive
Yes
No Respirations No
Yes
Heated humidified ventilation
Assume cardiac output
Insulate IV D5 NS
Cardiac monitor
Electrical complexes
Cardiac monitor
Nonperfusing rhythm
Heated humidified oxygen
Gentle evacuation
Central pulse
No (PEA)
Chest compression
Yes Hospital assessment
FIGURE 5-7 Prehospital life support. PEA, Pulseless electrical activity.
should attempt defibrillation initially with 2 watt sec/kg up to 200 watt sec. The energy requirement for defibrillation does not increase in hypothermia. If the patient does not respond, defer further attempts, and assume that the victim must be rewarmed at least past 30° C (86° F) before further attempts.7 Do not perform defibrillation if organized narrow electrical complexes are seen on the monitor. Most monitors and defibrillators have not been tested for operation at temperatures below 15.5° C (59.9° F). Standard monitor leads do not always stick well to cold skin, so benzoin may be useful. If this fails, needle electrodes may be necessary. Another option is to puncture the Gelfoam conventional monitor pad with a small-gauge injection needle.359 Unresponsive victims should be carefully assessed for a central pulse before assuming they have pulseless electrical activity (PEA). The lowest temperature at which mechanical reestablishment of cardiac activity has been successful is 20° C (68° F),61 and defibrillation attempts rarely succeed below 30° C (86° F). If resuscitation in the field is unsuccessful, rewarming and CPR should be continued during transport to the ED.268
MANAGEMENT IN THE EMERGENCY DEPARTMENT The history obtained from a hypothermic patient is often unreliable, so it is prudent to confirm hypothermia and monitor with continuous core temperature measurements. Diagnostic errors in the ED usually result from incomplete monitoring of vital signs. Doppler ultrasound may be necessary to locate a pulse and should be supported by continuous ECG monitoring. The physician should also address the requirements for resuscitation and initiate advanced life support when necessary (Box 5-5). Temperature Measurement Most hospitals have adequate equipment for accurate core temperature measurement.259 Rectal measurements are most practical clinically for mild cases but may not reflect cardiac or brain temperatures.133 An indwelling thermistor probe placed to a depth of 15 cm (6 inches) is fairly reliable unless adjacent to cold feces. Rectal temperature lags behind core temperature fluctuations and is also affected by lower-extremity temperatures (Table 5-3).364 Esophageal temperature measurements are far preferable in severe cases and when airway protection is provided with endotracheal intubation. Esophageal temperature approximates cardiac temperature. Because the upper one-third of the esophagus is near the trachea, the probe may read falsely high during heated 128
inhalation therapy if the probe is positioned too proximally. The probe should be placed 24 cm (9.5 inches) below the larynx. The greatest discordance between rectal and esophageal temperatures is noted during the transition phase between cooling and rewarming. Tympanic temperature theoretically approximates hypothalamic temperature and can be accurately measured with thermometers that are in contact with the tympanic membrane. Because these are impractical except in anesthetized patients, external auditory canal thermometers that measure infrared emission from the tympanic membrane are available. These are not actually “tympanic” thermometers, but this term is used extensively.379 Unfortunately, the external auditory canal thermometers are not very sensitive. Tympanic thermometers are inaccurate when compared with a true core temperature measured with a pulmonary artery catheter.85 Although bladder temperature measurement devices can be incorporated into the urinary drainage catheter, the readings are frequently unreliable. They are falsely elevated with heated peritoneal lavage and, more commonly, low as a result of coldinduced diuresis and crystalloid resuscitation. Initial Stabilization After core temperature measurement, all clothing should be gently removed or cut off with minimal patient manipulation.268 BOX 5-5 Resuscitation Requirements Thermal Stabilization • Conduction • Convection • Radiation • Evaporation • Respiration Maintenance of Tissue Oxygenation • Adequate circulation • Adequate ventilation Identification of Primary Versus Secondary Hypothermia Rewarming Options • Passive external rewarming • Active external rewarming • Active core rewarming
Type
Advantages
Considerations
Rectal
Convenient Continuous monitoring
Esophageal
Convenient Continuous monitoring
Tympanic
Approximates hypothalamic temperature via internal carotid artery Convenient Continuous monitoring
Insert 15 cm (6 inches) Lags during transition from cooling to rewarming Falsely elevated with peritoneal lavage Falsely low if probe is in cold feces or when lower extremities are frozen Insert 24 cm (9.5 inches) below larynx Tracheal misplacement Aspiration Falsely elevated with heated inhalation Probe: tympanic membrane perforation; canal hemorrhage Infrared: unreliable; cerumen effect
Bladder
Unreliable Falsely elevated with peritoneal lavage Falsely low with cold diuresis
Immediately insulate the patient with dry blankets. Apply a cardiac monitor, and insert intravenous catheters as needed. Arterial catheter insertion may help in managing selected profoundly hypothermic patients. Pulmonary artery catheters can precipitate cardiac arrhythmias and should be reserved for complex cases. Insertion of pulmonary artery catheters into cold vessels may perforate the pulmonary artery.46 Central venous catheters should not be inserted into the right atrium, because this could precipitate arrhythmias.312 A better option is temporary catheterization of the femoral vein. The accuracy of pulse oximetry during conditions of poor perfusion is unclear, because there are no studies in accidental hypothermia.190 In one study of hypothermic patients on CPB, the finger probes were inaccurate.43 The probe may be made more reliable if a vasodilating cream is applied first. In addition, there is a lag time in pulse oximetry with hypoxic desaturation in anesthetized hypothermic subjects. There is decreased failure of forehead pulse oximetry in comparison to fingertip readings.226 In theory, combining pulse oximetry with near-infrared spectroscopy could provide tissue perfusion information during hypothermic vasoconstriction. More practically, an accurate core and peripheral muscle temperature would prove just as useful. The value of end-tidal carbon dioxide measurements to assess adequacy of tissue perfusion and tracheal tube placement is established at normal temperatures. Most of these devices, however, measure only the carbon dioxide content of dehumidified air and thus cannot be used during airway rewarming. Laboratory evaluations to be considered, except in some cases of mild hypothermia, include blood glucose, arterial blood gases, complete blood cell count, electrolytes, BUN, creatinine, serum calcium, serum magnesium, serum amylase and lipase, PT, PTT, INR, platelet count, and fibrinogen level. A toxicologic screen should be considered if the level of consciousness does not correlate with the degree of hypothermia. Selective studies of thyroid function, cardiac markers, and serum cortisol levels are indicated.58 The indications for radiography should be liberalized from normothermia. Radiologic evaluation of poorly responsive patients must include cervical and other spine images to detect occult trauma. Chest radiographs may predict lung collapse during rewarming when cardiomegaly and redistribution of vascularity are already present. Abdominal imaging should be obtained when the physical examination is unreliable. Bowel sounds are usually diminished or absent in severe hypothermia, and rectus muscle rigidity is frequently present. Pneumoperitoneum, pancreatic calcifications, or hemoperitoneum may be
noted. Small bowel dilation is associated with cold-induced mesenteric vascular occlusion, and colonic dilation is often present in conjunction with myxedema coma. The use of focused abdominal sonography may be helpful.54 Nasogastric tube insertion should be performed after endotracheal intubation in moderate or severe hypothermia, because gastric dilation and poor gastrointestinal motility are common. Indwelling bladder catheters with urine meters are needed to monitor urine output and the cold diuresis.
Fluid Resuscitation Most fluid shifts are reversed by rewarming, and mild hypothermia usually requires only modest amounts of crystalloids. In more severe cases, volume shifts and elevated blood viscosity from hemoconcentration, lowered temperature, increased vascular permeability, and low flow state mandate aggressive fluid resuscitation. The viscosity of blood increases 2% per degree Celsius drop in temperature; therefore hematocrit values over 50% are commonly seen. Low circulatory plasma volume is often coupled with elevated total plasma volume during rewarming. Hemodilution is usually not a problem and is seen only during massive crystalloid resuscitation of actively hemorrhaging patients.32,56 Most patients are significantly dehydrated, with free water depletion elevating serum sodium concentration and osmolality. During the descent into a hypothermic state, normal physiologic cues for thirst become inactive and access to water is often difficult. Because hypothermia results in natriuresis, saline depletion may be present. Further causes of sodium losses include prior diuretic therapy and gastrointestinal losses. Preexisting total body sodium excess is seen with congestive heart failure, cirrhosis, and nephrosis. In these cases, serum sodium and osmolality values are often normal. Rarely, serum sodium level is low because of free water excess. Other causes include myxedema, panhypopituitarism, and inappropriate antidiuretic hormone secretion. Most adult patients with a core temperature below 32.2° C (90° F) should receive an initial fluid challenge with 250 to 500 mL of warmed 5% dextrose in normal saline solution. Theoretically, Ringer’s lactate solution should be avoided because a cold liver cannot metabolize lactate. In severe cases, some clinicians favor a mixture of crystalloids and colloids. The victim should be monitored for standard clinical signs of fluid overload, including rales, jugular venous distention, hepatojugular reflux, and S3 cardiac gallop. Persistent cardiovascular instability often reflects inadequate intravascular volume. As mentioned, a properly placed central venous pressure catheter, such as a femoral line that does not enter and irritate the right atrium, has a role. Pulmonary wedge pressure measurements are rarely indicated. The need for RBC transfusions is determined by the corrected hematocrit; blood dilution with warmed infusate does not cause significant hemolysis. In many cases, rapid volume expansion is critical. Circulatory volume is decreased and peripheral vascular resistance is increased. In neonates, adequate fluid resuscitation markedly decreases mortality. Adults receiving hemodynamic monitoring show improvement of cardiovascular efficiency during crystalloid administration. VF immediately after rescue is attributed to both core temperature afterdrop and vascular imbalance in patients who are moved suddenly from a horizontal supine position.218 The fluxing relationship between active vascular capacity and circulating fluid volume depends not only on the mechanism of cooling but also on the method of rewarming. Hypothermic patients, particularly those with frostbite, are at high risk for extremity compartment syndromes and rhabdomyolysis. Pelvic fracture belt slings should be considered only to temporarily stabilize coexistent exsanguinating major pelvic fractures.
Rewarming Options PASSIVE EXTERNAL REWARMING Because hypothermia is an extremely heterogeneous condition and evidence-based treatment guidelines do not exist, rigid treatment protocols are ill advised.295,299,380 A versatile approach to 129
CHAPTER 5 Accidental Hypothermia
TABLE 5-3 Core Temperature Measurements
PART 2 COLD AND HEAT
BOX 5-6 Rewarming Techniques Passive External • Thermal stabilization Active External • Radiant heat • Hot water bottles • Plumbed garments • Electric heating pads and blankets • Forced circulated hot air • Immersion in warm water • Negative-pressure rewarming Core • Inhalation rewarming • Heated infusions • Gastric and colonic lavage • Mediastinal lavage • Thoracic lavage • Peritoneal lavage • Diathermy • Hemodialysis • Venovenous extracorporeal blood rewarming • Arteriovenous extracorporeal blood rewarming • Cardiopulmonary bypass
rewarming can be developed after careful consideration of the observations from animal experiments, human experiments on mild hypothermia, and various clinical reports (Box 5-6).118,119,278 Treatment should be predicated on the presenting pathophysiology and the available resources and expertise. The initial key treatment decision is whether to use passive or active rewarming (Box 5-7). Noninvasive passive external rewarming (PER) is ideal for most previously healthy patients with mild hypothermia. The patient is covered with dry insulating materials in a warm environment to minimize the normal mechanisms of heat loss. When the wind is blocked, less heat escapes via radiation, convection, and conduction. Conditions with higher ambient humidity slightly limit respiratory heat loss. Aluminized body covers also reduce heat loss.82,143 Nevertheless, endogenous thermogenesis must generate an acceptable rate of rewarming for PER to be effective.260 Humans are functionally poikilothermic below 30° C (86° F), and metabolic heat production is less than 50% of normal below 28° C (82.4° F). Shivering thermogenesis is also extinguished below 32° C (89.6° F). This thermoregulatory neuromuscular response to cold normally increases heat production from 250 to 1000 kcal/hr unless glycogen is depleted before or during cooling. Older adult patients in whom mild hypothermia develops gradually are less acceptable candidates for PER. When rewarming times are markedly prolonged (over 12 hours), complications tend to increase. Patients who are centrally hypovolemic, glycogen depleted, and without normal cardiovascular responses should be stabilized and rewarmed at a conservative rate. In a multicenter survey, the rewarming rates for older adults in the first (0.75° C [1.35° F]), second (1.17° C [2.11° F]), and third (1.26° C [2.27° F]) BOX 5-7 Indications for Active Rewarming • Cardiovascular instability • Moderate or severe hypothermia (<32.2° C [90° F]) (poikilothermia) • Inadequate rate or failure to rewarm • Endocrinologic insufficiency • Traumatic or toxicologic peripheral vasodilation • Secondary hypothermia impairing thermoregulation • Identification of predisposing factors (see Box 5-2)
130
hours far exceeded 0.5° C (0.9° F) per hour, with no increase in mortality rate (Figure 5-8, online).59
ACTIVE REWARMING Active rewarming, which is the direct transfer of exogenous heat to a patient, is usually required with temperatures below 32° C (89.6° F).208 Rapid identification of any impediment to normal thermoregulation, such as cardiovascular instability or endocrinologic insufficiency, is essential.209 Intrinsic thermogenesis may also be insufficient after traumatic spinal cord transection or pharmacologically induced peripheral vasodilation. Some patient populations generally require active rewarming.63,195 For example, aggressive rewarming of infants minimizes energy expenditure and decreases mortality. In these circumstances, vigorous monitoring for respiratory, hematologic, metabolic, and infectious complications is essential.350 When active rewarming is needed, heat can be delivered externally or to the core. Active external rewarming (AER) techniques deliver heat directly to the skin. Examples include forcedair rewarming, immersion, arteriovenous anastomosis rewarming, plumbed garments, hot water bottles, heating pads and blankets, and radiant heat sources.349 During rewarming of hypothermic patients, there are metabolic pH and inflammatory interleukin fluxes.238,344 Cytokine production may be activated by accidental hypothermia.1
ACTIVE EXTERNAL REWARMING The interpretation of survival rates with AER is affected by various risk factors and patient selection criteria.63,317 Some experimental and clinical reports link AER with peripheral vasodilation, hypotension, and core temperature afterdrop, but previously healthy, young, and acutely hypothermic victims are usually safe candidates for AER.32 Heat application confined to the thorax may mitigate many of the physiologic concerns pertaining to the depressed cardiovascular and metabolic systems, which are unable to meet accelerated peripheral demands.340 Combining truncal AER with active core rewarming may further avert many potential side effects.73 Forced-Air Surface Rewarming Forced-air surface warming systems efficiently transfer heat.11,103,160,195,196 The Bair Hugger uses hot forced air circulated through a blanket. The air exits apertures on the patient side of the cover, permitting the convective transfer of heat.237,306 In one study that rewarmed accidental hypothermia victims in the ED, rewarming shock and core temperature afterdrop were not noted321 with the use of heated inhalation and warmed IV fluids. A group also treated with a convective cover inflated at 43° C (109.4° F) rewarmed 1° C (1.8° F) per hour faster than a group covered with a cotton blanket (1.4° C [2.5° F] per hour). Experimentally, resistive external heating is more effective than passive metallic-foil insulation.120 A study of full-body forced-air warming compared a commercially available convective blanket with simple air delivery beneath bedsheets.181 Directed 38° C (100.4° F) warm air under the sheets warmed standardized thermal bodies containing water very efficiently. Commercially available convective air rewarming devices (WarmTouch, whole-body blanket) are also effective. Another option is conductive warming with a warm water–filled heat exchange blanket (Blanketrol). The use of forced-air surface warming systems is most practical in the ED.193,211 Although these devices decrease shivering thermogenesis, afterdrop is minimized and heat transfer can be significant. Thermal injury to poorly perfused, vasoconstricted skin using some of the other external heat application techniques is a hazard in both adults and children.123,188 In particular, avoid resistanceheat electric blankets on which a patient lies, because vasoconstricted capillaries are compressed and burns occur easily. Another active external rewarming option is a thermoregulatory system that circulates warm water through energy transfer pads placed on the chest and lower limbs (Arctic Sun). The core temperature measured via probe is fed back to the control module.
Arteriovenous Anastomosis Rewarming The original description of this noninvasive AER technique was by Vangaard and colleagues345 in 1979. Exogenous heat is provided by immersion of the lower parts of the extremities (hands, forearms, feet, calves) in 44° to 45° C (111.2° to 113° F) water. The heat opens arteriovenous anastomoses (AVAs). These organs are 1 mm (0.4 inch) below the epidermal surface in the digits.17,71,243 Countercurrent heat loss is minimized because the superficial veins are not close to the arterial tree. To be efficacious, the cutaneous heat exchange area must include the lower legs and forearms, and the water must be 44° to 45° C (111.2° to 113° F). Advantages with AVA rewarming include patient comfort and decreased afterdrop after cooling.317 A permutation of AVA rewarming is negative-pressure rewarming. Under hypothermic conditions, the AVAs remain closed during peripheral vasoconstriction. In combination with localized heat application, application of subatmospheric pressure theoretically distends the venous rete and increases flow through the AVAs. To initiate negative-pressure rewarming, the forearm is inserted through an acrylic tubing sleeve device fitted with a neoprene collar. This allows an airtight seal to form around the forearm. After a vacuum pressure of −40 mm Hg is created, heat is applied over the dilated AVAs. The thermal load can be provided via an exothermic chemical reaction or a heated perfusion blanket. The clinical efficacy of AVA rewarming in accidental hypothermia is unclear. Studies concluding that heat exchange is ineffectual used cooler water applied only on the hands and feet.37,52 The potential for superficial burns of anesthetic, vasoconstricted skin is a consideration. Another caveat is hypotension precipitated in hypovolemic patients who remain semiupright with this technique. In one study, the rate of core rewarming increased dramatically,113 but another study comparing negativepressure rewarming with forced-air warming failed to replicate these results.329 Active Core Rewarming Various techniques that can effectively deliver heat to the core290,303,345 include heated inhalation, heated infusion, diathermy, lavage (gastric, colonic, mediastinal, thoracic, peritoneal), and extracorporeal rewarming. Average first-hour rewarming rates reported with some of these techniques in one multicenter study are listed in Figure 5-8, online. Although hemodynamic instability impacts the rewarming strategy, noninvasive techniques often succeed unless there are significant comorbidities.288 Airway Rewarming The effectiveness of the respiratory tract as a heat exchanger varies with technique and ambient conditions.241 Because dry air has low thermal conductivity, complete humidification coupled with an inhalant temperature of 40° to 45° C (104° to 113° F) is required.286 The main benefit of airway rewarming is prevention of respiratory heat loss. Heat yield can represent 10% to 30% of the hypothermic patient’s heat production when respiratory minute volume is adequate.28 The rate of rewarming is greater using an endotracheal tube (ETT) than by mask. In one series, the reported rewarming rate with a 40° C (104° F) aerosol was 0.74° C (1.33° F) per hour via mask and 1.22° C (2.2° F) per hour via ETT.244 In a multicenter survey,59 the average first- and second-hour rewarming rates in severe cases were 1.5° to 2° C (2.7° to 3.6° F) per hour. Because
100
O2 (% saturation)
Immersion in a 40° C (104° F) circulating bath presents difficulties in monitoring, resuscitation, treatment of injuries, and maintenance of extremity vasoconstriction to prevent core temperature afterdrop. In normothermic men with coronary artery disease, the cardiovascular stress and arrhythmogenic response to immersion in a hot tub are mild, less than those induced by exercise.4 In contrast, placing the hands and feet in warm water theoretically opens arteriovenous shunts and accelerates rewarming in acute hypothermia. The attraction to Scandinavian palmar heat packs may reflect this physiology.
of the decremental efficiency at higher temperatures, the rate is slower (10 kcal/hr) in mild cases.59 Thermal countercurrent exchange in the cerebrovascular bed of humans64 affects the efficiency and influence of heated-mask ventilation during hypothermia. Known as the rete mirabile, this system could preferentially rewarm the brainstem. Heated inhalation via face mask continuous positive airway pressure (CPAP) may correct the ventilation–perfusion mismatch.38 Heated humidified oxygen via face mask is not feasible in some patients with coexistent midface trauma. Heat liberated during airway rewarming is produced mainly from condensation of water vapor. The latent heat of vaporization of water in the lungs is slightly lower than 540 kcal/g H2O. This is multiplied by the liters per minute ventilation to calculate the quantity of heat transfer. When core temperature is 28° C (82.4° F), the rate of rewarming with heated ventilation at 42° C (107.6° F) equals endogenous heat production. Although the effect on overall thermal balance can be minimal, there may be preferential rewarming of thermoregulatory control centers.56 Heated humidified inhalation ensures adequate oxygenation, stimulates pulmonary cilia, and reduces the amount and viscosity of cold-induced bronchorrhea. Although preexisting premature ventricular contractions (PVCs) may reappear during rewarming, there is no evidence that inhalation rewarming precipitates new, clinically significant ventricular arrhythmias. Vapor absorption does not increase pulmonary congestion or wash out surfactant. When the pulmonary vasculature is heated, warmed oxygenated blood that returns to the myocardium could attenuate intermittent temperature gradients. The amplitude of shivering is also lowered, an advantage in more severe cases. This suppression could decrease heat production in mild hypothermia, although experimentally the core temperature continues to rise.52 There are numerous oxygenation considerations in hypothermia (see Box 5-1). The “functional” value of hemoglobin at 28° C (82.4° F) is 4.2 g/10 g in patients on CPB.93 The oxyhemoglobin dissociation curve also shifts to the left (Figure 5-9). This impairs release of oxygen from hemoglobin into the tissues. Although some patients can self-adjust their respiratory minute volume (RMV) for current carbon dioxide production, this may not be possible if there are additional toxins or metabolic depressants.56 Most humidifiers are manufactured in accordance with International Standards Organization (ISO) regulations. The humidifier will not exceed 41° C (105.8° F) close to the patient outlet with a 6-foot tubing length.353 If the decision is made to alter equipment, carefully monitor the temperature and do not exceed 45° C (113° F). The only report of thermal airway injury was in a patient ventilated via endotracheal tube for 11 hours with 80° C (176° F) inhalant. Strategies to circumvent the 41° C ceiling include reduction of tubing length, adding additional heat sources, disabling the humidifier safety system, and placing the temperature probe
NORMAL
50
T 37° C pH 7.40
0 0
50
100
PO2 (mm Hg) FIGURE 5-9 Oxyhemoglobin dissociation curve at 37° C (98.6° F). At colder temperatures, the curve shifts to the left.
131
CHAPTER 5 Accidental Hypothermia
Immersion
PART 2 COLD AND HEAT
outside the patient circuit.353 Label all modified equipment to avoid routine use. A volume ventilator with a heated cascade humidifier can also deliver CPAP or positive end-expiratory pressure (PEEP) if needed during rewarming. The airway rewarming rates clinically range from 1° to 2.5° C (1.8° to 4.5° F) per hour.59 In stable patients, circumventing the 41° C ceiling may not be worth the effort because the clinical benefit is modest.180 Heat and moisture exchangers function like artificial nares by trapping exhaled moisture and then returning it. They provide inadequate humidification to treat accidental hypothermia. With prolonged use, ETT occlusion and atelectasis are both problems.45 Airway rewarming is indicated in the ED when core temperature is lower than 32.2° C (90° F) on arrival. Although airway rewarming provides less heat than do other forms of active core warming, it prevents normal respiratory heat and moisture loss and is safe, fairly noninvasive, and practical in all settings. Heated Infusions Cold fluid resuscitation of hypovolemic patients can induce hypothermia. In one series of previously normothermic patients with major abdominal vascular trauma, the average postresuscitation temperature was 31.2° C (88.2° F) in those with refractory coagulopathies. IV fluids are heated to 40° to 42° C (104° to 107.6° F), although higher temperatures may be safe. The amount of heat provided by solutions becomes significant during massive volume resuscitations.27,313 One liter of fluid at 42° C (107.6° F) provides 14 kcal to a 70-kg patient at 28° C (82.4° F), elevating the core temperature almost 0.33° C (0.6° F). Significant conductive heat loss occurs through IV tubing, so long lengths of IV tubing increase heat loss, especially at slow flow rates.84 IV tubing insulators are available. There are various methods to achieve and maintain ideal delivery temperature of IV and lavage fluids in hypothermia, but there is no standardized approach.124,297 Blood preheated to 38° C (100.4° F) in a standard warmer is useful, but clotting and shortened RBC life are hazards with blood-warming packs. Local microwave overheating hemolyzes blood. An alternative is to dilute packed RBCs with warm calciumfree crystalloid. The Level 1 fluid warmer (Level 1 H-1200 Fast Flow Fluid Warmer with integrated air detector/clamp) warms cold crystalloid and blood via a heat exchanger at flow rates of up to 500 mL/min. A more portable and compact option is the Ranger. Unlike the Level 1, however, this unit must remain above the level of the patient, and the infusion capability is much lower. The Thermal Angel is a portable, lightweight, battery-powered infusion warmer that has the advantage of portability to the initial point of rescue or trauma. Microwave heating of IV fluids in flexible plastic bags is another option when more standardized heaters are unavailable. The plasticizer in the polyvinyl chloride containers is stable to microwave heating. Heating times should average 2 minutes at high power for a 1-L bag of crystalloid. The fluid should be thoroughly mixed before administration, to eliminate hot spots. Rapid administration of fluid into the right atrium at a temperature significantly different from that of circulating blood may produce myocardial thermal gradients.320 In one study, heated IV fluid, up to 550 mL/min, was administered through the internal jugular vein without complication. In an experimental canine model with adequate cardiac output, central infusion of extremely hot (65° C [149° F]) IV fluids accelerates rewarming without hemolysis.90,309 Using amino acid infusions may accelerate energy metabolism.305 Fever is common in patients receiving hyperalimentation. In patients recovering from elective surgery, however, amino acids have no significant thermogenic effect.139 The results might differ in energy-depleted patients with chronically induced accidental hypothermia. In summary, intravenous solutions and blood should be routinely heated during hypothermia resuscitations. Various blood warmers are available commercially, but countercurrent in-line warmers are the most efficient techniques.157 A mathematic model indicates that infusion heating devices are essential in trauma patients with high fluid requirements.27 132
HEATED IRRIGATION Gastrointestinal Irrigation Heat transfer from irrigation fluids is usually limited by the available surface area, so do not use irrigation as the sole rewarming technique. The irrigant should not exceed 45° C (113° F). Direct gastrointestinal irrigation is less desirable than irrigation via intragastric or intracolonic balloons because of induced fluid and electrolyte fluxes. Exceeding 200- to 300-mL aliquots may force fluid into the duodenum; therefore frequent fluid removal via gravity drainage minimizes “lost” fluid. A log of input and output is essential. This facilitates estimation of fluid balance during resuscitation and helps determine if irrigation should be abandoned in anticipation of dilutional electrolyte disturbances. To avoid these limitations, a double-lumen esophageal tube is available, as are other modified Sengstaken tubes.199 Patients should be tracheally intubated before gastric lavage. Because of the proximity of an irritable heart, overly vigorous placement of a large gastric tube is ill advised. In a multicenter survey, gastric, bladder, and colon lavage rewarmed severely hypothermic patients at 1° to 1.5° C (1.8° to 2.7° F) for the first hour and 1.5° to 2° C (2.7° to 3.6° F) for the second hour.59 Commercially available kits designed for gastric decontamination are convenient (Figure 5-10). The use of a Y connector and clamp simplifies the exchanges. Ideal dwell times for thermal exchange depend on flow rates and may average several minutes. In direct gastric lavage, warmed electrolyte solutions, such as normal saline or Ringer’s lactate, are administered via nasogastric tube.213 After 15 minutes, the solution is aspirated and replaced with warm fluids. Disadvantages include the small surface area available for heat exchange and the large amount of fluid escaping into the duodenum.36 Regurgitation is common, and the technique must be terminated during CPR. Esophageal and bladder heat exchange are also very limited.201,285,359,360 Aesthetic obstacles aside, heat transfer through colonic irrigation is negligible. Mediastinal Irrigation Mediastinal irrigation and direct myocardial lavage are alternatives in patients lacking spontaneous perfusion. A standard left thoracotomy is performed while CPR is continued. Opening the
Warm saline
15 min
Drainage
FIGURE 5-10 Gastric lavage.
Thoracic Lavage Irrigation of the hemithoraces is a valuable rewarming adjunct.14,34,35,189,356 An important semantic issue is that closed thoracic lavage via two thoracostomy tubes differs from open mediastinal and direct myocardial lavage. With the latter, closedchest CPR is not possible. Two large-bore thoracostomy tubes (36F to 40F in adults; 14F to 24F, ages 1 to 3; 20F to 32F, ages 4 to 7) are inserted in one or both of the hemithoraces. One is placed anteriorly in the second to third intercostal space at the midclavicular line, and the other in the posterior axillary line at the fourth to fifth intercostal space. Normal saline heated to 40° to 42° C (104° to 107.6° F) is then infused via a nonrecycled sterile system (Figure 5-11, A).185 A high-flow countercurrent fluid infuser heats to 40° C (104° F) and delivers normal saline in 1-L or preferably 3-L bags into the afferent chest tube.83,278 This author prefers connecting into the tubing with standard 0.19-inch internal-diameter suction connection tubing and a sterilized plastic graduated two-way connector, because this facilitates adaptation to any size chest tube (see Figure 5-11, A). The effluent is then collected in a thoracostomy drainage set. The reservoir must be emptied frequently. Alternatively, when a single chest tube is used, 200- to 300-mL aliquots are used for
irrigation, and suctioning is achieved through a Y connector. The Y connector is also useful for irrigating both hemithoraces with a single fluid warmer (Figure 5-11, B). Fluid can be infused into the anterior higher chest tube (afferent limb) and suctioned or gravity drained out the lower posterior tube (efferent limb) into a water-seal chest drain.122 Infusion inferoposteriorly with suction anteriorly can increase dwell times.159 The efficiency of thermal transfer varies with flow rates and dwell times. Once the patient is successfully rewarmed, the upper tube should be removed and the lower one left in place to allow residual drainage. Closed sterile thoracic lavage is a natural choice in the ED during potentially salvageable cardiac arrest resuscitations.369 Thoracic lavage is an option either as a bridge to CPB or when CPB is initially unavailable. In patients who are perfusing, this technique should be considered hazardous unless extracorporeal rewarming capability is immediately available. Many hypothermic trauma patients are irrigated successfully during surgery. The clinically reported infusion rates range from 180 to 550 mL/min. The overall rate of rewarming should easily equal or exceed that achievable with peritoneal lavage and is often 3° to 6° C (5.4° to 10.8° F) per hour. The surface area of the pleural space is well perfused. An added benefit is preferential mediastinal rewarming. In addition, closed-chest compressions during cardiac arrest can maintain perfusion. Open cardiac massage of a rigid, contracted heart may not be possible in severe cases before bypass, which is a problem with mediastinal irrigation.5,53,58 Various complications should be considered. Left-sided thoracostomy tube insertion into patients who are perfusing could easily induce VF. Patients with pleural adhesions or a history of pleurodesis have poor infusion rates, and subcutaneous edema may develop. If the fluids are infused under pressure without adequate drainage, intrathoracic hypertension or even a tension hydrothorax can develop and cause expected adverse cardiovascular effects.174,274 Peritoneal Lavage Heated peritoneal lavage is a technique available in most facilities (Figure 5-12). Heat is conducted intraperitoneally via isotonic dialysate delivered at 40° to 45° C (104° to 113° F).348 Before lavage is initiated, chest and abdominal radiographs should be obtained because subsequent films may reveal Warmed saline
Saline
Rib 2
AA
Heat exchanger
3
S V C
Lung
RB
4
Fluid warmer
T6
Air eliminator
Midclavicular line Postaxillary line
5 6
Saline out
B
Autotransfusion bag
A
Water seal chest drain FIGURE 5-11 Thoracic lavage. A, Cycle. B, Cross section.
133
CHAPTER 5 Accidental Hypothermia
pericardium is unnecessary unless an effusion or tamponade is present. The physician bathes the heart for several minutes in 1 to 2 L of an isotonic electrolyte solution heated to 40° C (104° F), then suctions and replaces warm fluids.34 The physician may attempt internal defibrillation after myocardial temperature reaches 26° to 28° C (78.8° to 82.4° F). Unless a perfusing rhythm is achieved, lavage is continued until myocardial temperature exceeds 32° to 33° C (89.6° to 91.4° F). A standard post-thoracotomy tube in the left side of the chest could provide an avenue for continued rewarming via thoracic irrigation. A median sternotomy also allows ventricular decompression and direct defibrillation.212 One potential disadvantage of both these techniques is that open cardiac massage of a cold, rigid, and contracted heart may not generate flow.5,53 Unless immediate CPB is an option, mediastinal irrigation and direct myocardial lavage are indicated only if cardiac arrest has occurred. In this circumstance, personnel skilled in the technique should also initiate all other available rewarming modalities.
PART 2 COLD AND HEAT
14F catheter
Peritoneum Fascia of linea alba
A Wire FIGURE 5-13 Peritoneal lavage. A 14F catheter is of a caliber that can infuse fluids rapidly. Catheter
Umbilicus
B
8F catheter
C FIGURE 5-12 Peritoneal lavage. A, Mini-laparotomy for peritoneal lavage. B, The catheter in place with the needle removed and the wire introduced. C, An 8F catheter is introduced over the wire, and the wire is then removed.
134
subdiaphragmatic air introduced during the procedure. The bladder and stomach must be emptied before insertion of the catheter. The two common techniques for introducing fluid into the peritoneal cavity are the mini-laparotomy and the percutaneous puncture. The “minilap” requires an infraumbilical incision through the linea alba. A supraumbilical approach is necessary if previous surgical scars, a gravid uterus, or pelvic trauma is identified. The peritoneum is punctured under direct visualization and dialysis catheter(s) inserted. A much simpler and more rapid technique is the guidewire, or Seldinger, variation of the percutaneous puncture. The site is infiltrated if necessary with lidocaine, and a small stab incision is made. An 18- to 20-gauge needle penetrates the peritoneum, and a guidewire is introduced. Entry into the peritoneum is usually recognizable by a distinct “pop.” A disposable kit is available (Arrow Peritoneal Lavage Kit [AK09000]). The 8F lavage catheter is inserted over the wire and advanced into one of the pelvic gutters. Double-catheter systems with outflow suction speed rewarming. Normal saline, lactated Ringer’s solution, or standard 1.5% dextrose dialysate solution with optional potassium supplementation can be used.82 Isotonic dialysate is heated to 40° to 45°C (104° to 113° F). Up to 2 L is then infused (10 to 20 mL/kg), retained for 20 to 30 minutes, and aspirated. The usual clinical exchange rate is 6 L/hr, which yields rewarming rates of 1° to 3° C (1.8° to 5.4° F) per hour. An alternative for severe cases is a larger catheter, as found in cavity drainage kits (Arrow 14F [AK-01601]) (Figure 5-13). The catheter can be placed with the Seldinger technique. The higher drainage capability markedly increases exchange rates and minimizes the dwell times necessary for maximal thermal transfer. The flow rate via gravity through regular tubing is approximately 500 mL/min, which can be tripled under infusion pressure. A unique advantage of peritoneal dialysis is drug overdose and rhabdomyolysis detoxification when hemodialysis is unavailable. In addition, direct hepatic rewarming reactivates detoxi fication and conversion enzymes. Peritoneal dialysis worsens preexisting hypokalemia. Vigilant electrolyte monitoring is essential before empirical modification of the dialysate. The presence of adhesions from previous abdominal surgery increases the complication rate and minimizes heat exchange. Peritoneal dialysis during standard mechanical CPR is as effective as partial cardiac bypass in resuscitating severely hypothermic dogs.364 In contrast to AER, peritoneal lavage rewarming did not require significantly greater quantities of crystalloids and bicarbonate. This exchange rate is rarely possible in humans. Bowel infarction may be a concern when using prolonged warm peritoneal dialysis in patients with severe hypothermia with inadequate visceral perfusion during CPR. Peritoneal lavage is invasive and should not be routinely used in treating stable, mildly hypothermic patients. This technique is
ENDOVASCULAR WARMING Another active rewarming option that is emerging is endovascular warming with commercially available temperature control devices. They are used in EDs for therapeutic cooling of resuscitated comatose cardiac arrest patients.367 Less invasive and technically easier than extracorporeal rewarming, endovascular systems that involve femoral vein catheterization may prove to be a promising alternative. The closedloop catheter has a temperature control element at the tip. Available models have a fail-safe feature on the console that must be circumvented to allow rewarming if the core temperature is below 30° C (86° F).203
EXTRACORPOREAL BLOOD REWARMING Table 5-4 summarizes the techniques for extracorporeal blood rewarming. Hemodialysis Standard hemodialysis is widely available, practical, portable, and efficient, and should be strongly considered in perfusing patients with electrolyte abnormalities, renal failure, or intoxication with a dialyzable substance.149,254,267 Two-way flow catheters allow the option of cannulation of a single vessel.205,327 A Drake-Willock single-needle dialysis catheter can be used with a portable hemodialysis machine and an external warmer. After central venous cannulation, exchange cycle volumes of 200 to 250 mL/min are possible. Although heat exchange is less than with standard two-vessel hemodialysis, the ease of percutaneous subclavian vein placement is a major advantage. Hemodialysis via two separate singlelumen catheters placed in the femoral vein can achieve continuous blood flow at 450 to 500 mL/min.135,136 In-line hemodialysis also TABLE 5-4 Techniques for Extracorporeal Blood
Rewarming
Technique
Comments
Cardiopulmonary bypass
Full circulatory support Perfusate temperature gradient: consider 5°-10° C (9°-18° F) Flow rates of 2-7 L /min (average, 3-5 L /min) Rate of rewarming, up to 9.5° C (17.1° F) per hour Consider if K <10 mmol/L, pH >6.5, at least 10°-12° C (50°-53.6° F) Percutaneous Seldinger technique to insert catheters Requires blood pressure of ≥60 mm Hg No need for perfusionist/pump/ anticoagulation Average flow rates of 225-375 mL/min Rate of rewarming, 3°-4° C (5.4°-7.2° F) per hour Consider for trauma Circuit not complex Efficient nonbypass modality Volume infusion to augment cardiac output Flow rates of 150-400 mL /min Rate of rewarming, 2°-3° C (3.6°-5.4° F) per hour Widely available Portable and efficient Single or dual catheter Exchange cycle volumes, 200-500 mL /min Rate of rewarming, 2°-3° C (3.6°-5.4° F) per hour Consider if there are electrolyte/toxicologic derangements
Continuous arteriovenous warming
Venovenous rewarming
Hemodialysis
Modified from Danzl DF: Hypothermia, Semin Resp Crit Care Med 23:57, 2002.
Water outlet
Cold blood inflow
CHAPTER 5 Accidental Hypothermia
indicated in combination with all available rewarming techniques in cardiac arrest patients.
Femoral artery Femoral vein
Warm blood outflow
Water inlet (40° C) Filter
FIGURE 5-14 Schematic of continuous arteriovenous rewarming.
simplifies correction of electrolyte abnormalities. Local vascular complications, including thrombosis of vessels and hemorrhage secondary to anticoagulation, may occur. Continuous Venovenous Rewarming In extracorporeal venovenous rewarming, blood is removed, usually from a central venous catheter, heated to 40° C (104° F), and returned via a second central or large peripheral venous catheter. Flow rates average 150 to 400 mL/min.116,131,319,336 The circuit is not complex and is more efficient than many other non-bypass modalities. There is no oxygenator, and because the method does not provide full circulatory support, volume infusion is the only option to augment inadequate cardiac output. Although the use of CAVR is limited by profound hypotension, high-flow venovenous rewarming may prove to be an alternative.162 In another variation of the extracorporeal venovenous circuit, blood is removed from the femoral vein, heparinized, and sent through a blood rewarmer via an infusion pump accelerator. It is neutralized with protamine before reinjection into the subclavian or internal jugular vein, which would preferentially rewarm the heart. Another option is to insert a femoral vein dual-lumen dialysis catheter. Continuous Arteriovenous Rewarming CAVR involves the use of percutaneously inserted femoral arterial and contralateral femoral venous catheters.95,96,98 This technique requires a blood pressure of at least 60 mm Hg. The Seldinger technique is used to insert 8.5F catheters. Heparinbonded tubing circuits obviate the need for systemic anticoagulation. CAVR has principally been performed on traumatized patients (Figure 5-14). The blood pressure of spontaneously perfusing traumatized hypothermic patients creates a functional arteriovenous fistula by diverting part of the cardiac output out of the femoral artery through a countercurrent heat exchanger (e.g., Level 1; FloTem IIe). The heated blood is then returned with admixed heated crystalloids via the femoral vein. The additional fluids are titrated and infused by piggyback until hypotension is corrected.251 The rate of rewarming exceeds that of hemodialysis. CAVR does not require the specialized equipment and perfusionist necessary for CPB. The average flow rates are 225 to 375 mL/ min, resulting in a rate of rewarming of 3° to 4° C (5.4° to 7.2° F) per hour. Because the catheters are 8.5F, the patient must weigh at least 40 kg. Coagulation begins to appear in the heparinized circuits at around 3 hours. Cardiopulmonary Bypass Partial or complete CPB should be considered in unstable, severely hypothermic patients.15,117,186,289,372 Favorable considerations include absence of severe head injury or asphyxia.314 Some 135
PART 2 COLD AND HEAT
centers initiate CPB only if the presenting arterial pH is above 6.5, serum potassium is below 10 mmol/L, and core temperature is above 10° to 12° C (50° to 54° F).142,337,355 Fischer’s considerations for CPB include a potassium level under 10 mmol/L in adults or under 12 mmol/L in children, coupled with a core temperature below 30° C (86° F). Patients are not resuscitated if extreme hyperkalemia is identified in a patient with a temperature over 30° C (86° F).92 A major advantage of CPB is preservation of oxygenated flow if mechanical cardiac activity is lost during rewarming.70,150,155,234 CPB is three to four times faster at rewarming than other active core rewarming (ACR) techniques, and it reduces the high blood viscosity associated with severe cases. CPB should also be considered when severe cases do not respond to less invasive rewarming techniques, in patients with completely frozen extremities, and when extensive rhabdomyolysis is accompanied by major electrolyte disturbances.169 Various extracorporeal rewarming techniques can be lifesaving in select profound cases of hypothermia.127 Althaus and colleagues describe complete recovery in three severely hypothermic tourists after prolonged periods of cardiac arrest and CPR.5 In another review of 17 cases, there were 13 survivors.318 Walpoth and co-workers354,355 report rewarming 32 patients with CPB, of which 15 are long-term survivors. The average age was 25.2 years. Their mean presenting esophageal temperature was 21.8° C (71.2° F), and the mean interval between discovery and CPB was 141 minutes. The standard femoral–femoral circuit includes arterial and venous catheters, a mechanical pump, a membrane or bubble oxygenator, and a heat exchanger (Figure 5-15). A 16F- to 30F venous cannula is inserted via the femoral vein to the junction of the right atrium and the inferior vena cava. The tip of the shorter 16F to 20F arterial cannula is inserted 5 cm (2 inches) or proximal to the aortic bifurcation. Antretter and colleagues8 use 32F venous and 28F arterial cannulas with the open surgical technique, and 21F venous and 19F arterial cannulas if inserted percutaneously. Closed-chest compressions can be maintained during percutaneous or open surgical technique insertion and may help decompress the dilated nonbeating heart. Transesophageal echocardiography can help evaluate ventricular load and valve function. Heated, oxygenated blood is returned via the femoral artery.20 Femoral flow rates of 2 to 3 L/min can elevate core temperature 1° to 2° C (1.8° to 3.6° F) every 3 to 5 minutes. In a review by Splittgerber and co-workers,318 the mean CPB temperature increase was 9.5° C (17.1° F) per hour. Most pumps can generate full flow rates up to 7 L/min. Long222 recommends considering
Oxygenator and vortex pump Portable bypass machine
Heat exchanger
the use of vasodilator therapy with IV nitroglycerin to facilitate perfusion. He initiates bypass flow rates at about 2 L/min and gradually increases to 4 to 5 L/min. Vasoactive agents may be needed to maintain the cardiac index at 30 L/min/m2 or more and a (low) systemic vascular resistance of 1000 dynes/sec × cm−5 or less.228 The optimal temperature gradient and bypass rewarming rates are unknown. One study of rewarming via CPB in a swine model cooled to 23° C (73.4° F) addresses this concern. An excessive temperature gradient between brain tissue and circulant adversely affected electroencephalographic (EEG) regeneration. The other theoretical concern is the possibility of increased bubbling if high perfusate temperature gradients are used. Most investigators use 5° C (9° F) gradients23 or 10° C (18° F) gradients.24 Eventually, neuromonitoring during rewarming will provide some answers. In severe cases, evoked cerebral responses before EEG regeneration could help assess the recovering brain.304 A variety of techniques decrease the need for IV anticoagulation with heparin, which previously limited clinical applicabil184 ity. Heparin-coated perfusion equipment was used successfully without systemic heparinization in a patient with hypothermic cardiac arrest (23.3° C [73.9° F]) and intracranial trauma.351 The use of nonthrombogenic pumps, coupled with enhanced physiologic fibrinolysis seen in the first hour of CPB, also succeeds experimentally. Complications with the standard technique include vessel damage, air embolism, hemolysis, DIC, and pulmonary edema (Box 5-8). Endothelial leakage increases compartment pressures and exacerbates frostbite. If adequate flow rates of 3 to 4 L/min (50 to 60 mL/kg/min) cannot be maintained, thoracotomy or a venous catheter with side holes, augmenting intravascular volume, should be considered. With all four of these techniques, there is no proof that rapid acceleration of the rate of rewarming improves survival rates in patients being perfused. The value of the maintenance of some degree of mild hypothermia after hypothermic cardiac arrest and extracorporeal rewarming is speculative. With accidental hypothermia, patients may have had neuroprotection before cardiac arrest from hypothermia. Potential complications of uncontrolled rapid rewarming in severe hypothermia include DIC, pulmonary edema, hemolysis, and acute tubular necrosis. As an alternative, a conservative core-rewarming approach can be highly effective for patients with severe hypothermia, despite hemodynamic instability.291 In hypothermic cardiac arrest, rewarming should be attempted via CPB and hemodialysis when CPR is not contraindicated (Box 5-9), unless frozen intravascular contents prevent flow.
Arterial line 16-20F
Venous line 16-30F
FIGURE 5-15 Femoral–femoral bypass.
136
BOX 5-9 Contraindications to Initiating
Complications • Vascular injury • Air embolism • Pulmonary edema • Coagulopathies (hemolysis, disseminated intravascular coagulation) • Frostbite tissue damage • Extremity compartment syndromes
• Do-not-resuscitate status is documented and verified. • Obviously lethal injuries are present. • Chest wall depression is impossible. • Any sign of life is present. • Rescuers are endangered by evacuation delays or altered triage conditions.
Cardiopulmonary Resuscitation in Accidental Hypothermia
Contraindications • Futile resuscitations • Lack of venous return • Intravascular clots or slush • Complete heparinization would be hazardous* • Cardiopulmonary resuscitation is contraindicated (see Box 5-9)
From Danzl DF, Pozos RS, Auerbach PS, et al: Multicenter hypothermia survey. Ann Emerg Med 16:1042, 1987. Developed in conjunction with the Wilderness Medical Society.
irradiation “until they squealed and suckled.” Subsequently, 20 of 28 human infants rewarmed with microwave irradiation at 90 to 100 watts survived. The temperature rose an average 1° C (1.8° F) after 6 to 7 minutes, and the average infant required 45 minutes to achieve a rectal temperature of 36° C (96.8° F). In an experimental study of men cooled to 35° C (95 ° F), warm water immersion rewarming is more rapid than radio-wave rewarming with 2.5 watts/kg.178 Both ultrasonic and low-frequency microwave diathermy can deliver large quantities of heat below the skin. As dosimetry guidelines develop, potential complications and ideal application sites for this experimental technique deserve further study in the hospital. In the field setting, potential problems with power supply and electronic and navigational interference compound the physiologic problems.
*Unless with athrombogenic tubing or adequate physiologic fibrinolysis.
Clotted atrial blood or failure to obtain venous return indicates that these techniques will be futile. If experienced personnel and necessary equipment are unavailable, all other rewarming techniques should be used in combination.23,350,370 Diathermy Diathermy, the transmission of heat by conversion of energy, is a potential rewarming adjunct in accidental hypothermia.140,220 Large amounts of heat can be delivered to deep tissues with ultrasonic (0.8 to 1 MHz) and low-frequency (915 to 2450 MHz) microwave radiation. Short-wave (13.56 to 40.68 MHz) modalities are high frequency and do not penetrate deeply. Contraindications include frostbite, burns, significant edema, and all types of metallic implants and pacemakers. Under ideal conditions in a laboratory study, radio-wave frequency (13.56 MHz) electromagnetic regional heating of hypothermic dogs after immersion does not damage tissue at 4 to 6 watts/kg and rapidly elevates core temperature.365 Zhong and colleagues381 successfully rewarmed 16 piglets with microwave FIGURE 5-16 Emergency department algorithm. ACR, Active core rewarming; AER, active external rewarming; CPB, cardiopulmonary bypass; PEA, pulseless electrical activity; PER, passive external rewarming.
Cardiopulmonary Resuscitation Basic and advanced life support recommendations in hypothermia continue to evolve (Figure 5-16).* Cardiac output generated with closed-chest compressions maintains viability in select patients with hypothermia.325 The optimal rate and technique are unknown. Definitive prehospital determination of cardiac *References 7, 67, 91, 180, 316, 323, 334.
Yes
Responsive No Respirations Yes
No Tracheal intubation and heated humidified oxygen
Cardiac monitor
Cardiac monitor Electrical complexes
Core temperature
Central pulse
Below 32.2° C (90° F) Above 32.2° C (90° F) PER
Yes
Arrest rhythm Attempt defibrillation
No (PEA)
ACR and truncal AER
All ACR and CPB
137
CHAPTER 5 Accidental Hypothermia
BOX 5-8 Extracorporeal Rewarming
PART 2 COLD AND HEAT
activity requires a cardiac monitor, because misdiagnosis of cardiac arrest is a hazard. Peripheral pulses are difficult to palpate when extreme bradycardia is present with peripheral vasoconstriction.130,366 Asystole may be as common a presenting rhythm as VF. In the field, differentiating VF from asystole may be impossible. Possible causes of VF include acid–base fluxes, hypoxia, and coronary vasoconstriction with increased blood viscosity. Chest compressions and various therapeutic interventions are also implicated, but not proven causes.121,265 The role of acid–base fluxes is not clear. Mild alkalosis appears somewhat protective against VF during controlled, induced hypothermia.200
RESPIRATORY CONSIDERATIONS When cardiopulmonary arrest develops during resuscitation, noncardiac causes are often pulmonary emboli or progressive respiratory insufficiency. Provision of adequate oxygen supply is essential during rapid rewarming. For each 1° C (1.8° F) rise in temperature, oxygen consumption increases up to three times (see Box 5-1).93 Endotracheal intubation and ventilation decrease atelectasis and ventilation–perfusion mismatch. Complete airway protection averts aspiration, which is otherwise common with depressed airway reflexes, bronchorrhea, and ileus. Carbon dioxide production also drops by one-half with an 8° C (14.4° F) fall in the temperature. During induced hypothermia, carbogen (1% to 5% carbon dioxide added to oxygen) facilitates acid–base management by allowing adjustment of the fractional inspired carbon dioxide concentration (FICO2) while adjusting the ventilation. Past controversy regarding the hazards of endotracheal intubation reflected coincidental episodes and a mis-citation by Fell and colleagues87 regarding a series of hypothermic overdoses reported by Lee and Ames.210 Fell and colleagues stated that “endotracheal intubation was followed by cardiac arrest in a large proportion of cases,” whereas Lee and Ames merely cautioned of that possibility. In a multicenter survey, endotracheal intubation was performed on 117 patients by multiple operators in various settings.59 No induced arrhythmias were recognized, which is consistent with several reports.209,244 Potential arrhythmogenic factors include hypoxia, mechanical jostling, and acid–base or electrolyte fluctuations. The indications for endotracheal intubation in hypothermia are identical to those in normothermia.54,107 It is required unless the patient possesses intact protective airway reflexes. Ciliary activity is depressed in hypothermia, frothy sputum produces chest congestion, and bronchorrhea resembles pulmonary edema. Fiberoptic or blind nasotracheal intubation may be preferable to cricothyroidotomy when cold-induced trismus or potential cervical spine trauma is present. Oral rather than nasal intubation is advisable in patients with coagulopathy, to avoid causing major epistaxis. Rapid-sequence intubation may be impossible when severe cold-induced trismus is present and the mandible will not move. In the milder cases, hypothermia prolongs the duration of neuromuscular blockade. Drug metabolism is also prolonged with vecuronium and atracurium. As a result, avoid using neuromuscular blockers.180 Efficacy, metabolism, and clearance are very unpredictable, and assessment of sedation adequacy is difficult.
BLOOD FLOW DURING CHEST COMPRESSIONS During normothermic conditions, blood flow partially results from phasic alterations in intrathoracic pressure and not just from direct cardiac compression. Niemann and co-workers261 demonstrated that antegrade flow occurs without left ventricular compression in a normothermic canine model. Closed-chest compressions increase intrathoracic pressure.227 When thoracic inlet venous valves are competent, the resultant pressure gradient between arterial and venous compartments generates supradiaphragmatic antegrade flow. Clinical observations challenge the “cardiac pump” model. This model is predicated on closure of the mitral valve and opening of the aortic valve during chest compression. This allows a forward stroke volume. During release of compression, transmitral flow 138
can fill the left ventricle. Optimal cardiac output is thus generated by achieving the maximal compression rate that allows maximal left ventricular end-diastolic filling. Interestingly, transesophageal echocardiography in a canine model demonstrates mitral valve closure during chest compression except during low-impulse (downstroke momentum) compressions. Compression of a cold, stiff chest wall may be equivalent to low impulse.53 In hypothermia, the role of a “thoracic pump” with the heart as a passive conduit is an attractive hypothesis. The phasic alterations in intrathoracic pressure generated by compressions are equally applied to all of the cardiac chambers and thoracic vessels. The mitral valve remains open during compression, and blood continues to circulate through the left side of the heart. Myocardial compliance can be severely reduced in hypothermia. Althaus and colleagues5 noted at thoracotomy in one of three survivors of hypothermia that “the heart was found to be hard as stone and it is hardly conceivable how effective external cardiac massage could have been.” Open cardiac massage can be combined with mediastinal irrigation when immediate cardiopulmonary bypass is an option.34-36 Chest wall elasticity is also decreased with cold, as is pulmonary compliance. If the abdominal muscles are not kneadable, anticipate that the stiff chest wall will prevent adequate ventilation. Lastly, more force is needed to depress the chest wall sufficiently to generate intrathoracic vascular compartment pressure gradients. Despite these potential physiologic explanations, a large number of neurologically intact survivors are reported after prolonged closed-chest compressions. The explanation lies in measuring intrathoracic pressures during hypothermic closedchest compressions. Perfusion enhancement maneuvers remain largely unstudied in hypothermia. Ancillary abdominal binding might favorably inhibit paradoxical diaphragmatic motion.53,261 Simultaneous compression and ventilation can increase flow in the heart’s left side. Ventilation with the proper carbogen concentration also allows high ventilatory rates while maintaining uncorrected PaCO2 at 40 mm Hg. Placement of a counterpulsation intra-aortic balloon is another option. Mechanical thoracic compression devices could be useful during prolonged resuscitations with limited availability of personnel. In addition, an automatic mechanical chest compression device may serve as a bridge while establishing the capability for CPB.366 During hypothermic cardiac arrest in swine, cardiac output, cerebral blood flow, and myocardial blood flow averaged 50%, 55%, and 31%, respectively, of those achieved during normothermic closed-chest compressions.230 Blood flow to these areas did not decrease with time, unlike in the normothermic group. No significant difference in flow generated appeared between normothermic and hypothermic swine at 20 minutes. Hypothermic rheologic changes, including increased viscosity, also affect flow. Peripheral vascular resistance is expected to increase during vasoconstriction, but in the swine there was no difference in systemic and organ vascular resistance between normothermic and hypothermic CPR.230 In a multicenter survey of 428 cases, 9 of the 27 patients receiving CPR initiated in the field survived, as did 6 of 14 patients with ED-initiated CPR.59 Based on these cases and a literature review, CPR standards in hypothermia are proposed (see Box 5-9). Because cardiac output is the product of heart rate and stroke volume, the optimal closed-chest compression rate should be the fastest rate allowing optimal ventricular filling. Many patients have recovered neurologically after slow compression rates. One recovered after 220 minutes at half the normal compression rate.263 The optimal rate probably has a direct linear relationship with the degree of hypothermia. Tissue decomposition, apparent rigor mortis, dependent lividity, and fixed, dilated pupils are not reliable criteria for withholding CPR. In addition, intermittent flow may provide adequate support during evacuation. Although one position paper implies otherwise, in the opinion of this author CPR should not be withheld only because continuous chest compressions cannot be ensured.42,76 Intermittent flow may be preferable to no flow. The lowest temperature documented in an infant survivor of
Cerebral Resuscitation The ability to reestablish cerebral blow flow with CPR and improve neurologic outcome is inversely proportional to the duration of cardiac arrest. Significant delay can markedly elevate the cerebral perfusion pressure (CPP) required to establish cerebral blood flow (CBF).19 It appears that thermal stabilization rather than aggressive field rewarming should be the focus, except for severely hypothermic victims or those in cardiac arrest. Mild hypothermia may be therapeutic and improve neurologic outcome after global cerebral ischemia. Hypothermia decreases glutamate release, metabolic demand, free radical formation, and release of inflammatory cytokines.109,294 In the prehospital setting, addressing disproportionate hypotension, hypoperfusion, and hypoxia is paramount. Once the airway is secured, elevating the head 5 to 10 degrees can attenuate intracerebral hypertension induced by global cerebral ischemia. Normally, CBF is independent of CPP over a range of pressures. After cerebral autoregulation is extinguished, CBF passively depends on the arterial blood pressure. When venous access is difficult, medications may be administered intratracheally or via the intraosseous route. Of interest, large internal jugular catheters may partially obstruct cerebral venous outflow.232 Because hypoxemia is the rule, supplemental oxygen should be initiated when available. The goal is normoxia. The prolonged use of 100% oxygen after the return of spontaneous circulation may increase oxidative brain injury by generating reactive oxygen species, including superoxide and hydrogen peroxide. The rescuer should avoid positive end-expiratory pressure unless it is essential to maintain normoxia, because it decreases cerebral venous outflow. Cerebral vasculature autoregulation may be lost after global brain ischemia, and yet hypocarbia-induced vasoconstrictive mechanisms remain intact. Therefore avoid protracted hyperventilation except in the rare case of a cranially traumatized hypothermic victim with impending uncal herniation. In the field, attempt to ventilate the patient at a rate that would maintain the uncorrected partial pressure of carbon dioxide (PCO2) between 35 and 40 mm Hg.231 Postischemic hyperglycemia is potentially detrimental, because glucose levels over 250 mg/dL are associated with lactate generation and exacerbation of metabolic acidosis. Cerebral resuscitation strategies in hypothermia reflect complex neurophysiology.294 The brain, although making up only 2% of total body weight, requires 15% of the cardiac output and consumes 20% of the available oxygen at 37° C. Cerebral blood flow depends on the CPP, which equals the mean arterial pressure minus the intracranial pressure. When the CPP drops below 50 to 60 mm Hg, CBF drops. Once CBF is below 20%, a cascade is initiated that includes the failure to maintain ionic gradients in neurons, cellular depolarization, and acidosis. Even when cold, neurons are more susceptible to hypoxic insult than are glial or endothelial cells.148,173 When reperfusion is reestablished, the initial transient hyperemic period is characterized by increased CBF with low oxygen consumption. This lasts for minutes and is followed by the “no reflow” phase, which lasts for hours. Reperfusion is also characterized by both cytotoxic edema during ischemia, and vasogenic edema caused by blood–brain barrier injury. Intraluminal vascular damage is caused by nitric oxide (NO) and reactive oxygen species (ROS), and proteases inflict abluminal injury.44 The decrease in CBF decreases mitochondrial ATP generation. Ionic gradients collapse across the neuronal membrane, as a result of failure of the Na–K pump. Sodium influx results in
depolarization, which causes axonal release of the excitatory neurotransmitter glutamate. Glutamate is the ultimate trigger of neuronal injury caused by N-methyl-D-aspartate receptor activation, because it allows cellular calcium influx.192 Second messengers in the cascade are signals during ischemia from trigger events that activate other second messengers or perpetrators of damage. Intracellular overload of calcium inhibits mitochondrial respiration. In addition, nitric oxide synthase generates NO and ROS, both of which damage DNA and increase cytokine levels. In the field, emphasis should be placed on avoidance of factors known to exacerbate adverse neuronal responses to cerebral ischemia: disproportionate hypotension, hypoperfusion, hyperglycemia, hypoxia, and hyperoxia.239
Resuscitation Pharmacology The pharmacologic effects of medications are temperature dependent. The lower the temperature, the greater is the degree of protein binding. Enterohepatic circulation and renal excretion are also altered, so abnormal physiologic drug responses should be anticipated. The usual clinical scenario consists of substandard therapeutic activity while the patient is severely hypothermic, progressing to toxicity after rewarming.204 Medications are not given orally because of decreased gastrointestinal function, and intramuscular medications are avoided because they may be erratically absorbed from vasoconstricted sites. The pharmacologic manipulation of respiratory drive, pulse, and blood pressure is generally not indicated except in profound cases. When a relative tachycardia is not consistent with temperature depression, the possibility of hypovolemia, hypoglycemia, or a toxic ingestion should be considered. Vasopressors are potentially arrhythmogenic, might lower VF threshold, and cannot increase peripheral vascular resistance if the vasculature is already maximally constricted.209 If intra-arterial pressure is not consistent with the degree of hypothermia, judicious use of inotropic agents may be necessary.266 Dopamine can be a successful adjunctive treatment.300 Dopamine reverses cardiovascular depression under hypothermic conditions, equivalent to up to 5° C (9° F) rewarming. Dopamine decreases systemic vascular resistance at low infusion doses and increases it at high infusion rates.266 Shock requiring vasoactive drugs is a risk factor for mortality.36 In severe cases, the target mean arterial pressure is around 60 mm Hg. Epinephrine and vasoconstrictors should probably be avoided.194,198 Balancing the need for flow versus pressure, Zandstra recommends labetalol and IV nitroglycerin. This therapy can be coupled with 2 to 4 mcg/kg of dopamine, which is less arrhythmogenic than are exogenous catecholamines.378 Epinephrine is not recommended by the American Heart Association for hypothermic cardiac arrest below 30° C (86° F). In porcine models, there is no evidence that repeated or highdose epinephrine during hypothermic CPR improves outcome.194,198 In the same model, a single 0.4 unit/kg dose of vasopressin below 30° C (86° F) improved defibrillation success.302 There is conflicting evidence regarding cardiovascular function after rewarming. In some studies, there is complete reversal of cold-induced changes, whereas in another, the physiologic response to norepinephrine is paradoxical.361 Patients with profound hypothermia after ethanol ingestion have been resuscitated with low-dose dopamine support. In frostbite victims, however, the use of catecholamines may jeopardize the extremities.222,223 Catecholamines also exacerbate preexisting occult hypokalemia. The effect of temperature depression on the autonomic nervous system is complex. In primates, cooling produces a biphasic response in plasma catecholamine concentrations. After an initial increase, the autonomic nervous system switches off at 29° C (84.2° F),41 suggesting that catecholamine support might be useful below that temperature. The initial rise in catecholamine levels could also be caused by acute respiratory acidosis, which stimulates the sympathetic nervous system.31 Low-dose dopamine (1 to 5 mcg/kg/min) or other catecholamine infusions are generally reserved for disproportionately severe hypotensive patients who do not respond to crystalloid resuscitation and rewarming. 139
CHAPTER 5 Accidental Hypothermia
accidental hypothermia is 15.2° C (59.4° F); in an adult, 13.7° C (56.7° F); and in induced hypothermia, 9° C (48.2° F).51,59,106,258,264 One patient recovered after 6.5 hours of closed-chest compressions.215 In Saskatchewan 1994, a 2-year-old child reportedly recovered from a core temperature of 13.9 ° C (57° F). Remarkably, a physician who authored the report was successfully resuscitated from 13.7° C (57° F) after she received 165 minutes of CPR and then CPB.106
PART 2 COLD AND HEAT
THYROID The most dramatic Rip Van Winkle–type of rude awakening from hypothermic myxedema coma was Dr. Richard Asher’s patient in the 1950s. He was successfully metabolically aroused from a 7-year, 30° C (86° F) slumber. Ironically, so was a quiescent oat cell carcinoma. Cold induces stimulation of the hypothalamic-pituitary-thyroid axis. Unless myxedema is suspected, empirical therapy is not recommended. A history of neck irradiation, radioactive iodine, Hashimoto’s thyroiditis, or surgical treatment of hyperthyroidism should heighten the clinician’s suspicion of myxedema. Failure to rewarm despite an appropriate course of therapy is a further clue.225 Myxedema coma is usually precipitated in older adult patients with chronic hypothyroidism who are stressed by trauma, infection, anesthesia, or medication ingestion. Typical nonspecific laboratory abnormalities include hyponatremia, anemia, and liver enzyme and lipid elevations. If myxedema coma is suspected, thyroid function studies, including serum thyroxine (T4) by radioimmunoassay, triiodothyronine (T3) resin uptake, and thyroidstimulating hormone level, should be obtained and serum cortisol level measured. Given the appropriate index of suspicion, the physician should administer 250 to 500 mcg levothyroxine (T4) intravenously over several minutes without waiting for confirmatory laboratory results. Daily injections of 100 mcg are required for 5 to 7 days. The clinician should consider adding at least 100 to 250 mg of hydrocortisone to the first 3 L of intravenous fluid. Absorption of T4 is erratic if the drug is given orally or intramuscularly. The onset of action of T3 is more rapid, which jeopardizes cardiovascular stability; therefore T3 is avoided in acute replacement therapy. The onset of action of T4 is 6 to 12 hours, evidenced by continuous improvement of the vital signs during rewarming. Up to one-half of the T4 is eventually converted by the peripheral tissues into T3.
spontaneously during rewarming, and digitalization or other pharmacologic intervention is not warranted. Electrophysiologic studies show that the interval prolongation present on His bundle electrocardiography is unresponsive to atropine. Mesenteric embolization is a potential hazard when the rhythm converts back to sinus rhythm. Hypothermia renders the negative inotropic effects of calcium channel blockers redundant.56 In summary, all new atrial arrhythmias usually convert spontaneously during rewarming and should be considered innocent. Attention is directed toward correcting acid–base, fluid, and electrolyte imbalances and avoiding administration of atrial antiarrhythmics.
VENTRICULAR ARRHYTHMIAS Because preexisting chronic ventricular ectopy may be suppressed in a cold heart, the physician noting ectopy during rewarming is placed in a quandary. The history from the hypothermic patient may be unproductive, and the past cardiac history is often unavailable. Transient ventricular arrhythmias should generally be left untreated. In one study of 22 continuously monitored patients with hypothermia, supraventricular arrhythmias were common (9 cases) and benign.284 Ventricular extrasystoles developed in 10 patients, but none experienced ventricular tachycardia or VF during rewarming. The terminal rhythm in the 8 who died while being monitored was asystole and not VF. The energetics of the fibrillating hypothermic ventricle suggest that asystole may consume less energy and be more protective. Pharmacologic options are limited, because hypothermia induces complex physiologic changes that result in abnormal responses.374 Drug metabolism and excretion are both progressively decreased. In normothermia, class IA ventricular antiarrhythmics have negative inotropic and indirect anticholinergic effects, and they moderately decrease conduction velocity (Box 5-10). Procainamide increases the incidence of VF during hypothermia. Quinidine has been useful during induced profound
CORTICOSTEROIDS Acute cold stress and many coexisting disease processes stimulate cortisol secretion. The free active fraction of cortisol decreases as the temperature drops because of increased protein binding, and cortisol utilization is similarly decreased. The increase in adrenocorticotropic hormone (ACTH) and adrenal steroid secretion may also be a neurogenic or an emotional response in the conscious subject to an unpleasant environment. Experimentally, inhibition of ACTH secretion during hypo thermia is mediated by decreased hypothalamic secretion of arginine vasopressin. This decreases pituitary responsiveness to corticotropin-releasing factor, inhibiting corticotropin release. Thus exogenous arginine vasopressin could prove helpful during rewarming. Cold exposure also induces adrenal unresponsiveness to ACTH. As a result, false diagnosis of decreased adrenal reserve is possible and does not represent functional adrenal insufficiency, because ACTH levels return to normal after rewarming. Serum cortisol levels are commonly elevated. Secondary adrenal insufficiency resulting from panhypopituitarism may also coexist with myxedema. Empirical administration of corticosteroids is indicated if hypoadrenocorticism is suspected on the basis of a previous history of corticosteroid dependence, suggestive physical findings, or an inexplicable failure to rewarm. The use of narcotic antagonists in hypothermia is reported. Naloxone may reduce the severity of hypothermia in drug overdoses and in spinal shock and appears to have activity at the µ-opioid receptor sites.56
Resuscitation Complications ATRIAL ARRHYTHMIAS All atrial arrhythmias, including atrial fibrillation, should have a slow ventricular response with the temperature depression. Atrial fibrillation is commonly noted below 32° C (89.6° F) in accidental hypothermia victims. Atrial fibrillation usually converts 140
BOX 5-10 Antiarrhythmic Agents Class I. Sodium Channel Blockers IA. Conduction and depolarization moderately slowed, and action potential duration (APD) and repolarization prolonged • Disopyramide • Procainamide • Quinidine IB. Conduction and depolarization minimally slowed, and APD and repolarization shortened • Lidocaine • Mexiletine • Moricizine • Phenytoin • Tocainide IC. Conduction and depolarization markedly slowed, and APD and repolarization prolonged • Encainide • Flecainide Class II. β-Adrenergic Blockers Class III. Antifibrillatory Properties (APD Prolonged) • Amiodarone • Bretylium • D-sotalol Class IV. Calcium Channel Blockers • Diltiazem • Verapamil Unclassified • Adenosine • Magnesium sulfate
The ideal ventricular antiarrhythmic would do the following: • Cause no further decrease in conduction velocity • Shorten the action potential duration (APD) • Lengthen the APD only in warmer regions of the myocardium to reduce dispersion • Possess direct antifibrillatory properties
hypothermia, preventing VF during cardiac manipulation at 25° to 30° C (77° to 86° F). No reports detail the effects of disopyramide. The role of the class IB agent lidocaine for prophylaxis or treatment is unresolved. In animal studies, lidocaine and propranolol have minimal hemodynamic effects in hypothermia. If normothermic effects persisted during hypothermia, the class IB agents would appear attractive because they minimally slow conduction while shortening the action-potential duration (APD). The class III agent bretylium tosylate, a unique bromobenzyl quaternary ammonium compound, has been effective in several animal studies and ineffective in others.78,326 It is not commercially available. This class of agents seems most ideal pharmacologically because it possesses direct antifibrillatory properties. The ability to prolong the APD is temperature dependent. Ideally, a drug would lengthen the APD only in warmer regions of the myocardium to reduce dispersion (Box 5-11). Two cases of chemical ventricular defibrillation after infusion of bretylium (10 mg/kg) in accidental hypothermia are reported.54,191 In the first study to evaluate the effects of bretylium administered after induction of hypothermia, Murphy and co-workers252 noted that only 1 of 11 dogs given bretylium (mean, 40.5 mg/kg) before five invasive maneuvers developed VF. No dog, including control subjects, showed fibrillation during endotracheal intubation. Of note in discussions regarding prophylaxis, 3 of the 11 dogs converted to VF during the drug infusion. The effect of bretylium on plasma catecholamines and electrically induced arrhythmias has also been studied. Because catecholamine levels increase during cooling, the demonstrated protection appears to result from alteration of electrophysiologic properties of the cardiac tissues. Amiodarone is another class III drug that possesses direct antifibrillatory activity. In a canine model of severe hypothermic VF, neither bretylium nor amiodarone improved resuscitation.326 The safety of the class III antiarrhythmic agent D-sotalol is problematic.22 It has temperature-dependent effectiveness and lengthens prolonged action potentials more efficiently at long pacing cycle lengths. Also of note, magnesium sulfate at a dose of 100 mg/kg IV can spontaneously defibrillate most patients on CPB at 30° C (86° F) with induced hypothermia. Emergency transvenous intracardiac pacing of bradyarrhythmias is extremely risky with cold hearts because it commonly precipitates VF. New arrhythmias that develop after rewarming may, on rare occasions, require pacing. Transcutaneous pacing (TCP) with low-resistance electrodes seems far preferable before stabilization.144 In a canine model, TCP restored and maintained hemodynamic stability and rewarmed hypothermic animals twice as rapidly as it did the controls.69 In summary, there are no commercially available ventricular antiarrhythmics proved safe and effective in accidental hypothermia.
SEPSIS In hypothermia, the classic signs of infection, including erythema and fever, are absent.229 Rigors and shakes resemble shivering. The initial history, physical, and laboratory data are often unreliable, so repeated evaluations and comprehensive culturing are mandatory in the ED. The 10% subset of patients with sepsis syndrome who present with a hypothermic response have a significantly increased frequency of shock and death, and this secondary hypothermia does not appear to be protective. Hypothermia compromises host defenses and results in serious bacterial infections. These significant infections can be
accompanied by minimal inflammatory response. Some common causative organisms include gram-negative bacteria, grampositive cocci, oral anaerobes, and Enterobacteriaceae.214 The core endotoxin components of gram-negative bacteria normally signal macrophages. At a normal or elevated temperature, active cytokine triggers include tumor necrosis factor, interleukin-1, and interleukin-6. The potential role of antiendotoxin monoclonal antibodies in patients with accidental but not cytokine-induced hypothermia is unresolved. Bone marrow release and circulation of neutrophils are compromised for up to 12 hours. In addition, human and porcine neutrophils are susceptible to hypothermia. In vitro, neutrophil migration and bacterial phagocytosis are reduced at 29° C (84.2° F). Neutrophilic extermination of various bacteria, including Staphylococcus aureus and Streptococcus faecalis, is also impaired. Acquired neutrophil dysfunction occurs. In addition, hypothermia is associated with decreased neutrophil levels in neardrowned children. As a clinical demonstration of the importance of these factors, therapeutic maintenance of hypothermia to control cerebral edema in near drowning is abandoned because of the substantial incidence of infectious complications. The incidence of infection varies dramatically with the victim’s age and the clinical series reported.214,363 In one large group of infants, over one-half were septic. Although there were no reliable indicators of infection, some suggestive clues emerged. Serum glucose and leukocyte abnormalities, anemia, uremia, and bradycardia were often identified. In addition to Staphylococcus and Streptococcus, the predominant organisms were Haemophilus and Enterobacteriaceae. Lung infections, usually in the right upper lobe, were reported in many hypothermic infants by El-Radhi and colleagues.79 Evaluation of the gastric aspirate was another diagnostic predictor of sepsis in the majority of infected infants. In several studies, sepsis was found in a large percentage of hypothermic infants. In this age-group, empirical broad-spectrum antibiotics are warranted. In adults, the incidence of infection ranges from less than 1% to over 40%, depending on patient selection criteria.58 In the urban series of Lewin and co-workers,214 serious soft tissue or pulmonary infections were present in one-half the patients. Occult bacteremia was present in less than 1% of White’s series363 of 102 patients, and results were negative in all of the 46 lumbar punctures. In other studies of hypothermic older adult patients admitted to hospitals, most have had evidence of probable or definite infections.60 In summary, unlike children and older adults, most previously healthy young adults do not need empirical antibiotic prophylaxis. Nevertheless, treatment indications should be liberalized from normothermia. They should include failure to rewarm, and any suspicion or evidence of aspiration, myositis, chest film infiltrate, bacteriuria, or persistent altered mental status. In choosing broad-spectrum coverage, the physician should consider altered drug interactions, volumes of distribution, protein binding, hepatic metabolism, and renal excretion.
Forensic Pathology Macromorphologic and micromorphologic lesions are variable and nonspecific in hypothermia, and there is no single pathognomonic finding at autopsy.216,280,339 Establishing hypothermia as the primary cause of death requires an adequate history of exposure and the absence of other lethal findings at necropsy.5,161 Unnatural deaths in nursing home patients, for example, may be significantly underreported for these reasons.49 Macroscopic skin changes can suggest the diagnosis. Hyperemia of the dorsa of the hands and knees is commonly found. Nonpathognomonic findings have been identified in the pancreas, lungs, and heart. Pancreatic findings include fat necrosis, aseptic pancreatitis, and hemorrhage. Pulmonary changes consist of intra-alveolar, interstitial, and intrabronchial hemorrhages. An eye that has been directly exposed to the environment could be a chemical indicator of both the environmental and victims temperatures at the time of death. Vitreous humor chemistry profiles at autopsy can reveal that glucose concentration and total carbon dioxide content vary inversely with temperature, with 141
CHAPTER 5 Accidental Hypothermia
BOX 5-11 Antiarrhythmic Characteristics
PART 2 COLD AND HEAT
To function optimally “as the water stiffens” requires an understanding of the principles of heat conservation and loss.176 Welltrained and educated urban adults can participate in prolonged Arctic maneuvers safely.310,311,333 To maintain core temperature in the narrow band necessary for peak functioning in cold environments, appropriate adaptive behavioral responses are essential.145 Autonomic and endocrinologic mechanisms are only supplemental. Studies of human cold adaptation reach highly variable conclusions. Explanations for these discrepancies include changes in core and shell temperatures and in metabolic rates before and after cold adaptation. Hypothermic, insulative, isometabolic cold adaptation may be associated with local cold adaptation of the extremities.375 Excellent physical conditioning with adequate rest and nutrition is paramount.26 Hikers and skiers must be accompanied by a partner and should wear effective thermal insulation. Wet inner garments must be changed promptly. Persons who exert themselves, including long-distance skiers, should switch garments depending on current exertional heat production.146,148 Because dehydration must be avoided, drinking from a cold stream is preferable to snow ingestion. Significant energy is needed to convert ice at 0° C (32° F) into water. All areas with a large surface area–to–volume ratio should be well insulated.331 Excellent synthetic insulating materials include Gore-Tex, Flectalon, Thinsulate, and taslanized nylon. Under certain circumstances, insidious hypothermia may develop during exposure to cold water because of the effects of increased insulation on compensatory physiologic events.12,177 The army mnemonic COLD, in reference to insulation with clothing, means clean, open during exercise to avoid sweating, loose layers to retain heat, and dry to limit conductive heat losses. For a complete discussion of preventive measures, see Chapters 8 and 9. Prevention of urban accidental hypothermia requires continuous public education. For example, the optimal safe indoor temperature recommendation for older adults has risen to 21.1° C (70° F). Energy assistance and temporary sheltering are effective measures, and selective heating of sleeping quarters and use of electric blankets are economic suggestions. Prewarming the bed and bedroom at night may be the best overall advice to older adults.
are warm and dead.”248 Clearly, some victims are indeed “cold and dead,” and it would be useful to safely identify them.10 Survival is difficult to predict because human physiologic responses to temperature depression vary so widely.236,240,273 The type and severity of the underlying or precipitating disease process are two determinants.346 Age extremes, although not statistically correlated with survival, are commonly associated with severe illnesses. In a multicenter survey, however, there were no significant age differences in mortality.59 Gender, trauma, infection, and toxin ingestions affected survival differently in multiple, uncontrolled clinical studies.141 There were no clinically significant differences in male versus female profiles in the multicenter survey.59 From a large hypothermia database, a hypothermia outcome score could enable multiple observers at different sites to assess treatment modalities and outcome predictors.291 Prehospital cardiac arrest, low or absent blood pressure reading, elevated BUN, and the need for either endotracheal or nasogastric intubation in the ED were significant predictors of outcome after multivariate analysis.55,179 In a multiple regression analysis of 234 cases in Swiss clinics,221 the biggest negative survival factors were asphyxia, slow rate of cooling, invasive rewarming, asystole, and development of pulmonary edema or adult respiratory distress syndrome. The largest single-hospital series of adult hypothermic cardiac arrest patients rewarmed with CPB is reported from Finland. Patients with cold exposure or immersion without suffocation or asphyxia tolerated prolonged CPR before CPB.314 Positive predictors of survival include rapid cooling rate, presence of VF during cardiac arrest, and narcotic or ethanol intoxication. In a study of 29 patients below 30° C (86° F), mode of cooling was the only independent risk factor.273 In a study of CPB survivors, 15 of the 32 patients are longterm survivors.355 Their neuropsychological functioning after prolonged prehospital circulatory arrest is very encouraging. These patients were not asphyxiated before becoming hypothermic. Vretenar and colleagues352 reviewed the literature regarding the outcomes of 68 other patients resuscitated with CPB. The survival rate was 60%, and the coldest survivor had been 15° C (59° F). In a series of 26 patients given extracorporeal rewarming, those with nonasphyxiated deep accidental hypothermia had a reasonable prognosis.86 There is a need for a valid triage marker of death, because vital organ damage is difficult to predict. In one retrospective analysis of primarily avalanche burial victims, extreme hyperkalemia was noted on initial examination, and resuscitation proved fruitless.296 In the Mt Hood tragedy, the nonsurvivors were also hyperkalemic (serum potassium level greater than 10 mmol/L).127 Although a serum potassium level of 10 mmol/L appears to be a reasonable ceiling for viability, a child at 14.2° C (57.6° F) with a potassium level of 11.8 mmol/L did well.70 In both of these reports, asphyxia and compression injury may have been contributory. Other indicators of a grave prognosis include a core temperature below 12° C (53.6° F), arterial pH below 6.5, or evidence of intravascular thrombosis (direct visualization; fibrinogen below 50 mg/dL).
Outcomes
REFERENCES
Partially in reaction to the dramatic reports of reanimations, the historic standard of care has been that “no one is dead until they
Complete references used in this text are available online at www.expertconsult.com.
values significantly higher in the winter. An elevated vitreous glucose in a nondiabetic victim should suggest hypothermia. The total urinary catecholamine, particularly epinephrine, content was high in one group of casualties known to be hypothermic. Erosions of the gastric mucosa, termed Wischnewsky spots, are also frequently found.330,338,371 In addition, exposure to extreme cold should be suspected when unusual intravascular hemolysis, which is seen after freezing of blood, is observed in a corpse. Fatty degeneration in renal tubule epithelia may help confirm the diagnosis.279
PREVENTION
142
CHAPTER 6
Immersion Into Cold Water GORDON G. GIESBRECHT AND ALAN M. STEINMAN
The authors of this chapter hail from two different countries that view and measure temperature differently. The United States uses ° F (Fahrenheit), whereas the country up north uses ° C. (Some people think that the letter C stands for “Celsius,” but it actually means “Canadian.”) The author from up north has provided a conversion chart to allow neighbors from either side of the border to get on the same thermal wavelength (Box 6-1). Immersion in cold water is a hazard for anyone who participates in recreational, commercial, or military activities in the oceans, lakes, and streams of all but the tropical regions of the world. Recreational aquatic activities include swimming, fishing, sailing, power boating, ocean kayaking, white-water rafting, canoeing, ocean surfing, windsurfing, waterskiing, diving, hunting, and using personal watercraft. In addition, winter activities like driving on icy roads and snowmobiling can involve cold-water exposure as a result of accidental entry into lakes and streams.1 Commercial activities that involve water include fishing, shipping, offshore oil drilling, and diving. Military operations over cold water include Coast Guard (Figure 6-1), Navy, and Marine Corps missions. Army, Air Force, and Marine Corps forces may encounter cold-water exposure during winter operations on land. The definition of cold water is variable. The temperature of thermally neutral water, at which heat loss balances the heat production of a nude subject at rest (i.e., not shivering), is approximately 33° to 35° C (91.4° to 95° F).16,18 Hypothermia eventually results from immersion in water at less than this temperature. For practical purposes, significant risk for immersion hypothermia usually begins in water colder than 25° C (77° F),114,162,163 and it is quite significant in water colder than 15° C BOX 6-1 The Official Canadian Temperature
Conversion Chart
10° C (50° F) Americans shiver uncontrollably. Canadians plant gardens. 0° C (32° F) American water freezes. Canadian water gets thicker. −18° C (0° F) New York City landlords finally turn on the heat. Canadians have the last cookout of the season. −51° C (−60° F) Mt St. Helens freezes. Canadian Girl Guides sell cookies door to door. −114° C (−173° F) Ethyl alcohol freezes. Canadians get frustrated when they can’t thaw the keg. −273° C (−460° F) Absolute zero; all American atomic motion stops. Canadians start saying, “Cold, eh?” −295° C (−500° F) Hell freezes over. A U.S. hockey team beats Canada in the Olympic gold medal game.
(59° F). Table 6-1 shows the variation in water temperature throughout the year at various sites in North America.180 Figure 6-2 shows typical worldwide sea-surface temperatures for April, with data from 2005.126 With the use of 25° C (77° F) as the defining point for cold water, the risk of immersion hypothermia in North America is nearly universal during most of the year. Cold-water immersion is associated with two significant medical challenges: near drowning and hypothermia. This chapter discusses the physiologic responses to and treatment of immersion hypothermia, the risk of near drowning with respect to the physiologic consequences of sudden immersion in cold water, and the problems of survival in rough seas. Controversies are also identified and discussed. Chapter 5 discusses land-based hypothermia; Chapter 75 provides a more complete discussion of drowning; and Chapter 77 discusses diving injuries. Since the previous edition of this textbook was published, many audiovisual resources have been produced; several are listed in the Video Resources section at the end of this chapter.
History and Epidemiology The history of human association with the sea and with inland waters provides abundant examples of the effects of accidental cold-water immersion. Case studies demonstrate the scope of the problem. Perhaps the most famous occurrence was the sinking of the Titanic in 1912. After striking an iceberg at approximately 11:40 PM on April 14, the ship sank in calm seas, but the water temperature was near 0° C (32° F). Of the 2201 people on board, only 712 were rescued, all from the ship’s lifeboats. The remaining 1489 people died in the water, despite the arrival of a rescue vessel within 2 hours. Nearly all of these people were wearing “life preservers,” yet their causes of death were officially listed as drowning.119 However, it is more likely that their deaths were caused by immersion hypothermia. Survivors reported hearing victims’ screams for periods long enough (i.e., more than 1 hour) to indicate that the individuals in the water survived for a period of time sufficient to result in severe hypothermia.102,110
FIGURE 6-1 Canadian Coast Guard rescue boat in rough seas. (Courtesy Canadian Coast Guard.)
For online-only figures and videos, please go to www.expertconsult.com
143
PART 2 COLD AND HEAT
RECREATIONAL ACTIVITIES AND COLD WATER
Case 6-3 “SKATING” ON THIN ICE
A Canadian Red Cross Report stated that, from 1991 to 2000, there were 5900 water-related deaths in Canada. Two hundred and eighty-three (21%) of recreational boating drownings occurred in “extremely cold” water, which means that it was colder than 10° C (50° F). Of the 14% of all boating drownings in which the victims were wearing personal flotation devices (PFDs), most of these occurred in cold water, and death resulted from hypothermia. Of note is that 232 snowmobilers drowned after breaking through the ice, and 218 individuals died after falling through the ice during other activities. Cases 6-1 to 6-4 illustrate potential problems that might occur with immersion hypothermia during recreational boating, hiking, snowmobiling and other activities.
In the winter of 1997-1998, four people died when their snowmobile broke through the thin ice of Lake Scugog, which is near Toronto, Ontario, Canada. The deaths occurred, ironically, during Snowmobile Safety Week in North America. The Canadian Safety Council reported that, in 1997, 101 people were killed in snowmobile mishaps, the majority of them by drowning and hypothermia after crashing through ice on frozen rivers and lakes.1
Case 6-1 LONGTERM IMMERSION IN MODERATELY COLD WATER On February 28, 2009, four friends who were all former or current football players in their mid-twenties set out on a fishing trip in a 21-foot boat into the Gulf of Mexico west of Tampa Bay, Florida. According to the survivor’s account,148 their boat capsized in a storm before they could return to shore, and the four men were thrown into the 18° C (65° F) water. Weather conditions were 4.3-m (14-foot) seas and 15 to 18 m/sec (30 to 35 knot) winds. None of the men were wearing PFDs at the time of the capsizing. One of the survivors dove under the boat to retrieve three keyhole PFDs and one seat cushion. Despite their large size (≈190 cm [74.8 inches] tall and ranging from 98 to 120 kg [216 to 265 lb] in weight) and high level of muscle mass and physical fitness, the men all developed hypothermia as a result of the combination of a low level of body-fat insulation, the cold water temperature, the effect of the wind on their wet clothing, and the strenuous work to remain on the boat or to get out of the water. Two victims died after about 13 hours, a third died after 25.5 hours, and the lone survivor was rescued after 43 hours by the U.S. Coast Guard. The first casualty was the lightest (≈98 kg [216 lb]) and wore only swimming trunks and a keyhole PFD; he had discarded his t-shirt, wind pants, and jacket to try to dive under the boat for supplies. The second casualty, who died at about the same time, was the heaviest (≈120 kg [265 lb]), but he had spent far more time immersed in the water than the others had. The third casualty survived another 12 hours, but he perished nearly 18 hours before the lone survivor was rescued. That casualty had also taken off his wind jacket and pants, which were later lost, so that he could dive under the boat. During the first 13 hours, he struggled to help the other victims while he was in the water, and he had little insulation from the seat cushion, which he wore on his back; he later switched to the keyhole PFD that had been worn by the first casualty. These early conditions likely put him behind the survival curve of his remaining companion. The survivor (≈109 kg [240 lb]) had the double advantage of less direct water exposure (he spent more time positioned on top of the boat, often holding onto the motor) and more insulation (i.e., sweatpants, sweatshirt, water-resistant and fleece-lined hooded coat, skullcap, and gloves). He had a core temperature (Tco) of 31.9° C (89.5° F) after 43 hours at sea (Figure 6-3, online). This case will be referenced throughout this chapter. Case 6-2 PANIC IN ICE WATER In February 1990, four teenage boys broke through the ice on Convict Lake in California. After one boy escaped and summoned help, a series of adults—including two lay and three professional rescuers—approached and also broke through the ice. It was not until a properly equipped rescue team arrived “that a safe rescue attempt could be made … on one lone adult. In just fifteen minutes, three boys and four of their five adult rescuers were dead.”48 Despite the common belief at the time, the victims did not perish as a result of hypothermia but rather from cold- and panic-induced incapacitation and drowning. 144
Case 6-4 PROBLEMS WITH COLD-WATER RESCUE In the winter of 1988, two men died of hypothermia when their nine-man rowing scull sank during a winter storm on a small lake in western Canada. The nine rowers were immersed in 4° C (39.2° F) water. They struggled to hang on to their overturned vessel in 0.6 to 1.0 m (1.97- to 3.28-foot) waves and 30 km/hr (18.7 mph) winds for more than 50 minutes before rescuers could reach them. One man drowned just before rescue; the others were all conscious when they were pulled from the water. However, during the 13-minute boat transport to shore, three of the thinnest victims lost consciousness, and one of these men suffered cardiopulmonary arrest. His Tco in the hospital 44 minutes after rescue was 23.4° C (74.1° F); subsequent resuscitation efforts were unsuccessful. The remaining seven survivors were resuscitated from Tcos of as low as 25° C (77° F). This case illustrates the rapidity of onset of immersion hypothermia in lean subjects and the potentially serious consequences of cardiovascular instability, circumrescue collapse, and post-rescue Tco afterdrop in individuals with immersion hypothermia (see Physiologic Responses to Cold-Water Immersion with the Head Above Water, later).58 Case 6-5 DANGERS OF FISHING IN COLD WATER In December 2004, the fishing vessel Northern Edge capsized near Nantucket, Massachusetts, in 4° C (39.2° F) water and 3- to 4-m (9.84- to 13.12-foot) seas. Five of the six crewmembers lost their lives.184 In several similar cases in the same region, seven fishermen on three different vessels lost their lives during a 30-day period in the winter of 2004-2005.181 In June 2003, the charter fishing vessel Taki Tooo, which was carrying 17 passengers and crew, capsized in the turbulent waters of the Tillamook River bar on the Oregon coast, with the loss of 11 lives. The water temperature was 10° C (50° F).183 In April 2001, the fishing vessel Arctic Rose sank in the Bering Sea of Alaska, with a loss of 15 crewmembers.184 The vessel sank so quickly that there was no time for either a distress call to be made or for the crewmen to don survival suits. Case 6-6 COLD-WATER FISHING FATALITIES A 1999 U.S. Coast Guard Fishing Vessel Casualty Task Force Report181 found that, in just 2 months (December 1998 and January 1999), 20 commercial fishing vessels were lost at sea. During these mishaps, 21 persons on board died, mainly from exposure to cold water as a result of the vessel sinking or capsizing or from persons falling overboard. From 1994 to January 1999, U.S. Coast Guard statistics show that 396 fishermen lost their lives while fishing. Of these, 298 died from cold-water immersion as a result of falling overboard or of the vessel sinking, capsizing, or flooding. In 1998, the death rate for fishermen was 179 per 100,000 workers; this is 16 times higher than the rates for firefighters and police officers.
COMMERCIAL ACTIVITIES ON COLD WATER Numerous examples of maritime occupational accidents exist. In 1982, the offshore mobile oil-drilling platform Ocean Ranger collapsed in mountainous seas near Newfoundland, Canada; the water temperature was −1° C (30.2° F). Eighty-four workers were plunged into the water, and, despite the presence of a rescue vessel, all of them died. Immersion hypothermia was a significant factor in these deaths, although the inabilities of the workers to
0 7 4 11 14 10 21 17 3 2 26 24
Kodiak, Alaska Victoria, British Columbia Astoria, Oregon San Francisco, California San Diego, California Mobile, Alabama Miami, Florida Norfolk, Virginia Cape May, New Jersey Traverse City, Michigan Puerto Rico Honolulu, Hawaii
0 7 5 11 14 10 21 16 3 1 26 24
(32) (44.6) (41) (51.8) (57.2) (50) (69.8) (60.8) (37.4) (33.8) (78.8) (75.2)
February 2 (35.6) 7 (44.6) 7 (44.6) 12 (53.6) 15 (59) 14 (57.2) 23 (73.4) 15 (59) 5 (41) 1 (33.8) 26 (78.8) 24 (75.2)
March 4 (39.2) 9 (48.2) 10 (50) 12 (53.6) 16 (60.8) 21 (69.8) 25 (77) 18 (64.4) 10 (50) 1 (33.8) 26 (78.8) 24 (75.2)
April 7 (44.6) 10 (50) 13 (55.4) 12 (53.6) 17 (62.6) 23 (73.4) 27 (80.6) 20 (68) 14 (57.2) 1 (33.8) 26 (78.8) 25 (77)
May 9 (48.2) 11 (51.8) 16 (60.8) 12 (53.6) 18 (64.4) 28 (82.4) 29 (84.2) 24 (75.2) 19 (66.2) 3 (37.4) 27 (80.6) 25 (77)
June 12 11 19 13 20 29 30 26 23 5 27 26
(53.6) (51.8) (66.2) (55.4) (68) (84.2) (86) (78.8) (73.4) (41) (80.6) (78.8)
July 12 11 21 13 20 29 30 26 23 10 27 26
(53.6) (51.8) (69.8) (55.4) (68) (84.2) (86) (78.8) (73.4) (50) (80.6) (78.8)
August 10 11 17 12 20 27 29 25 21 10 28 27
(50) (51.8) (62.6) (53.6) (68) (80.6) (84.2) (77) (69.8) (50) (82.4) (80.6)
September 7 10 13 12 18 23 27 25 17 6 27 26
(44.6) (50) (55.4) (53.6) (64.4) (73.4) (80.6) (77) (62.6) (42.8) (80.6) (78.8)
October 4 9 9 11 16 19 25 21 11 5 27 25
(39.2) (48.2) (48.2) (51.8) (60.8) (66.2) (77) (69.8) (51.8) (41) (80.6) (77)
November
2 8 5 11 15 14 23 21 6 4 26 25
(35.6) (46.4) (41) (51.8) (59) (57.2) (73.4) (69.8) (42.8) (39.2) (78.8) (77)
December
FIGURE 6-2 Worldwide sea surface temperatures for April 2005. (From the National Center for Environmental Prediction, Space Science and Engineering Center, University of Wisconsin–Madison. http://www.ssec.wisc.edu/data/sst/latest_sst.gif.)
Temperatures of <25° C (77° F) are noted in red.
(32) (44.6) (39.2) (51.8) (57.2) (50) (69.8) (62.6) (37.4) (35.6) (78.8) (75.2)
January
Site
TABLE 6-1 Mean Water Temperatures in ° C (° F)
CHAPTER 6 Immersion Into Cold Water
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PART 2 COLD AND HEAT
suits, inflatable life rafts) is primarily a response to the needs of people who work in cold-water environments. The value of various types of protective clothing is examined later in this chapter.
VEHICULAR ACTIVITIES ON ICE
FIGURE 6-4 Sinking fishing vessel. (Courtesy U.S. Coast Guard.)
combat rough seas and to maintain airway freeboard (i.e., the distance between the water surface and the mouth) were also major problems.127 Fishing vessel mishaps are a common cause of immersion hypothermia. Cases 6-5 to 6-6 illustrate the problems that face the commercial fishing industry (Figure 6-4).
MILITARY ACTIVITIES AND COLD WATER The extensive use of combat ships and aircraft in World War II, particularly in the north Pacific and north Atlantic oceans, provided many examples of accidental immersion in cold water. Molnar reviewed several hundred of these cases.124 Among them was the following: “A ship was rammed, and it sank in 3 minutes. Thirty survivors were picked up from rafts after exposure of 1.5 to 4 hours. Some drowned and others died of exposure because the water was 4° C (7.2° F) with high seas and a wind velocity of scale 7. Some of the survivors who held on to ropes couldn’t let go and rescuers had to cut frozen rope to release them. It appears miraculous how the survivors could have endured such cold water. Most of those who were rescued were in an unconscious state and, when they became conscious, complained of numbness of extremities and hands.” The Falklands War in 1982 provided further examples of immersion hypothermia related to naval combat. The Argentinian cruiser General Belgrano sank in approximately 5° C (9° F) water, which resulted in the deaths of many sailors. Some of the deaths from cold occurred even after the sailors had managed to emerge from the water into life rafts. Maritime military operations are not the only source of hypothermia casualties in the armed forces; land operations, either during combat or training, also have immersion hypothermia risks. In March 1995, four U.S. Army Rangers died and four others were hospitalized during a training mission in a Florida swamp. The water at the exercise site was deeper and colder than was customary for this exercise. Consequently, the Rangers were forced to spend more than 6 hours in cold and wet conditions, much of the time partially immersed in the 15° C (59° F) water. Night conditions and difficulties encountered during the medical evacuation of the accident victims contributed to the hypothermia deaths.17,186 In March 2001, two U.S. Coast Guard crewmen drowned after immersion in cold water, when their four-man vessel capsized in the waves of the Niagara River bar in Lake Ontario. The water temperature was 2° C (3.6° F). All of the crewmen were wearing dry suits with insulation as well as PFDs, but they were without insulated headgear. They left the boat to swim towards a buoy. Vigorous swimming caused water intrusion into two of the dry suits, as did the coxswain’s use of a neck ring device before capsizing. This leakage resulted in severe immersion hypothermia and subsequent drowning.182 The relatively high fatality rate from accidental immersion in cold water in various military, commercial, and recreational settings has stimulated technologic advances in protective clothing and rescue devices. The current availability of commonplace items of survival equipment (e.g., wet suits, dry suits, survival 146
Motor vehicle submersions account for approximately 10% of all drownings, including approximately 400 fatalities in North America each year.177,201 Although most of these deaths occur in open water during spring, summer, or fall, many also occur during the winter, when vehicles break through the ice while traversing either makeshift (e.g., ice fishing) or official (e.g., winter roads) transport routes. In 2005, a heavy machine operator was maintaining an icy road when his snowplow broke through the ice, and he drowned.91 The ice-cold water temperature was cited as a contributing factor to his death. In summary, numerous case histories and statistical evidence document the significance of cold-water immersion as a cause of the environmental emergencies of drowning and hypothermia. Although drowning is relatively easy to prevent (e.g., with the use of PFDs, water safety training, and the restriction of alcohol use), hypothermia is not easy to prevent. Hypothermia is now more widely recognized than in the past, but the prevention of immersion hypothermia is still a difficult and often expensive proposition. Therefore, in regions with cold water (which includes most of the North American continent), cold-water safety, knowledge of cold-water risks, and the use of appropriate flotation and protective clothing are essential.
Physiologic Responses to Cold-Water Immersion With the Head Above Water The effect of sudden cold-water immersion on humans is poorly understood by the general public as well as by medical and rescue personnel. Many individuals believe that an individual who falls into ice water will die of hypothermia within minutes, even if that person is dressed in winter clothing. In a series of surveys of continuing medical education attendees,47 75% of respondents felt that, under these conditions, a victim would experience life-threatening hypothermia in less than 30 minutes. As discussed later in this chapter, most adults can survive for an hour or more if they take appropriate action. The improper assumption of rapid and impending death only serves to induce panic, poor decisions, and exhaustion as a result of thrashing about, thereby causing problems for both primary victims and for the persons trying to rescue them. The primary pathophysiologic effects of hypothermia are a decrease in tissue metabolism and the gradual inhibition of neural transmission and control. However, during the initial stages of cooling of an intact and conscious victim, secondary responses to skin-temperature cooling predominate. Sudden immersion in cold water results in an immediate decline in skin temperature, which, in turn, initiates shivering thermogenesis with increases in metabolism, ventilation, heart rate, cardiac output, and mean arterial pressure. As body temperature declines and shivering ceases, metabolism, heart rate, mean arterial pressure, and cardiac output decrease proportionally with the fall in Tco, whereas hematocrit and total peripheral resistance increase. Renal diuresis and extravascular fluid shifts can lead to a considerable loss of intravascular volume, thus decreasing systemic perfusion. A more detailed description of the pathophysiologic effects of systemic hypothermia is provided in Chapter 5: Accidental Hypothermia. The following section pragmatically describes the effects of the pathophysiologic changes that accompany cold-water immersion and the impact of these changes on survival. The body’s responses and mechanisms of death during coldwater immersion can be divided into four phases: (1) initial immersion and the cold shock response; (2) short-term immersion and the loss of performance; (3) long-term immersion and the onset of hypothermia; and (4) circum-rescue collapse just before, during, or after rescue. Each phase is accompanied by specific survival hazards for the immersion victim that originate
PHASE 1: THE COLD SHOCK RESPONSE (0 TO 2 MINUTES) The cold shock response occurs within the first few minutes of cold-water immersion and depends on the extent and rate of skin cooling. The responses are generally those that affect the respiratory system, heart, and the body’s metabolism (Figure 6-5).36,175 Rapid skin cooling initiates an immediate gasp response, an inability to hold one’s breath, and hyperventilation. The gasp response may cause drowning if the head is submersed during the initial entry into cold water. The subsequent inability to hold one’s breath may further potentiate drowning in high seas. Subsequent hyperventilation will normally diminish within seconds to minutes, but it could be increased and exaggerated indefinitely as a result of emotional stress and panic. Uncontrolled hyperventilation can cause numbness, muscle weakness, or fainting, which may lead to drowning. Any of these respiratory responses can
lead to pulmonary aspiration of water. Panic may ensue, with subsequent drowning. These responses may be viewed on several video links listed in the Video Resources section at the end of this chapter. Skin cooling initiates peripheral vasoconstriction as well as increased cardiac output, heart rate, and arterial blood pressure. Increased workload on the heart may lead to myocardial is chemia and arrhythmias, including ventricular fibrillation. Sudden death can occur either immediately or within a matter of minutes after immersion as a result of syncope or convulsions, which can lead to drowning, vagal cardiac arrest, or ventricular fibrillation in susceptible individuals.* Cold shock can occur in water colder than 20° C (68° F), with symptoms increasing as water temperature decreases to freezing. Staged entry into cold water attenuates respiratory responses because of a gradual increase in thermal stimulation. The best advice to combat this phenomenon is, when possible, to control entry into cold water by entering slowly and most importantly by *References 23, 44, 103, 118, 167.
FIGURE 6-5 Possible cold shock responses. ↑, Increase; ↓ decrease. (From Edmonds C, Lowry C, Pennefather J: Cold and hypothermia. In Diving and subaquatic medicine, Oxford, UK, 1992, Butterworth-Heinemann.)
RAPID SKIN COOLING STIMULATION OF PERIPHERAL RECEPTORS
GASP REFLEX AND HYPERVENTILATION
HYPOCAPNIA
PERIPHERAL VASOCONSTRICTION
↑ HYPERTENSION (arterial and venous pressure)
INABILITY TO HOLD BREATH
Respiratory alkalosis
↑ Filling pressure
↑ Cardiac output
Inspiratory shift
Ventricular fibrillation
↓ Cerebral blood flow
TACHYCARDIA
↑ WORK OF HEART
Vessel rupture
↓ Coronary blood flow
↓ Serum and body fluid Ca2+
Dyspnea
Cerebrovascular accident
Tetanic spasms Convulsions
↑ Ventricular irritability
Panic Cerebral hypoxia
Arrhythmias/ ventricular fibrillation
Swim failure Disorientation Loss of consciousness
Myocardial ischemia
INHALATION OF WATER
Stimulation of nasal and glottal receptors
Drowning
Vagal arrest
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CHAPTER 6 Immersion Into Cold Water
from or are influenced by a variety of pathophysiologic mechanisms. Deaths have occurred during all four phases of immersion.
Ventilation volume (liters • min–1)
execute a plan of action: (1) try to enter the water without submersing the head; (2) escape (i.e., pull oneself out of the water, inflate, and board a life raft); (3) minimize exposure (i.e., get as much of one’s body as possible out of the water and onto a floating object); (4) ensure flotation if one must remain in the water (i.e., don or inflate a PFD); and (5) call for assistance (i.e., activate signaling devices). It may be difficult to execute these actions when cold shock responses predominate. However, after respiratory effects are under control, immediate action should be taken. If self-rescue is not possible, actions to minimize heat loss should be initiated by remaining as still as possible in the heat escape lessening position (HELP), in which the arms are pressed against the chest while the legs are pressed together, or by huddling with other survivors (Figure 6-8, online).86 Drawstrings should be tightened in clothing to decrease the flow of cold water within clothing layers. Many of these responses can be viewed on several video links in the Video Resources section at the end of this chapter.
Non-staged
60 50 40 30 20
Staged
10 0
Respiratory frequency (breaths • min–1)
PART 2 COLD AND HEAT
70
50
PHASE 3: ONSET OF HYPOTHERMIA (IMMERSION OF MORE THAN 30 MINUTES)
Non-staged
45 40 35 30 25 20
Staged
15 –20
0
30
60
90
120
150
180
Immersion time (s) FIGURE 6-6 Respiratory responses (minute ventilation and respiratory rates) to sudden and graded immersion into cold water. (From Hayward JS, French CD: Hyperventilation response to cold water immersion: Reduction by staged entry, Aviat Space Environ Med 60:1163, 1989.)
keeping the head from being submersed. One should never dive into cold water! After cold-water immersion, it is important to focus on surviving the first minute by not panicking and by consciously getting one’s breathing under control. Figure 6-6 shows that minute ventilation and breathing frequency increase dramatically with rapid immersion in cold water. These responses are blunted by more than 50% with graded immersion.
PHASE 2: COLD INCAPACITATION (5 TO 15 MINUTES) For those who survive the cold shock response, significant cooling of peripheral tissues—especially in the extremities— continues, with most of the effect occurring during the first 15 minutes of immersion. This cooling has a direct deleterious effect on neuromuscular activity.186 This effect is especially significant in the hands, where blood circulation is negligible,34 which leads to finger stiffness, poor coordination of gross and fine motor activity, loss of power,* and swim failure (Figure 6-7, online). It has been shown that this effect is primarily the result of peripheral rather than central cooling.63 The loss of motor control makes it difficult if not impossible to execute survival procedures, such as grasping a rescue line or hoist. The ultimate cause of death is drowning, either through the failure to initiate or maintain survival performance (i.e., keeping afloat, swimming, or grasping onto a life raft) or excessive inhalation of water under turbulent conditions. These phenomena have obvious survival implications. It is of course advisable to avoid cold-water exposure completely. If cold-water immersion occurs, it is best to quickly determine and *References 40, 51, 133, 134, 191.
148
Most cold-water deaths likely result from drowning during the first two phases of cold-water immersion, as discussed previously. In general, true hypothermia usually only becomes a significant contributor to death if immersion lasts more than 30 to 60 minutes. A recent survey indicates that even medical practitioners greatly underestimate the time required for a person to become hypothermic in cold water.47 In fact, 75% of respondents felt that a properly clothed adult would become hypothermic after less than 15 minutes in ice water (0° C [32° F]) (Figure 6-9, online). An individual who survives the immediate and shortterm phases of cold-water immersion faces the possible onset of hypothermia, because continuous heat loss from the body eventually decreases Tco. Many predictive models to determine the Tco response to cooling are based on the relationships between body composition, thermoregulatory response (i.e., shivering thermogenesis), clothing and insulation, water temperature, and sea conditions (see Cold-Water Survival, later).* Even in ice water, a victim may not drown when he or she becomes unconscious as a result of hypothermia (≈30° C [86° F]) if a PFD is worn or if some other factor prevents the need for vigorous exercise to prevent drowning. If the head is kept above water, the victim could still survive for up to 1 hour before the heart stops as long as the sea is relatively calm and waves do not wash over the mouth. It is important for members of the public to be educated about the fact that they are not necessarily going to die if they are suddenly immersed in cold water (Box 6-2). The relative contributions of the first three phases to death in cold water of varying temperatures are estimated schematically in Figure 6-10. In colder water, if no flotation is worn (top panel), death occurs as a result of cold shock or cold incapacitation. Only if flotation is worn (bottom panel) will a victim survive long enough to die as a result of hypothermia (Box 6-3). BOX 6-2 The 1-10-1 Principle If you fall into ice-cold water, remember that you have 1 minute—10 minutes—1 hour.* • You have 1 minute to get your breathing under control, so don’t panic. • You have 10 minutes of meaningful movement to get out of the water or to attain a stable situation. • You have up to 1 hour until you become unconscious from hypothermia if you don’t panic or struggle unnecessarily. If you are wearing a PFD, you may have another hour until your heart stops beating as a result of hypothermia. *Times are subject to individual variability and factors such as body size, water temperature, and amount of the body immersed.
*References 90, 163, 197, 202, 207.
Relative contribution to death (%)
100.0 90.0 80.0 70.0 Cold incapacitation Cold shock Hypothermia
60.0 50.0 40.0 30.0 20.0 10.0 0.0 0
5
A
10
15
20
Water temperature (° C) CAUSE OF DEATH (WITH FLOTATION)
Relative contribution to death (%)
100.0 90.0 80.0 70.0 60.0
Cold incapacitation Cold shock Hypothermia
50.0 40.0 30.0 20.0 10.0 0.0 0
B
5
10
15
20
Water temperature (° C)
FIGURE 6-10 Estimation of the relative contributions of cold shock, cold incapacitation, and hypothermia to death in water at different temperatures. A, Estimation if no flotation is available. B, Estimation if flotation is available.
PHASE 4: CIRCUM-RESCUE COLLAPSE Anecdotal cases of fatalities among immersion hypothermia victims have been noted during the immediate pre- and postrescue periods, despite the survivor being recovered in an apparently stable and conscious condition. The hypothermic victim may experience symptoms that range from fainting to cardiac arrest. These events are often referred to as cases of “rewarming shock” or “post-rescue collapse.” Golden and colleagues73 noted that deaths can occur either shortly before rescue, during rescue, or after rescue, and they have used the term circum-rescue collapse to describe these events. Deaths have occurred within minutes before rescue, while climbing out of the water, while BOX 6-3 Controversy Box: Time to Hypothermia Most people greatly underestimate the amount of time required to become hypothermic in very cold water. This is important, because if a victim thinks that hypothermia will set in very quickly, panic is more likely. A proper understanding of the fact that cold shock is initially the greatest threat will help the victim to focus more on controlling the gasp reflex and to get control of his or her breathing.
being hoisted onto a helicopter, within a few minutes of entering a warm compartment of a rescue vessel, 20 to 90 minutes after rescue, in a hospital after transport, and during the 24-hour period after rescue.71,73,100,116 Three causes of circum-rescue collapse have been proposed: (1) afterdrop, which is a continued drop in Tco after recovery; (2) collapse of arterial pressure (Figure 6-11, online); and (3) factors that potentiate the risk of ventricular fibrillation (e.g., hypoxia, acidosis, rapid changes in pH). These causes are discussed further later in this chapter. When rescue is imminent, mental relaxation and the decreased output of stress hormones may result in a drop in blood pressure, which may cause fainting and drowning. The act of rescue itself may also cause sudden collapse. Pulling a victim out of the water in a vertical position removes hydrostatic squeeze around the lower limbs and may cause blood pooling in these extremities, with subsequent decreased blood pressure. Extra cardiac work or rough handling may induce reflex cardiac arrest of the cold heart. Afterdrop is a well-known phenomenon that occurs after the removal of a victim from cold-water immersion. Tco continues to decline (i.e., afterdrop) in both animate and inanimate objects, although cold-water immersion has ended.* Afterdrop of as much as 5° to 6° C (9° to 10.8° F) has been observed in humans (Figure 6-12, online).6,43,161 This afterdrop was long proposed to be the major cause of post-rescue death, because further cooling of the heart might result in a temperature at which ventricular fibrillation or cardiac arrest could occur.13 Golden and colleagues73 discount the importance of this phenomenon and propose the collapse of arterial pressure as the cause of death during rescue. They correctly point out that after drop that occurs in victims who were hypothermic yet warm enough to climb on board a ship without assistance would be unlikely to cause enough myocardial cooling to result in cardiac arrest or ventricular fibrillation. Those clinicians also propose that removal from cold water results in a precipitous fall in blood pressure, inadequate coronary blood flow, and myocardial is chemia, which possibly precipitate ventricular fibrillation. This mechanism is likely the main factor in both pre-rescue collapse and collapse that occurs during rescue. A fall in blood pressure before removal from the water may be the result of reduced sympathetic tone or catecholamine secretion when rescue is imminent. Hypotension during and shortly after rescue may be caused by a sudden decrease in hydrostatic pressure on the body (i.e., removal of the hydrostatic squeeze of water pressure that exists during immersion), hypovolemia, or impaired baroreceptor reflexes. However, this mechanism cannot fully account for all of the other post-rescue deaths that occur 20 minutes to 24 hours after rescue. The importance of continued myocardial cooling cannot be discounted. Fibrillation of a cold heart can be initiated by mechanical stimuli, hypoxia, acidosis,131 and rapid changes in pH.101 In dogs, myocardial cooling from 30° to 22° C (86° to 71.6° F) has been shown to cause a five-fold decrease in the electrical threshold for ventricular fibrillation.25 It is also likely that an increase in the rate of myocardial cooling may stimulate fibrillation. On the basis of the large afterdrop values described previously, it is plausible that continued Tco cooling in significantly hypothermic victims could result in ventricular fibrillation, caused primarily by spontaneous fibrillation of the cold myocardium or secondary to a cold-induced increase in sensitivity to other fibrillation stimuli. Finally, death may occur within minutes to hours after rescue. A rescued victim may be severely compromised with cold alkaline or acidic blood in the extremities, a heart that is extremely prone to failure, a decrease in or a loss of consciousness, or low blood volume (hypovolemia). Sudden redistribution of blood to the extremities (especially the lower extremities) may cause collapse as a result of decreased blood pressure and cardiovascular instability, sudden return of metabolic by-products to the irritable heart, or continued decrease in temperature (afterdrop) of an irritable heart. The Tco will continue to drop, and the heart will *References 2, 13, 20, 57, 75, 141, 147, 194.
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CHAPTER 6 Immersion Into Cold Water
CAUSE OF DEATH IN COLD (NO FLOTATION)
PART 2 COLD AND HEAT
react with profound tachycardia or fibrillation. Up to 20% of persons who are recovered alive die as a result of circum-rescue complications, either before or during rescue, or within hours after rescue.
Factors That Affect Cooling of the Body’s Core Normal body Tco fluctuates around 37° C (98.6° F). The clinical definition of hypothermia is a Tco of 35° C (95° F) or lower; however, any exposure to cold that lowers the Tco to less than a normal level results in the body becoming hypothermic. Although various temperatures and terms have been used to classify different levels of hypothermia, the following classifications (Figure 6-13) will be used here. With mild hypothermia (Tco = 32° to 35° C [89.6° to 95° F]), thermoregulatory mechanisms continue to operate fully, but ataxia, dysarthria, apathy, and even amnesia are likely. With moderate hypothermia (Tco = 28° to 32° C [82.4° to 89.6° F]), effectiveness of the thermoregulatory system (i.e., shivering thermogenesis) diminishes until it fails; there is a continued decrease in the level of consciousness, and cardiac dysrhythmias may occur. With severe hypothermia (Tco <28° C [82.4° F]) consciousness is lost, shivering is absent, acid–base disturbances develop, and the heart is susceptible to ventricular fibrillation or asystole. Death from hypothermia is generally a result of cardiorespiratory failure. If a victim of cold-water immersion can avoid drowning during the initial few minutes after water entry, the prevention of hypothermia becomes an important problem. Survival time in cold water, which is based on the pathophysiologic effects of decreasing Tco, is not a precise calculation. Large individual variations among survivors with regard to body morphology and state of health and fitness, in combination with many exogenous variables that affect cooling rate (e.g., clothing, water temperature, sea state, flotation, behavior), preclude exact predictions of survival time. However, sufficient experimental data and case history findings exist to allow for generalizations. At a Tco of 34° C (93.2° F), there is a significant deleterious effect on manual dexterity and “useful function” in cold water.24,132 If a survivor is trying to combat rough seas, this level of dysfunction may potentiate drowning. At a Tco of 30° C (86° F), unconsciousness is probable. Even if a survivor is wearing a self-righting PFD that has been designed to maintain airway freeboard in an
Classifications
Core temperature
unconscious person, drowning is probable at this Tco in all but the calmest seas. At a Tco of less than 25° C (77° F), ventricular fibrillation or asystole often occur spontaneously.29 Of these three Tcos, 30° C (86° F) is the most practical for defining the limits of survival in cold water.* The rate of body Tco cooling during cold-water immersion depends on the following variables: water temperature and sea state; thermal protection; body morphology; amount and surface area of the body immersed in water; behavior (e.g., excessive movement) and posture (e.g., HELP, huddle) of the body in the water; shivering thermogenesis; and other nonthermal factors.
WATER TEMPERATURE AND SEA STATE These variables are critically important to the intensity of the cold shock response, the onset of physical and mental impairment, and the rate of Tco cooling. Figure 6-14 graphically illustrates the inverse linear relationship between water temperature and Tco cooling rate.82 Water conducts heat away from the body approximately 25 times as fast as does air at the same temperature.125
THERMAL PROTECTION A large number of studies over the past few decades have evaluated the relationships of different types of protective clothing with heat loss and cooling rates.† Nearly all of these studies have been conducted in calm water or in laboratory settings. As illustrated by the cooling rate data in Tables 6-2 and 6-3, such studies have generally shown that, in calm water, intact “dry” and insulated garments provide better protection than do “wet” insulated garments and that well-insulated garments provide significantly better protection than do poorly insulated garments. Figure 6-15, online shows various types of cold-water protective garments. Although calm-water studies have value in that they compare the relative degree of protection afforded by different types of protective clothing, many immersion accidents occur in rough water.143,168,169 In this environment, a survivor’s cooling rate may be affected by swimming to maintain airway freeboard, passive *References 18, 29, 158, 159, 163. † References 5, 35, 83, 89, 98, 99, 109, 132, 150, 158, 159, 166, 170, 172, 173, 175, 198, 203.
Patient’s ability to rewarm without external heat source
Clinical presentation
Normal
Above 35° C (95° F)
Cold sensation; shivering
Mild
35-32° C (95–90° F)
Good
Moderate
32-28° C (90–82° F)
Limited
Below 30° C (86° F) shivering stops; loss of consciousness
Severe
Below 28° C (82° F)
Unable
Rigidity Vital signs reduced or absent Severe risk of mechanically stimulated (rough handling) ventricular fibrillation (VF)
Below 25° C (77° F)
Unable
Spontaneous ventricular fibrillation (VF); cardiac arrest
Physical impairment • Fine motor • Gross motor
Mental impairment • Complex • Simple
Bold text shows the major thresholds between stages of hypothermia.
FIGURE 6-13 Classification of levels of hypothermia on the basis of core temperature and clinical presentation.
150
Flight suit Float coat
0.06
Shorty wet suit Aviation coveralls
Cooling rate (° C min–1)
0.05
Boatcrew coveralls Wet suit
0.04
Calm Rough
Dry suit Survival suit
0.03
0
1
2
3
4
Cooling rate (° C/hr)
0.02
FIGURE 6-16 A comparison of mean rectal temperature cooling rates in lean male subjects in calm versus rough seas at 10.7° C (51.3° F). The flight suit, when used as a control garment, is equivalent to lightweight clothing. (From Steinman AM, Hayward JS, Nemiroff MJ, et al: Immersion hypothermia: Comparative protection of anti-exposure garments in calm vs rough seas, Aviat Space Environ Med 58:550, 1987.)
0.01
0
5
10
15
20
25
Water temperature (° C) FIGURE 6-14 Relationship between water temperature and mean rectal temperature cooling rate in lightly clothed nonexercising males and females during immersion in seawater. (From Hayward JS: The physiology of immersion hypothermia. In Pozos RS, Wittmers LE, editors: The nature and treatment of hypothermia, Minneapolis, 1983, University of Minnesota Press.)
body movements caused by waves, flushing of cold water through “wet” suits, and leakage of cold water into “dry” suits. For example, subjects in a wave tank demonstrate higher energy expenditure and faster cooling rates than do subjects in calm water.81 Several experimental studies have demonstrated
TABLE 6-2 Mean Linear Cooling Rates for Lean Men
Dressed in Various Types of Garments in Calm Water at 10° C (50° F)
Type of Protective Clothing Control (equivalent to ordinary street clothes) “Wet” Design Thermal float coat (loose-fitted, 5.4-mm [0.21-inch] closed-cell, foam-insulated jacket) Short wet suit (custom-fitted, 3.2-mm [0.13-inch] closed-cell, foam that covers the arms, the trunk, and the upper thighs) Insulated coveralls (loose-fitted, 3.2-mm [0.13-inch] closed-cell foam that covers the extremities and the trunk) Full wet suit (custom-fitted, 4.8-mm [0.19-inch] closed-cell foam that covers the extremities and the trunk) “Dry” Design Immersion suit (loose-fitted, 4.8-mm [0.19-inch] closed-cell foam with sealed openings)
Cooling Rate Given as ° C/hr ± Standard Deviation (° F/hr ± Standard Deviation) 3.2 ± 1.1 (5.8 ± 2.0) 1.6 ± 0.6 (2.9 ± 1.1)
significantly faster cooling rates for human volunteers wearing “wet” protective garments in rough or turbulent water142,158,203 as compared with persons in calm water. Even “dry” suits have shown degradation of protection in rough water. In a study of dry immersion suits in 16° C (60.8° F) water, Ducharme and Brooks found that wave heights of up to 70 cm (28 inches) resulted in a 14% decrease in total suit insulation and an average 45% decrease in thermal resistance at the head and trunk regions of the suits.31 Figure 6-16 shows a comparison of cooling rates for lean males dressed in the various types of protective clothing shown in Figure 6-15 in both calm and rough waters at approximately 10° C (50° F).158 The most dramatic differences occurred in the loose-fitted “wet” protective clothing (e.g., float coat, insulated coveralls), where cooling rates nearly doubled in rough seas as compared with those seen in calm seas. This was primarily caused by the flushing of cold water through the garments. However, even the tight-fitted full “wet” suit allowed for a 30% faster cooling rate in rough water as compared with that seen in calm water. The “dry” suit, which did not leak, showed no significant difference between calm and rough seas.
TABLE 6-3 Comparison of Mean Cooling Rates
for Thin Men (Mean Body Fat = 9.1%) Wearing Various Types of Protective Clothing in Calm Water at 11.8° C (53° F)
1.2 ± 0.4 (2.2 ± 0.7) Clothing Type 1 ± 0.4 (1.8 ± 0.7) 0.7 ± 0.3 (1.3 ± 0.5)
0.5 ± 0.3 (0.9 ± 0.5)
From Steinman AM, Hayward JS, Nemiroff MJ, et al: Immersion hypothermia: Comparative protection of anti-exposure garments in calm versus rough seas, Aviat Space Environ Med 58:550, 1987.
Dry, closed-cell foam insulation (4.8-mm [0.19-inch] thick) Wet, closed-cell foam insulation (4.8-mm [0.19-inch] thick) Dry and uninsulated (watertight shell over lightweight clothing) Control (lightweight clothing alone)
Ratios as Compared With Control
Mean Cooling Rate Given as ° C/hr (° F/hr)
Direct
Inverse
0.31 (0.56)
0.14
7.35
0.54 (0.97)
0.23
4.26
1.07 (1.93)
0.47
2.15
2.3 (4.14)
1
1
From Hayward JS: Design concepts of survival suits for cold-water immersion and their thermal protection performance. In 17th symposium of the SAFE (Survival and Flight Equipment) Association. Van Nuys, Calif. 1979.
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CHAPTER 6 Immersion Into Cold Water
0.07
of Protective Clothing in Rough Seas
Estimated Survival Time (hr) (95% Confidence Interval)
Clothing Type
Time to Incapacity (hr) (Temperature = 34° C [93.2° F])
Time to Unconsciousness (hr) (Temperature = 30° C [86° F])
Time to Cardiac Arrest (hr) (Temperature = 25° C [77° F])
0.4-1.3 0.9-2.7
0.8-2.6 1.6-5.2
1.3-4.3 2.5-8.4
Control (lightweight clothing) Torn, non–foam-insulated, dry coveralls (50.8 mm [2-inch] tear in left shoulder) Closed-cell foam-insulated, wet coveralls (3.2-mm [0.13-inch] thick insulation in loose-fitted coveralls) Closed-cell foam-insulated, custom-fitted wet suit (4.8-mm [0.19-inch] thick insulation; tight-fitted) Intact, non-foam–insulated, dry coveralls (watertight shell over thick, fiberfill, insulated underwear)
1-2.9
1.9-6
3-9.9
1.6-4.7
3.1-9.9
4.9-16.2
2.9-8.8
5.7-18.2
9.1-30
From Steinman AM, Kubilis P: Survival at sea, report no. CG-D-26-86, United States Coast Guard. 1986, National Technical Information Service.
Estimated survival times in rough seas, on the basis of experimental data, were published for thin males wearing different types of protective clothing in 6° C (42.8° F) water.159 Table 6-4 shows these times for three different levels of survival. Underlying these estimations are the following assumptions: 1. Cooling rates are linear.89,158,159,163 2. Initial Tco is 37.5° C (99.5° F). 3. Survivors are able to maintain airway freeboard until unconsciousness occurs at a rectal temperature of 30° C (86° F). 4. Self-righting flotation maintains airway freeboard when survivors are unconscious. By comparing these estimated survival times with those of Figure 6-17 (i.e., calm-water survival times), the reader must recall that Figure 6-17 concerns only survival to a Tco of 30° C (86° F). Furthermore, the zone in the graph must be adjusted downward for rough seas and for survivors wearing only lightweight clothing, and it should be adjusted upward for survivors wearing insulated clothing. For 6° C (42.8° F) water, the survival times (to a Tco of 30° C [86° F]) correlate well between Figure 6-17 and Table 6-4. We must emphasize that the estimates in Table 6-4 pertain to lean individuals with a mean body fat level of only 11.1%. Because many populations of adults (e.g., offshore oil workers) in the 30- to 50-year-old age range average 25% to 30% body fat, the estimates of “time to unconsciousness” and “time to cardiac arrest” must be considered conservative for a broader spectrum of adults. A recent video production called Cold Water Boot Camp (see Video References section at the end of this chapter) tested various flotation ensembles, including closed-cell and inflatable PFDs, heavy dry suits, and lighter extended-wear (paddling) dry suits. Figure 6-18 schematically shows that Tco and survival time decrease as the amount of thermoprotection and flotation decreases (Box 6-4).
BOX 6-4 Controversy Box: Flotation Clothing Impedes
Escape from Submersed Vehicles
In many winter road jurisdictions, workers are mandated to wear thermoprotective flotation jackets or overalls. Some workers resist wearing this clothing because of fears that clothing buoyancy may impede exit by forcing the occupant upward against the roof of the vehicle and that increased bulk may impede passage through a window or hatch. Flotation jackets or overalls do not pose an exit threat and should be considered safe for ice road use. Inflatable PFDs have been considered as an option, but, because they may be inflated prematurely before exit, they might impede exit and are not recommended for vehicle use in any situation.59
152
BODY MORPHOLOGY (SIZE AND COMPOSITION) Children cool faster than adults because children have a greater surface area–to–mass ratio. Cooling rate is generally proportional to surface area, whereas the amount of heat that can be lost is proportional to mass. Thus, a large surface area–to–mass ratio favors cooling. Similarly, smaller adults generally cool faster than do larger adults, and tall, lanky individuals cool faster than do short, stout individuals. Body composition is also important. 12 11 10
Death from hypothermia highly probable
9 Survival time (hr)
PART 2 COLD AND HEAT
TABLE 6-4 Estimated Survival Times for Lean Subjects (Mean Body Fat = 11.1%) Wearing Various Types
8 7 6
rs
ole
5
ow
4
Sl
3
e Av
2
co
rag
t Fas
1 0 0
5
10
rs
ole
o ec
lers
coo
Death from hypothermia highly improbable 15
20
25
Water temperature (° C) FIGURE 6-17 Predicted calm-water survival time (defined as the time required to cool to 30° C [86° F]) in lightly clothed, nonexercising humans in cold water. The graph shows a line for the average expectancy and a broad zone that indicates the large amount of individual variability associated with different body sizes, builds, fatness levels, physical fitness levels, and states of health. The zone would include approximately 95% of the variations expected for adult and teenage humans under the conditions specified. The zone would be shifted downward by physical activity (e.g., swimming) and upward slightly for heavy clothing or protective behaviors (e.g., huddling with other survivors, adopting a fetal position in the water). Specialized insulated protective clothing (e.g., a survival suit or wet suit) is capable of increasing survival time from 2 to 10 times (or more) the basic duration shown here. For the zone in which death from hypothermia is highly improbable, cold shock on initial immersion can potentiate death from drowning, particularly for those who are not wearing flotation devices. (From the U.S. Coast Guard: Addendum to the National Search and Rescue (SAR) Manual, COMDTINST M16120.5 and COMDTINST M16120.6. 1995.)
Core temperature
Flotation Moderate thermal protection
Flotation No thermal protection No flotation No thermal protection Time
FIGURE 6-18 Schematic estimation of core temperature and survival times with varying flotation devices and thermal protective clothing.
Subcutaneous fat is a very efficient insulator against heat loss, and cooling rate is inversely related to skinfold thickness. For example, subjects in the tenth percentile for skinfold thickness wearing light clothing in 5° C (41° F) water have nine times the cooling rate of subjects in the ninetieth percentile for skinfold thickness.132 Figure 6-19 shows the linear relationship between change in Tco and mean skinfold thickness.101 Shivering, which is a primary defense against Tco cooling, also varies with skinfold thickness. At a given skin temperature, the shivering response is less in humans with greater amounts of subcutaneous fat.108 In moderately cold water temperatures (18° to 26° C [64.4° to 78.8° F]), Tco cooling has been shown to proceed at the same rate in high- and low-fat individuals because of greater shivering thermogenesis in the low-fat subjects. However, at colder water temperatures (8° C [46.4° F]), Tco cooling is attenuated by greater amounts of subcutaneous fat and body mass as a result of increased insulation.53 In general, for a survivor who is immersed in cold water, the Tco cooling rate is fairly linear after Tco begins to decline. This has been shown to be true for mildly hypothermic experimental subjects. The only data that exist for severely hypothermic
Fall in Tre ° C
2.0
humans are those from the infamous Dachau concentration camp atrocities, in which conscious victims were inhumanely cooled to death in ice water.2 Because these unfortunate victims were emaciated and ill, these data do not apply to healthy cold-water immersion subjects and should be considered atrocious. The advantage of body fat as an insulator against cold has been discussed previously in the section about pathophysiology and cooling rates. With the use of an extrapolation of a linear cooling rate to 30° C (86° F), Figure 6-17 shows predicted calmwater survival times of lightly clothed, nonexercising humans in cold water. The graph shows a line for the average survival expectancy. A broad zone indicates the large amount of individual variability associated with different body sizes, builds, and degrees of fatness. The zone would include approximately 95% of the variation expected for adult and teenage humans under the conditions specified. For the zone in which death from hypothermia is highly improbable, cold water still potentiates death from drowning as a result of cold shock (as discussed previously) during the first few minutes of immersion, especially for those who are not wearing PFDs. It is important to note that Figure 6-17 discusses only calm-water survival times. Because roughwater conditions decrease survival times, as will be discussed later in this chapter, Figure 6-17 may be useful for estimating maximum survival times for an individual who is immersed in cold water. Search and rescue organizations might find such a maximum survival time helpful, because they often use the longest possible survival time to decide when to terminate a search effort.
AMOUNT OF BODY IMMERSED Because of the difference in thermal conductivity between air and water (as discussed previously), heat loss from body surfaces immersed in cold water is far greater than from body surfaces exposed to cold air, even considering the effect of windchill. Thus, immersed victims should attempt to get as much of their bodies out of the water as possible (Figure 6-20). This issue is discussed in greater detail in Cold-Water Survival, later in this chapter.
HEAD IMMERSION Exposure of the dorsal head to cold water may increase a survivor’s rate of cooling and adversely affect mental performance. Survival may depend on the ability to conduct multiple tasks to avoid drowning and hypothermia. The ability to carry out these tasks involves both physical components, which are affected by local muscle and nerve temperature,63 and mental components, which are affected by brain temperature;50 both may be adversely affected by hypothermia. Head immersion has traditionally been of concern in survival situations.69 In the absence of water in the airways, heat is lost
1.5
1.0
0.5
0.05
0.10
0.15
0.20
0.25
Reciprocal of mean skinfold thickness mm–1
FIGURE 6-19 The relationship between subcutaneous fat thickness in 10 men and the decline in rectal temperature during 30-minute immersions in stirred water at 15° C (59° F). Skinfold thickness is given as a mean of readings at the biceps, the abdomen, and subscapular and subcostal sites. Tre, Rectal temperature. (From Keatinge WR: Survival in cold water, ed 2, Oxford, 1969, Blackwell Scientific Publications.)
FIGURE 6-20 Nick Schuyler sitting atop an overturned boat, awaiting rescue. He survived for 43 hours in 18° C (64° F) water, whereas his three companions perished after 13 to 25 hours. His position on top of the boat decreased his heat loss, and his bright-colored jacket and keyhole personal flotation device resulted in him being seen by U.S. Coast Guard personnel. (Courtesy U.S. Coast Guard.)
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CHAPTER 6 Immersion Into Cold Water
Flotation High thermal protection
Esophageal temperature (° C)
PART 2 COLD AND HEAT
through the head either via convection (heat loss from the blood that perfuses the scalp) or conduction (direct heat loss through bone and soft tissue).206 One hypothesis predicts substantial heat loss through the head because of abundant scalp vascularity and because the scalp vasculature does not vasoconstrict in response to cold as do superficial blood vessels in other body areas.45 Alternatively, heat loss from the back of the head might be minimal, because dorsal head and neck immersion would only involve an additional 3% to 5% of the body surface area.107 In addition, conductive heat loss directly through the scalp and skull is likely to be minimal.206 A few studies have addressed the head cooling of animals in water22 or of humans in cold air,45,139 but only one human study has included cold-water exposure of the head. Alexander reported the data regarding head cooling from studies carried out on prisoners of war in Dachau during World War II.2 These studies were horrific, reprehensible, and grossly unethical, and the results are considered invalid and unusable because of the emaciated condition of the prisoners as well as questions regarding the protocol and accuracy of the results. Few experimental data are available to evaluate the effects of mild hypothermia on mental performance. A few medical studies have evaluated the impairment of memory among divers during cold-water dives.9,190,193 Two other studies involved cognitive testing during hypothermia without direct head cooling.19,50 Lockhart and colleagues111 recently evaluated the effects of dorsal head and neck immersion among human subjects immersed in 10° C (50° F) water on Tco cooling rates and mental performance. Dorsal head and neck immersion (with the body insulated) resulted in a cooling rate of 0.4° ± 0.2° C/hr (0.7° ± 0.4° F/ hr). Body immersion with the head, neck, and upper thorax out of the water resulted in a cooling rate of 1.5° ± 0.7° C/hr (2.7° ± 1.3° F/hr). Immersion of both the whole body and the dorsal head and neck nearly doubled the cooling rate to 2.8° ± 1.6° C/ hr (5.0° ± 2.9° F/hr) (p <0.0002). In addition, there were significant correlations between diminished cognitive performance and decreasing Tco. The time required to correctly complete the Stroop Color-Word Test increased as Tco decreased (p <0.001). The number of correct responses decreased with Tco for digit symbol coding (p <0.02), backward digit span (p <0.05), and paced auditory serial addition testing (p <0.05). Figure 6-21 demonstrates the effects of different PFDs on the position of the head in water. Giesbrecht and co-workers46 repeated the head-cooling study with the use of subjects immersed in 12° C (53.6° F) whose
38.0 37.5
†
37.0 36.5
†
*
36.0
*
35.5 35.0
**
34.5 34.0 33.5 –20
–10
0
10
20
30
Time (min) Body insulated, head out Body insulated, dorsal head in Body exposed, head out Body exposed, dorsal head in FIGURE 6-22 Core-temperature response to immersion in 12° C (54° F) water with the head out or the dorsum immersed in body-insulated and body-exposed conditions; shivering was inhibited with meperidine to mimic a severely nonshivering victim. (From Giesbrecht G, Lockhart T, Bristow G, et al: Thermal effects of dorsal head immersion in cold water on nonshivering humans, J Appl Physiol 99:1958, 2005.)
shivering thermogenesis had been inhibited with intravenous meperidine to model severe hypothermia.67 When the body was insulated, there was no Tco cooling with the head out of the water, and immersing the dorsum of the head had no further effect. However, when the body was not insulated but instead exposed to the cold water, Tco decreased at 3.6° C/hr (6.5° F/hr). In this condition, also immersing the dorsum of the head significantly increased the rate of Tco cooling to 5.0° C/hr (9° F/hr) (Figure 6-22). These results did not confirm the supposition of proportionately greater heat loss from the head. The measured heat loss from the head in both head-immersed conditions was only about 60 kJ as compared with 18 kJ to 33 kJ in the two head-out conditions. By contrast, total body heat loss in the body-exposed configurations was about 1100 kJ and 1260 kJ, respectively, for head-out and back-of-the-head-in conditions. Thus the head accounted for only about 3% and 5% of the total body heat loss, respectively, in the body-exposed conditions. The majority of the difference in heat loss in the body-immersed conditions came from immersion of the anterior thorax rather than from the dorsal head and neck. Nevertheless, it is important to recognize that, although there was not a significant increase in heat loss through the head, there was a disproportionate increase in Tco cooling. Although the mechanisms for this disparity have not yet been determined, the implications are clear for manufacturers and survivors. During long-term cold-water immersion, it is advantageous to keep the head out of the water. If this is not possible (i.e., most survival suits place the victim in a supine position), the survival ensemble should include a hood with as much insulation as is practical (Box 6-5).
BEHAVIOR AND POSTURE OF THE BODY IN COLD WATER
FIGURE 6-21 Effectiveness of various types of personal flotation devices for keeping the head and the upper chest out of the water. Top left, Type I jacket; top right, Type 3 jacket; bottom left, typical keyhole inflatable jacket; bottom right, waist-mounted inflatable device. (Courtesy Gordon G. Giesbrecht.)
154
Behavioral variables also affect Tco cooling rate. Hayward and colleagues used infrared thermography to demonstrate that, despite marked peripheral vasoconstriction, heat losses are high in the groin, the lateral and central thorax, and the neck.85 In the groin and neck, which are regions with relatively thin layers of peripheral soft tissue, blood flow through the large and relatively superficial femoral vessels, carotid arteries, and jugular veins potentiates heat flow to the cold water. In the lateral and central thorax, the relative absence of tissue (muscle and subcutaneous fat) insulation in combination with the high thermal conductivity
Heat Through Your Head
This common belief has caused many incorrect and even dangerous actions, such as going to extreme lengths to retrieve hats or to removing clothing when immersed to place it on the head for thermal protection. In a cold-water immersion scenario, 90% to 95% of heat loss occurs through the cold-exposed body. It has been demonstrated that, under similar thermal stresses, relative heat loss from the head (per unit of surface area) is not that much higher than that from other areas of the body. However, under certain conditions, increased heat loss from the head can cause a disproportionate decrease in body Tco. Thus head contact with cold water should be minimized whenever possible by changes in posture and maximum practical insulation.
of rib bone potentiates heat loss from the relatively warm lungs to the cold environment. Furthermore, exercise or excessive movement in the water greatly increases heat loss from active muscles. The effect of activity on total heat balance depends on the balance among the many factors illustrated in Figure 6-23. In normothermic circumstances, heat produced locally in peripheral muscles is transferred to the core via venous return. By contrast, during cold-water immersion, physical activity may actually increase heat loss through increased blood flow to the periphery. This is especially true when immersed victims engage in excessive movement in the water (e.g., swimming, performing the vigorous extremity movements that are necessary to maintain airway freeboard in rough seas). Hayward and colleagues86 demonstrated that minimizing both voluntary activity and exposure of major heat loss areas of the skin to cold water are the most effective ways to minimize a decline in Tco. They showed that treading water and drownproofing significantly increased the cooling rate. Despite increased metabolic heat production during exercise, the increased surface heat loss resulted in faster Tco cooling during exercise in cold water. They also developed two well-known cold-water survival techniques: HELP and the group huddle (Figure 6-8). These adaptive behaviors reduce Tco cooling by 69% and 66% of that of control conditions, respectively.82 When the sea is not calm, it may be difficult to perform the group huddle with complete thermal efficiency. However, other advantages of this position include the maintenance of group contact and morale. Sagawa and colleagues concluded that the lowest water temperature in
which humans could maintain normal Tco by generating body heat through muscular activity is 25° C (77° F), although there may be individual variations.145
EXERCISE Normally the advice is to not exercise while awaiting rescue in cold water. This is because of the understanding that, although metabolic heat production will increase, exercise increases blood flow to muscles and causes increased heat loss to the water, with a net result of increased Tco cooling. A recent study by Færevik and colleagues39 was conducted in subjects wearing neoprene survival dry suits in a wave tank with water temperature of 0° C (32° F) and air temperature of 5° C (23° F). When subjects remained still, Tco dropped more during 3 hours of immersion than it did during 6 hours of immersion during which they performed leg exercises for 5 minutes every 20 minutes (Figure 6-24). Thus, if enough insulation is worn, the heat of exercise can be contained within the insulation, which attenuates the drop in Tco.
SHIVERING Shivering is a thermoregulatory function during which involuntary muscle contraction increases heat production in an effort to prevent or minimize Tco cooling. Shivering intensity increases as Tco and skin temperatures decrease. Generally shivering intensity is maximal at a Tco of 32° to 33° C (89.6° to 91.4° F) and a skin temperature of approximately 20° C (68° C). However, shivering heat production is lower at any given skin temperature among individuals with higher levels of subcutaneous fat.108,199 Thermal balance during shivering depends on the same factors as it does during voluntary activity (see Figure 6-23). Figure 6-25, online illustrates how shivering heat production can maintain Tco in cold air and how it can arrest the fall in Tco in both warm and cool water. In colder water, the combination of shivering thermogenesis and body insulation (as a result of peripheral vasoconstriction) may result in maintenance of a steady-state Tco, albeit below normothermic levels. At even lower water temperatures, Tco will continue to decrease. This decrease accelerates when shivering thermogenesis eventually stops as a result of hypothermia-induced thermoregulatory impairment (this occurs when Tco <≈30° C [86° F]). The power of shivering is especially important during consideration of the clinical
37.8
↑ Convective heat transfer (blood flow) to core
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FIGURE 6-23 Factors that influence total thermal balance during increases in metabolic heat production (i.e., voluntary exercise and involuntary shivering).
A, Non exercise B, Intermittent leg exercise
FIGURE 6-24 Rectal temperature for six subjects during immersion in 0° C (32° F) water and −5° C (−23° F) air. A, No exercise, and B, intermittent leg exercise for 5 minutes every 20 minutes (mean ± standard deviation). *, There is a significantly higher rectal temperature in condition B as compared with condition A from 40 to 180 minutes. (From Faierevik H, Reinertsen RE, Giesbrecht GG: Leg exercise and core cooling in an insulated immersionsuit under severe environmental conditions, Aviat Space Environ Med 81:1, 2010.)
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CHAPTER 6 Immersion Into Cold Water
BOX 6-5 Controversy Box: You Lose Most of Your
PART 2 COLD AND HEAT
classification of hypothermia and rewarming therapies, because this valuable heat source is an efficient mechanism for rewarming the core during postimmersion recovery and resuscitation. This is discussed in more detail in Rescue and Management, later in this chapter.
NONTHERMAL FACTORS Underwater divers often experience “symptomless” or “undetected” hypothermia. Several factors contribute to increased cooling. Heat is lost through direct conduction to cold water and through the breathing of compressed air. Breathing compressed air at depth alters human thermoregulation. Mekjavic and colleagues studied the effects of hyperbaric nitrogen at 6 atm;117 these researchers also simulated inert gas or “nitrogen” narcosis with the inhalation of 30% nitrous oxide.136 They demonstrated a decrease in the Tco threshold for shivering and an increase in the rate of Tco cooling of up to twofold under these conditions. In a separate study, this group demonstrated qualitatively similar effects of insulin-induced hypoglycemia.137 Hypercapnia and hypoxia may also be present in various underwater scenarios. Hypercapnia has been shown to lower the shivering threshold94 and to transiently inhibit shivering. Both hypercapnia94 and hypoxia95 have also been shown to accelerate Tco cooling. Alcohol consumption is frequently associated with immersion hypothermia, because ethanol impairment of mental and motor performance is often the cause of accidental immersion. Social drinking can result in carelessness. Intoxicated mariners or others near water often fall from a boat, ship, gangway, wharf, or bridge into the water. Drunken drivers capsize or collide. On the basis of the frequency of occurrence alone, the consequences of alcohol ingestion warrant special considerations. Studies of the effects of moderate doses of ethanol (i.e., blood alcohol levels of 50-100 mg/dL, which is the range associated with legal impairment) on cold stress have established the following: 1. The rate of heat loss is not significantly increased. Alcohol has a primary vasodilatory effect under normothermic conditions.38,83,100 Under hypothermic conditions, where vasoconstriction predominates, alcohol lowers the vasoconstriction threshold during the moderate cold stress of 28° C (82.4° F) water immersion, but does not affect the shivering threshold or the rate of Tco cooling.93 2. The rate of heat production is slightly decreased. For immersion in water colder than 28° C (82.4° F), a moderate ethanol dose inhibits the metabolic response to cold.42,115 Shivering thermogenesis is reduced in cold water by approximately 10% to 20%. 3. The cooling rate is not significantly increased.42,93,115 Because the body’s cooling rate in cold water is influenced more by the rate of heat loss than by the rate of heat production, the slight reduction in shivering thermogenesis induced by moderate ethanol ingestion is outweighed by factors that affect heat loss (e.g., peripheral vasoconstriction, body fat). Because these do not vary with alcohol use when the person is cold stressed, the cooling rate does not change. 4. Fatigue potentiates thermoregulatory impairment by alcohol. Exhaustive exercise leading to fatigue (which is characterized by hypoglycemia and the depletion of glycogen reserves) in combination with a moderate dose of ethanol significantly reduces resistance to cold.78,96 Alcohol inhibits gluconeogenesis,76,96 so the ability to provide glucose to maintain shivering is reduced. If a person enters cold water in this condition, his or her cooling rate is likely to be greater than in the absence of ethanol. 5. The perception of cold is diminished. Experimental studies of humans in cold water show that moderate alcohol dose to some extent relieves feelings of intense cold.42,101 This cognitive alteration may be functionally related to the reduced shivering response. 6. Cold-induced diuresis is increased. Alcohol inhibition of antidiuretic hormone augments immersion diuresis.26 During the first hour of cold-water immersion, the urine flow rate can be more than six times normal (i.e., up to 156
approximately 8 mL/min). For longer immersions (i.e., >1 hour), alcohol potentiates the development of dehydration and hypovolemia. For most humans, high doses of alcohol (i.e., blood levels of >200 mg/dL) have an anesthetic effect. The major impairment of mental, motor, and involuntary function (including thermoregulation) occurs. Alcoholics who “pass out” in cold locations (i.e., “urban hypothermia”) rapidly and passively become hypothermic.28,121 When highly intoxicated persons enter cold water (usually by falling in), hypothermia is seldom a problem, because such persons usually drown quickly.
Cold-Water Survival Cold-water survival depends on avoidance of drowning and hypothermia and on the many factors related to these risks, including the following: ability to control the cold shock response; ability to swim and maintain airway freeboard; the availability and type of a PFD; availability of a life raft or other floating object to increase buoyancy; behavior of the survivor in water; decision to swim for shore or to wait for rescue; availability of signaling devices (e.g., whistles, flares, strobe lights, radios, mirrors) and the ability to use them; and proximity of rescue personnel.154,155,159
ABILITY TO CONTROL THE COLD SHOCK RESPONSE As previously discussed, sudden immersion in cold water initiates a cardiorespiratory cold shock response that significantly potentiates the risk of drowning. This response and the resulting incapacitation that can accompany it have been suspected as the primary causes of drowning after short-term (i.e., <10 minutes) immersion in cold water.165 Abrupt tachycardia and hypertension induced by sudden immersion in cold water can produce incapacitating cardiac dysrhythmias in susceptible individuals and myocardial infarction or cerebrovascular accident in persons with arterial disease or hypertension.165 In addition, reflex gasping and hyperventilation165,174 significantly shorten the duration of breath holding.84,88,165 Figure 6-26 illustrates this phenomenon. Loss of breath-holding capacity can have severe consequences for survivors attempting underwater egress from a submerged vehicle or from a capsized vessel or aircraft or for survivors who are simply trying to maintain airway freeboard in a rough sea or a white-water river.88,144,169 Respiratory difficulties induced by the cold shock reflexes make breathing while swimming extremely difficult. Golden and Hardcastle have demonstrated a “swim stroke/respiration asynchrony” that leads to water inhalation and swimming failure.70 Golden and colleagues have shown that even persons who are considered good swimmers (at least in warm water) can only swim for a few minutes in cold water. Swimming ability and survival time in cold water are further diminished by the subjective perception of shortness of breath and panic reactions from unexpected cold-water immersion.165 The work that is required to swim in cold water is greater than that in warm water because of the former’s higher viscosity (e.g., water at 4.7° C [40.5° F] has a viscosity that is 67% higher than that of water at 23.7° C [74.7° F]).104 The increased work of swimming in cold water potentiates the onset of fatigue. The combination of all of these factors may incapacitate even physically fit and capable swimmers. Keating and colleagues observed sudden incapacitation in two experimental subjects (who were good swimmers) who were immersed in 4.7° C (40.5° F) water.104 One subject inhaled water because of respiratory difficulty and fatigue after swimming for 7.5 min and had to be pulled from the water. The second subject lasted only 1.5 min before he “floundered and sank without managing to reach the side of the pool, which was about one meter from his head, and had to be pulled” out of the water. The observed frequency of such swimming failures and unexpected submersions has led the U.S. Coast Guard to coin the term “sudden disappearance syndrome” to describe the phenomenon.178 The magnitude of the cold shock response can be attenuated through increased insulation, graded immersion (see Figure 6-6),
110 Second submersion (after habituation and hyperventilation)
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40
Drowning is the most immediate survival problem after water entry. To maintain airway freeboard and to avoid drowning, a survivor must possess the physical skills and psychological aptitude to combat the effects of wave action.155,169 Although a PFD assists with maintenance of airway freeboard, waves can still submerge a survivor’s head, even in moderately calm seas.65,154,178 To reduce risk of drowning in rough seas, a survivor can increase effective airway freeboard by partially exiting the water (e.g., clinging to an overturned vessel or other debris floating in the water) or by climbing totally out of the water onto a life raft or a capsized vessel. In both of these environments, the survivor may still have to cope with the effects of cold wind, spray, and waves (Figure 6-27; see also Figure 6-20).
30
BEHAVIOR OF THE SURVIVOR IN THE WATER
Breath-hold duration (sec)
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Water temperature (° C) FIGURE 6-26 Effect of water temperature on maximum breath-hold duration in young, physically fit human subjects (80 men and 80 women). The first submersion was sudden after sitting comfortably in air at a mean temperature of 11.3° C (52.3° F). The second submersion followed 2 minutes of acclimatization to the water. The last 10 seconds of the acclimatization was accompanied by 10 seconds of hyperventilation. (From Hayward JS, Matthews BR, Overweel CH, et al: Temperature effect on the human dive response in relation to cold-water near-drowning, J Appl Physiol 56:202, 1984.)
and habituation to cold immersion. Tipton and colleagues demonstrated that habituating subjects to 10° C (50° F) water resulted in a 16% reduction in respiratory rate during the first 30 seconds of immersion in 10° C (50° F) water and a 26% reduction in respiratory rate during the 30 sec to 180 sec interval after immersion in 10° C (50° F) water. Tidal volume and heart-rate response demonstrated similar declines in habituated subjects.171 Habituation through cold-water survival training may thus be an important safety measure for workers in cold-water environments. Protective clothing also diminishes the cold shock response that occurs as a result of the initial immersion in cold water. Clothing (e.g., well-fitted wet suits, dry suits with adequate seals) that limits the amount and ingress velocity of water that reaches a subject’s skin significantly decreases cardiorespiratory reflex responses to sudden immersion.118,172,173,175 Tipton and Golden demonstrated that subjects who were wearing wet suits that protected the torso but that left the limbs exposed had significantly reduced respiratory reflex responses but not reduced heart-rate responses as compared with control subjects with neither torsos nor limbs protected. They concluded that the limbs may be more important than the torso with regard to the cardiac response to sudden cold-water immersion.172 Tipton and colleagues also demonstrated that even loose-fitting and poorly insulated clothing can attenuate the magnitude of the cold shock response as compared with immersion in swimming trunks only.173 When volunteers were immersed in 10° C (50° F) water wearing either conventional clothing or conventional clothing plus windproof/showerproof foul-weather clothing,
Survivor location has a significant effect on Tco cooling rate and survival time. The U.S. Coast Guard and other rescue organizations recommend that a survivor of a maritime accident in cold seas get as much of his or her body out of the water as possible to minimize the cooling rate and maximize survival time.159,178 This recommendation derives from the higher thermal conductivity of water as compared with air at the same temperature. However, survivors who are exposed to cold air are still at risk from hypothermia as a result of convective, evaporative, and radiant heat losses. In a rough sea environment, wind increases the magnitude of convective heat loss, and spray and periodic wetting from breaking waves result in conductive heat loss.162,164 Steinman and colleagues confirmed these observations.159 The cooling rates of thin male subjects wearing different types of protective clothing were compared for three survival situations: 1. Immersion in 6° C (42.8° F) water with 1.5 m (4.9 ft) breaking waves. 2. Exposure to 7.7° C (45.9° F) air, continuous water spray at 6° C (42.8° F), continuous 28 to 33 km/h (17.40 to 20.50 mph) wind, and occasional breaking waves while sitting atop an overturned boat (see Figure 6-27). 3. Exposure to 7.7° C (45.9° F) air and occasional breaking waves while sitting in an open one-man life raft. The results of the study are shown in Figure 6-28. For each type of garment worn, cooling rates were considerably faster in the water than atop the boat (despite the effects of wind, spray, and breaking waves) or within the raft. These experimental conditions were tragically reproduced in real life for the four football players whose boat capsized in the Gulf of Mexico, as described previously. Only one of the men
FIGURE 6-27 Testing protective clothing atop an overturned boat with exposure to wind, spray, and breaking waves. (Courtesy Allen M. Steinman.)
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CHAPTER 6 Immersion Into Cold Water
cardiopulmonary and thermal responses were significantly less than those found with swimming trunks alone. Mental preparation should be used to avoid panic, to decrease emotional response, and to make a conscious effort to control breathing.
PART 2 COLD AND HEAT
Environment Water 5.82
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FIGURE 6-28 Mean linear cooling rates (° C/hr) for lean males in three survival environments: (1) water = immersion in 6.1° C (43.0° F) breaking waves; (2) boat = 5-min immersion in 6.1° C (43.0° F) water followed by exposure to 7.7° C (45.9° F) air atop an overturned boat with continuous 28 to 33 km/hr (17.4 to 20.5 m/hr) wind, water spray, and occasional breaking waves; and (3) raft = exposure to 7.7° C (45.9° F) air in an open, one-man life raft preceded by 5-min immersion in 6.1° C (43.0° F) water. AC, Air-crew coveralls; BC, boat-crew coveralls; FS, flight suit (lightweight clothing); NI, intact, non–foam-insulated “dry” coveralls; NX, NI with a 5-cm tear in the left shoulder, thus permitting water to leak into the suit and degrade its insulation; WS, wet suit. Blank squares indicate combinations of garments and environments that were not tested. (From Steinman AM, Kubilis P: Survival at sea: The effects of protective clothing and survivor location on core and skin temperature, USCG Rep No. CG-D26-86, Springfield, Va., 1986, National Technical Information Service.)
survived the heavy seas, high winds, and 18° C (65° F) water. He survived for 43 hours, primarily by getting out of the water and sitting atop the capsized boat (see Figure 6-20). The other three men spent a lot more time immersed and wore less insulation; thus they cooled faster and perished (see Survival Modeling, later, for further discussion). Survivors should attempt to get as much of their bodies out of the water as possible, even if it means exposure to cold wind and spray. Even rescue and medical personnel who frequently work in wilderness environments poorly understand this recommendation. A widespread misunderstanding of the concept of windchill128 causes many to conclude that survivors have higher heat losses if they are exposed to wind, especially if they are wet, than if they are immersed in water.159 The term windchill, which was originally used by Siple and Passel151 to describe the increase in heat loss from unprotected skin exposed to wind, is frequently used in the communication media without regard to the difference between exposed and unexposed skin. This leads many to erroneously believe that windchill temperature applies to both clothed and unclothed areas of the body. Furthermore, common experiences during recreational activities at the beach, lake, or swimming pool, where people subjectively feel colder after leaving the water (because of evaporative heat loss from the skin) than they do while swimming, reinforce this misunderstanding. This has occasionally led survivors to abandon a position of relative safety atop a capsized vessel and to reenter the water, usually with tragic results. The sensation of coldness, which is skin dependent, does not reliably convey information about rate of heat loss when two radically different environments (e.g., air and water) are compared.
DECISION TO SWIM FOR SHORE OR TO WAIT FOR RESCUE During cold-water immersion, physical activity increases heat loss through increased blood flow to the periphery. This is especially pertinent when immersed victims engage in excessive movement in the water (e.g., swimming, performing the vigorous extremity movements necessary to maintain airway freeboard in rough seas). The decision to swim for shore or to wait for rescue is crucial for a survivor of cold-water immersion. The increased cooling rate associated with swimming might lead one to conclude that holding still is preferable to an attempt to swim for safety. However, if the survivor can make it to shore or even to shallow water, survival is likely to be prolonged, despite the risk of lower 158
Tco. Lonsbury and co-workers specifically evaluated this issue by comparing the cooling rates and swimming distances for both novice and expert swimmers in a swimming plume.32 Experimental subjects, who were wearing average clothing (i.e., no specific insulation against cold-water immersion) and PFDs, were immersed in 10° C (50° F) water and either remained still in a HELP position or swam against a current that was matched with their swimming ability. Swimming resulted in a 17% faster rate of Tco cooling as compared with holding still. The novice swimmers traversed about 800 m (2625 ft) and the expert swimmers about 1400 m (4593 ft) during their swims. Thus, swimming may well have allowed the subjects to achieve safety ashore, despite the faster cooling rate. The researchers also found that the probability of a successful survival outcome depended on the decision to swim for safety early during a survival event. If the subjects had cooled for 30 minutes before attempting to swim, the likelihood of success was significantly reduced. The decision to swim or to remain still ultimately depends on the immersed individual’s understanding of the many variables that affect a successful outcome, including the following: body morphology and cooling rate; water temperature; wave conditions and currents; proximity of shore; proximity of rescue personnel; swimming ability; and availability of signaling devices, flotation devices, and protective clothing. There is no uniformly correct answer to the question, “Should I swim for it?” Each survival situation must be evaluated individually; a suggested algorithm appears in Figure 6-29 (also see Box 6-6).
SURVIVAL MODELING When a rescue organization is tasked with searching for victims in cold water, it is important to have an accurate estimate of how
BOX 6-6 Controversy Box: Always Stay with Your Boat For many scenarios in which warmer water temperature allows for longer survival and in which rescue is likely to occur, this is good advice. However, in colder water in secluded areas, the decision is not as clear, especially if rescue is unlikely. First, the decision to swim to safety should be made only if the victim is wearing a PFD, if the likelihood of rescue is low, and if the victim can reach shore within 45 minutes. With a PFD, if swim failure occurs, the victim will still remain afloat. Without a PFD, swim failure will result in drowning (see Figure 6-29).
CHAPTER 6 Immersion Into Cold Water
Accidental cold-water immersion
Don’t panic, breathing under control
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Decide early Commit to decision FIGURE 6-29 Algorithm for making the decision to stay or swim when immersed in cold water. PFD, Personal flotation device.
long the victims might survive and thus continue to warrant search resources. Various prediction models have been devised to assist with these difficult estimates. The Cold Exposure Survival Model was devised by Tikuisis to provide a sophisticated set of survival-time estimates for individuals who are immersed in cold, rough seas and for survivors who are partially immersed or exposed to cold wind under wet conditions.162,163 The model was developed on the basis of experimental data about cooling with different types of flotation devices and thermal protective clothing (Figure 6-30),158,159 shivering control and capacity,38 body composition (Figure 6-31), and other factors. The Cold Exposure Survival Model has been used for many years by both the Canadian and U.S. Coast Guards. Recently, the U.S. Coast Guard started using a new decision tool: the Probability of Survival Decision Aid (PSDA), which was developed by Xu and colleagues.205 Although the Cold Exposure Survival Model is based on a one-cylinder model, which assumes that most heat loss comes from the torso in cold victims, the PSDA includes six cylinders that represent the head, torso, arms, hands, legs, and feet. For example, Figure 6-32 shows predicted survival times for victims in varying water temperatures. Presently the PSDA predicts the time required for Tco to drop to 34° C (93.2° F) (i.e., functional time) and to 30° C (86° F) (i.e., survival time). When the PSDA was applied to the four football players whose boat capsized (as described previously in Recreational Activities and Cold Water), the survival time predictions for the first and third fatalities (13.5 and 25.7 hours, respectively) were very close to the actual survival times of approximately 13.0 and 25.5 hours. The heaviest victim (the second fatality) died much sooner (13.5 hours) than was predicted (37.3 hours). However, his symptoms were much different and indicated that more than hypothermia was involved. Instead of the expected hypothermia-induced gradual loss of physical abilities and the expected level of mental abilities and responsiveness, he was very agitated and aggressive, and he vigorously and continuously tried to get away from the boat. He eventually took off his lifejacket and forcefully dove under the surface and drowned. Therefore, it is likely that some other factors also contributed significantly to his death.
Because this victim spent so much more time immersed in the water than did the others, he may have ingested significant amounts of seawater; this was described and would be consistent with some of his actions and symptoms. Finally, the lone survivor lasted longer than predicted with a Tco of approximately 32° C (89.6° F) after 43 hours; the PSDA predicted he would cool to 28° C (82.4° F) after 41 hours. Interestingly, at this point, he was still shivering vigorously, likely as a result of his excellent physical condition; normally he would have been expected to stop shivering many hours before rescue. This long-lasting and high-intensity shivering heat production would have a significant affect in attenuating the drop in Tco. Predictive modeling has many inherent complications, but the PSDA results indicate the value of modeling as well as of providing some insight into the thermophysiology and pathophysiology present during this epic struggle.
SIGNALS Effective signals can greatly increase the chance of survival by bringing rescue and shortening the duration required to survive. Figures 6-33 and 6-34 show various types of signals, including dye, smoke, group formations, streamers, and flares. One inherent signal can be the clothing that is worn. It is a great advantage to wear colorful PFDs or other colorful clothing. For example, the U.S. Coast Guard rescue personnel found Nick Schuyler after 43 hours of immersion in the Gulf of Mexico because of his bright orange jacket (see Figure 6-20).
Physiologic Responses to Cold Water Submersion With the Head Under Water Drowning is covered in detail in Chapter 75: Submersion Injuries and Drowning. However, a brief discussion is included here to provide a more complete discussion of cold-water immersion. There have been several recent advances in our understanding of why individuals can survive cold-water submersion for as long as 66 minutes8 with full or partial neurologic recovery (i.e., coldwater near drowning). The most important factors in these unusual cases are low water temperature and subsequent brain 159
MECHANISMS FOR BRAIN AND BODY COOLING Children have an advantage in cold-water submersion incidents, because their greater surface area–to–mass ratio allows for faster conductive cooling, which provides cerebral protection on the
basis of decreased cerebral metabolic requirements of oxygen (CMRO2). The mammalian dive reflex, which initiates intense bradycardia and shunts blood flow to important core organs such as the heart and brain, has also been implicated. A third factor that has recently been explored is the possibility that cold-water ventilation may result in rapid and extensive cooling during submersion. The effectiveness of the human dive reflex, especially the breath-hold response, is controversial. Nemiroff, who reported one of the largest series of successful resuscitations of submersion victims, feels the dive reflex plays an important role, particularly in children and infants and especially in neonates.129,130 Hayward and colleagues88,138 feel that the enhanced success of resuscitation associated with cold-water submersion is more a result of hypothermia than of the dive reflex.
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PART 2 COLD AND HEAT
cooling. This principle has been used in clinical practice for years. For example, cardiopulmonary bypass used to cool neurosurgical patients to a Tco of approximately 9° C (48.2° F) made it possible to arrest brain blood flow for at least 55 minutes, with full neurologic recovery.135 The full explanation for these recoveries relates to both (1) the mechanisms for and amounts of brain and body cooling and (2) the mechanisms for the protective effect of this cooling.
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FIGURE 6-30 Prediction of survival time (ST) for an average individual under varying degrees of clothing protection (see Figure 6-15). A, For immersion in rough seas versus water temperature, low = nude, flight suit, float coat, aviation coveralls, boat-crew coverall, or torn coverall); medium = short wet suit or full wet suit; and high = dry coverall or dry suit. B, For exposure to air at 20 km/hr (12.4 m/hr) under wet conditions versus air temperature, low = nude, flight suit, or aviation coverall; medium = float coat, boat-crew coverall, short wet suit, full wet suit, dry coverall, or torn coverall; and high = dry suit. (From Tikuisis P: Predicting survival time at sea based on observed body cooling rates, Aviat Space Environ Med 68:441, 1997.)
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FIGURE 6-31 Predicted survival time (ST) for individuals wearing boatcrew coveralls (see Figure 6-15) for A, immersion in rough seas versus water temperature; and B, exposure to air at 20 km/hr (12.4 miles/hr) under wet conditions (i.e., clothing wetness of 1550 g/m2) versus air temperature. The lower and upper boundaries of the shaded regions represent predictions for lean and fat individuals, respectively. (From Tikuisis P: Predicting survival time at sea based on observed body cooling rates, Aviat Space Environ Med 68:441, 1997.)
CHAPTER 6 Immersion Into Cold Water
100 0C 5C 10C 15C
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35
Immersion time (hr) FIGURE 6-32 Effect of water temperature on predicted number of survivors using the Probability of Survival Decision Aid. (From Xu X, Amin M, Santee WR: Probability of Survival Decision Aid (PSDA), USARIEM Technical Report T08-05. Natick, Mass., 2008, U.S. Army Research Institute of Environmental Medicine.)
It is important to note that the protective effect of cooling depends on the Tco at cessation of oxygen delivery and the subsequent rate and extent of the decrease of Tco. Because Tco is likely to be near normal at the onset of an accidental submersion, rapid cooling after the onset of ischemia is important for survival. Conduction alone probably cannot account for the rapid decrease in Tco that occurs during cold-water submersion incidents. Conn and colleagues studied cold-water (4° C [7.2° F]) drowning in shaved and anesthetized dogs, and found that submersed dogs continued to breathe the cold water for an extended period of time.22 Tco decreased by 11° C (19.8° F) after 4 minutes in the completely submersed dogs as compared with only 3° C (5.4° F) in the control dogs, which were immersed with their heads out and did not breathe cold water. It is likely that the rapid cooling was the result of convective heat exchange in the lungs as
FIGURE 6-34 Differences in visibility in water based on suit color (top) and whether a group is stationary in a star formation (middle) or kicking the legs (bottom). (Courtesy Gordon G. Giesbrecht.)
compared with only surface conduction in the control dogs. The general conclusion that brain cooling is accelerated considerably by respiration of cold water has been proposed by others54,68,74 and mathematically predicted by Xu and colleagues.206 Although breath holding may occur during submersion, a physiologic break point occurs, at which time involuntary breathing movements predominate.4 This factor, when coupled with unconsciousness, could reasonably be expected to result in the respiration of water, at least under certain circumstances. Experimental and anecdotal evidence in humans is rare. However, one helicopter crash survivor reported that, after being trapped underwater for some time, he recalled feeling that he was about to die and that he was breathing water in and out just before escaping the cockpit.12 Whether or not this occurred has not been confirmed.
MECHANISMS FOR THE PROTECTIVE EFFECT OF BRAIN COOLING
FIGURE 6-33 Dye marker (top) and smoke flare (bottom) signals. (Courtesy Gordon G. Giesbrecht.)
Hypothermia provides an advantage during anoxic periods, such as cold-water submersion, because of what is known as the “metabolic icebox.” Whole-body or focal hypothermia has long been used to extend biologic survival time during surgery under ischemic conditions. Cerebral protection under hypothermic conditions has commonly been attributed to decreased cerebral metabolic requirements for oxygen, according to the temperature coefficient (Q10) principle. Although the Q10 of the whole body is about 2, the Q10 of the brain increases from approximately 3 between 27° and 37° C (80.6° and 98.6° F) to 4.8 between 17° and 27° C (62.6° and 80.6° F).120 On the basis of these values, if the brain could survive an ischemic insult for 5 minutes at 37° C (98.6° F), cooling to 27° C (80.6° F) or to 17° C (62.6° F) would provide 15 and 72 minutes of protection, respectively, based 161
140 Survival time (min)
PART 2 COLD AND HEAT
160
120 100 80 60 40 20 0 7
17
27
37
Core temperature (° C) FIGURE 6-35 Schematic presentation of survival time at different core and brain temperatures. A, Prediction based on a temperature coefficient (Q10) of 2. B, Prediction based on a Q10 of 3. C, Prediction based on the Q10 effect plus other factors, such as changes in neurotransmitter release (i.e., glutamate and dopamine). Actual survival times are from both neurosurgical and accidental hypothermia cases. Most of these cases fall outside of the range predicted based on Q10 alone; thus some other factors must also contribute to survival.
solely on the decreased CMRO2 (Figure 6-35). Although long survival times at brain temperatures of less than 20° C (68° F) may be predicted on the basis of increasing Q10 and diminishing CMRO2, some additional mechanisms may be required to explain intact survival after prolonged submersion, when reported Tcos are often above 30° C (86° F). These factors are schematically shown in Figure 6-36, online. Since the early 1990s, several studies that have been directed mainly toward the protection of the brain during or after cerebral ischemic events have demonstrated that even moderate brain cooling of 3° to 5° C (5.4° to 9° F) provides substantial cerebral protection from ischemic insult.* Submersion likely promotes cerebral death as tissue ischemia depletes high-energy phosphates and leads to membrane depolarization. This stimulates release into the extracellular space of excitatory neurotransmitters such as glutamate and dopamine, which mediate postsynaptic depolarization and cause calcium entry into the cell. Calcium influx mediates production of oxygen and hydroxyl free radicals (which may be involved in reperfusion injury) and release of free fatty acids, which results in eicosanoid synthesis.176 Various animal studies have shown that cooling the brain by only 3° to 5° C (5.4° to 9° F) before ischemia delays terminal depolarization and does the following: reduces the initial rate of rise of extracellular potassium;97 results in complete suppression of glutamate release and 60% reduction in the peak release of dopamine;15 attenuates ischemia-induced damage to endothelial cells;29,30 reduces hydroxyl radical production;66 and improves postischemia glucose use.64 These results relate to mechanisms other than decreased CMRO2, which may explain cerebral protection during cold-water near drowning. In summary, these findings indicate the following: (1) if the brain cools even by only 3° to 5° C (5.4° to 9° F), it is protected in excess of what would be predicted from decreased CMRO2 alone; (2) protection results from additional protective mechanisms of cooling related to neurotransmitter release, calcium flux, eicosanoid synthesis, and perhaps other phenomena; (3) the mammalian dive reflex may result in cold-induced circulatory adjustments that favor conservation of oxygen for the heart and the brain; and (4) cold-water ventilation may accelerate brain cooling and provide further protection.
IMPLICATIONS FOR SURVIVAL The paradox of whether Tco cooling is an advantage or a disadvantage depends on whether there is cessation of oxygen delivery, *References 14, 15, 64, 123, 146, 204.
162
and, if so, what Tco is when anoxia occurs and how much the Tco subsequently declines. These factors are schematically illustrated in Figure 6-36, online. If oxygen delivery is not compromised (i.e., during immersion hypothermia), then Tco cooling will eventually lead to death from cardiac arrest. However, if oxygen delivery is compromised (i.e., during submersion hypothermia and coldwater near drowning), Tco and brain cooling will prolong survival as compared with a condition in which Tco cooling does not occur (i.e., myocardial infarction). These factors are important to understanding whether children have a survival advantage over adults during cold stress. Because children cool faster, their body size would be an advantage when oxygen supply is compromised during cold-water submersion. However, when the oxygen supply is uninterrupted during head-out immersion or in cold air, the small body size becomes a disadvantage, because the onset of severe hypothermia is not as fast.
Rescue (Self-Initiated or Assisted) SELF-RESCUE FROM OPEN WATER OR AN ICE HOLE Most people have a poor understanding of how their bodies will react during cold-water immersion. Although there is individual variability, the following general principles apply. First, get breathing under control, because gasping and hyperventilation may result in gulping water or even drowning. One should be able to control breathing within 30 seconds to 2 minutes. In icecold water, loss of arm control and of the ability to grasp is progressive and begins to occur within the first 3 to 15 minutes. In open water, self-rescue may involve pulling oneself onto a floating object and out of the water as much as possible. If a person has fallen through the ice, it is usually best to turn and face the direction from which he or she came. The ice traveled over has already been proved capable of holding one’s weight. Swim to the ice ledge on the entry side of the hole. The self-rescue exit is illustrated in Figure 6-37 and can be seen in Cold Water Boating, listed in the Video References
Hold on
Kick your feet to get horizontal
Kick and pull
Slide along: DO NOT STAND
FIGURE 6-37 Self-rescue technique after falling through ice. Place the arms on the ice and kick the feet (i.e., flutter kick) until the body is horizontal with the water surface, then kick vigorously with the legs and pull the body along the ice surface. Slide or roll away from the hole, and do not stand up until it is certain that the ice is thick enough to hold body weight. (Courtesy Wilderness Medicine Newsletter. Available at http://www.wildernessmedicinenewsletter.com.)
Assess the Situation 1. Assess the victim’s physical and emotional condition. 2. Assess the ice and water conditions (e.g., ice thickness, water current). 3. Assess the equipment that you have that might be useful in a rescue. 4. Assess the rescue skills that are possessed by you and by those who are with you. Follow the Rescue Sequence The rescue sequence progresses from lowest-risk actions to highest-risk actions. Low-risk actions should be taken first. Progression to higher-risk actions is dictated by training level and available equipment. 1. Shore-assisted rescues involve talking, throwing, and reaching; untrained bystanders should limit themselves to these techniques. 2. Platform-assisted rescues involve working from or with a flotation platform (e.g., an inflatable boat or other buoyant device). 3. Finally, in a “go” rescue, the rescuer approaches and contacts the victim. This should only be done by trained personnel wearing PFDs and thermally protective dry suits (Figure 6-38). Rescuers should always perform the lowest-risk rescue first and then contact professional authorities, if possible.
UNTRAINED BYSTANDER RESCUE Every year, newspaper articles describe the death of well-meaning bystanders who rush to help victims who have fallen through the ice. It is extremely important that the untrained bystander apply the acronym STOP to his or her actions: stop, think, observe, and plan. Stop the urge to rush up to help the victim,
A
B
ASSISTED RESCUE OF A VICTIM WHO HAS FALLEN THROUGH THE ICE Self-rescue and assisted rescue both have three guidelines: (1) acknowledge the danger of the situation; (2) assess the situation; and (3) follow the rescue sequence. Recognize the Danger 1. Recognize that ice conditions are unsafe and that no one else should approach the area. 2. Recognize that the victim is in an urgent situation that is potentially life threatening but that, if proper action is taken, there is more time than might be expected to make safe and effective decisions. 3. Recognize your own limitations in terms of training and equipment.
C FIGURE 6-38 The professional rescue of a volunteer from ice water. A rescue sling is placed around the victim’s chest (A), and the rescuer then enters the water to help the victim out of the water (B). Both individuals are then pulled along the ice to safety (C). (Courtesy Gordon G. Giesbrecht.)
163
CHAPTER 6 Immersion Into Cold Water
section at the end of this chapter. It is initiated by putting the arms up on the ice and getting as much of the upper body out of the water as possible. Kick the legs vigorously to bring the body into a horizontal position. Next, kick and pull yourself forward and get on top of the ice. Once up on the ice edge, it is best to crawl or roll away from the hole until the ice is thick enough to stand on. Use ice picks, car keys, a knife, or any other available object to get a better grip on the ice. Once on solid ice, remember that hypothermia and frostbite pose threats to survival. The first thing to do is to wring the water out of clothing. It might seem that this would make one colder, but wringing out the clothing increases its insulation value, which is best in the long run. Next, decide whether to stay and try to get warm and dry by a fire or to seek shelter. If shelter is reasonably close (i.e., <30 min of exposure to the cold air), it may be beneficial to walk to safety. If it is more than 30 minutes away, it may be better to stay and build an emergency fire and campsite. It is extremely important to protect the hands from becoming frostbitten. Wring water from gloves or mittens. If the fingers are still very cold, place each hand in the opposite armpit. If necessary, pull the arms inside the jacket to place the hands directly against the skin of the armpit. When the hands have recovered, it is imperative to start a fire to warm up and dry the clothing. Although a person who cannot get out of the cold water unaided might not yet be very hypothermic, physical incapacitation will get worse within 10 to 15 minutes. Consciousness will remain for an hour or so, until Tco decreases from 37° C to about 30° C (99° F to about 86° F), so one should work to extend survival time to widen the window of opportunity for rescue. Recall the 1-10-1 principle for responses during cold-water immersion (but remember that time estimates are subject to individual variability): you have 1 minute to get your breathing under control, 10 minutes of meaningful movement, and 1 hour until you become unconscious as a result of hypothermia. Swimming should be minimized, because it causes the body to lose heat much faster than does remaining as still as possible, and it also causes exhaustion. Clothes should be kept on in the water, because they help to conserve body heat. Although the air initially trapped in clothing will eventually be forced out, it helps with flotation while it remains. Wet clothing does not cause a person to sink. The main effect of water in clothing is that its inertia makes movement difficult. The weight of water in clothing becomes a problem only when trying to exit the water. In all cases (even if wearing a thermal protection suit or a PFD), use the ice edge for support. Extend the arms over the ice and press the legs together to help to conserve body heat. Keep the head and upper body as far out of the water as possible to conserve as much body heat as possible. Remain as still as possible. This will decrease heat loss, but it may also result in the arms freezing to the ice. After about 1 hour, when consciousness is lost from severe hypothermia, drowning occurs unless the head is prevented from slipping beneath the water. If one is frozen to the ice, drowning will be prevented, and a victim might survive yet another hour before the heart stops beating (generally at a Tco <25° to 28° C [77° to 82° F]). Thus, this could double the survival time and perhaps allow rescue.
PART 2 COLD AND HEAT
because you are likely to fall through the ice and become another victim. Think and observe the victim and the surrounding conditions, including any material that might be used in a rescue attempt. Finally, plan how to assist the victim out of the water. Untrained bystanders should limit themselves to techniques that progress from talking to throwing to reaching. Talk Encourage the victim to calm down and not panic. Direct the victim to an area of strong ice, and instruct the victim to execute a self-rescue by placing the arms on the ice, kicking until the body is horizontal on the water surface, and then kicking and pulling up onto the ice. Direct the victim to crawl and roll away from the hole until stronger ice is reached. Throw Any buoyant item can be thrown to the victim to assist him or her with remaining buoyant, especially if the ice is continually breaking and not providing a secure base of support. If possible, tie a rope or cord to the object; this could allow you to pull the victim out of the water. If only a cord or rope is available, tie a large loop at the end to make it easier for the victim to hold on to it. After the rope has been grabbed, instruct the victim to put the loop over his or her body and under the arms, to put an arm through the loop and bend the elbow around the rope, or to simply hold onto the loop. Reach It may be possible to reach a victim with some implement, such as a tree branch, a ladder, or anything else that can be pushed out on the ice. Care must be taken to not get too close to the hole when trying to reach the victim with any implement. Any rescue that requires the rescuer to approach the hole in the ice should be left to trained personnel. An untrained bystander who cannot perform a rescue with the use of these techniques should help the victim to widen the window of opportunity for trained rescuers to arrive. Instruct the victim to stop struggling and to hold his or her arms still on the ice. The objective is to let the arms freeze to the ice. Make sure that someone contacts emergency personnel. Wait with the victim, and provide continuous encouragement that he or she can survive; let him or her know that help is on the way.
RESCUE BY TRAINED PERSONNEL These paragraphs are not meant to provide in-depth training for professional rescue workers but rather to describe some of the basics of high-risk rescues. The techniques used by any professional rescuer should follow the policies and procedures of their local jurisdictions.
Trained personnel should first use the lower-risk techniques that were described earlier. If these do not work, personnel should implement the higher-risk techniques described by many ice-rescue training institutions.48 Briefly, trained rescuers must not go on the ice unless they are wearing a thermal protective dry suit and a PFD. The rescuers should also be secured by a safety rope that is operated by a trained colleague. Platform-assisted rescues involve working from or with a flotation platform, such as an inflatable boat or another buoyant device. These techniques involve pushing or being transported on the buoyant platform. The first choice is to push the platform toward the victim and to use it as a reaching device. Alternatively, the rescuer can make contact with the victim directly from the platform. Finally, during a “go” rescue, the rescuer approaches and contacts the victim directly. Standard lifesaving techniques should be used to ensure that a panicking victim does not pose a threat to the rescuer. After the victim is securely contacted, the victim and the rescuer can be pulled toward shore by the attendants on shore (see Figure 6-38).
RESCUE FROM OPEN WATER Retrieval of a victim from cold-water immersion must be performed with caution. Sudden reduction of the “hydrostatic squeeze” applied to tissues below the water’s surface may potentiate hypotension, especially orthostatic hypotension.73 Because a hypothermic patient’s normal cardiovascular defenses are impaired, the cold myocardium may be incapable of increasing cardiac output in response to a hypotensive stimulus. A victim’s vertical posture may also potentiate hypotension. Hypovolemia as a result of combined cold- and immersion-induced diuresis as well as increased blood viscosity potentiate these effects.27 Peripheral vascular resistance may be incapable of increasing, because vasoconstriction is already maximal as a result of cold stress. The net result of the sudden removal of a hypothermic patient from the water is similar to sudden deflation of antishock trousers on a patient in hypovolemic shock: abrupt hypotension. This has been demonstrated experimentally in mildly hypothermic human volunteers,72 and it has been suspected as a cause of post-rescue death in many immersion hypothermia victims.73,157 Accordingly, rescuers should attempt to maintain hypothermic patients in a horizontal position during retrieval from the water and aboard the rescue vehicle (Figure 6-39).3,73,157 If rescuers cannot recover the patient horizontally, they should place the victim in a supine posture as soon as possible after removal from cold water (Box 6-7).157 Helicopter hoist extractions can be performed directly by a rescue swimmer (Figure 6-40) or with a rigid litter from a boat (Figure 6-41, online). FIGURE 6-39 Single (A) and double (B and C) sling techniques affect how vertical the victim is during extraction from the water. The rescue slings provide a leverage advantage, especially when there is high freeboard (A and B). A wet victim is wrapped in a makeshift vapor barrier to minimize evaporative and convective heat loss during boat transport (D). (Courtesy Gordon G. Giesbrecht.)
A
B
C
D
164
BOX 6-8 Controversy Box: Prehospital Warming is
Although severe hypothermia is a critical condition, rescue and treatment do not necessitate rapid and reckless actions. Rescuers and medical providers should take the time required to safely remove the victim from the cold stress and then do as much as possible to be gentle and to keep the patient horizontal. The patient’s core has been cooling gradually for a long time (i.e., hours or even days), and a delay of a few minutes to get organized for treatment will not make the patient’s condition worse. However, rushing may result in patient jostling that induces ventricular fibrillation and cardiac arrest.
For many decades, it was believed that warming would cause massive vasodilation and result in cardiac arrest as a result of a precipitous drop in blood pressure or Tco or the return of noxious metabolites from the periphery. Many studies have demonstrated that a very cold patient will display intense vasoconstriction such that only massive heating from warm-water immersion could override this thermoregulatory response. Any heat source (other than a warm water bath) that is available in a prehospital setting will likely be safe. Thus it is now widely accepted that gradual core rewarming through the application of heat to the chest and axillae is valuable as long as cardiovascular stability is maintained.
Presents an Emergency That Must be Dealt With Quickly
The patient’s Tco may continue to decline—depending on the quality of insulation provided, the patient’s endogenous heat production, active or passive manipulation of extremities, and the site of Tco measurement—even after he or she has been rescued as a result of the physiologic processes described earlier as “afterdrop.” To diminish this effect, the patient’s physical activity must be minimized. Conscious patients should not be required to assist with their own rescue (e.g., by climbing up a scramble net or a ship’s ladder) or to ambulate when they are out of the water (e.g., by walking to a waiting ambulance or helicopter).49,122,157 Physical activity increases afterdrop, presumably by increasing perfusion of cold muscle tissue with relatively warm blood.11,52,53,55 As this blood is cooled, venous return (the circulatory component of afterdrop) contributes to a decline in myocardial temperature, thereby increasing the risk for ventricular fibrillation.87 Experiments on moderately hypothermic volunteers with esophageal temperatures of 33° C (91.4° F) demonstrated a threefold greater afterdrop during treadmill walking than while lying still.10,56 Such an exercise-induced enhancement of afterdrop could precipitate post-rescue collapse. Throughout the rescue procedures and during subsequent management, hypothermic patients must be handled gently.3,77,122 Excessive mechanical stimulation of the cold myocardium is another suspected cause of death after rescue.110,192 Several extraction techniques are presented in Figure 6-39 and can be seen on the videos in the Video References section at the end of this chapter. The technique depends on the number of rescuers, the design of the boat platform and the resultant freeboard, and the equipment on hand. Victims can be pulled by their clothing or PFDs; placed into single or double rescue slings, rescue nets, or even hoists; and extracted either head first or horizontally. It is easier to be gentle and to keep the victim horizontal if there are low gunnels or if the boat has a rescue port on the side. If possible, the method that will be used to package the patient (see Packaging, later) should be prepared ahead of
Dangerous and Should Be Avoided
time. Regardless of the technique used, care should be taken to be as gentle as possible and to lift the patient directly into the packaging system.
Medical Management This section describes prehospital management of hypothermia with specific reference to immersion pathophysiology. The hospital management of both accidental immersion and land-based hypothermia is described in Chapter 5: Accidental Hypothermia. Prehospital management of hypothermia patients, both in the field and during transportation to a site of definitive medical care, varies with the patient’s level of hypothermia, the rescuer’s level of training, the resuscitative equipment available, type of transportation, and time required for delivery to definitive care. Medical personnel must exercise good clinical judgment to balance all of these factors to select appropriate therapeutic modalities (Box 6-8). The primary goals of prehospital management of victims of accidental immersion hypothermia are prevention of cardiopulmonary arrest; prevention of continued Tco decline; moderate safe core rewarming, if practicable; and transportation to a site of definitive medical care.* Aggressive rewarming in the field has been contraindicated in the past, because the means to either diagnose or manage the many potential complications of severe hypothermia are unavailable in this setting.122 However, in the prehospital scenario of cold-water immersion, there is no source of heat that could be considered aggressive. Figure 6-42 indicates the levels of aggressiveness and effectiveness of various sources of heat for hypothermia and frostbite treatment. When transportation to a site of definitive care will take more than 30 minutes or is impossible, rewarming in the field with the use of the principles and techniques of management described in the following paragraphs may be appropriate (Box 6-9).
EXAMINATION, TRIAGE, AND LIFE SUPPORT Because hypothermia affects virtually every physiologic process, rescuers should manage a severely hypothermic patient as they would a victim of multiple trauma.156,157 Rescuers should not focus solely on Tco to the exclusion of other potentially life-threatening problems. Conversely, when the incident includes cold exposure, care must be taken to not focus solely on trauma injuries. Several *References 33, 79, 105, 112, 152, 157. BOX 6-9 Controversy Box: Afterdrop Is an Artifact
and Is Unimportant
FIGURE 6-40 A U.S. Coast Guard helicopter hoist rescue with a rescue swimmer and a victim. (Courtesy Gordon G. Giesbrecht.)
Rescuers and emergency medical personnel should be aware that Tco will continue to drop after an individual has been removed from the cold stress (see Figure 6-12). Although some decrease is inevitable, the understanding is that anything that increases blood flow to cold tissue (e.g., the legs) will increase afterdrop. Thus, patients should be kept from walking and remain horizontal, and the arms and legs should not be rubbed or massaged in an effort to warm the patient.
165
CHAPTER 6 Immersion Into Cold Water
BOX 6-7 Controversy Box: A Hypothermic Patient
PART 2 COLD AND HEAT
Power source
Heat level/ aggressive
Heat source Prehospital
Treatment effectiveness
Hospital
Hypothermia
Frostbite
XX
XXX
Fire Nonelectric
Chemical pack
–
√
IV fluid
√
–
√ –
–
√
√
√
√
Low-to-moderate heat
Warm sweet drink Inhalation warming
Non-aggressive
Warm water bottles Warm body Charcoal HeatPac
–
√√
√
Electric blanket
Electric blanket
√
√
Water blanket
Water blanket
√
√
Forced air warming
√√
√
XX
– – – –
Electric Forced air 120 VAC warming Warm shower Warm bath
Warm bath Lavage CAVR Fem-fem
XXX
High heat
√√√ √√√
Aggressive
√, Effectiveness
–
√√√ √√√√
Bypass –, Not effective or applicable
–
X, Harmful
FIGURE 6-42 Heat sources that could be used for hypothermia rewarming classified by location, heat level or aggressiveness, and treatment effectiveness for hypothermia and frostbite.
patients have died of hypothermia when treatment focused only on non–life-threatening physical injuries. It is rarely possible to measure Tco in the field. However, a diagnosis can be made on the basis of the patient’s history (to confirm that the main insult is cold exposure) and his or her signs and symptoms (see Figure 6-13). Generally, if a patient is mentally alert and shivering vigorously, he or she can be considered mildly hypothermic. If shivering is waxing and waning or absent or if consciousness is diminished or absent, he or she can be considered moderately to severely hypothermic. In accordance with standard emergency medical procedures, the ABCs of first aid—airway, breathing, and circulation—are essential.3,157 Rescuers should ensure an open airway and confirm the presence of adequate ventilation and circulation. If the patient is severely hypothermic, respirations and pulse may be slow, shallow, and difficult to detect3,156; therefore, rescuers should take 30 to 45 seconds to assess these vital signs.3 If neither the pulse nor breathing is detectable, rescuers should commence cardiopulmonary resuscitation (CPR) in accordance with normal basic life support protocols.3,156 Figures 6-43 and 6-44 are treatment algorithms for field treatment and medically equipped emergency personnel.152 Cardiac rhythm should be carefully monitored. Percutaneous electrodes may be required to overcome interference from muscle fasciculations or shivering.3 Endotracheal intubation and administration of heated and humidified air or oxygen are useful for management of apnea or hypoventilation and for reduction of further respiratory heat loss.3 Mouth-to-mouth or mouth-to-mask ventilation also provides heated and humidified air. If oxygen is available, it may supplement mouth-to-mouth or mouth-to-mask ventilation. Mouth-to-mouth or mouth-to-mask ventilation has the added advantage of providing a small amount of carbon dioxide for the patient’s inspired gases. This may be useful for prevention of hypocapnea as a result of relative hyperventilation in a severely hypothermic victim whose metabolic production of carbon dioxide is diminished.28 This is important because hypocapnea may decrease the threshold for ventricular fibrillation. Hypothermic patients with any detectable pulse or respiration do not require the chest compressions of CPR, although severe bradycardia and bradypnea may be present.3,156 This differs from 166
HYPOTHERMIA: FIRST-AID PREHOSPITAL CARE Rescue/examine
Responsive?
Yes
No
Respiration?
Yes Assume cardiac output
Shivering?
Yes
No
Pulse? (Check for 60 sec)
Spontaneous rewarming (insulate, vapor barrier, provide fuel)
Heat optional
No Ventilate 3 minutes
Heat desirable
Yes
No
Continue ventilation if still apneic
CPR
Heat if possible Hospital FIGURE 6-43 Algorithm for field treatment of a hypothermic victim.
BOX 6-10 Controversy Box: CPR Should be Started
Rapidly if a Pulse Cannot be Found Quickly
Rescue/examine
A hypothermic patient has been cooling for a long time, and it will likely not affect the outcome if a few minutes are taken to ensure that the heart is not functioning before commencing CPR. Premature chest compressions can cause an irritable heart to fibrillate. An initial pulse check should be done for 60 seconds. If no pulse is found, 3 minutes of rescue breathing might oxygenate the heart enough to strengthen contractions. If a pulse still cannot be found after another 60-second check, it can be assumed that the heart is not functioning, and chest compressions can be started in accordance with local jurisdiction protocols (see Figure 6-43).152
Responsive?
Yes
No
Respiration?
Yes Assume cardiac output
Shivering?
Yes
No
Spontaneous rewarming (insulate/ vapor barrier)
Heat if possible
No Ventilate 1–2 minutes
Cardiac monitor
Non-arrest rhythm
Arrest rhythm
Ventilate if apneic
Cardiac monitor
Central pulse
PEA
CPR
Yes
Heat if possible Hospital FIGURE 6-44 Algorithm for emergency medical treatment of a hypothermic victim.
normothermic CPR protocols, with which chest compressions may be indicated if bradycardia fails to provide sufficient cardiac output or systolic blood pressure.3 Because the metabolic requirements of hypothermic patients are reduced, bradycardia and bradypnea may still meet tissue oxygen requirements.29,49 Inappropriate administration of chest compressions in an attempt to augment cardiac output may precipitate ventricular fibrillation from mechanical stimulation of the irritable myocardium29 (Box 6-10). If a victim of cold-water immersion is found floating face down, drowning should be suspected and managed accordingly (see Chapter 75: Submersion Injuries and Drowning). In this case, correction of anoxia is paramount, and consideration of hypothermia is of secondary importance.3,130 Normal advanced cardiac life support protocols should not be routinely applied to severely hypothermic patients in cardiac arrest, because management beyond basic life support differs from that used for normothermic patients.3,29 Defibrillation and pharmacologic interventions are usually ineffective for myocardial temperatures of less than 30° C (86° F).3,7,29 Furthermore, repeated defibrillatory shocks may damage the myocardium.3,156 Defibrillation should be limited to three shocks at 200, 300, and 360 joules, consecutively, for patients who are colder than 30° C (86° F).3 Administered medications are ineffective, and they may accumulate to toxic levels,
because drug metabolism by the hypothermic liver and kidneys is reduced.29,196 For hypothermic patients with a Tco of more than 30° C (86° F), normal advanced cardiac life support protocols may be used.3 All intravenous fluids should be warmed before administration. However, it may be necessary to extend the recommended interval for intravenous medications because of the patient’s reduced metabolic rate. For the unconscious hypothermic patient who is not in cardiopulmonary arrest, endotracheal or nasotracheal intubation should be performed gently. The insertion of pacemaker wires and central venous catheters has been suspected of precipitating ventricular fibrillation, but prior ventilation with 100% oxygen has been associated with a decreased risk for this complication.27,28 Rescuers should not withhold endotracheal intubation, if indicated, for fear of precipitating ventricular fibrillation.3 If the patient does not require immediate life support intervention, a thorough and systematic examination must be performed as quickly as possible before the initiation of treatment for hypothermia. Because severely hypothermic patients may have a markedly depressed mental status, they may not respond normally to painful stimuli. Victims of immersion hypothermia may have suffered trauma before entering or while in the water. Central nervous system, skeletal, and soft-tissue injuries may be overlooked unless a careful examination occurs. Attention should be paid to the patient’s mental status and other central nervous system signs. Rescuers should evaluate the level of consciousness, presence or absence of shivering, and pupillary size and light reflex. Pupils may appear fixed and dilated in an unconscious and severely hypothermic patient, thus simulating the appearance of death. The diagnosis of death should not be made in a hypothermic patient, particularly in a field setting, unless resuscitation efforts fail after adequate rewarming efforts. The vital signs should be carefully measured, with particular attention paid to the Tco. A low-reading thermometer that is capable of recording down to 20° C (68° F) is required. Esophageal temperature at the level of the atria is the most clinically useful Tco obtainable, because this site most closely parallels cardiac temperature.56,87 However, most rescue personnel are almost never equipped to measure esophageal temperature. Rectal temperature is the most easily obtained Tco, yet rescuers often show reluctance to obtain a recording from this site in the field, and incorrect thermometer placement may cause an erroneous reading. If neither esophageal nor rectal temperature is taken, oral or axillary temperature is of limited value. Neither of these will accurately reflect Tco in a victim of immersion hypothermia. Facial cooling affects oral temperature, and cold skin temperature affects axillary recordings. However, the patient’s Tco will not be lower than that indicated by an oral or axillary recording. Thus, rescuers can use even superficial temperatures in a limited way to monitor the patient’s status, although this is not ideal. Hemorrhage should be controlled in the usual manner. Antishock trousers are normally contraindicated, because they are likely to be ineffective in the face of the maximal vasoconstriction already present in a severely hypothermic patient.29 Because hypothermia itself can cause hypotension without massive fluid losses, antishock trousers should be used only if they are required for temporary stabilization of a suspected pelvic fracture.29 167
CHAPTER 6 Immersion Into Cold Water
HYPOTHERMIA: EMS PREHOSPITAL CARE
PART 2 COLD AND HEAT
INSULATION, STABILIZATION, AND REWARMING After recovery of the patient from the water and management of immediate life-threatening emergencies, the next objectives are prevention of further heat loss and efforts at moderate rewarming (i.e., 1° to 2° C/hr [1.8° to 3.6° F/hr]). Strategies for moderate rewarming in the field vary with the equipment available, training of rescue personnel, environmental conditions, and length of time required for transport to a site of definitive care. Maximum insulation of the whole body from any further environmental cooling is an obvious first requirement. The main goals for rescue personnel are to maintain or improve cardiorespiratory stability and to minimize Tco afterdrop, which can depress cardiac temperature and potentiate ventricular fibrillation. Packaging The purpose of packaging a patient in the field or during prehospital transport is to minimize all sources of heat loss (i.e., evaporation, conduction, convection, and radiation). Rescuers should maintain the patient in a horizontal position to prevent hypotension, and movement of the patient must be kept to a minimum. Clothing should be cut away if it is wet and if the patient is in a sheltered area. The patient’s skin should be dried with gentle blotting motions (no rubbing), and the patient should be protected by dry and insulating clothing and blankets, a sleeping bag, or a specialized rescue bag (Figure 6-45). This protection must include the head and neck. Incorporation of a windproof and waterproof layer or vapor barrier is of value for prevention of convective and evaporative heat loss. This is particularly important for patients who require helicopter evacuation, because downwash from helicopter rotor blades can reach wind speeds in excess of 160 km/hour (100 mph), thereby potentiating significant heat loss from windchill. It is important to note that the vapor barrier should also protect the insulation from becoming wet. Therefore, if the patient is dry, the vapor barrier can be wrapped around the outside of the insulation. However, if the patient is wet and his or her clothing cannot be changed (i.e., a survivor picked up by a small rescue boat), the vapor barrier should be placed around the patient inside the insulation layers. Spontaneous Rewarming Patients who are only mildly hypothermic (i.e., exposed to cold water for a relatively short time, fully conscious, and vigorously shivering with a Tco of >32° to 33° C [89.6° to 91.4° F]) are usually capable of rewarming themselves without difficulty. Heat production from shivering can reach levels that are five to six times that of the resting metabolic rate.38 Shivering is thus a highly effective means of rewarming, particularly if rescuers insulate the patient’s
BOX 6-11 Controversy Box: Airway Warming
Effectively Warms the Core
It is important for an emergency medical provider to know that airway warming does not significantly warm the body core (see Figure 6-12). However, the method does have some advantages. Most of the heat transfer occurs in the upper airways and may warm certain areas in the brainstem. Moisture loss is eliminated. It is important to know that some additional warming techniques—preferably application of heat to the chest and axillae—are necessary to actually raise the temperature of the heart.
head and body with vapor-barrier garments to minimize evaporative heat loss.56 Vigorous shivering has been shown to be capable of producing rewarming rates of as high as 3° to 4° C/hr (5.4° to 7.2° F/hr).49,56,62 Patients who are conscious and vigorously shivering are generally not a medical emergency and usually do not require immediate transportation for definitive care. However, rescuers should be aware that prolonged periods of shivering consume the patient’s endogenous energy reserves. Thus rescuers should administer oral glucose-containing fluids to conscious patients who have adequate cough and gag reflexes. Attention to energy reserves in unconscious and severely hypothermic patients is also important. Warmed intravenous glucose solutions are useful for these patients as part of definitive resuscitative and rewarming protocols, which are described later in this chapter.3,29 Alcoholic beverages are contraindicated in all cases. Inhalation Warming Rescuers should attempt to minimize respiratory heat losses. Hypothermic patients lose up to 11 to 13 kcal/hr through inhalation of relatively cold and dry air and through exhalation of water-saturated air at near Tco.65,200 Administration of heated and humidified air or oxygen at approximately 42° to 46° C (108° to 115° F) can result in net positive gain of 17.1 kcal/hr. Although this is a relatively small amount of heat compared with the total kilocalories required to completely rewarm the hypothermic patient, heated and humidified ventilation is of value for insulating the airway from further evaporative heat loss. However, some studies have shown that inhalation rewarming reduces metabolic heat production provided by shivering.54 In experimental subjects whose shivering was pharmacologically inhibited, inhalation warming did not appear to provide any advantage over spontaneous rewarming.67 Other suggested benefits of inhalation warming include rehydration, stimulation of mucociliary activity in the respiratory tract, and direct heat transfer from the upper airways to the hypothalamus, brainstem, and other brain structures. Any warming of the respiratory, cardiovascular, or thermoregulatory centers could be of benefit. Although research continues regarding efficacy of airway rewarming, most hypothermia treatment protocols continue to recommend inhalation warming as an adjunct to overall rewarming strategies.* Warmed Intravenous Fluids Administration of warmed intravenous fluids is beneficial for reversing hypothermia-induced dehydration and hypovolemia.29,156 Replacement of fluids before rewarming has been shown in dogs to augment cardiac output.140 Dextrose 5% in water or normal saline and normal saline alone are preferable to lactated Ringer’s solution, because a hypothermic liver may be unable to metabolize lactate normally.157 Administration of 300 to 500 mL should occur fairly rapidly, with the remainder of the liter administered over the next hour.5 In no case should cold intravenous fluids be administered. Plastic intravenous fluid bags can be easily carried inside of a rescuer’s clothing (preferably next to the skin) to keep the fluids warm and to supply some perfusion pressure (Box 6-11).
FIGURE 6-45 Packaging of a cold-stressed volunteer. Clothing was removed, the skin was dried with blotting motions, and the volunteer was then placed in an insulated bag and wrapped with a vapor barrier. (Courtesy Gordon G. Giesbrecht.)
168
Body-to-Body Rewarming Body-to-body warming of the hypothermic patient has long been advocated as an acceptable field treatment. Sir John Franklin, in *References 3, 27, 29, 33, 49, 157, 195.
FIGURE 6-46 Placement of a charcoal heater on the chest. Warming ducts are wrapped over the shoulders and touching the neck, under the axillae, and over the chest. This configuration provides heat to two of the three main areas for heat transfer to a cold patient.
his 1823 text Narrative of a Journey to the Shores of the Polar Sea in the Years 1819, 20, 21, describes this technique for resuscitation of an expedition member who was recovered from ice water.41 When wrapped together in a blanket or sleeping bag, a rescuer can donate body heat to a hypothermic patient. However, experimental studies on human volunteers have failed to demonstrate a rewarming advantage with this technique for shivering individuals. When subjects were cooled to an average Tco of 34.6° C (94.3° F), body-to-body rewarming proved no better than did shivering alone.62 In this study, the heat donated by the rescuers was only sufficient to offset the heat lost by the inhibition of shivering. Several theoretic arguments mediate against the routine use of body-to-body rewarming for shivering patients in the field: (1) the large heat loss of an immersion hypothermic victim (e.g., 300 kcal in cooling an average normothermic adult to a Tco of 33° C [91.4° F]) is unlikely to be reversed by the relatively small amount of heat provided by the donor (i.e., a resting, nonshivering adult produces only about 100 kcal/hr);62 (2) rescuers provide a relatively small surface area that is in direct contact with the hypothermic victim through which to donate heat; (3) peripheral vasoconstriction in the victim will limit heat flow to the core;37 and (4) external heat from body-to-body contact will inhibit the hypothermic victim’s endogenous heat production through shivering.56 However, for severely hypothermic and nonshivering victims or for victims whose shivering thermogenesis is inhibited by alcohol, medications, age, or anything else, body-to-body rewarming may be used. Furthermore, body-to-body rewarming may provide important psychological support to the patient. For these reasons, rescuers should weigh the likelihood of effective rewarming against the advantages and disadvantages of body-to-body rewarming when devising a field rewarming strategy for any particular hypothermic patient. Heating Pads The application of external moderate heat sources to hypothermic patients has been a traditional method of field rewarming. Particularly when they are applied to the patient’s thorax, neck, and groin (i.e., areas with high potential for conductive heat transfer),85 hot water bottles, chemical and charcoal heat packs (Figure 6-46), heating pads, and other warmed objects have been used to attempt to stabilize the patient’s Tco. If a patient is shivering vigorously, the Tco will warm at a similar rate as with external heat.* For more severely hypothermic patients who are not shivering, these types of external heat sources would help to stabilize and even increase the patient’s Tco, which would likely remain low if no heat were added. A recent study demonstrated that charcoal heating provides a significant rewarming advantage for hypothermic subjects when shivering was pharmacologically inhibited.92 *References 21, 56, 80, 113, 160.
Arteriovenous Anastomoses Rewarming The arteriovenous anastomoses (AVA) rewarming technique relies on the physiologic AVAs that exist in human digits and on the superficial venous rete in the forearms and the lower legs. Warming these areas opens the AVA and increases superficial venous return via the rete. Warmed venous blood thus reaches the core without excessive countercurrent heat loss to cold arteries (i.e., superficial veins are not in close contact with arteries). As a result of the pioneering work of Vanggaard and Gjerloff,189 who proposed AVA rewarming, the Royal Danish Navy has been using this technique since 1970.187 Recent experimental studies have confirmed the efficacy of this technique.188 Mildly hypothermic subjects with an esophageal temperature of 34.2° C (93.6° F) whose hands, forearms, feet, and lower legs were immersed in either 42° C (108° F) or 45° C (113° F) water had a smaller postcooling afterdrop as compared with shivering alone (0.4° C [0.7° F] as compared with 0.6° C [1.1° F]) and a significantly faster rate of rewarming (6.6° C/hr [11.9° F/hr] and 9.9° C/hr [18° F/hr]) as compared with shivering alone (3.4° C/hr [6.1° F/hr]). Although this technique may be difficult to implement in some field settings, it may be practical for mildly hypothermic victims on rescue vessels or other vehicles where a source of warm water is available. As with heating pads and other sources of external heat, however, rescuers should be concerned about the possibility of thermal burns. In the previously described study, no burns were observed in the experimental subjects, even when their extremities were immersed in 45° C (113° F) water, although some subjects complained of initial discomfort at this temperature. Rescuers opting to use AVA rewarming should perhaps start with a water temperature of 42° C (108° F) and gradually raise the temperature to 44° C (111° F).188 Another concern with AVA rewarming concerns potential cardiovascular instability. Hypotension may occur as a result of an increase in peripheral blood flow in a hypovolemic patient. If the patient is required to be in a semi-upright position to receive AVA rewarming, orthostatic hypotension could potentially add to cardiovascular instability. No experimental data support these potential cardiovascular problems, but studies of AVA rewarming have only been performed on mildly hypothermic subjects.188 Further research is required to evaluate the efficacy and safety of AVA warming on severely hypothermic patients. Forced Air Warming Forced air warming (FAW) is a technique that was derived from a treatment modality used to prevent or reverse hypothermia in surgical patients.106,149 Convective heat transfer is provided by warm air blown into warming covers over the patient’s body. Both experimental and clinical data support the efficacy of this technique on mild, moderately, and severely hypothermic patients. In mildly hypothermic experimental subjects, FAW was associated with a 30% smaller afterdrop as compared with shivering alone. Furthermore, during the initial 35 minutes of rewarming, shivering patients experienced net heat loss of 30 to 50 W as compared with net heat gain from FAW of 163 to 237 W.61 In moderately to severely hypothermic patients with a mean rectal temperature of 28.5° C (83.3° F) who were treated in an emergency department, FAW (when used in conjunction with warmed intravenous fluids and inhalation warming) achieved a rewarming rate of 2.4° C/hr (4.3° F/hr), which was nearly twice that of patients treated only with warmed intravenous fluids and inhalation warming (1.4° C/hr [2.5° F/hr]).153 In another series of experiments involving human subjects, a FAW device designed for field use was associated with significantly higher Tco rewarming rate (5.8° C/hr [10.4° F/hr]) as compared with shivering alone (3.4° C/hr [6.1° F/hr]), but it showed 169
CHAPTER 6 Immersion Into Cold Water
Rescuers should be aware of several potential hazards with this rewarming technique. Hypothermic skin is very sensitive to heat and easily injured. All sources of external heat must be separated from direct contact with the patient’s skin to prevent severe thermal burns.156 Third-degree burns have resulted from the application of a lukewarm hot-water bottle directly to a hypothermic child’s skin.129 Furthermore, heat packs that make use of burning charcoal as a heat source can create a carbonmonoxide hazard within an enclosed space.160
Core temperature (° C)
PART 2 COLD AND HEAT
REWARMING
40 35 30
Start cooling
High heat
Shivering
Shivering or moderate heat Invasive heat
End cooling
High heat
Moderate heat
Nonshivering 25
End cooling
No heat
20 Time
FIGURE 6-47 Schematic illustration of the effectiveness of various rewarming techniques under shivering and nonshivering hypothermic conditions. The dashed line indicates the approximate core temperature at which shivering is spontaneously abolished.
no advantage over shivering with regard to decreasing afterdrop.35 When shivering was inhibited with meperidine in human volunteers,57 FAW was associated with 50% decrease in afterdrop and 600% increase in rewarming rate as compared with spontaneous rewarming alone.67 A different prototype FAW device that made use of a collapsible rigid patient cover and that was evaluated experimentally on nonshivering human volunteers was associated with smaller afterdrop and faster rewarming rate as compared with spontaneous rewarming alone.60 In summary, FAW has shown significant promise as both a field and hospital treatment modality. It is a safe and noninvasive technique that can both decrease afterdrop and increase the Tco warming rate of immersion hypothermic patients. Figure 6-47 schematically illustrates Tco responses to various rewarming methodologies under mild (i.e., shivering intact) and severe (i.e., shivering absent) hypothermic conditions.
TRANSPORTATION Stabilization, insulation, and rewarming of the hypothermic patient should be started during transport of the patient to an appropriate medical center for definitive rewarming. If possible, the receiving facility should be selected on the basis of its knowledge of and experience with management of hypothermic patients. In the same manner that victims of multiple trauma are most appropriately managed in trauma centers, severely hypothermic patients are best managed in hospitals equipped to handle potential complications and to provide core rewarming therapies. For example, a hospital with cardiac bypass rewarming capabilities may be a better choice for management of a severely hypothermic patient than a hospital without such qualifications, even if the former may require a longer transport time.
170
FIGURE 6-48 Norwegian ice breaker.
During transport to a site for definitive medical care, emergency medical personnel should frequently monitor the patient’s Tco and other vital signs. In addition, they should attach an electrocardiography monitor and continue administration of warmed intravenous fluids, heated and humidified air or oxygen, and other rewarming efforts discussed previously. Rescuers should maintain the hypothermic patient in a supine posture, and they should restrict the voluntary movements of conscious individuals. At the receiving facility, rescuers should ensure that the patient is carried (rather than allowed to walk) to the treatment location. In summary, prehospital rescue and management of immersion hypothermia victims requires understanding the physiologic events that occur during cooling and recovery. With such understanding, medical personnel can better prepare for and manage this potentially difficult environmental emergency. When prehospital care is performed safely and effectively, definitive hospital care is more likely to have a successful outcome. Finally, it should be noted that, if you are from a Nordic country, you are oblivious to cold, and this chapter is likely irrelevant to you (Figure 6-48).
VIDEO RESOURCES 1. Cold Water Boot Camp. Available at www.coldwaterbootcamp.com 2. Cold Water Boating (©2008—State of Alaska, Department of Natural Resources, Division of Parks and Outdoor Recreation, Office of Boating Safety). Available at www.expertconsult.com. 3. The Cold, Hard Facts of Winter Roads Safety (©2007—Manitoba Infrastructure and Transportation/University of Manitoba). Available at www.expertconsult.com.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
36
CHAPTER 7
Nonfreezing Cold-Induced Injuries
20
CHRISTOPHER H.E. IMRAY AND JOHN W. CASTELLANI
Nonfreezing cold-induced injury (NFCI) is a clinical syndrome that results from damage caused to tissues exposed to cold temperatures at or above the freezing point of water (0° to 15° C [32° to 59° F]). NFCI does not involve tissue freezing, which distinguishes it both clinically and pathologically from frostbite.36 The earliest descriptions of this syndrome had their origins in the military. Baron Dominique Jean Larrey, Napoleon’s chief surgeon, used the word congelation to describe the nonfreezing injuries together with frostbite casualties that occurred during the 1812 assault on Russia.92 Historically, infantry regiments have been decimated by cold and wet conditions, and many medical advances in understanding the pathophysiology and clinical course of NFCI have occurred after wars.2,35 However, it has been observed that the continuity of research tends to lag during the periods between major military campaigns.98 Developments in prevention of cold injury have flourished as new clothing and footwear have been designed, but little progress has been made in the treatment of NFCI. There is a rise in the number of people pursuing recreational activities in harsh environments, and as a consequence, civilian NFCI is becoming more prevalent. However, because many physicians are unfamiliar with NFCI, it may go undiagnosed during assessment of the cold-exposed victim.98 This results in unnecessary hospital admissions and potentially harmful and expensive therapy.41 Proper education and awareness of the hazards innate to the cold environment should mean that NFCI is preventable in most circumstances. This chapter explores the history, epidemiology, pathophysiology, and current prevention and treatments of NFCI, as well as pernio (chilblains), cryoglobulinemia, and cold urticaria.
Epidemiology Individuals suffering cold and wet extremities for extended periods are at risk for NCFI. During the 1800s, NFCI was observed more frequently when the temperature hovered around the freezing point—when the ground was muddy rather than frozen.43,91 Standing or sitting for long periods, wearing constrictive footwear, malnutrition, fatigue, or the blunt trauma of marching on cold, wet feet all added to the severity of injury.92 Original animal studies that modeled NFCI demonstrated that cold temperatures near the freezing point were more likely to cause injury when the extremities were wet than when they were dry.10,91 Ambient temperature and wind speed can both influence cooling.32,114 With “shelter limb” (dependency without cold) and “paddy foot” (wet but not cold), one observes an injury that has no apparent distinguishing differential feature from NFCI. This suggests that neither cold nor wet is a prerequisite to developing the injury. It appears that NFCI is a reperfusion injury that develops after a sustained period of peripheral vasoconstriction.98
MILITARY In combat settings, there is rarely the time, equipment, or opportunity to apply appropriate remedies to NFCI. In the 1854 Crimean War, cold injury was documented more often among “the men in the trenches [who] were so restricted in their movements.… Frequently this position happened to be the bottom of a trench knee-deep in mud and water or half-filled with snow.”91 In November 1944, during World War II, American forces sustained
11,000 cases of trench foot.110 Evaluation of possible risk factors for cold injury during the 1982 war in the Falkland Islands has been published. A year after exposure, there were no cases of cryoglobulinemia or hematologic evidence to suggest that any of the men who developed cold injury had abnormal circulating proteins, plasma hyperviscosity, or indicators of alcohol abuse.20 In the 1990s, both the U.S. Army and the Israel Defense Forces recorded that the majority of nonfreezing cold injuries occurred during routine training exercises, rather than during combat operations.26,68,73
ETHNICITY Historically, the first reports of increased susceptibility in certain ethnic groups (blacks) to cold-weather injury came from the American Civil War.87 It was also noted that there was an increased incidence of cold injuries among blacks in the cold winter conflict in the Ardennes in 1944 during World War II.110 A major retrospective study looking at 2143 U.S. Army cold-weather injury hospital admissions between 1980 and 1999 found that the injury rates for men and women were 13.9 and 13.3 per 100,000 soldiers, respectively.26 Increased rank and experience were associated with a decrease in cold-weather injuries. There were 3.3 times more blacks hospitalized than whites, (95% confidence interval [CI], 3.1-3.7), and infantry and gun crews appeared to be at greater risk. There was a marked reduction in the number of soldiers admitted to the hospital between 1980 and 1999, from greater than 30 cases per 100,000 soldier years to almost zero. Young male African Caribbeans in the British Army have been found to have a 30 times greater chance of developing peripheral cold injury and are more severely affected than are their white counterparts following similar climatic exposure, using similar clothing and equipment. Pacific Islanders carry a 2.6 times increased risk, whereas being a Gurkha appears to be protective.15 Peripheral vascular responses to a local cold stress were studied in four groups of Indians: South Indians, North Indians, Gurkhas, and high-altitude natives of 3,500 meters (11,483 feet). The heat output and cold-induced vasodilation (CIVD) were highest in high-altitude natives, with the lowest observed in South Indians.67
PREVALENCE In most North Atlantic Treaty Organization (NATO) countries, prevalence of NFCI injuries appears to be static or decreasing among military personnel. However, in the British military, there appears to be a marked increase in the incidence of reported cold-weather injury. Over a 4-year period, the reported rate increased from 9 per 1000 to 30 per 1000 recruits, with the majority of cases (90%) originating during field-based training. Independent factor analysis demonstrated that African Caribbeans were 13.2 (95% CI, 9.5-18.4, probability [p] <0.01) times more likely to report cold injury and 27.3 (95% CI, 16.3-45.9, p <0.01) times more likely to be medically discharged than were whites.113 The rise in NFCI in the military of the United Kingdom (UK) may be caused by increased exposure, lower threshold to diagnose the condition, increased awareness, or recruiting of a different and more sensitive population. Alternatively, the rise may be caused by a type I statistical error (poor specificity of the tests used to diagnose NFCI or excessive credulity) or a type II error
For online-only figures, please go to www.expertconsult.com
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PART 2 COLD AND HEAT
(poor sensitivity of the tests used to diagnose NFCI). Perhaps other countries are failing to diagnose and report the condition.52
CIVILIAN The environmental conditions that can produce NFCI in military settings are also found in the context of wilderness medicine. Outdoor recreation may lead to cold, dehydrated, exhausted, and wet hikers exposed to the elements for an extended period. These individuals may be unwilling or unable to take the time and effort to care for their wet boots and socks, and they may be unaware of the risks inherent in the situation. Other civilian populations at risk for NFCI include the homeless,116 older adults,83 and alcoholics.98 Personal Administration Proper protective equipment and appropriate use are important factors reducing the incidence of NFCI. Factors affecting the incidence of frostbite are closely related to those affecting NFCI. A surprisingly high incidence of frostbite has been reported in mountaineers. In one study, the mean incidence was 366 per 1000 population per year. Mild (grade 1) injury (83.0%) and hand (26.4%) and foot (24.1%) involvement were most common. There was a significant relation between lack of proper equipment (odds ratio 14.3) or guide (p <0.001) and the injury. Inappropriate clothing, lack or incorrect use of equipment, and lack of knowledge of how to deal with cold and severe weather were claimed to be the main reasons for the injury.47 Cold injury is uncommon in Antarctica. Despite this, it warrants a continued high profile, because under most circumstances, it may be regarded as an entirely preventable occurrence.16 It has been suggested that prolonged heavy load carriage during a 109-day Arctic expedition may have impaired blood flow or nerve conduction in the hands and inhibited cold acclimatization. However, a different response was observed in the feet, where there was improvement in cold acclimatization despite development of moderate trench foot.77 Civilian Case Reports Laden and colleagues64 reported cold injury to a diver’s hand after a 90-minute dive in 6° C (42.8° F) water. With the advent of “technical diving,” characterized by going deeper for longer (often in cold water), and adventure tourism, it was suggested that this extremely painful condition was likely to increase in prevalence. Older adult patients commonly present to the hospital following their collapse and a period of distressing immobilization on the floor. A case of bilateral trench foot in an older adult immobile patient has been reported.112
Skin—A Thermoregulatory Organ Thermoregulation is a major function of skin in humans, and it is achieved by large fluxes in cutaneous blood flow.65 The metabolic requirements of skin are fixed and relatively modest; the observed large fluctuations in cutaneous blood flow are primarily determined by the individual’s thermoregulatory needs. Arteriovenous anastomoses (AVAs) abound in the extremities. The AVAs are coiled muscular-walled vessels approximately 35 µm in diameter and have little basal tone. They are under dual control. First, there is central hypothalamic control via the sympathetic nervous system. Second, there is direct local control allowing dilation under warm conditions and constriction with a cold stimulus. The two effects may be additive. Cutaneous vessels are controlled by sympathetic adrenergic vasoconstrictor fibers, and vascular smooth muscles have both α- and β-receptors. When core temperature exceeds 37.5° C (99.5° F), the hypothalamus reduces vasoconstrictor drive to the AVAs and vasodilation occurs. As a result, a lowresistance shunt in the dermal venous plexus opens, which in turn increases local heat loss. Under cold conditions there is an increase in sympathetic tone, resulting in local arteriovenous vasoconstriction and reduction in cutaneous blood flow. Under basal conditions, a 70-kg (154.3-lb) person has a total cutaneous blood flow of 200 to 500 mL/min. With external 172
heating to maintain skin temperature at 41° C (105.8° F), this may increase to 7000 to 8000 mL/min, whereas cooling the skin to 14° C (57.2° F) may diminish it to 20 to 50 mL/min. Heat is dissipated by four processes: radiation, conduction, convection, and evaporation. Cutaneous vascular tone is inversely related to ambient temperature. Cold-induced vasoconstriction is attenuated by α2-receptor blockers and by sympathetic inhibition. Reduction in ambient temperature results in insertion of more α2-receptors from the myocyte Golgi apparatus into the plasma membrane, raising affinity for the sympathetic neurotransmitter norepinephrine. At the same time, endothelial nitric oxide synthase (eNOS) activity declines, resulting in vasoconstriction of AVAs. Core temperatures have a strong influence over cutaneous sympathetic vasomotor activity. Vascular endothelium regulates local vascular tone by secreting vasoactive agents, including the vasoconstrictor endothelin and the vasodilators nitric acid and prostacyclin. Endothelin causes long-lasting vasoconstriction and is elevated in hypoxia, preeclampsia, and hemorrhagic stroke.
ORTHOSTASIS Orthostasis causes immediate reduction in local blood flow. Indeed, cutaneous perfusion is reduced by approximately twothirds as a result of the poorly understood arteriolar-venous response. It is believed that this response helps maintain central arterial pressure during standing and also reduces dependent edema formation. Long periods of sitting or standing tend to exacerbate this response.
COLD-INDUCED VASODILATION When the hand or foot is cooled to 15° C (59° F), maximal vasoconstriction and minimal blood flow occur. If cooling continues to 10° C (50° F), vasoconstriction is interrupted by periods of vasodilation and an associated increase in blood and heat flow. This CIVD, or “hunting response,” occurs in 5- to 10-minute cycles to provide some protection from the cold. Prolonged repeated exposure to cold increases CIVD and offers some degree of acclimatization. Inuit, Sami, and Nordic fishermen have a very strong CIVD response and very short intervals between dilations, which may contribute to maintenance of hand function in the cold environment.44 CIVD responses are more pronounced when the body core and skin temperatures are warm (hyperthermic state) and suppressed when they are cold (hypothermic state), when compared with normothermia.22,23,78 Cheung and Mekjavic17 investigated whether CIVD responses of one finger can predict the responses of other fingers and also whether the CIVD of fingers could predict CIVD responses of the feet and toes. They found that CIVD is highly variable across the fingers and is not a generalizable response across either digits or limbs. Paradoxical CIVD will normally prevent tissue damage, but in conditions such as Raynaud’s disease, the vessels of the toes and fingers exhibit an exaggerated and sustained vasoconstriction response, resulting in blanching, numbness, and paresthesias and in severe cases tissue loss. Subjects with a weak CIVD to experimental cold-water immersion of the fingers in a laboratory setting have been shown to have a higher risk for local cold injuries when exposed to cold in real life.24 There is a strong relationship between the mean temperature of the fingers during cold-water immersion and toes during cold-air exposure (correlation coefficient for bivariate analysis [r ] = 0.83, p <0.01), showing that a weak CIVD response in the hand correlates with a weak response in the foot.105 Felicijan and colleagues33 found evidence for significant enhancement of the CIVD response after brief high-altitude acclimatization and that these changes were especially prominent in the feet of Alpinists when compared with controls. Temperatures of the extremities can drop surprisingly quickly in the field. Toe temperatures of 10 subjects were monitored in the field in Arctic Norway (minimum air temperature −27° C [−16.6° F]). The lowest skin temperature recorded was 1.9° C (35.4° F). The mean estimated time for toe temperature to cool from 25° C (77° F) to 5° C (41° F) was 109 minutes (standard
Trench Foot (Immersion Foot) PATHOPHYSIOLOGY Continuous exposure to a cold, wet environment causes skin breakdown, directly cools nerves in the area of exposure, and causes prolonged vasoconstriction. NFCI is primarily caused by prolonged vasoconstriction, which in turn causes direct injury to the vessels (and endothelium) that supply blood to nerves, fat, and muscle cells.49,72,98 Pain, fear, constrictive footwear, and immobility interact in maintaining vasoconstriction through a heightened sympathetic nervous system response or by mechanically limiting blood flow (Figure 7-1). Nerve cooling has been suggested as a contributing factor in the development of NFCI. Large myelinated fibers (C fibers) are most susceptible to prolonged cold exposure.53,61,62,88 In severe nonfreezing cold injury, there is characteristic peripheral nerve damage and tissue necrosis.54 Clinical sensory tests indicate damage to both large- and small-diameter nerves. The prolonged cold injury affects blood vessels serving these large myelinated fibers, with subsequent ischemia causing decreased oxygen to the nerve, resulting in the appearance of a primary nervous system injury58,59 (Figures 7-2 to 7-5). Vasoconstriction is mediated by presynaptic vesicle release of norepinephrine and neuropeptide Y from sympathetic nerve fibers that interact postsynaptically on smooth muscle at α2C6,18 and Y195 receptors. Recent work100 demonstrated that coldinduced vasoconstriction is mediated by Rho kinase. The prolonged decrease in blood flow caused by vasoconstriction causes
Local nerve cooling
Cold-wet exposure
Swelling and breakdown of skin
Vasoconstriction
Pain and fear
↓ Local blood flow
Local nerve damage
Constrictive footwear Immobility
Ischemia
Endothelial damage
Sensory impairment
Loss of vasodilation
Cold sensitization
FIGURE 7-1 Schematic of factors and mechanisms that contribute to nonfreezing cold injuries.
Percent of NBF baseline
120 100 80
Control Experimental
60 40 20 0
100 min
200 min
250 12h D1 D2 D3 D5 min
Time (min, hr and day) FIGURE 7-2 Laser Doppler mean nerve blood flow (NBF) in control and experimental animals at 10-minute intervals during nerve cooling and rewarming (up to 250 minutes) and at follow-up examination immediately before sacrifice (at various times up to 5 days). Note that the nerve blood flow falls steeply over 20 minutes and reaches its nadir (25% of baseline) 180 minutes after the onset of cooling. Nerve blood flow remains significantly reduced up to 5 days after cold injury. (Modified from Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)
direct injury to capillary endothelium. Studies indicate that the endothelial lining separates from underlying cells, leaving “gaps.”31 Leukocytes and platelets fill in these gaps and accumulate to further decrease capillary blood flow, leading to ischemia and eventual tissue hypoxia (Figure 7-6, online). The degree and duration of cold exposure determine severity of the injury. Animal models have been developed to understand the underlying pathophysiology of NFCI. Thomas and co-workers99 developed a rat model of NFCI by immersing the tail in 1° C (33.8° F) water for 6 to 9 hours and characterized the loss of CIVD and a prolonged decrease in tail blood flow followed by an increase in blood flow above baseline. This pattern is similar to that clinically observed in humans during the prehyperemic phase followed by the hyperemic phase. In rats, absence of CIVD with prolonged cold exposure is similar to this prominent and consistent finding of NFCI in humans. Stephens and associates95 used the rat tail model in an attempt to elucidate possible mechanisms that cause vascular endothelial damage. Their preliminary data suggest that acute cold-water exposure causes loss of nitric oxide–dependent endothelial function and possibly a change in smooth muscle contractility. Using a rabbit hind limb model, Irwin53 demonstrated that cold-water immersion damaged large myelinated fibers while sparing small myelinated and unmyelinated fibers. Nonfreezing cold injuries affect many different types of tissue. Pathologic examination of specimens displays a variety of lesions in skin, muscle, nerves, and bone.8,9,38 Muscles exhibit separation of cells and damage to muscle fibers, described as acidophilic and hyalinized (Zenker’s hyaline degeneration). The myoplasm within muscle loses its cross striation, and the healing muscle appears to undergo fibrous tissue replacement. One of the major pathologic processes in cold injury is progressive microvascular thrombosis following reperfusion of the ischemic limb, with cold-damaged endothelial cells playing a central role in the outcome of these cold-injured tissues.71 Reperfusion of previously ischemic tissues causes free radical formation, leading to further endothelial damage and subsequent edema. With restoration of blood flow, there is reintroduction of oxygen species within cells that further damages cellular proteins, DNA, and the plasma membrane. Free radical species may also act indirectly in redox signaling to initiate apoptosis. Leukocytes may accumulate in small capillaries, obstructing them and leading to more ischemia.59 In an in vivo rabbit hind limb model subjected to 16 hours of cold immersion (1° to 2° C [33.8° to 35.6° F]), there was 173
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deviation [SD], 10.2) at an ambient temperature of −21° C (−5.8° F). One subject experienced a toe temperature below 5° C (41° F) for 2.9 hours during a 27-hour period. Surprisingly, none of the subjects demonstrated clinical signs of cold injury, but this does not mean that this exposure was without risk.101 The cutaneous microcirculation of skin was assessed in patients with sequelae from local cold injuries. All patients reported cold intolerance 3 to 4 years after the primary cold injury (sustained during military service).4 The transcutaneous oxygen tension was decreased, but oxygen reappearance time, oxygen recovery index, postocclusive reactive hyperemia, and venoarterial reflex were normal. No capillary nailfold abnormalities were found. Local cold injuries appear to cause disturbances in the CIVD, impaired cold tolerance, and increase the risk for future cold injuries. There is evidence to suggest disturbances of reflex mechanisms mediated by the central nervous system. Neurophysiologic factors seem more important than ischemic mechanisms in the pathophysiology of late sequelae with peripheral cold-weather injuries.
PART 2 COLD AND HEAT
V A M
A
B
C
D
E
FIGURE 7-3 Sciatic nerve epineurial microvessels before, during, and following nerve cooling (1° to 5° C [33.8° to 41° F]). A, Normothermia. Arteriole (A), venule (V), and metarterioles (M) have a normal appearance. B, One hour after the commencement of nerve cooling the diameter of both the arteriole and venule are reduced by approximately 40%. Under a dissecting microscope, erythrocytes present a granular appearance in both vessels (arrows). Note occlusive aggregations (open arrow) in metarteriole and the suggestion of leukocyte clumping in the venule (arrow head). C, Two hours after nerve cooling, segmental occlusive aggregates are seen in the venule (arrows). The arterioles contain prominent rouleaux (open arrows). D, Three hours after nerve cooling, there is stasis of flow in both vessels. An occlusive aggregate (arrow) is now seen in the arteriole, and those in the venule have extended (open arrows). E, After 1 hour of nerve rewarming (37.5° C [99.5° F]), the venule still exhibits multiple segmental occlusions (arrows). Erythrocyte granulations (open arrows) in the arteriole indicate poor reperfusion. Bars represent 100 mm. (From Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)
A
B
C
D
FIGURE 7-4 Electron micrographs of endoneurial vessels in cooled sciatic nerve. A, An empty capillary with a degenerating pericyte 1 hour after nerve rewarming. Bar represents 2 µm. B, Aggregating platelets (arrows) 24 hours after cooling. Bar represents 2 µm. C, Platelets, adherent to the endothelium of a venule, show varying degrees of degranulation without pseudopod formation, 48 hours after nerve cooling. Two red blood cells are trapped within this platelet thrombus. Bar represents 1 µm. D, A thrombus formed of platelets, red blood cells, and fibrin 5 days after nerve cooling. The blood vessel wall is necrotic. Bar represents 2 µm. (From Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)
174
B
FIGURE 7-5 Electron micrographs of cooled sciatic nerve fibers. A, A rat sciatic nerve fiber, 12 hours after nerve cooling, illustrating myelin unraveling and intramyelinic edema (arrow). B, A rat sciatic nerve fiber 2 days after cooling, exhibiting a shrunken axon and marked periaxonal edema. Bars represent 1 µm. (From Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)
reduction in the number of myelinated nerve fibers of all sizes, most marked in large-diameter fibers, a feature consistent with ischemic neuropathy and reperfusion injury.54 Unmyelinated fibers showed only minor damage. The resulting evidence has suggested that both of these mechanisms may contribute to the nerve injury. There is further extensive supporting evidence that established NFCI is associated with histologic and/or clinical evidence of nerve damage.27,30,59,76 Das and colleagues25 demonstrated that quinacrine, an antioxidant, decreased damage to cell membrane phospholipids upon rewarming and reperfusion, although more recent studies97 have shown no benefit from antioxidant use. Most importantly, both these studies used models that assumed that cold-induced nerve injury, rather than capillary or endothelial damage, is the primary cause of NFCI.
CLINICAL PRESENTATION Trench foot and immersion foot are clinically and pathologically indistinguishable but have different etiologies. The term trench foot originated during the trench warfare of World War I,110 when soldiers wore wet boots and socks for prolonged periods.5 Immersion foot was first medically documented during World War II among shipwreck survivors whose feet had been continuously immersed in cold water.21 Both injuries occur when tissue is exposed to cold and wet conditions at temperatures ranging from 0° to 15° C (32° to 59° F). Colder temperatures decrease the time required to induce NFCI.10,92 Severe nerve damage from immersion foot has been seen after exposure periods of 14 to 22 hours.103,104 Immersion foot injury may extend proximally and involve the knees, thighs, and buttocks, depending on the depth of immersion.111 Clinically, NFCI is insidious in onset, with progression from initial exposure through three distinctive phases (prehyperemic, hyperemic, posthyperemic). These phases have variable time courses and may overlap. Prehyperemic Phase During the prehyperemic phase, the affected limb, both during and immediately after cold exposure, appears blanched, yellowish white, or mottled but seldom blistered (Figure 7-7).104 Whayne and DeBakey110 state that the degree of edema during this prehyperemic stage is less severe if the feet are intermittently rewarmed during the course of exposure. Whereas muscle cramps are common, pain is rare.43,92 The single most important diagnostic criterion is loss of a sensory modality, most typically complete local anesthesia, which is distinct from premonitory feelings of extreme cold in the affected periphery, almost invariably in the feet although hands can also be affected. With further exposure, the cold sensation leads to complete anesthesia with loss of proprioception, resulting in numbness and gait disturbances. This sensation has been described as “walking on air” or “walking on
cotton wool.”104 Capillary refill is sluggish, and pedal arterial pulses are usually absent, except through Doppler examination.70 Intense vasoconstriction is the predominant feature of this stage.46 Hyperemic Phase Within several hours after rewarming, the extremities become hot, erythematous, painful, and swollen (Figures 7-8 to 7-11; Figure 7-9, online), with full bounding pulses.109 Impairment of the microcirculation is evident through delayed capillary refill98 (Figure 7-12, online) and petechial hemorrhages.45 Sensation returns first to proximal regions and then extends distally, rapidly progressing to a severe, burning, or throbbing pain and reaching maximal intensity in 24 to 36 hours.103,104 Affected areas have marked hyperalgesia to light touch. This pain is aggravated by heat and dependent positioning and often worsens at night, when even the pressure of sheets may become unbearable.46 After 7 to 10 days, the nature of the pain changes to “shooting or stabbing.”103 The sensory deficits usually diminish, but paresthesias continue, and anesthesia may be extensive on the toes and plantar foot surfaces.111 Vibratory sensation is reduced or lost, whereas proprioception is usually retained. Anhidrosis coincides with the extent of sensory loss.98 Vascular injury is evident in vessel reactivity. Skin temperature gradients are absent, with digits often as warm or warmer than the groin or axillae. When the affected limbs are lowered, blood pools, turning the extremity a deep purple-red color, whereas
FIGURE 7-7 Prehyperemic phase of immersion foot. These feet are still mostly numb and very cold to the touch. (British Crown Copyright/ MOD.)
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A
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blanching occurs when the limb is raised. Tense edema becomes marked during this stage. Blisters containing serous or hemorrhagic fluid may form, indicating more severe injury.98 The superficial epidermis becomes thick, indurated, and desquamated. Eschars form (Figures 7-13 and 7-14) and eventually
FIGURE 7-8 Hyperemic phase of nonfreezing cold injury. This person spent 18 hours during the winter bailing out a boat that threatened to capsize in Prince William Sound, Alaska. (Courtesy James O’Malley, MD.)
slough, leaving a pink dermis (Figure 7-15). In more severe cases, the skin may become gangrenous (Figure 7-16). This is rare, and with appropriate care, gangrene is usually minimal.1,109,110 Muscles may show weakness with impaired electrical responses, slowing of plantar deep tendon reflexes, and intrinsic muscle atrophy.103,104 In milder cases, this stage peaks at 24 hours; in more severe cases, the hyperemic phase may take 6 to 10 weeks to resolve.98 Posthyperemic Phase The posthyperemic phase lacks obvious physical signs. In mild cases, this phase may be absent104; in other cases, it may last weeks, months, or years after the hyperemic phase has subsided.70,103 The extremities transition from a consistent warmth to noted coolness, with affected areas becoming cold sensitive, remaining so for hours after exposure despite normal warming processes. After 6 to 10 weeks, patients often complain of spontaneous hyperhidrosis, and sweat rashes are common in areas with heavy perspiration.103 On a warm day, socks are quickly soaked; extremities may sweat excessively, even when cold. Hyperhidrosis predisposes to chronic paronychial infections. Sweating may be more pronounced at the margins of anhidrotic and analgesic areas.104 During the posthyperemic phase, the paresthesias and extreme pains typical of the hyperemic phase have usually resolved, replaced by dull aches and anesthesia that may persist for months to years.110 Recurrent edema of the feet, return of paresthesia,
FIGURE 7-13 Severe nonfreezing cold injury. This Argentinian soldier had been unable to care for his feet for many weeks. (British Crown Copyright/MOD.)
FIGURE 7-10 Hyperemic phase of immersion foot. The characteristic redness of the stage is absent because of the pigmented skin, but the feet are swollen and painful. (British Crown Copyright/MOD.)
FIGURE 7-11 Hyperemic phase in moderately severe nonfreezing cold injury. Swollen, red, and persistent pain in the feet of an infantry soldier from the Falklands War. (British Crown Copyright/MOD.)
176
FIGURE 7-14 Severe nonfreezing cold injury in an Argentinian mine layer who wore his boots for 47 straight days during the Falklands War. (Courtesy M.P. Hamlet.)
FIGURE 7-15 Severe nonfreezing cold injury in a British sailor during World War II. (Courtesy M.P. Hamlet.)
and further blistering are common, especially after long walks. Intrinsic muscle and ligament atrophy tend to resolve,104 but in severe cases, fibrous scarring may lead to rigidity and permanent contracture of the toes.111 Decalcification of bones similar to that seen with osteoporosis is frequently observed.102 Immobility and pain in severe cases may lead to prolonged convalescence of 6 or more months.111 In the most severe cases, gangrene can develop, and ablative surgery in the form of amputations of digits or even major lower limb amputation becomes necessary. Neuropathic tissue is susceptible to local trauma, ulceration, and eventually local osteomyelitis and sinus development (Figures 7-17 to 7-19). Appearance and behavior of the neuropathic foot have many similarities to those of the diabetic foot. In the diabetic foot, infections tend to be polymicrobial with Staphylococcus aureus, Staphylococcus epidermidis, and Enterococcus and Streptococcus species being most commonly isolated from bone culture. However, aerobic gram-negative rods (such as Pseudomonas aeruginosa) and obligate anaerobic species may be found.52 Partial foot amputations may result in significant alterations in functional biomechanics of the foot. Because this is often associated with alterations in the sensory nerve supply to the feet, ongoing disabling problems can persist (Figure 7-20).52 More Severe Injuries NFCI can vary in severity from mild to severe. In severe cases, cold sensitization is so serious that individuals are unable to work outside. There is often persisting edema and hyperhidrosis, making the individual susceptible to fungal infections. Chronic pain may resemble causalgia or reflex sympathetic dystrophy. The profound sensory neuropathic foot can develop ulcerations
FIGURE 7-16 The Argentinian mine layer seen in Figure 7-14, several weeks later. (Courtesy M.P. Hamlet.)
FIGURE 7-18 Same patient as in Figure 7-17, 24 months after nonfreezing cold injury with chronic discharging sinuses from osteomyelitis of the first metatarsal. (Courtesy Christopher H.E. Imray, MD.)
and tissue loss, ultimately resulting in either minor or major lower limb amputation. Ongoing care with a foot specialist who can arrange for custom-made shoes and insoles appears to improve functional outcome. Multidisciplinary team approaches to coordinating care leading to healing of the ulcerated neuropathic foot using patella weight-bearing orthoses has been described.63 NFCI pain is often so severe as to require tricyclic antidepressants, which may need to be instituted at an early stage.51,98 Failure to do so increases the risk for developing severe chronic pain resistant to all subsequent treatment modalities. Early involvement of
FIGURE 7-19 Magnetic resonance imaging scan of the patient in Figures 7-17 and 7-18, 24 months after nonfreezing cold injury with chronic discharging sinuses from osteomyelitis of the first metatarsal head. (Courtesy Christopher H.E. Imray, MD.)
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FIGURE 7-17 Patient 24 months after nonfreezing cold injury. Amputation of third, fourth, and fifth toes on the left foot. (Courtesy Christopher H.E. Imray, MD.)
PART 2 COLD AND HEAT
Sympathectomy Recovery during the posthyperemic phase may be hastened with physiotherapy and exercise to rehabilitate atrophied intrinsic muscles.110,111 Lumbar sympathectomy has been theorized to reduce disabling contracture by decreasing vascular tone, increasing circulation, and hastening collagen and fibrous tissue absorption. In severe cases of NFCI exhibiting atrophic rigid feet, small case studies have shown symptomatic improvement after sympathectomy,111 but other clinicians feel that there is little therapeutic advantage to the procedure.109 Tissue-Freezing Complications Frostbite and NFCI injuries do not necessarily occur in isolation, so when assessing an individual, both diagnoses need to be entertained. Following exposure to severe cold, careful appraisal of the injury allows selection of optimal treatment.
A
B FIGURE 7-20 A guillotine transmetatarsal amputation of the left foot was undertaken 6 months after severe nonfreezing cold injury. The patient was treated with delayed primary split-skin grafting. This photograph was taken 12 months after the original injury and shows that the split-skin graft has taken, but is now ulcerated as a result of the shear forces generated by walking on the insensate tissue. A, Transverse view from the bottom of the foot. B, Lateral view. (Courtesy Christopher H.E. Imray, MD.)
pain specialists is important. It is essential to control pain following NFCI at the earliest opportunity.
TREATMENT Hypothermia The treatment required for the general effects of cold is different from that needed for localized NFCI. Core temperature must be raised while the extremities are kept cool.109-111 Injured feet should be elevated and exposed to steady cool air from a fan.109,111 Extremity cooling lowers metabolic requirements to a point where vascular oxygen supply can sustain tissue demand. Continuous cooling brings rapid improvement in pain, edema, and vesiculation.109,111 Local cooling should be continued until pain is relieved, circulation has recovered, and hyperemia subsides.111 The affected extremities should never be rubbed, which may compound the injury.2 Rewarming Treatment is limited to symptomatic relief and reversing ischemia while minimizing progression of disease. Rewarming injured tissues increases metabolic demand of damaged cutaneous cells to a greater extent than can be provided by the supply capability of the injured subcutaneous blood vessels.111 Tissue anoxia and endothelial cell injury, coupled with reflex vasodilation, lead to fluid transudation, increasing edema, skin necrosis, and worsening pain.109,111 178
Drugs Diagnosis of NFCI is often difficult or delayed. In view of involvement of the α-receptors in the control of peripheral circulation and the apparent noradrenergic sensitization,36 it was believed that vasodilators or α-blocking drugs might be beneficial. However, there is no evidence to support this approach. Because painful rewarming and persistent pain are features of NFCI, it is important to attempt to alleviate pain at an early stage. Although simple analgesics may be of benefit, Thomas and Oakley98 observed that quinine sulfate (200 to 400 mg, given at night) appeared more successful than regular analgesics, although others have since commented that they are not useful. Since 1982, the standard treatment in the armed forces of the United Kingdom, first proposed by Riddell,85 has been amitriptyline hydrochloride, in doses of 50 to 100 mg given at night. Incremental increases in dosage may be required with both drugs if pain breaks through after initial relief.37
ASSESSING THE SEVERITY OF NONFREEZING COLD-INDUCED INJURY Following the initial injury, there develops increased sensitivity to cold. There are often few objective clinical signs of a nonfreezing cold injury. A careful history of cold exposure, clear history of the typical rewarming symptoms and signs, detailed examination, and special investigations combine to build a case consistent with NFCI. Corroborative evidence of an appropriate cold exposure and symptoms consistent with NFCI from medical records is vital. Special Investigations Infrared thermography can be used to assess the individual’s response to a standardized cold stress and may be helpful in confirming the diagnosis, assessing the severity of injury, and monitoring recovery from NFCI (Figure 7-21). Although the infrared thermography test is used extensively by the UK military, it is not widely used elsewhere.50,57 There appears to be significant intraindividual variability in the responses of some individuals to the current infrared thermography test. As a result, interest is shown in the use of gentle exercise before the infrared thermography cold sensitivity test and also in the use of laser Doppler flowmetry to try to improve the assessment used to classify nonfreezing cold injury.29 Careful experimental design to validate any potential new tests against suitable controls, both preexposure and postexposure, will be required.
PREVENTION The simplest way to prevent NFCI is to avoid prolonged exposure to cold, wet environments. This can be difficult to achieve. During military conflict, completing the assigned mission may require performing in a cold, wet environment for sustained periods of time in cramped, immobile positions. During mountain rescues, individuals may be so focused on helping to save others that they do not take adequate care to prevent NFCI. Prevention can be achieved by encouraging activities that promote blood flow to the feet, rotating personnel out of cold,
34 32 30 28 26 24 20.9° C FIGURE 7-21 Infrared thermography in the assessment of the consequences of nonfreezing cold injury. The upper sequence of three images was taken from an uninjured, asymptomatic control; the lower sequence from a patient who had sustained nonfreezing cold injury and subsequently complained of sensitivity. In both the control and patient, the first (left) image was taken after resting in ambient air temperature of 30° C (86° F). The second (center) image was taken immediately after the foot had been immersed in water at 15° C (59° F) for 2 minutes. The final (right) image was taken 5 minutes after removal from the water, again in 30° C (86° F) air. The upper series shows feet that were warm at rest, which rewarmed briskly after mild cold stress, and recovered almost completely within 5 minutes after removal from the water. The lower series shows a severe degree of cold sensitization; the feet were much colder than the surrounding air at rest, and once cooled, took a long time to rewarm, remaining much cooler than the control foot at 5 minutes after immersion. The scale at far right indicates the color– temperature relationship. (Copyright British Crown Copyright/MOD. Reproduced with the permission of Her Britannic Majesty’s Stationery Office. From Thomas JR, Oakley HN: Nonfreezing cold injury. In Pandolf KB, Burr RE, editors: Textbook of military medicine: Medical aspects of harsh environments, vol 1, Washington, DC, 2002, Office of the Surgeon General, Borden Institute, pp 467-490.)
wet environments on a regular basis, keeping feet dry by early changing of wet socks, maintaining core body temperature by limiting sweat accumulation into clothing and dressing in layers, and by educating people about the early signs and symptoms of nonfreezing cold injuries. Changing socks two to three times during the day is mandatory in cold, wet environments. The military suggests that optimal care entails air drying feet for at least 8 hours out of every 24.14,116 Vapor-barrier boots do not allow sweat to evaporate, and in some situations, this increases maceration.3 These boots should be taken off each day, wiped to remove moisture and debris, and allowed to dry. Footwear should not constrict blood flow; sizing is important as is educating the user not to tie his or her shoelaces too tightly. Prophylactic treatment with topical skin silicone preparations (antiperspirants) has proved effective.40 The effect is believed to be caused by prevention of hyperhydration of the stratum corneum.14,28 However, stickiness, adherence of sand and grit to the foot, and product bulkiness make this technique marginally acceptable to infantry soldiers in combat situations.40 In small clinical trials, silicone ointment applied only to the sole of the foot instead of to the entire foot (thus reducing surface area exposed to dirt retention, amount of material transported by the soldier, and expense) was sufficient to prevent NFCI.28 As a consequence of the apparent increasing incidence of NFCI in the British military, preventive steps are being taken. These include improved education of recruits and existing personnel about prevention measures and equipment and early recognition. Well-designed equipment, supplied to appropriate personnel, and used in a timely and appropriate way should reduce the incidence of injury. The severity of current UK military NFCI events appears to be relatively mild in comparison with civilian NFCI injuries (see Figures 7-17 to 7-19) and military historical controls (see Figures 7-13 to 7-16). This raises the question of whether (1) there is a
continuous spectrum of disease, (2) there is a bimodal distribution of the disease with milder and more severe forms of NFCI, or (3) the commonly presenting form is the same disease process that has been investigated in the past. Perhaps the lack of clarity lies in the UK military’s decision to use infrared thermography as one of the bases for diagnosis, severity, and progression of NFCI. There appears to be a lack of published control data on subjects’ prior response to cold exposure, so that the test cannot be compared with the normal variability in the population. One approach would be to screen potential recruits. This requires a test with high sensitivity and specificity. However, individual variation in the control of peripheral blood flow is so great that no assessment currently available meets these requirements.12,22,24,98 Reducing the incidence of cold injury in military training requires striking a delicate balance between training, realism, and safety. Training in demanding environments runs real risks of injuring personnel, but the benefits to soldiers in their necessary field skills are vital if they are to avoid future NFCI.98
Pernio (Chilblains) Pernio (perniones), or chilblains, are localized, inflammatory, bluish red lesions caused by an abnormal reaction to a cold, damp environment. This mild form of cold injury is prevalent in the temperate climates of northwestern Europe,66 and it is found worldwide throughout temperate and northern zones.41,69,70,79 Pernio is less common in very cold climates where well-heated houses and adequate warm clothing are common.80 In a study of 111 patients, 67 (60.4%) were males and 44 (39.6%) were females. Eighty-nine (80.2%), 90 (81.1%), and 90 (81.1%) patients had onset in relation to lower temperature (<10° C [50° F]), relatively low atmospheric pressure (<1500 kPa), and higher relative humidity (>60%), respectively. Susceptibility to chilblains appeared to increase when ambient temperature was less than 10° C (50° F) and relative humidity more than 60%.84 Acute pernio has a seasonal incidence, with reversible symptoms more common in cold weather. The acute form is seen primarily in schoolchildren and young adults under the age of 20 years, with the highest incidence in adolescent females.66 It can occur in mildly cold settings such as logging, kayaking, snowmaking,46 winter horseback riding, and hiking.82 Pernio can be caused by brief (30 minutes) cold exposure, often appearing several hours after exposure, with the skin lesions fully developed within 12 to 24 hours.79 Characteristic locations for these lesions are the feet, hands, legs, and thighs. Single or multiple, erythematous, purplish, edematous lesions form, with vesicles in severe cases. Symptoms include intense pruritus, burning, or pain, often worsened by subsequent warmth. The lesions of acute pernio are self-limited and usually resolve within a few days to 3 weeks,80 occasionally leaving residual hyperpigmentation.19 Although the healing process appears to occur as the plaques resolve, pain often persists. Subsequent mild cold exposure may trigger paresthesias, edema, and skin scaling.46 Chronic perniosis usually progresses over several winters after repeated episodes of acute pernio, rarely progressing from the initial injury to chronic irreversible skin changes within a single season.66 Repeated episodic seasonal lesions may become edematous, with permanent discoloration and subcutaneous nodule formation. The nodules are firm and painful, ultimately rupturing, which provides pain relief and leaves a shallow ulcer with pigmented atrophic skin. These ulcers may grow larger and coalesce, remaining open, which leads to permanently swollen extremities, scaly pigmented skin, and unremitting pain aggravated by light pressure. Pernio is believed to be caused by prolonged cold-induced vasoconstriction with subsequent hypoxemia and vessel wall inflammation.41,55 Subcutaneous arterial vasoconstriction is documented by both pathologic66 and arteriographic studies.93 Histologic examinations show a lymphocytic vasculitis and papillary dermal edema with pervasive inflammatory changes.41,55,66 The differential diagnosis includes lupus erythematosus, Raynaud’s disease, polycythemia vera, atheromatous embolization, erythema nodosum, and livedo vasculitis with ulcerations. 179
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36.0° C 36
PART 2 COLD AND HEAT
Treatment of pernio is accomplished by drying and gently massaging the affected skin. Active warming above 30° C (86° F) significantly worsens the pain and should be avoided.46 Although therapeutic regimens in the literature include nicotinic acid,42 ultraviolet irradiation,48 thymoxamine,56 intravenous calcium combined with intramuscular vitamin K,34 corticosteroids,39 and sympathectomy in severe cases,66 few have proved to be either effective or universally accepted. Recently, nifedipine (20 mg, 3 times daily) has been shown to be effective for treatment of severe perniosis. Patients treated had a significantly reduced time for clearance of lesions, decreased pain and irritation of existing lesions, and less development of new pernio.41,86 Preventing pernio is relatively simple. Recommended prophylactic measures include minimizing cold exposure with suitable clothing when outdoors and maintaining adequate warm temperatures indoors.
Cryoglobulinemia Cryoglobulins are cold-precipitable serum immunoglobulins.96 These cryoimmunoglobulins were first reported in a patient with multiple myeloma115 and were subsequently recognized to occur in a diverse group of hematologic malignancies, acute and chronic infections, and collagen vascular diseases.94,106 Cryoglobulins are classified as three types. Type I cryoglobulins (10% to 15% of total) are composed of a monoclonal immunoglobulin, primarily IgG. Type II cryoglobulins (50% to 60% of total) are polyclonal, most frequently IgG and IgM. The IgM fraction usually has rheumatoid factor activity. Type III cryoglobulins (25% to 30% of total) are also composed of polyclonal IgG and IgM fractions. In general, the higher the protein concentration, the higher the temperature at which precipitation begins. Of clinical relevance is the composition of the cryoprecipitate. For example, IgM is intrinsically more viscous than is IgG, and patients with monoclonal IgM cryoglobulin have an amplified hyperviscosity. Because extremity temperatures can reach 30° C (86° F), in vivo cryoprecipitation may directly contribute to impaired capillary blood flow.46 There are many clinical conditions that are associated with cryoglobulinemia.96 Infections (viral, bacterial, fungal, parasitic), hematologic diseases (chronic lymphocytic leukemia, multiple myeloma), and autoimmune diseases (rheumatoid arthritis, pulmonary fibrosis, inflammatory bowel disease) are all associated with cryoglobulinemia. Hepatitis C is considered a principal trigger of cryoglobulinemia. Serum cryoglobulin values do not usually correlate with clinical severity or disease prognosis96 but may serve as a marker of the disease. Cryoglobulinemia is characterized by a clinical triad of purpura, weakness, and arthralgias. A large clinical trial showed that two-thirds of patients diagnosed with cryoglobulinemia initially presented with symptoms of skin lesions or Raynaud’s disease–like vasomotor attacks. Mucosal bleeding, visual disturbances, and abdominal pain were less common. Cold sensitivity was apparent in less than one-half of these patients.13 Symptoms associated with cryoglobulins include typical Raynaud’s phenomenon, dependent purpura, cutaneous vasculitis with ulceration, retinal hemorrhages, coagulopathies, glomerulonephritis, renal failure, and cerebral thrombosis. Treatment of cryoglobulinemia should be directed at the severity of the symptoms and to the disease causing the cryoglobulinemia. Because hepatitis C virus (HCV) is implicated in many cases of types II and III cryoglobulinemia, targeting HCV is the treatment of choice to eliminate cryoglobulinemia. Interferon, prednisone, and ribavirin have all been used to treat HCV and associated cryoglobulinemia. For non–HCV-associated cryoglobulinemia with mild to moderate symptoms (purpura, arthralgia, sensory neuropathy), immunosuppression with corticosteroids and analgesics is the treatment of choice.96 A low-antigencontent diet (rice, fresh vegetables, fruit, tea) has been shown to improve purpura.81 With severe manifestations of disease such as renal failure, neurologic impairment, disabling paresthesias or myalgias, plasmapheresis may be helpful in reducing the cryoimmunoglobulin concentration below a critical point to alleviate symptoms.13 Plasmapheresis is used in conjunction with corticosteroids or other drugs, because discontinuing 180
FIGURE 7-22 Cold urticaria. The hives occurred within minutes of holding an ice cube against the skin. (From Habif TP: Clinical dermatology, ed 4, Philadelphia, 2004, Mosby, with permission.)
plasmapheresis treatment usually causes reappearance of the cryoglobulinemia.96
Cold Urticaria Cold urticaria is a physical urticaria characterized by development of either localized or generalized wheals and itching after skin exposure (air, liquid, object) to cold89 (Figure 7-22). It most frequently affects young adults with a duration of 4 to 5 years, although primary cold urticaria can occur at any age. Women are twice as likely to be affected.90 The incidence rate is approximately 0.05% of the population. Symptoms are usually limited to cold-exposed skin areas.89 Local symptoms include redness, itching, wheals, or edema of the exposed skin. The wheals last approximately 30 minutes. Systemic reactions can also occur, and symptoms of this include fatigue, headache, dyspnea, and hypotension. Swimming in cold water is the most common trigger of severe reactions. This may lead to hypotension, fainting, shock, and possibly death.7,45 Suffocation may also occur after consuming cold drinks as a result of pharyngeal angioedema.89 Secondary urticaria occurs in 5% of patients with cold urticaria.45 The wheals are more persistent and may be associated with purpura and vasculitis on skin biopsy. This disorder is associated with an underlying disorder such as cryoglobulinemia, cold agglutinins, paroxysmal hemoglobinuria, or connective tissue disease.107 In addition, there is a rare autosomal dominant familial form that has its onset in infancy and is associated with arthralgias and leukocytosis.108 The cause of cold urticaria is unknown. Cold urticaria has been associated with viral or bacterial infections,89,90 as well as infections of the upper respiratory tract, teeth, and urogenital tract. It has been reported to involve the release of histamine,60 leukotrienes, and other mast-cell mediators,90 possibly mediated by IgE and IgM. Support for an IgE-mediated mechanism comes from successful treatment11 using an anti-IgE (omalizumab). The diagnosis of cold urticaria is made through the ice cube test in the majority of patients,74 in which a hive is induced by holding an ice cube to skin for 3 to 5 minutes. If the results are equivocal, a cold-water immersion test of submerging a forearm for 5 to 15 minutes in water at 0° to 8° C (32° to 46.4° F) establishes the diagnosis. Treating cold urticaria with antihistamines is the most effective option. However, to sufficiently reduce symptoms may require dosing up to four times the recommended dose.75,89,90 In addition, other therapies include leukotriene antagonists, cyclosporine, corticosteroids, and anti-IgE.90 Individuals with severe reactions should have an emergency kit containing corticosteroids, antihistamines, and epinephrine. Based on the finding that infectious disease may be a trigger for cold urticaria, earlier treatment with antibiotics for infectious diseases may also be warranted.90
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 8
Frostbite LUANNE FREER AND CHRISTOPHER H.E. IMRAY
Frostbite is a true freezing injury, and depending on the severity, ice crystals will tend to form in deep and/or superficial tissues. The degree of injury is a complex interaction of many factors, including environmental (e.g., temperature, windchill, length of exposure, altitude) and individual (e.g., genetics, comorbidities, medications and drugs, clothing, skin products, previous frostbite injury, among other factors). This chapter reviews current understanding of the history, epidemiology, physiology, pathophysiology, classification, risk factors, clinical presentation, field and hospital evaluation and treatment, prevention, and consultation strategies for the management of frostbite. Although the principles of prevention and treatment of frostbite transfer from urban to wilderness settings, the time to definitive treatment is often prolonged and resources are almost always limited in the wilderness setting; therefore, wherever possible, we incorporate special considerations for wilderness management of frostbite injuries. Hypothermia and nonfreezing cold-induced injuries are discussed in Chapters 5 and 7.
History of Frostbite A 5000-year-old pre-Columbian mummy discovered in the Chilean mountains is widely recognized as the earliest documented evidence of frostbite.138 In 218 BC, Hannibal lost nearly one-half of his army of 46,000 to cold injuries in only 15 days when they crossed the Pyrenean Alps. Dr. James Thatcher wrote in 1778 that 10% of George Washington’s army had been left to perish in the winter cold during his campaign against the British soldiers.151 Despite the fact that frostbite was a known consequence of military campaigns in the cold for thousands of years, the first authoritative report of mass casualties was by Baron Larrey,93 surgeon-in-chief of Napoleon’s army during the invasion of Russia in the winter of 1812-1813. Larrey introduced the concept of friction massage with ice or snow, avoidance of heat in thawing, and the idea that cold injuries were similar to burn injuries. These concepts are better understood against the background as viewed by Larrey;93 soldiers with cold injuries rapidly rewarmed their extremities over roaring fires (65° to 75° C [149° to 167° F]) after long marches, only to renew the trek and refreeze their extremities the next day. Larrey recognized that warming was good, but he cautioned against the use of excessive heat and ultimately recognized the freeze–thaw–freeze cycle. Napoleon left France with 250,000 men and returned 6 months later with only 350 effective soldiers. The remainder were casualties to cold or starvation.93 During both world wars and the Korean conflict, at least 1 million cases of frostbite occurred.129,130,167,184 High-altitude frostbite, first described in 1943, was recognized from the treatment of aviators in World War II, when gunners of aircraft flying between 7620 and 10,668 m (25,000 and 35,000 feet) fired machine guns through open waist pots, removing their bulky mittens and jackets to improve the dexterity that they felt was crucial to saving their lives.184 Until the 1950s, treatment of cold injuries basically followed Larrey’s guidelines. In 1956, experimental laboratory work encouraged Merryman, the Public Health Service district medical officer in Tanana, Alaska, to try rapid rewarming at 37.8°C (100° F) on a patient with frostbite and hypothermia.20,117 This was the genesis and has become the cornerstone of the method currently used in Alaska and popularized by Mills.117,119
Epidemiology No comprehensive statistical data are available on the incidence of frostbite, but it is much more prevalent during military campaigns and is a known hazard for mountain climbers and polar explorers. The typical frostbite victim is working or recreating in cold and/or high-altitude environments, is homeless, or is accidentally trapped outdoors in the winter;86,89,133 is 30 to 49 years old;136,181 and in more than half of urban cases, is intoxicated.115,177
CIVILIAN In the nonadventurer U.S. civilian population, Mills had collected 500 cases in Alaska by 1963, Cook County Hospital in Chicago recorded 843 cases from 1962 to 1972, and Detroit Receiving Hospital reported on 154 patients treated between 1982 and 1985.12,64,90,117 The incidence of frostbite in Finland, calculated in a 9-year retrospective query of hospital admissions, was 2.5 cases per 100,000 inhabitants.76
MILITARY AND OCCUPATIONAL The mean annual incidence of frostbite in the Finnish military was reported as 1.8 per 1000, with the head, hands, and feet most commonly affected.95 In a more recent study of almost 6000 Finnish military recruits, 44% reported at least one episode of frostbite during their lifetime, and the annual incidence was 2.2%; the head, hands, and feet were the sites most commonly afflicted.38 Among refugees navigating a high-altitude military line of control during December 1988 to March 2003, 2564 cases of frostbite were treated at local hospitals in Muzaffarabad, Azad Kashmir.81
MOUNTAINEERING A 10-year retrospective survey of medical records of the British Antarctic Survey revealed that the incidence of frostbite was approximately 65.6 per 1000 per year.23 During a 10-year period in the Karakorum mountains, 1500 cases of frostbite were treated at tertiary care medical facilities; all victims were males ages 17 to 43 years. The incidence is unknown because the total number of potential exposures was unrecorded.61 In a questionnaire-based study of 637 mountaineers, the mean incidence of frostbite was 366 per 1000 population per year,60 and out of 2219 south-side Mt Everest climbers in 7 years (2001 to 2007), the base camp medical clinic at Mt Everest saw 35 cases of frostbite (and estimates at least a comparable number did not seek treatment at the facility).47
Anatomy and Physiology Physiologically, humans are tropical beings, better suited to losing heat than retaining it. When naked and at rest, a person’s neutral environmental temperature is 28° C (82.4° F); with an environmental drop of only 8° C (14.4° F), metabolic rate must double to avoid lowering of body temperature. The rate at which heat is lost by radiation is a function of the temperature of the cutaneous surface, which in turn is primarily a function of the rate of blood flow through the skin. Heat is poorly conducted from warmer internal tissue to the cutaneous surface because adipose tissue is a good heat insulator. As a result, the cutaneous circulation is key to the development of frostbite. Because of its role in thermoregulation, normal
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blood flow of skin far exceeds its nutritional obligation. The skin holds a complex system of capillary loops that empty into a large subcapillary venous plexus containing the majority of the cutaneous blood volume. Under normothermic conditions, 80% of an extremity’s blood volume is in the veins of skin and muscle. Skin blood volume depends in part on tone in resistance and capacitance vessels, and tone in turn depends largely on ambient and body temperature. Under basal conditions, a 70-kg (154.3-lb) person has a total cutaneous blood flow of 200 to 500 mL/min. With external heating to maintain skin temperature at 41° C (105.8° F), this may increase to 7000 to 8000 mL/min, whereas cooling the skin to 14° C (57.2° F) may diminish it to 20 to 50 mL/min. Blood flow through apical structures such as the nose, ears, hands, and feet varies most markedly because of the richly innervated arteriovenous connections. Blood flow to hand skin can be increased from a basal rate of 3 to 10 mL/min/100 g of tissue to a maximum of 180 mL/min/100 g of tissue. This cutaneous vascular tone is controlled by both direct local and reflex effects. Indirect heating (warming a distant part of the body) results in reflex-mediated cutaneous vasodilation, whereas direct warming results in vasodilation dominated by local effects. When both types (central and peripheral) of heating or cooling are present, their effects are additive. Cutaneous vessels are controlled by sympathetic adrenergic vasoconstrictor fibers, and vascular smooth muscles have both α- and β-receptors. Vasodilation in the hands and feet is passive, so maximal reflex vasodilation occurs after sympathectomy. When the hand or foot is cooled to 15° C (59° F), maximal vasoconstriction and minimal blood flow occur. If cooling continues to 10° C (50° F), vasoconstriction is interrupted by periods of vasodilation and an associated increase in blood and heat flow. This cold-induced vasodilation (CIVD), or “hunting response,” recurs in 5- to 10-minute cycles to provide some protection from the cold. There is considerable individual variation in the amount of CIVD, and it is believed this might explain some of the variation in susceptibility to frostbite. Prolonged repeated exposure to cold increases CIVD and offers some degree of acclimatization. Inuit, Sami, and Nordic fishermen have a strong CIVD response and very short intervals between dilations, which may contribute to maintenance of hand function in the cold environment.57 Normal skin maturation and tissue function rely on main tenance of permeability and integrity of all tissue membranes. A steady-state relationship of prostaglandins (PGs), particularly PGE2 (vasodilator) and PGF2α (vasoconstrictor), is crucial for normal skin function. An imbalance may disrupt cell membrane equilibrium. This relationship is controlled through PGE2-9-ketoreductase and nicotinamide adenine dinucleotide phosphate (NADPH). Low concentrations of PGE2-9-ketoreductase found in normal skin emphasize an active biologic presence. It is not difficult to imagine why frostbite tends to affect tissues that are acral and receive diminished blood supply as a result of vasoconstriction (e.g., fingers, toes, ears, nose), thereby conserving heat for the core. The nose and corneas may be difficult to protect from cold wind and are particularly vulnerable; face coverings such as a balaclava and goggles should be considered in extreme conditions. In addition, men who jog, ski, or otherwise exercise in the cold may be prone to penile frostbite, especially if fast speeds create a headwind. Clothing then becomes moist with sweat in the groin, and the tip of the penis is vulnerable, especially if unprotected by a wind-resistant or windproof outer layer.47,66
Pathophysiology of Frostbite The pathophysiology of frostbite has been categorized in several different ways, illustrating the numbers of variables that affect the extent and depth of tissue damage. Frostbite may be divided into four pathologic phases: prefreeze, freeze–thaw, vascular stasis, and late ischemic. Overlap occurs among these phases. The changes during each phase vary with rapidity of freezing and duration and extent of injury. Some feel that it is conceptually clearer to divide pathologic changes occurring in frostbite into two categories: those resulting 182
from direct cellular injury and those from indirect cellular effects, or progressive dermal ischemia,125 a similar pathophysiology seen in thermal burn patients.109,110,150
DIRECT CELLULAR INJURY Regardless of the classification scheme, researchers agree that the changes caused by direct injury include the following:196,197 • Extracellular ice formation • Intracellular ice formation • Cell dehydration and shrinkage • Abnormal intracellular electrolyte concentrations • Thermal shock • Denaturation of lipid–protein complexes Cells subjected to a slow rate of cooling (hours) develop ice crystals extracellularly in the cellular interspaces. Rapid cooling (seconds to minutes) produces intracellular ice crystals, which are more lethal to the cell and less favorable for cell survival. In a clinical cold injury, the slower rate of freezing does not produce intracellular crystals;112,113 however, the extracellular ice formed is not innocuous. It draws water across the cell membrane, contributing to intracellular dehydration. The theory of cellular dehydration was originally proposed by Moran124 in 1929 and subsequently supported by Merryman’s study of “ice-crystal nucleation.”112,113,115 Cellular dehydration produces modification of protein structure by high electrolyte concentration, alteration of membrane lipids, alteration of cellular pH, and imbalance of chemical activity.106,107,116 This phenomenon subsequently permits a marked and toxic increase of electrolytes within the cell, leading to partial shrinkage and collapse of its vital cell membrane. These events are incompatible with cell survival. Not all the water within a cell is freezable. A small amount of unfrozen water, “bound water,” constitutes up to 10% of the total water content and is held tightly in the protein complex within the cell. No matter how rapid or marked the cold injury, this bound water remains liquid. At temperatures below −20° C (−4° F), approximately 90% of available water is frozen.194 Although the theory of ice crystal disruption of cell structure is attractive, it has yet to be conclusively proved. Thermal shock defines the phenomenon of sudden and profound temperature change in a biologic system. Precipitous chilling has been theorized to be incompatible with life, but the severity of this phenomenon is debatable. Another poorly understood concept is the manner in which subzero temperatures produce denaturation of lipid–protein complexes. One proposed theory hypothesizes the detachment of lipids and lipid protein from cell membranes as a consequence of the solvent action of a toxic electrolyte concentration within a cell.99,100 There is no direct evidence supporting an alteration of enzyme activity during freezing, but DNA synthesis is inhibited.74 On the other hand, there is indirect evidence of ox liver catalase inactivation caused by denaturation and structural alteration of lactic acid dehydrogenase after freezing and thawing.102,166
INDIRECT CELLULAR DAMAGE/PROGRESSIVE DERMAL ISCHEMIA Indirect cellular damage secondary to progressive microvascular insults is more severe than is the direct cellular effect. This is supported by the observation that skin tissue subjected to a standard freeze–thaw injury, which consistently produced necrosis in vivo, survived as a full-thickness skin graft when transplanted to an uninjured recipient site.190 Conversely, uninjured full-thickness skin did not survive when transferred to a recipient area pretreated with the same freezing injury. Thus, direct skin injury is reversible. The progressive nature of injury is probably secondary to microvascular changes. Approximately 60% of skin capillary circulation ceases in the temperature range of 3° to 11° C (37.4° to 51.8° F), whereas 35% and 40% of blood flow ceases in arterioles and venules, respectively.148 Capillary patency is initially restored in thawed tissue, but blood flow declines 3 to 5 minutes later. Three nearly simultaneous phenomena occur after thawing: momentary and initial vasoconstriction of arterioles and venules, resumption of capillary circulation and blood flow, and showers of emboli coursing
Reports in the 1940s documenting the histopathology of frostbite injury to the skin were not comprehensive. Historically, studies by several investigators have been limited to skin biopsies without documentation of location, exposure time, temperature, or time elapsed since the injury.159 More recently, experimental studies have been able to document the histopathology of skin changes under controlled conditions. In 1988, Schoning and Hamlet161,162 used a Hanford miniature swine model for frostbite injury (−75° C [−103° F] exposure for up to 20 minutes) to note progressive epithelial damage. Early changes included vacuolization of keratinocytes, and there was loss of intercellular attachments and pyknosis over a period of 1 week or more. This subsequently progressed to advanced cellular degeneration and formation of microabscesses at the dermoepidermal junction. Later changes included epithelial necrosis and regeneration, either separately or together within the same tissue. Such histopathologic data favor the current standard of conservative delayed-surgical management of frostbite injury. However, Marzella and associates104 used a New Zealand white rabbit ear model of frostbite injury and proposed that the skin necrosis induced by frostbite injury was merely a reflection of damage to the target cell—the endothelial cell. After sub mersion of a shaved rabbit ear in 60% ethyl alcohol at −21° C (−5.8° F) for 60 seconds, the entire microvasculature demonstrated endothelial damage within 1 hour; erythrocyte extravasation occurred within 6 hours. These early vascular changes in the rabbit ear model are in contradistinction to the timing of vascular changes in the Hanford miniature swine model reported by Schoning and Hamlet.162 These clinicians performed biopsies on animals exposed to frostbite injury (−75° C [−103° F] for up to 20 minutes) and evaluated the specimens for vascular inflammation, medial degeneration, and thrombosis. The earliest change documented both grossly and microscopically was hyperemia. Within 6 to 24 hours, leukocyte migration and vasculitis were noted. However, the most severe vascular changes of thrombosis and medial degeneration were not observed for 1 to 2 weeks after the injury. Whether or not changes in the epidermis are primary or secondary to damage of underlying endothelial cells, it is clear that these tissues have potential, although limited, capacity for regeneration. Human experience clearly suggests that robust local tissue inflammation and coagulation stimulate microvascular thrombosis and progressive cell death.125 A perfect representative animal model for frostbite has yet to be found. A wide range of animal models is used to create and assess the condition. Developing a consistent reproducible and appropriate model would facilitate frostbite research.171 As early as 1991, Manson and co-workers101 proposed that frostbite is characterized by acute tissue injury induced by freezing and thawing. Initial complete ischemia is followed by reperfusion and later, tissue necrosis. They suggested that the vascular events supported the hypothesis that free radical–mediated reperfusion injury at thawing might contribute to tissue necrosis after frostbite in a manner similar to that seen after normothermic ischemia. Supporting evidence included electron micrographs showing the appearance of severe endothelial cell injury beginning during freezing and extending through early reperfusion. Later, neutrophil adhesion, erythrocyte aggregation, and microvascular stasis were seen.
Definitions and Classifications Classically, frostbite has been described by its clinical presentation, but this can be difficult to predict in the field and before rewarming.85,117 Mills124,126 favors the use of two simple classifications: mild (without tissue loss) and severe (with tissue loss.) Historically, and following the classification of thermal burn injury, frostbite has been divided into “degrees” of injury based on acute physical findings after freezing and rewarming. Frostnip (Figure 8-1, online ; also see Figure 9-8) is superficial and associated with intense vasoconstriction. It is characterized by discomfort in the involved parts. Symptoms usually resolve spontaneously within 30 minutes, and no tissue is lost. There is some question whether this qualifies as cold-induced injury, because neither frozen extracellular water nor progressive tissue loss is routinely demonstrated. 183
CHAPTER 8 Frostbite
through microvessels.197 Ultimately, there is progressive tissue loss caused by progressive thrombosis and hypoxia. This is similar to the tissue loss seen in the distal dying random flap and the no-reflow phenomenon. For both of these, in addition to the effect of arachidonic acid metabolites, oxygen free radicals have been shown to be detrimental and to contribute to tissue loss. It has been proposed that this may be the case with frostbite injury.19 Emerging concepts, perhaps including the deleterious role of protein kinase C in reperfusion injury, will no doubt be incorporated into our understanding of frostbite injury as scientific understanding evolves. Considerable evidence points to the primary alteration of the cold injury being injury to vascular endothelium.196 Seventy-two hours after a freeze–thaw injury, there is loss of vascular endothelium in the capillary walls, accompanied by significant fibrin deposition. The endothelium may be totally destroyed, and fibrin may saturate the arteriole walls.122,196,197 Ultrastructural derangement of endothelial cells after the thaw period has been observed by electron microscopy in capillaries of the hamster cheek pouch following subzero temperatures.144 The endothelial injury was confirmed by demonstrating fluid extravasation from vessels almost immediately after thawing.197 As in other forms of trauma, vascular endothelial cells swell and protrude inward into the lumen until they lyse. Venules appear more sensitive to cold injury than do other vascular structures, partly because of lower flow rates. Arterioles, with a rate of flow almost twice that of venules, are less damaged by freezing and develop stasis later than do venules. Capillaries manifest the fewest direct effects of cold injury, but their flow is quickly arrested as a result of their position between arterioles and venules. Generalized stasis and cessation of flow are noted at the point of injury within 20 minutes after freeze and thaw. “White thrombi” (blood cells and fibrin) follow platelet thrombi as blood flow progressively slows. Sludging and stasis result in ultimate thrombosis. Microangiography after cold injury shows that although spasm of the arterioles and venules exists, it is not marked enough to completely account for the decreased flow of progressive microvascular collapse.9 In the 1950s, Kulka87,88 observed that vascular thrombosis after cold injury advanced from the capillary level to that of the large vessels and ultimately resulted in ischemic death of progressively larger areas. Viable dermal cells may be observed histologically in cold-injured tissues for up to 8 days or until there occurs occlusion of local vessels. This emphasizes that a major role is played by vascular insufficiency and that direct injury to cellular structures and mechanisms may be reversible. Because Cohnheim had shown changes in cold injury to be similar to changes seen in other inflammatory states, Robson and Heggers150 postulated that the progressive ischemia seen in frostbite might be caused by the same inflammatory mediators responsible for progressive dermal ischemia in the burn wound. They evaluated blister fluid from patients with hand frostbite, measuring levels of PGE2, PGF2α, and thromboxane B2 (TXB2). Levels of the vasoconstricting, platelet-aggregating, and leukocytesticking prostanoids (PGF2α and thromboxane A2 [TXA2]) were markedly elevated. The investigators postulated that massive edema after cold injury was due either to leakage of proteins caused by release of these prostanoids or to leukocyte sludging in the capillaries and increased hydrostatic pressure. Studies have confirmed the similarity between cold injury and the burn wound.19 Severe endothelial damage was observed by researchers studying a minimal cold-injury model in the hairless mouse.13 In addition, the sequence of endothelial damage, vascular dilation, vascular incompetence, and erythrocyte extravasation was confirmed. This led to speculation that arachidonic acid metabolites, which may originate from severely damaged endothelial cells, are important in progressive tissue loss. Significantly absent from in vivo and microscopic observations were vascular spasm, thrombosis, and fibrin deposition, all of which have previously been implicated as pathophysiologic mechanisms. A rabbit ear model demonstrated increased tissue survival after blockade of the arachidonic acid cascade at all levels.145 The most marked tissue salvage resulted when specific TXA2 inhibitors were used. This has now been shown to be effective in clinical situations.64
PART 2 COLD AND HEAT FIGURE 8-2 A Nordic skier with first-degree frostbite (central pallor having cleared after rewarming) of the abdominal skin. This skier reported having skied for 90 minutes in −23.3° C (−10° F) temperature, unaware that his shirt, underneath a parka, had come untucked from his trousers. (Courtesy Luanne Freer, MD.)
First-degree injury shows numbness and erythema. There may initially be a white or yellowish, firm plaque in the area of injury. There is no tissue loss, although edema is common (Figure 8-2). Second-degree injury results in superficial skin vesiculation (Figure 8-3). Clear or milky fluid is present in the blisters, surrounded by erythema and edema. Third-degree injury shows deeper blisters, characterized by purple, blood-containing fluid (Figure 8-4). This indicates that the injury has extended into the reticular dermis and beneath the dermal vascular plexus. Fourthdegree injury is completely through the dermis, and involves relatively avascular subcuticular tissues (Figure 8-5). This tends to cause mummification, with muscle and bone involvement (Figure 8-6). Less severe bone injury in children may affect the growth plate and result in developmental digital deformities.16,22 Cauchy and colleagues26 proposed a different classification of frostbite injury for the hand and foot that is based on the risk for
FIGURE 8-3 A climber with second-degree frostbite of the fifth finger sustained after only several seconds’ exposure to −45.6° C (−50° F) windchill when gloves were briefly removed to handle placement of a carabiner to the fixed rope. Clear bullae developed after rewarming. (Courtesy Luanne Freer, MD.)
FIGURE 8-5 A climber with fourth-degree or severe frostbite injury just hours after rewarming. Note absence of any blistering. Fingers are insensate, and capillary refill is absent. (Courtesy Luanne Freer, MD.)
amputation of the affected part. An early prognosis for frostbite patients may be delayed by the lack of useful clinical guidelines; this new classification scheme (Tables 8-1 to 8-3) is intended to help resolve such issues. The four severity levels proposed provide earlier prediction of the final outcome of frostbite injury by using a technetium-99m (99mTc) bone scan in conjunction with the clinical findings on presentation. It was noted that the probability of bone amputation for the hand and foot could also be correlated to the extent of frostbite injury seen at the time of initial presentation and early 99mTc bone scanning. In a review of 70 cases of severe frostbite injury, the probability of bone amputation was 1% for the distal phalanx, 31% for involvement of the middle phalanx, 67% for the proximal phalanx, and 98% and 100%, respectively, for involvement of the metacarpal/metatarsal and carpal/tarsal bones (see Table 8-3). Grade 1 lesions do not require hospitalization or bone scans. Grade 2 lesions may require brief hospita lization and bone scans. Rapid rewarming and treatment with antibiotics and oral vasodilators appear to be sufficient for healing. Grade 3 lesions are connected with a significant risk for amputation and require rapid rewarming, antibiotics, aspirin, and intravenous (IV) vasodilators. Grade 4 lesions have high risk for amputation and complications such as thrombosis, sepsis, and other systemic problems (see Table 8-3). Cauchy’s clinical/99mTcbased classification scheme appears particularly useful in its ability to predict at a very early stage subsequent outcome from a frostbite injury.
Contributing Factors TEMPERATURE AND WINDCHILL Air alone is a poor thermal conductor, and cold air alone is not nearly as dangerous a freezing factor as is a combination of wind and cold.194 Wind velocity in combination with temperature establishes the windchill index. For example, an ambient
FIGURE 8-4 A climber with second-, third-, and fourth-degree frostbite of the hand. Note fingers 1 to 4 with hemorrhagic bullae over the areas of third-degree injury, clear bullae over the dorsum of the hand with second-degree injury, and deeply violaceous and unblistered fourth-degree injury of the distal phalanx of the fifth finger. (Courtesy Luanne Freer, MD.)
184
FIGURE 8-6 Photographs of 8-week follow-up of hand pictured in Figure 8-5, showing complete mummification and autoamputation of remaining digits. (Courtesy Luanne Freer, MD.)
Grade 1
Grade 2
Grade 3
Grade 4
Extent of initial lesion at day 0 after rapid rewarming Bone scanning at day 2
Absence of initial lesion
Initial lesion on distal phalanx
Initial lesion on carpal/tarsal
Useless
Blisters at day 2
Absence of blisters
Hypofixation of radiotracer uptake area Clear blisters
Initial lesion on intermediary (and) proximal phalanx Absence of radiotracer
Prognosis at day 2
No amputation
Tissue amputation
Sequelae
No sequelae
Fingernail sequelae
Hemorrhagic blisters on the digit Bone amputation of the digit Functional sequelae
Absence of radiotracer uptake area on the carpal/tarsal Hemorrhagic blisters over carpal/ tarsal Bone amputation of the limb± systemic involvement± sepsis Functional sequelae
From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ Med 12:248, 2001.
TABLE 8-2 Management of Frostbite Injuries of the Extremities On day 0, treatment consists of rapid rewarming for 2 hours in 38° C (100.4° F) water bath, with intravenous infusion of 400 mg chlorohydrate of vasodilator (buflomedil) and 250 mg aspirin. Subsequent treatment depends on the extent of the initial lesion, as follows: Grade 1* Absence of Initial Lesion
Grade 2 Initial Lesion Over Distal Phalanx
Grade 3 Initial Lesion Over Intermediary (and) Proximal Phalanx
Grade 4 Initial Lesion Over Carpal/Tarsal
No hospitalization Oral treatment for 1 week (aspirin, vasodilator) —
Hospitalization 2 days Possibly a bone scan at day 2
Hospitalization 8 days Bone scan at day 2
Hospitalization intensive care unit Bone scan at day 2
Oral treatment for 3 weeks (aspirin, vasodilators), dressing — —
IV administration for 8 days (aspirin, vasodilators), dressing Bone scan near day 8 Bone amputation near day 30
Recovery with moderate sequelae
Bone amputation of the digit with functional sequelae
IV administration for 8 days (aspirin, vasodilators), dressing Possibly antibiotics Early bone amputation near day 3 if sepsis Bone amputation of the limbs with systemic involvement
— — Recovery
From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ Med 12:248, 2001. IV, Intravenous. *See Figure 8-2.
temperature of −6.7° C (−19.9° F) with a 45-mph wind has the same cooling effect as does a temperature of −40° C (−40° F) with a 2-mph breeze184,186,189 (Figure 8-7, online). Thus, it is important to think in terms of heat loss, not cold gain. Frostbite occurs when the body is unable to conserve heat or protect against heat loss.
TABLE 8-3 Probability of Amputation Based
on the Extent of the Initial Lesion Extent (Level of Involvement)
Probability of Bone Amputation (95% CI)
Hand
5 4 3 2 1
(carpal/tarsal) (metacarpal/metatarsal) (proximal phalanx) (intermediary phalanx) (distal phalanx)
100— 100— 83 (66;100) 39 (25;52) 1 (00;03)
Foot
5 4 3 2 1
(carpal/tarsal) (metacarpal/metatarsal) (proximal phalanx) (intermediary phalanx) (distal phalanx)
100— 98 (93;100) 60 (45;74) 23 (10;35) 0—
Hand and foot
5 4 3 2 1
(carpal/tarsal) (metacarpal/metatarsal) (proximal phalanx) (intermediary phalanx) (distal phalanx)
100— 98 (95;100) 67 (55;79) 31 (22;41) 1 (00;02)
From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ Med 12:248, 2001. CI, Confidence interval.
CONDUCTION The type and duration of cold contact are the two most important factors in determining the extent of frostbite injury.184,186,189 Touching cold wood or fabric is not nearly as dangerous as is direct contact with metal, particularly by wet or even damp hands.51 This is a result of differences in thermal conductivity between the materials. Deep, loose snow, which traditionally has been thought to insulate from the cold, may actually contribute to frostbite. Temperature measured beneath deep snow is frequently much lower than that on the surface. Washburn189 recounts one expedition to Mt McKinley, Alaska, when members of his party found it extremely difficult to keep their feet warm, despite a clear, sunny, −16° C (3.2° F) day with little wind. One member inadvertently dropped a thermometer in the snow and noted that it registered −25.6° C (−14.1° F). Feet must be dressed for the temperature at their level, not for surface temperature protection.189
ALTITUDE Ambient temperature drops by approximately 1.0° C (1.8° F) for every 150 m (492 feet) of height gain. Many serious cases of frostbite originate at high altitude, but it is difficult to sort out the independent risk for hypobaria/hypoxia versus cold exposure. Hashmi and colleagues61 reported 1500 cases of highaltitude frostbite and observed a “very steep upward curve” beyond a height of 5182 m (17,000 feet) above sea level. CIVD has been shown to be diminished in non-native visitors to high altitude.52 Some important sequelae of high-altitude acclimatization, namely erythrocytosis (an increase in red blood cells to maintain oxygen transport in the hypobaric environment) and high-altitude dehydration, result in hyperviscosity that may make frostbite more likely. Garvey and associates50 demonstrated that 185
CHAPTER 8 Frostbite
TABLE 8-1 Proposed Classification for Severity of Frostbite Injuries of the Extremities
PART 2 COLD AND HEAT
erythremia in the setting of a hypobaric environment provoked procoagulability in a rhesus monkey model. Recent evidence using a real-time video-imaging technique compared the sublingual microcirculation at sea level and at altitude.103 The study showed significant reduction in microcirculatory flow index (MFI) at high altitude (4900 m [16,076 feet]) when compared with sea level in small (<25 µm) and medium (26 to 50 µm) blood vessels (Figure 8-8). Larger vessels were not studied because of the relative paucity of their representation in the vascular bed studied. The results also showed further reduction in MFI within small and medium vessels at extreme altitude (6400 m [20,997 feet]). The very marked slowing of blood flow in the microcirculation at high altitude is easily appreciated (clips can be seen online at http://www.sdfimaging. net/dsmsealevelmicrocirc.wmv and http://www.sdfimaging.net/ dsm6400metermicrocirc.wmv). Stagnant hypoxia may occur in tissues as a result of reduced microcirculatory blood flow and consequent failure of oxygen mass transfer. Furthermore, disparity of oxygen supply and demand at a microvascular level could lead to heterogeneous tissue oxygenation and cellular hypoxia.73 These preliminary data are the first evidence demonstrating clear reduction in microcirculatory blood flow at altitude and may in part explain the apparent increased incidence of frostbite at extreme altitude, because a reduction in flow will be associated with reduction in heat transfer. Further studies to assess the potential reversibility with supplemental oxygen are indicated. Hypoxic neurologic dysfunction is a feature among nonsurvivors at extreme altitude; failure to adequately protect extremities may contribute to the high incidence of frostbite at extreme altitude.42 Inadequate fluid intake and poor nutrition are also possible risk factors.121,142
FIGURE 8-9 Sherpa climber on day 4 of treatment for second-degree frostbite from propane leak in backpack on Mt Everest. (Courtesy Luanne Freer, MD.)
COOLANTS Not all victims of frostbite are exposed to cold environments. Case reports cite toxic dermatologic effects of propane, butane, chloroethane, and liquid oxygen47,91,164,179,183 application to the skin, either intentionally, but exceeding time exposure for cryotherapy, or accidentally (Figure 8-9), as in the case of severe frostbite requiring skin grafting in a child improperly using a toilet air freshener containing propane and butane.91 Careless use of ice to cool a soft tissue injury can result in frostbite,55 and patients should be instructed to place a towel or other fabric between ice packs and bare skin to prevent this complication.
Clothing
A
The degree of inadequacy of protective clothing varies with conditions and may contribute to insufficient conservation of body heat.33 Tight-fitting clothing may produce constriction, which hinders blood circulation and lessens the benefit of heat-retaining air insulation. Wet clothing transmits heat from the body into the environment, because water is a thermal conductor superior to air by a factor of about 25.85 Clothing that transmits moisture away from the body may be protective if an outer wind-resistant layer decreases heat loss. However, this wind-resistant layer must retain the same transmission capabilities; otherwise, clothing will still become moist. Clothes that decrease the amount of surface area may decrease frostbite risk. Mittens are more protective than gloves, because gloves have a greater surface area and prevent air from circulating between fingers. Poorly fitted boots notoriously generate frostbite injuries, even when worn with excess socks (Figures 8-10 and 8-11; Figure 8-10, online). Although up to 40% of total body heat loss can occur through exposed head and neck areas,178 a more recent study has refuted the widely held belief that the head loses proportionally more heat than does the rest of the body. In fact, any uncovered part of the body loses heat in proportion to the body surface area exposed; appropriate protection is important for all exposed skin.140
SKIN WETNESS/UNWASHED SKIN
B FIGURE 8-8 Sublingual microcirculatory flow at sea level (A) and 4900 m (16,076 feet) (B). There is a significant reduction in microcirculatory flow index at high altitude (4900 m) when compared with baseline in small (<25 µm) and medium (26 to 50 µm) blood vessels, Caudwell Xtreme Everest Expedition. (From Martin DS, Ince C, Goedhart P, et al: Abnormal blood flow in the sublingual microcirculation at high altitude. Eur J Appl Physiol 106:473, 2009.)
186
Development of frostbite does not depend simply on ambient temperature and duration of exposure. Along with windchill, humidity and wetness also predispose to frostbite. Skin wetting adds an increment of heat transfer through evaporation and causes wet skin to cool faster than dry skin.123 More important, water in the stratum corneum can terminate supercooling by triggering water crystallization not only in this layer but also in the underlying tissue. Skin wetness is therefore conducive to frostbite because it allows crystallization to terminate supercooling after approximately one-half of the exposure time required by dry skin. This substantiates the following clinical observation: “It has been found that supercooling displays itself in greater degree in skin that remains unwashed. Washing the skin
Impaired local circulation is a primary contributor to frostbite. Cigarette smoking causes vasoconstriction, decreased cutaneous blood flow, and tissue loss in random skin flaps.94 Reus and colleagues147 documented that smoking induced arteriolar vasoconstriction and decreased blood flow in a nude subject. Although red blood cell velocity increased, the net effect was a decrease in blood flow in the cutaneous microcirculation during and immediately after smoking. Curiously, habitual heavy smokers show higher scores on the Resistance Index of Frostbite (RIF), which correlates with lower risk for frostbite.29 Empirically, one could conclude that smoking, which induces vasoconstriction, should place one at increased risk for frostbite, and research supports this.30,38,61
COMORBIDITIES Drugs known to have vasoactive properties may predispose to or compound frostbite injury. Disease states that alter tissue perfusion, such as diabetes, atherosclerosis, arteritis, and Raynaud’s disease, predispose to frostbite (Figure 8-12).34,88
PREVIOUS FROSTBITE INJURY
FIGURE 8-11 Subject on South Col, Mt Everest (7950 m [26,083 feet]) with excess socks in hand, about to descend, Caudwell Xtreme Everest Expedition. (Courtesy Christopher H.E. Imray, MD.)
encourages freezing, whereas rubbing the skin with spirit and anointing it with oil discourages it. The capacity to supercool greatly would seem to be connected with relative dryness of the horny layers of the skin. It is well known that Arctic explorers leave their skin unwashed.”96
ALTERED MENTAL STATUS (ALCOHOL, DRUGS, MENTAL ILLNESS) Putting on clothes in response to cold is not a reflex but requires a conscious decision. When the ability to decide or to act is impaired, there is a risk for cold-induced injury; not surprisingly, alcohol has been implicated in up to 53% of nonmilitary frostbite cases.177 Once the injury had occurred, alcohol intake probably did not significantly alter the course of events. Barillo and associates7 experimentally demonstrated increased mortality and a detrimental effect of ethanol on tissue perfusion associated with severe murine frostbite. Alcohol consumption promotes peripheral vascular dilation and increases heat loss, making an exposed part more susceptible to frostbite.149 In one series of 20 urban frostbite patients, all had overt or covert psychiatric disease.135 This prompted a retrospective review that suggested that between 61% and 65% of victims of urban frostbite suffer from psychiatric disease, and some centers now advocate psychiatric screening in all cases of urban frostbite injury.
On the basis of clinical observations, an individual who has experienced prior cold injury is placed in a high-risk category during subsequent cold exposure.118,193 For undefined reasons, cold injury sensitizes an individual, so that subsequent cold exposure, even of a lesser degree, produces more rapid tissue damage.84 Cold-induced neuropathy may play an important role in the long-term sequelae of cold sensitivity after local cold injury. An alteration in somatosensory function was found, and this was more pronounced in lower limb injuries.4
IMMOBILITY Military studies emphasize that long periods of immobility contribute to the extent of cold injury.84,85 Motion produces body heat and improves circulation, especially in endangered limbs.
GENETIC PREDISPOSITION The deletion genotype (DD) for the angiotensin I–converting enzyme (ACE) has been associated with increased vascular reactivity in vivo and in vitro.18,65 Kamikomaki77 proposed that a case of frostbite in a climber with ACE DD allele was caused by genetic propensity for vasoconstriction.
FATIGUE During World War II and the Korean conflict, clinical studies indicated that cold injuries occurred with higher frequency among soldiers in retreat.129,130,193 Fatigue and apathy also increase the incidence of cold injury. When warfare is proceeding toward defeat, or in conditions of starvation, soldiers often become indifferent to personal hygiene and clothing, and the frequency of frostbite increases.83 Overexertion increases heat loss. A large amount of body heat can be expanded by panting, and perspiration further compounds the problem of chilling. Both panting and sweating consume energy, which compounds the fatigue factor.
FIGURE 8-12 A 54-year-old man had an acute primary episode of Raynaud’s disease after surfing for 80 minutes in water that was 21° C (69.8° F). The distinctive asymmetric pallor of the terminal phalanges of the fourth digit on the right hand persisted for 40 minutes. A sharp demarcation between the second and third phalangeal joints was evident, but no other symptoms were apparent. The pallor spontaneously resolved without cyanosis or redness of the affected area. Medical evaluation subsequently revealed no disorder known to cause secondary Raynaud’s phenomenon. (From Bluto MJ, Norman DA: Acute episode of Raynaud’s disease, N Engl J Med 347:992, 2002.)
187
CHAPTER 8 Frostbite
SMOKING
PART 2 COLD AND HEAT
Civilian clinical studies are inadequate for statistical evaluation of factors such as race and previous climatic environmental exposure.84,109,111 In a recent study, blacks were found to have difficulty generating increased metabolic rate (measured by 2 ] and rectal temperature) after acute oxygen consumption [ VO cold exposure, and researchers suggest this group may be at greater risk for cold injury.40 Military studies suggest that women30 and blacks30,52 may be more susceptible to cold injury. One author postulates that blacks are three to six times more susceptible to frostbite than are whites because blacks tend to initiate shivering at lower core temperatures and tend to have long, thin fingers and toes, as well as thin arms and legs, which do not conserve heat as efficiently as do their white counterparts. In testing, black fingers cool faster when immersed in cold water and reach a lower temperature before hunting reaction ensues.52 Individuals with type O blood52 and from warmer climatic regions in the United States tend to be more susceptible.193 An increased incidence of frostbite was reported in nearly 6000 military recruits with cold-provoked white finger syndrome and in those with hand/arm vibration in both exposure classes analyzed.38,128 A low RIF, determined in a simple laboratory test, may be indicative of increased risk for cold injuries during operations in the field.29
Clinical Presentation In most patients, the initial clinical observation is coldness of the injured part, and more than 75% complain of numbness. The involved extremity feels clumsy or “absent” because of ischemia following intense vasoconstriction. When numbness is present initially, it is frequently followed by extreme pain (76% of patients) during rewarming. Throbbing pain begins 2 to 3 days after rewarming and continues for a variable period, even after dead tissue becomes demarcated (22 to 45 days). After about a week, the victim usually notices a residual tingling sensation, a result of ischemic neuritis, which explains why this sensation tends to persist longer than other symptoms. Severity of the injury usually defines the extent of neuropathologic damage. Because different injuries are influenced by so many environmental and individual factors, there may be a great deal of variation in symptoms. In patients without tissue loss, symptoms usually subside within 1 month, whereas in those with tissue loss, disablement may exceed 6 months. In all cases, symptoms are intensified by a warm environment. Other sensory deficits include spontaneous burning and electric current–like sensations. The burning sensation, which is frequently early in presentation, subsides within 2 to 3 weeks and is usually not present in victims with tissue loss. In victims without tissue loss, the burning sensation may resume on wearing shoes or increasing activity. The electric current–like shock is almost universal (97%) in patients with tissue loss. It usually begins 2 days after injury, lasts for about 6 weeks, and is particularly unpleasant at night. All frostbite victims experience some degree of sensory loss for at least 4 years after injury and perhaps indefinitely. The clinical appearance of frostbite depends on how quickly the injured patient presents to care, and it is important to note that this appearance may initially be deceiving.12,129 Patients in the Alps who arrive by helicopter within minutes of their injury may present quite differently than do Himalayan climbers, who have nearly all rewarmed during self-descent and may be fortunate to arrive at definitive care even several days after injury. Regardless of venue, only a few patients arrive with tissue still frozen. At first, the extremity appears yellowish white or mottled blue. It may be insensate and may appear frozen solid, regardless of the depth of the injury. With rapid rewarming there is almost immediate hyperemia, even in some of the most severe injuries. Sensation returns after thawing and persists until blebs appear. At this point, some effort may be made to assess the severity of the injury. After the extremity is rewarmed, edema appears within 3 hours and lasts 5 days or longer, depending on the severity of the case.129 Vesicles or bullae appear 6 to 24 hours after rapid rewarming.112,130 Clear bullae confer a better prognosis than hemorrhagic bullae, which indicate deeper injury. During the first 9 to 15 days, severely frostbitten skin forms a black, hard, and 188
A
B FIGURE 8-13 Photo of climber 24 hours (A) and approximately 2 weeks after (B) deep frostbite injury to fingers, showing eschar formation. (Courtesy Luanne Freer, MD.)
usually dry eschar, whether or not vesicles are present (Figure 8-13).130 Mummification forms an apparent line of demarcation in 22 to 45 days.129
Field Treatment In 1957, Hurley68 stated, “Tissue cells can be affected by freezing in three different ways: (1) a certain number of cells are killed; (2) a certain number remain unaffected; and (3) a large number are injured but may recover and survive under the right circumstances.” Clearly, the major treatment effort must be to salvage as many cells in the third group as possible. Frostbite treatment is directed separately at the pre-thaw and post-thaw intervals.
SELF-RESCUE IN THE FREEZING ENVIRONMENT The International Commission for Alpine Rescue (ICAR) gives specific recommendations for self-rescue to those working, recreating, or otherwise exposed to a cold environment (Box 8-1). These guidelines advise seeking shelter from cold and wind, drinking warm fluids, removing wet clothing, taking ibuprofen, and attempting self-rewarming for 10 minutes. If at high altitude, supplemental oxygen is advised, and if sensation does not return, the victim is advised to discontinue any further exposure and seek treatment.172 Although these guidelines may seem common sense to most, climbers appreciate these guidelines for safety and self-rescue when in an exposed, potentially dangerous, and remote setting.
IN THE PREHOSPITAL FREEZING ENVIRONMENT The Alaska State guidelines for field treatment and transport of patients with frostbite recommend the following: If transport time will be short (1 to 2 hours at most), the risks posed by improper rewarming or refreezing outweigh the risks of delaying treatment for deep frostbite. If transport will be prolonged (more than 1 to 2 hours), frostbite will often thaw spontaneously. It is more important to prevent hypothermia than to rewarm frostbite rapidly in warm
BOX 8-2 Alaska State Guidelines for Prehospital
Emergency Treatment In the Open With Possible Onset of Frostbite • Move out of the wind/consider turning back/drink fluids (warm if possible) • Remove boots—but consider possible problems with replacement if swelling occurs • Remove socks/gloves if wet. Exchange for dry clothing • Warm by placing foot/hand in companion’s armpit/groin for 10 minutes only • Replace boots • Give one dose of aspirin or ibuprofen to improve circulation (if available and not contraindicated) • Don’t rub the affected part because this may cause tissue damage • Don’t apply direct heat If there is sensation, the victim can continue to walk If there is no sensation, the victim should go to the nearest warm shelter (hut/base camp) and seek medical treatment At high altitude, give oxygen if available
First Responder/Emergency Medical Technician— I, II, III/Paramedic/Small Bush Clinic Evaluation and Treatment A. Anticipate, assess, and treat the patient for hypothermia, if present. B. Assess the frostbitten area carefully because the loss of sensation may cause the patient to be unaware of soft tissue injuries in that area. C. Obtain a complete set of vital signs and the patient’s temperature. D. Remove jewelry and clothing, if present, from the affected area. E. Obtain a patient history, including the date of the patient’s last tetanus immunization. F. If there is frostbite distal to a fracture, attempt to align the limb unless there is resistance. Splint the fracture in a manner that does not compromise distal circulation. G. Determine whether rewarming the frostbitten tissue can be accomplished in a medical facility. If it can, transport the patient while protecting the tissue from further injury from cold or impacts. H. If the decision is made to rewarm frostbitten tissue in the field, you should prepare a warm water bath in a container large enough to accommodate the frostbitten tissues without them touching the sides or bottom of the container. The temperature of the water bath should be 99° to 102° F (37° to 39° C). • Generally, patients with frostbite do not require opiates for pain relief; they occasionally need non-opiate pain medication or anxiolytics. If possible, consult a physician regarding the administration of oral analgesics, such as acetaminophen, ibuprofen or aspirin. Aspirin or ibuprofen may help improve outcomes by blocking the arachidonic acid pathway. • Immersion injury or frostbite with other associated injuries may produce significant edema and high pain levels. These patients may need opiate pain medications for initial treatment. In this case, advanced life support personnel should administer morphine or other analgesics in accordance with physician-signed standing orders or online medical control. I. A source of additional warm water must be available. J. Water should be maintained at approximately at 99° to 102° F (37° to 39° C) and gently circulated around the frostbitten tissue until the distal tip of the frostbitten part becomes flushed. K. Pain after rewarming usually indicates that viable tissue has been successfully rewarmed. L. After rewarming, let the frostbitten tissues dry in the warm air. Do not towel dry. M. After thawing, tissues that were deeply frostbitten may develop blisters or appear cyanotic. Blisters should not be broken and must be protected from injury. N. Pad between affected digits and bandage affected tissues loosely with a soft, sterile dressing. Avoid putting undue pressure on the affected parts. O. Rewarmed extremities should be kept at a level above the heart, if possible. P. Protect the rewarmed area from refreezing and other trauma during transport. A frame around the frostbitten area should be constructed to prevent blankets from pressing directly on the injured area. Q. Do not allow an individual who has frostbitten feet to walk except when the life of the patient or rescuer is in danger. Once frostbitten feet are rewarmed, the patient becomes nonambulatory.
of Potential Frostbite
Adapted from Syme D (for ICAR Medical Commission): Position paper: On-site treatment of frostbite for mountaineers. High Alt Med Biol 3:297, 2002. ICAR, International Commission on Alpine Rescue.
water. This does not mean that a frostbitten extremity should be kept in the cold to prevent spontaneous rewarming. Anticipate that frostbitten areas will rewarm as a consequence of keeping the patient warm and protect them from refreezing at all costs.31 The Joint Commission of Health and Human Services, emergency medical services, and public health departments for Alaska have published further guidelines for prehospital and bush clinic care of frostbite. These guidelines are widely regarded as stateof-the-art recommendations and appear in Box 8-2. If a patient is referred from a nearby location, no attempt at field rewarming is indicated. Vigorous rubbing is ineffective and potentially harmful. The extremity should not be intentionally rewarmed during transport and should be protected against slow partial rewarming by keeping the patient away from intense campfires and car heaters. All constrictive and wet clothing should be replaced by dry, loose wraps or garments. The extremity is padded and splinted for protection, and ibuprofen 400 mg twice daily (which may be more beneficial than aspirin because aspirin may block more of the inflammatory cascade than is helpful) may be initiated. Although there is a correlation between the length of time tissue is frozen and the amount of time required to thaw that tissue, there is no direct correlation between the length of time tissue is frozen and subsequent tissue damage. Still, “rapid” transport of frostbite patients (within 2 hours) is appropriate. Otherwise, rapid rewarming should be instituted (goal to see blush of rewarming and/or 15 minutes immersed in rewarming fluid) and the victim transported with protective, dry, nonadherent dressings to prevent refreezing. Appropriate and adequate analgesia should be administered (opiates either IV or intramuscularly [IM]) may be required). Blisters should be left intact. Patients with long transport times are at greater risk for (refreezing) recurrent injury. All efforts should be made to prevent subsequent refreezing, because this creates an infinitely worse result than does delayed thawing (Figures 8-14 to 8-16; Figure 8-16, online). A victim who must walk through snow should do so before thawing frostbitten feet (see Figure 8-10). During transport, the extremities should be elevated and tobacco smoking prohibited.119 Alcohol ingestion is contraindicated. The Wilderness Medical Society convened a panel of experts to review recent literature and ICAR and Alaska State guidelines in order to apply evidence grades based on the quality of supporting evidence, and balance between the benefits and risks for each modality according to methodology stipulated by the American College of Chest Physicians. A document of these graded guidelines is projected to be published in 2011.
Treatment of Frostbite
From Department of Health and Social Services, Division of Public Health Section of Community Health and EMS: State of Alaska cold injuries guidelines, 2003 version rev 2005. http://www.chems.alaska.gov.
189
CHAPTER 8 Frostbite
BOX 8-1 Guidelines From ICAR for Self-Treatment
PART 2 COLD AND HEAT
Definitive Treatment IMMEDIATE TREATMENT
A
B FIGURE 8-14 A, Day 2 after exposure: field rewarming of frostbite injury to Mt Everest summiteer at 6400 m (20,997 feet); B, day 3: field treatment of frostbite injury at 5300 m (17,388 feet). (Courtesy Christopher H.E. Imray, MD.)
A
B FIGURE 8-15 A, Six weeks after injury: third toe is showing signs of recovery; B, 10 weeks after injury: primary closure was achieved with full-thickness skin cover, to optimize the functional result. (Courtesy Christopher H.E. Imray, MD.)
190
Once in the emergency department, if tissues are still frozen, rapid rewarming should be started immediately. Any associated traumatic injuries or medical conditions should be identified. Systemic hypothermia should be corrected to a core temperature of at least 34° C (93.2° F) before frostbite management is attempted. Fluid resuscitation is usually not a problem with isolated frostbite injuries, although one case of rhabdomyolysis and acute renal failure has been reported.152 Treatment is directed at the specific pathophysiologic effects of the frostbite injury, either blocking direct cellular damage or preventing progressive microvascular thrombosis and tissue loss. Direct cellular damage is treated by rapid thawing of all degrees of frostbite with immersion in gently circulating water warmed to between 40° and 42° C (104° and 107.6° F).84 Adherence to this narrow temperature range (as long as it is easy to monitor in the hospital) is important, because rewarming at lower temperatures is less beneficial for tissue survival48,64 and rewarming at higher temperatures may compound the injury by producing a burn wound.120 Frozen extremities should be rewarmed until the involved skin becomes pliable and erythematous at the most distal parts of the frostbite injury. This usually takes less than 30 minutes. Active motion during rewarming is helpful, but massage may compound the injury. Extreme pain may be experienced during thawing, and unless otherwise contraindicated, parenteral analgesics are administered. Rapid return of skin warmth and sensation with the presence of an erythematous color is a favorable sign, whereas the persistence of cold, anesthetic, and pale skin is unfavorable. Rapid rewarming reverses the direct injury of ice crystal formation in the tissue. However, it does not prevent the progressive phase of the injury. McCauley and associates109,110 have designed a protocol based on the pathophysiology of progressive dermal ischemia that has been quite successful in minimizing production of local and systemic thromboxane by injured tissues. All but the most minor frostbite cases should be admitted to the hospital. Victims with minor injuries should be admitted if, after rapid rewarming, a warm environment cannot be ensured for the patient. No patient should ever be discharged into subfreezing weather. Even with a warm car waiting, the patient should be allowed to leave only with proper clothing (such as stocking cap, wool mittens, and wool socks). Because the majority of frostbite injuries necessitate admission to the hospital, a discussion of the protocol is warranted. White or clear blisters, which represent more superficial injury, are debrided to prevent further contact of PGF2α or TXA2 with the damaged underlying tissues. Unlike the clear blisters, hemorrhagic blisters reflect structural damage to the subdermal plexus. It may be worthwhile to aspirate the thromboxane-containing fluid out of these blisters, but debridement may promote desiccation of the deep dermis and allow conversion of the injury to a full-thickness injury. Therefore hemorrhagic blisters are left intact. A specific thromboxane inhibitor, like Aloe vera gel, is placed on the wounds to prevent further formation of this vasoconstricting mediator,63 and dressings should accommodate for expected increasing edema. Aspirin was originally given systemically to block production of PGF2α and TXA2. The correct dose of aspirin to block PGF2α is difficult to determine, so it has been replaced with ibuprofen by many clinicians. Aspirin may, however, still have a useful antiplatelet action if ibuprofen is not available. Ibuprofen not only inhibits the arachidonic acid cascade but has the additional benefit of fibrinolysis. Oxygen should be used to achieve normoxia in a hypoxic patient and is used for frostbite injuries occurring at extreme altitude.
Evaluation and Treatment in the Hospital OVERALL STRATEGY Frostbite is a thermal injury affecting the vasculature, microvasculature, and tissues of the extremities and as such shares many
INITIAL ASSESSMENT OF FROSTBITE AND OTHER INJURIES A rapid and detailed clinical assessment of the patient on arrival in the emergency department is mandatory. The standard approach of assessing the airway, breathing, and circulation clearly takes precedence over assessment of the frostbite injury. History and examination may reveal coexisting problems, and although the frostbite injuries may be visually distressing and severe, it is possible that there are more serious injuries or medical conditions that need to be treated first. Particular attention needs to be paid to hypothermia, limb fractures, the peripheral circulation, and any coexisting trauma. Coexisting medical conditions such as poor glycemic control and alcohol/drug use need to be considered. Principles Hurley68 stated in 1957 that frostbite will result in three zones of tissue injury: dead tissue, normal living tissue, and an interface zone. If we develop this concept further, immediately after the index frostbite injury the size of the interface zone will be maximal and is potentially salvageable. Weeks after injury, the interface zone will be negligible; as a result, the interface zone has a “dynamic” component.47,68 The aim of early evaluation of the frostbite injury is to try to determine the exact extent of the three zones so that a subsequent multifaceted management plan may be directed to optimize tissue salvage in the dynamic interface zone. The initial injury, individual’s response, ambient temperature, and time from initial cold injury at the presentation at the hospital all contribute to how extensive the intermediate potentially salvageable interface zone will be. The patient who is transferred from the mountainside directly to the emergency department by helicopter will have a relatively large potentially salvageable interface zone when compared with a patient who has undergone a much more lengthy evacuation from a remote climbing region of the Himalayas.
PATIENT CARE Specialist Nursing Care Almost all urban patients with significant frostbite should be admitted to the hospital, given that alcohol intoxication, psychiatric illness, and homelessness are common features of the urban frostbite patient; immediate discharge is rarely prudent. Overall goals of hospital treatment include keeping the patient quiet, well nourished, suitably hydrated, and pain-free. Wound care must be meticulous to avoid further trauma. Injured extremities should be elevated above heart level to attempt to minimize edema. Physiotherapy is important, and the patient should be encouraged to mobilize as soon as possible.192 Extremities should be treated with clean dressings and twice-daily whirlpool baths with antiseptics such as chlorhexidine or povidone-iodine. Topical Aloe vera gel should be applied every 6 to 8 hours through resolution of blisters. This encourages the eschars created by the blisters to separate from underlying healthy tissue. Although patients may be nursed anywhere that these objectives can be achieved, vascular surgery or plastic surgery/burns wards (with multidisciplinary input) tend to be most appropriate for the more severe injuries. Frostbite blisters have been shown to contain high concentrations of the vasoconstricting metabolites of arachidonic acid, PGF2α and TXB2 which are known to mediate dermal ischemia in burns and pedicle flaps. It is suggested that they may play a role in the pathogenesis of frostbite, and so early debridement, either with needle aspiration or surgical debridement, is indicated.150
TECHNIQUES TO EVALUATE TISSUE PERFUSION Over the years, several diagnostic tests have been used to attempt to predict severity and prognosis of frostbite injury. These include plain radiographs, infrared thermography, angiography,56 triplephase bone scanning,27 laser Doppler, digital plethysmography,146 and magnetic resonance imaging/magnetic resonance angiography (MRI/MRA). It appears that the most promising approaches are triple-phase bone scanning10,27 and MRI/MRA.8 Early diagnostic angiography (before tissue plasminogen activator [t-PA]) may become the most appropriate first-line investigation for the patient presenting acutely with severe frostbite injury without significant comorbidities.165 Duplex Ultrasonography Duplex ultrasonography uses B-mode, pulsed wave Doppler ultrasonography to visualize the blood flow within a vessel and color flow Doppler imaging to visualize the structure and hemodynamics within a vessel. In a modern vascular unit, there is a move toward using duplex ultrasound examination as the firstline investigative examination, reserving angiograms for situations in which a therapeutic intervention is required. Ease of access, portability, and the ability to make repeat examinations give the technique certain advantages over other imaging modalities. Many remote research stations and even large expeditions may have portable ultrasound machines. Duplex imaging has been used in the field at altitudes as high as 7950 m (26,083 feet) (Figure 8-17, online). Ultrasound has been used to determine the need for sympathetic blockade after frostbite.146 Magnetic Resonance Angiography MRI/MRA investigation has a theoretical advantage over 99mTc bone scanning because it allows direct visualization of vessels (both patent and occluded), as well as imaging of surrounding tissues. It has been suggested that it shows a more clear-cut line of demarcation of ischemic tissue.8 The other advantage of MRA over angiography is that it is noninvasive. However, there are relatively few accounts of its use in frostbite evaluation in the literature. Technetium-99m Scanning The first description of 99mTc scanning for assessment of bone viability in patients with frostbite injuries was in 1976.98 The degree of accretion of the 99mTc was found to depend on integrity of the vascular supply. It was successfully used to distinguish viable from nonviable bone. However, Miller and Chasmar114 found that very early 99mTc bone scanning in frostbitten patients was not as accurate an indicator of the ultimate extent of tissue loss as was scanning at 5 days after injury. They also noted that lesions appeared to fluctuate in extent over a 3-week period. Cauchy and colleagues25,26 recognized that existing frostbite classifications were based on retrospective diagnoses and were not useful for predicting the extent of final tissue loss and prognosis for frostbite patients. The 3- to 6-week waiting period often necessary to determine severity of the lesion and resultant need for amputation often caused considerable distress for patients. They suggested a new classification system that begins at day 0 (just after rewarming) and is based mainly on the topography of the lesion and on early bone scan results. This appears to be a very useful classification for the physician and patient, in that it allows accurate determination at a very early stage of the likely extent of subsequent tissue loss (see Tables 8-1 to 8-3). An interesting insight into some of the possible mechanisms involved in certain frostbite injuries was described by Salimi and co-workers,156 who designed an experimental model to study the pathogenesis and treatment of frostbite. Using 99mTc radionuclide imaging, they monitored the evolution and extent of tissue damage relative to temperature, rate of freezing, and controlled rewarming. Characteristic serial changes were demonstrated on sequential scans. Initial nonperfusion was followed by perfusion and finally again by nonperfusion; this occurred in all areas in which necrosis subsequently developed. The reappearance of nonperfusion corresponded to vascular injury. Vessel thrombosis 191
CHAPTER 8 Frostbite
clinical features with both vascular injuries and burn wounds. This section discusses the aspects of definitive patient care, including complete patient assessment, specific evaluation of the frostbite injury regarding perfusion and tissue viability, and optimal medical management, including proper selection of candidates for endoluminal treatments such as catheter-directed thrombolysis. Early and late reconstructive surgery, ablative surgery, rehabilitation, and frostbite prevention strategies are discussed.
PART 2 COLD AND HEAT
was found on pathology examination and may be related to reperfusion injury. These clinically relevant observations gave evidence to support the concept of temporal “perfusion flux” in blood flow to a frostbitten extremity. The initial reduction is often followed by a temporary hyperperfusion phase before the final infarction phase (probably secondary to endothelial dysfunction and thrombin accumulation). Consequently, measurement of tissue perfusion at a single time point may not be as accurate in predicting outcome as originally believed. Additional supporting evidence for perfusion flux in frostbite comes from Cauchy and associates,25,27 who performed a more detailed analysis of two-phase 99mTc bone scans. Sensitivity of the technique was enhanced by performing a second scan more than 5 days after rewarming. Comparative analysis of the two scans demonstrated that some of the lesions continued to evolve between day 2 and day 8. Based on this finding, they suggested that the outcome of lesions could still be modified during this period. However, in the case of severe sepsis, the results of the first bone scan can be used as an indication for emergency amputation.26 Although the large retrospective study of Cauchy and colleagues using two-phase bone scintigraphy suggested that nonuptake (or low uptake) in frostbite lesions had a strong correlation with the subsequent need for amputation, another prospective study has questioned some aspects of the technique.10 This study compared 22 controls with 20 patients with frostbite. Serial scintigraphy using 99mTc was performed in some patients. In line with the perfusion flux concept, the study suggests that scintigraphy results are somewhat more variable than previously suggested and that moderate to severe frostbite lesions can be classified as having infarcted, ischemic, or hibernating (viable) tissue, similar to the classification employed when using myocardial scintigraphy. Absence of uptake of 99mTc, even after the initial 10 days in this study, did not necessarily indicate infarction and the need for amputation, because many such lesions retain potential for vasodilation and recovery. Triple-phase bone scanning (using 99mTc) has now become more widely used in specialty units, often within the first few days of presentation. This technique assesses tissue viability in an effort to allow early debridement of soft tissue and early coverage of ischemic bony structures.58 There are few prospective data on the efficacy of 99mTc scanning in predicting the outcome of frostbite injuries. However, it remains a very useful way of assessing potential tissue loss69 (Figures 8-18 to 8-21).
MEDICAL MANAGEMENT Drugs used in the management of frostbite are summarized in Table 8-4. Tetanus Prophylaxis Frostbite should be considered to be a high-risk injury. Tetanus prophylaxis status should be completed in all patients according to currently accepted guidelines.32 Heparin Heparin is a naturally occurring anticoagulant that prevents formation of clots and extension of existing clots within blood vessels. Although true thrombi are not present in dilated, erythrocyte-filled vessels immediately after thawing, they form over the next few days. Heparin has been suggested as a possible treatment for frostbite.163 Lange and Loewe92 demonstrated its usefulness in experimental frostbite. Subsequent investigations have been unable to substantiate these findings, and there is no evidence that heparin alters the natural history of frostbite.16 However, most experts would agree that deep vein thrombosis (DVT) prophylaxis is indicated in any relatively immobile frostbite patient. Indications and Recommendations for Antibiotics There has long been awareness of the potential for infectious complications in frostbite patients.134 The metabolic requirements of infected and healing tissue are increased over those of normal 192
A
B FIGURE 8-18 Frostbitten left hand of a climber (A) taken 36 hours after injury, while climbing in Antarctica (B) Note the discoloration and blister formation, iodine warming towels, and aseptic techniques used in tented field hospital. The digital image was reviewed within 6 hours by Christopher H.E. Imray, MD, in the United Kingdom, and management advice was given over the Internet. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)
tissue. Consequently, should the marginally perfused interface zone become infected, the resulting tissue loss is likely to be increased. Although there is little published evidence with regard to the use of antibiotics in the frostbite patient, antibiotics are widely used. When the skin is edematous, penicillin is administered prophylactically because edema inhibits the skin’s inherent streptococcal properties.125 If there are clinical signs of infection, antibiotic use is absolutely indicated. Wound cultures should be taken from infected tissue to guide therapy, but while awaiting identification of species and sensitivities, practitioners should be aware that the common causative organisms include Staphylococcus aureus, β-hemolytic streptococci, gram-negative rods, and anaerobes. Empiric use of antibiotics to cover these likely organisms should be considered pending culture results. In a 12-year retrospective study, factors found to correlate significantly with amputation were duration of exposure, lack of proper attire, remote geographic location, presence of wound infection, and delay in seeking treatment. Prophylactic systemic antibiotics did not decrease the incidence of wound infection.181 This paper supports the approach of deferring the use of anti biotics until a clinically relevant infection develops. Topical: Aloe vera Experimental evidence from the frostbite rabbit ear model has suggested a clearly defined role for thromboxane as a mediator of progressive dermal ischemia in frostbite injuries. Rapid rewarming helps to preserve tissue by limiting the amount of direct
CHAPTER 8 Frostbite
A
FIGURE 8-21 Hands of patient in Figures 8-18 to 8-20 after 5 days of intravenous iloprost. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)
B FIGURE 8-19 Condition of hands of patient in Figure 8-18 on patient’s arrival in the United Kingdom, 5 days after initial injury. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)
cellular injury. Selective management of blisters helps protect the subdermal plexus, and application of Aloe vera cream (e.g., Dermaide Aloe cream or gel) combats the local vasoconstrictive effects of thromboxane (Figure 8-22). Animal studies suggest thromboxane appears to be a mediator of progressive dermal ischemia in frostbite. In a rabbit ear frostbite model, Heggers and associates64,109 compared the effect of (1) the antiprostanoids (methylprednisolone), (2) aspirin combined with Aloe vera, (3) methimazole, and (4) a control group that received no therapy. Methimazole treatment gave 34.3% tissue survival; Aloe vera, 28.2% survival; aspirin, 22.5% survival; and methylprednisolone, 17.5% survival. In a human study of 154 patients with frostbite, there was significant improvement in outcome and reduction in amputation rates of treated patients compared with controls (p < 0.001). It was concluded that morbidity of progressive dermal ischemia in frostbite may be decreased by therapeutic use of inhibitors of the arachidonic acid cascade.
ANTIPROSTAGLANDIN AGENTS
L
L
Nonsteroidal antiinflammatory drugs, such as ibuprofen, act as a necessary adjuvant to rewarming, because they inhibit inflammatory reactions and pain by decreasing prostaglandin synthesis.64 Oral administration of ibuprofen decreases systemic levels of thromboxane. Ibuprofen 400 mg may be given by mouth and should be continued at a dose of 12 mg/kg of body weight per day. McCauley and co-workers111 treated 38 patients with frostbite in a protocol designed to decrease production of thromboxane locally and prostaglandins systemically. All patients recovered
R
Marker
R
FIGURE 8-20 Technetium-99m bone scans performed on arrival of patient in Figures 8-18 and 8-19 in the United Kingdom. The scans show minimal perfusion to the terminal phalanges in the left hand, suggesting that amputation of the distal phalanges is likely to be necessary. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and nonfreezing cold injuries, Postgrad Med J 85:481, 2009.)
FIGURE 8-22 Aloe vera cream being applied at the Everest Base Camp Medical Clinic. Note the care being taken to apply nonconcentric dressings to allow for edema formation. (Courtesy Suzanne Boyle, MD.)
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PART 2 COLD AND HEAT
TABLE 8-4 Frostbite Management: Drugs, Doses, and Modes of Action and Rationale* Intervention
Dose
Action
Aspirin Ibuprofen Aloe vera gel or cream Oxygen Hyperbaric oxygen therapy Iloprost Nitroglycerin Papaverine Reserpine Buflomedil Pentoxifylline 10% Dextran 40 t-PA LMW heparin
75-250 mg orally once daily 400 mg bid or tid orally With dressing changes every 6 hr 2 L/min above 4000 m (13,123 ft) or when SpO2 is below 90% 2-2.5 atm 1-2 hr daily
Antiplatelet agent, improve rheology Antiprostaglandin effect Topical antiprostaglandin effect Improve tissue oxygenation Improve tissue oxygenation, improve rheology
2-10 mg/hr IV titrated against side effects 100 mcg IA single dose 300 mg over 1hr IA 0.1 to 0.25 mg once daily 400 mg IV or 300 mg bid orally 400 mg tid orally for 2-6 weeks 20 mL bolus, 20 mL/hr IV 1 mg/hr IA or IV Prophylactic dosage subcutaneously Therapeutic dosage subcutaneously
Vasodilator, improve rheology Vasodilator Vasodilator Vasodilator Vasodilator, improve rheology Vasodilator, improve rheology Improve rheology Thrombolytic agent DVT prevention, anticoagulant Maintain patency of recently thrombolysed vessels
Tetanus prophylaxis
bid, Twice a day; DVT, deep vein thrombosis; IA, intra-arterially; IV, intravenously; LMW, low molecular weight; SpO2, oxygen saturation as measured by pulse oximetry; tid, 3 times a day; t-PA, tissue plasminogen activator. *This table is intended to be used as a potential frostbite formulary reference, not as a protocol for treatment. See text for further discussion.
without significant tissue loss. Increased tissue survival was demonstrated experimentally with preservation of the dermal microcirculation by using antiprostaglandin agents and thromboxane inhibitors.
VASODILATORS The equation determining fluid flow within a tube was first described by the French physician and physiologist Jean Poiseuille in the 1840s. He demonstrated that flow was related to perfusion pressure, radius,4 length, and viscosity. In a frostbite patient, each of these parameters (other than length) can be optimized using appropriate medical interventions. Iloprost Prostaglandin E1 (PGE1) is a vasoactive drug that dilates arterioles and venules, reduces capillary permeability, suppresses platelet aggregation, and activates fibrinolysis. Its intra-arterial use has been effective in treating ischemic peripheral vascular disease. The potentially beneficial effect in treating frostbite injuries with intra-arterial PGE1 was first assessed in an animal model.195 PGE1 reduced the magnitude of frostbite injury when the injured limb was slowly rewarmed. The data suggested a possible role for the use of PGE1 in frostbite patients who have not undergone rapid rewarming. Since the first description of its use in patients,59 PGE1 has been used with some success in frostbite injuries.69,192 Further experimental evidence implicates an inflammatory process in the underlying mechanism of tissue injury. It has been postulated that progressive ischemic necrosis is secondary to excessive TXA2 production, which upsets the normal balance between prostacyclin (prostaglandin I2) and TXA2.132 A recent study24 printed as a research letter showed a pro mising decrease in the digit amputation rate with the use of intravenous iloprost in severe frostbite injuries. The clinicians compared results of a trial of 47 frostbite patients who were rapidly rewarmed, received 250 mg of aspirin and 400 mg IV buflomedil, and who were then randomized to receive 250 mg aspirin per day, plus either buflomedil, iloprost, or r-TPA with iloprost. The iloprost group had the lowest overall amputation rate, and though the ideal dose is undetermined, this encouraging data will most likely lead to more clinical research and hope for future frostbite victims. Iloprost is best given as an IV infusion either through a peripheral or central line in a specialist vascular or highdependency unit. The diluted iloprost should be delivered by an accurate rate delivery system such as a syringe driver. The infusion is started at a rate 2 mg/hr and incrementally increased up to 10 mg/hr; titrated against the side effects of facial flushing, 194
headache, nausea, and flulike symptoms; and infusion is usually run for 5 days.69,70 Reserpine Reserpine is a powerful vasodilator that acts by inhibiting uptake of norepinephrine into storage vesicles.137 For frostbite, it is used intra-arterially. The first description in the treatment of frostbite was by Snider and colleagues.169 An animal study suggested that a regional “medical sympathectomy” may be beneficial in reducing tissue loss following frostbite, especially when rapid rewarming cannot be performed.168 Pentoxifylline Pentoxifylline, a methylxanthine-derived phosphodiesterase inhi bitor, has been widely used to treat intermittent claudication, arterial disease, and peripheral vascular disease and has yielded some promising results in human frostbite trials.62 It increases blood flow to the affected extremity, increases red cell deformability, decreases platelet hyperactivity, helps normalize the prostacyclin–to–TXA2 ratio, and has been shown to enhance tissue survival. Pentoxifylline is also presumed to lower pathologically increased levels of fibrinogen and so may protect against vascular endothelial damage. The drug’s efficacy has been demonstrated in animal studies and approaches the effectiveness of Aloe vera. The combination of pentoxifylline and Aloe vera appears to be synergistic.116 A similar synergy of aspirin and pentoxifylline was demonstrated in an animal study.143 Hayes and co-workers62 have proposed a treatment using pentoxifylline in conjunction with the traditional therapy of rewarming, soaks, pain management, and vesicle debridement. They recommend pentoxifylline in the controlled-release form of one 400-mg tablet 3 times a day with meals, continued for 2 to 6 weeks. Controlled studies of pentoxifylline in the management of frostbite have yet to be performed. Buflomedil Buflomedil hydrochloride is a vasoactive drug that may have a number of effects, including inhibition of α-receptors, inhibition of platelet aggregation, improved erythrocyte deformability, nonspecific and weak calcium antagonistic effects, and oxygensparing activity.28,105,108 A case series of 20 patients reported that early administration of IV buflomedil appeared to reduce the risk for subsequent amputation.45 However, buflomedil has not been shown to reduce microcirculatory damage from acute experimentally induced freeze injury.37 Although buflomedil does not have U.S. Food and Drug Administration (FDA) approval, it has been used extensively in France to treat frostbite, with considerable beneficial effect.26
Low-Molecular-Weight Dextran It has been observed that shortly after thawing, cold-injured vessels become dilated and filled with clumps of erythrocytes. These clumps can be easily dislodged by gentle manipulation and do not represent true thrombosis. Although the mechanism that leads to erythrocyte clumping is not completely understood, it may reflect cold-induced increase in blood viscosity. This suggests that use of low-molecular-weight (LMW) dextran may be beneficial for early treatment of frostbite. Although no controlled clinical trial of LMW dextran has been reported, there has been experimental evidence to support its use. Weatherly-White and colleagues190 demonstrated that use of LMW dextran, 1g/kg/day, protected against tissue loss in the rabbit ear model. This led to the suggestion that the use of 1 L of 6% dextran IV on the day of injury, followed by 500 mL on each of 5 successive days, might be of benefit.151 The extent of tissue necrosis was also found to be significantly less than in controls when hemodilution with dextran was combined with water bath rewarming with our present understanding of the etiology of frostbite and introduction of newer techniques such as t-PA, there appear to be fewer instances when LMW dextran may be used and have a demonstrable benefit.
ENDOVASCULAR INTERVENTIONS Thrombolysis With Tissue Plasminogen Activator Treatment of embolic and thrombotic peripheral vascular disease has changed radically over the last 10 years. In 1963, Fogarty and co-workers43 reported treating acute occlusion of a peripheral vessel by a remote embolectomy catheter technique. The artery is surgically opened distant to the site of the embolus. A deflated catheter balloon is passed from the proximal artery beyond the embolus, the balloon is then inflated, and the catheter withdrawn, removing the embolus. More recently, catheterdirected thrombolysis has been used to clear distal arteries and the microvasculature using a thrombolytic agent such as t-PA. Found in vascular endothelial cells, t-PA has fibrinolytic action and plays an important role in the dynamic balance between clot formation and lysis. Plasminogen and t-PA bind to the fibrin surface of the thrombus, resulting in production of plasmin and subsequent dissolution of the thrombus. t-PA has been used extensively in coronary, cerebrovascular, and peripheral arterial disease.131 A small retrospective study reported successful use of catheterdirected intra-arterial t-PA to reduce amputation rates in frostbite.17 Among the six patients who received t-PA within 24 hours of injury, 6 of 59 (10%) affected fingers or toes were amputated, compared with 97 of 234 (41%) among those who did not receive t-PA. It was postulated that rapid clearance of the microvasculature improves tissue salvage. The protocol in this study employed a 2- to 4-mg bolus of t-PA after the catheter was secured and total maximum dose of 1 mg/hr run continuously while simultaneous heparin was given at 500 units/hr through the access sheath and continued for 72 to 96 hours. When there was evidence of digital flow by angiography, t-PA was discontinued. The clinicians noted that there was limited benefit for administration of t-PA when treatment was started more than 24 hours after the initial injury. Twomey and associates176 reported another series using 0.15 mg/kg IV t-PA bolus, followed by 0.15 mg/kg/hr infusion over the next 6 hours to a total dose of 100 mg. Heparin was started after completion of the t-PA infusion, and the partial thromboplastin time was adjusted to two times that of normal control. Coumarin was initiated 3 to 5 days after t-PA and continued for 4 weeks in this study, which found decreased amputation rates similar to those in the study by Bruen and colleagues.17 Successful use of the combination of intra-arterial t-PA and vasodilators infused coaxially has recently been described.36 After proper rewarming, the patient undergoes an arteriogram to assess perfusion and document vascular flow cutoff if present. Clinicians describe a response rate of approximately 80% if treatment can be started early.
Current Strategy for Imaging and Thrombolysis in the Acute Phase of Frostbite It is important to realize that the role of thrombolytic therapy in the treatment of frostbite is evolving rapidly. The aim of t-PA treatment is to attempt to clear the microvascular thrombosis. However, there are both risks and benefits to t-PA therapy, and an appropriate balance needs to be struck. The Patient t-PA should be considered for patients with a “significant” deep frostbite injury presenting to an appropriately equipped unit within 24 hours of the injury. A significant frostbite injury will vary from individual to individual, dominant versus nondominant hand, occupation, hands versus feet, and existing comorbidities. The injury will usually extend proximal to the proximal interphalangeal joints. Experienced clinicians familiar with the techniques need to evaluate each injury to determine whether intervention with t-PA is justified. Tissue Plasminogen Activator in the Field If a frostbite patient is being cared for in a remote area, transfer to a facility with t-PA administration and monitoring capabilities should be considered if the injury has occurred recently and the patient will arrive in the specialist unit within the first 24 hours of the injury. Use of t-PA in the field setting is currently not recommended because it may not be possible to detect and treat bleeding complications. The Hospital Unit The hospital unit needs intensive care monitoring capabilities and the hospital should be familiar with intra-arterial angiography and t-PA. A review of absolute and relative contraindications of t-PA should be undertaken. The Massachusetts General Hospital group has proposed a screening and treatment tool for thrombolytic management of frostbite, including a protocol165 (Table 8-5). Choice of Imaging in the Patient Presenting Within 24 Hours of Injury Angiography or 99mTc scanning should be used to evaluate the initial injury and monitor progress after t-PA per local protocol and resources. Angiography is an invasive procedure but allows both diagnostic and therapeutic measures to be carried out, unlike 99mTc scanning, which is only diagnostic. Logical practice TABLE 8-5 A Proposed Screening and Treatment
Tool for the Use of Thrombolysis in Cases of Frostbite
Treatment Screen (Four “Yes” Answers Required to Proceed to Angiography) Are the patient’s gas exchange and hemodynamics stable? Is flow absent after rewarming (no capillary refill or Doppler signals)? Was the cold-exposure time less than 24 hr? Is the warm-ischemia time less than 24 hr? Treatment Protocol Perform angiography with intra-arterial vasodilators If there is still no flow after angiography with vasodilators, infuse tissue plasminogen activator (t-PA) with systemic heparinization, with priority to the hands—other sites receive a systemic dose Repeat angiography every 24 hr Indications for Stopping the Infusion of t-PA When restored flow has been confirmed by angiography or clinical examination If a major bleeding complication occurs After 72 hr of treatment Postlysis Anticoagulation One month of subcutaneous low-molecular-weight heparin at a prophylactic dose From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.
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CHAPTER 8 Frostbite
BLOOD VISCOSITY
PART 2 COLD AND HEAT
dictates that angiography be used to monitor intra-arterial t-PA and 99mTc scanning used to monitor IV administration of t-PA. There is no evidence to demonstrate superiority of one imaging modality over the other.
A series of case reports suggests significant beneficial effects from HBO.5,44,127,185,187 The role of HBO in frostbite therapy warrants further investigation because it is a relatively safe and inexpensive treatment.188
Choice of Imaging in the Patient Presenting After 24 Hours of Injury In patients with delayed presentation (greater than 24 hours from the time of injury), 99mTc25-27 or MRA8 can be used to predict at an ultraearly stage the likely levels of tissue viability/amputation where t-PA is not being considered.
Epidural Spinal Cord Stimulation An anecdotal case series that described epidural spinal cord stimulation versus conventional treatment reported good therapeutic effects in four young patients with frostbite of the lower limbs. The authors state the mechanism of action is unknown but the treatment is reported to have resulted in rapid recovery, reduced pain, and more peripheral level of amputation.3
Papaverine Papaverine is a powerful topical and intravascular vasodilator that is used clinically as a smooth muscle relaxant in microvascular surgery and has been used to treat cerebral vasospasm.78 The exact mechanism of action remains to be determined, but it appears that inhibition of the enzyme phosphodiesterase, thus causing elevation of intracellular cyclic adenosine monophosphate levels, may be key. This might improve outcomes in early frostbite. When used in conjunction with intra-arterial t-PA in older patients, papaverine appears to cause a less pronounced drop in systemic blood pressure than does intra-arterial nitroglycerin in older adults.35
ADJUNCTIVE TREATMENTS Sympathectomy Cutaneous vessels are controlled by sympathetic adrenergic vasoconstrictor fibers, and vascular smooth muscles have both α- and β-receptors. Because vasodilation of the extremities is passive, maximal reflex vasodilation occurs after sympathectomy. The role of sympathectomy, either surgical (open or minimally invasive) or chemical, has yielded mixed results. Early sympathectomy, performed within the first few hours of injury, increases edema formation and leads to increased tissue destruction. However, if performed 24 to 48 hours after thawing, it is believed to hasten resolution of edema and decrease tissue loss.173 Sympathectomy may have a role in preventing some long-term sequelae of frostbite, such as pain (often caused by vasospasm), paresthesias, and hyperhidrosis.173 In a study of 66 persons with frostbite, 15 patients with acute, bilaterally equal severe injuries were treated with immediate intra-arterial reserpine in one limb and ipsilateral surgical sympathectomy. Efficacy of therapy was assessed by comparison of the sympathectomized limb with the contralateral untreated limb. There was no conservation of tissue, resolution of edema, pain reduction, or improved function in sympathectomized limbs compared with those treated with intra-arterial reserpine. One patient demarcated more rapidly, and one other patient appeared to be protected from recurrent injury. Sympathectomy was not effective therapy for acute frostbite, even when achieved early with intraarterial reserpine. Late protection against subsequent cold injury appears to be the only benefit of surgical sympathectomy for frostbite.14 Because surgical sympathectomy is irreversible, great caution should be exercised when considering its use, particularly with the advent of alternative IV vasodilators. Many would argue there is now no role for its use in the early management of frostbite. Hyperbaric Oxygen Evaluating the effectiveness of use of hyperbaric oxygen (HBO) in the management of frostbite is difficult. Several animal studies have demonstrated it to be of no benefit,125 yet two recent studies in humans have yielded excellent results.41,185 Although the proposed mechanisms of action are multiple, the major changes are postulated to occur in the microcirculation. HBO reportedly increases erythrocyte flexibility and decreases edema formation in postischemic tissues, and it is bacteriostatic. Such actions may counteract the vascular congestion, platelet aggregation, and infiltration of leukocytes seen in the microcirculation of frostbite patients. Finderle and Canker41 report successful HBO treatment of a patient at 2.5 atm for 90 minutes daily for 28 sessions in a multiplace chamber, without significant tissue loss; this treatment started 12 days after injury. HBO may also act as an antioxidant. 196
Surgical Treatment The conventional teaching is that early surgical intervention has no role in the acute care of frostbite. However, early surgical intervention in the form of fasciotomy is required for compartment syndrome in the immediate post-thaw scenario (secondary to a reperfusion injury) or for ischemia from a constricting eschar or subeschar infection.53 Decompressing escharotomy incisions are rarely necessary to increase distal circulation. If such escharotomies are necessary to decompress digits and facilitate joint motion, incisions along the transaxial line have been suggested as being the most appropriate.111 However, many plastic and vascular surgeons would consider using transaxial with axial incisions on the trunk and axial fasciotomy type of incisions in the limbs (Figure 8-23). It is important that incisions avoid injury to the underlying structures. Occasionally, early amputation is indicated if liquefaction, moist gangrene, or overwhelming infection and sepsis develop.1 There is rarely any urgency to intervene, and so amputation should be undertaken by a surgeon with appropriate experience, usually 4 to 8 weeks after the injury. In the vast majority of cases, it is a failure to delay surgery that is the major source of avoidable morbidity. The functional end result of any surgery needs to be considered. Ideally, when major limb loss is foreseen, early involvement of a multidisciplinary rehabilitation team will result in better long-term function.72 A conservative approach was reported as being successful in what must be one of the largest number of cases (847) of frostbite dealt with simultaneously (2-week period) during the IndoPakistan conflict in 1971.6 A combination of LMW dextran, an antiinflammatory agent (oxyphenbutazone), and a vasodilator (isoxsuprine hydrochloride) was used for the third- and fourthdegree injuries, improving limb salvage in comparison with historical controls. Surgical intervention is normally reserved for late treatment of frostbite. This is most often necessary if frostbite is very severe or if treatment has been delayed. Aggressive therapeutic measures can often prevent or reduce progressive injury and
FIGURE 8-23 Axial fasciotomies on the dorsum of the left hand. (Courtesy Christopher H.E. Imray, MD.)
TELEMEDICINE
FIGURE 8-24 Bilateral below-knee amputation for frostbite in a homeless patient. (Courtesy Christopher H.E. Imray, MD.)
gangrene. If gangrene ensues, amputation or debridement with resurfacing may be necessary (Figure 8-24). Surgery should be accomplished only after the area is well demarcated, which generally requires 4 to 8 weeks. Historically, aggressive early debridement and attempted salvage have been thought to jeopardize recovering tissue and add to tissue loss. Gottlieb and associates54 and Greenwald and colleagues58 have taken a much more aggressive approach to coverage of severe frostbite injury. Using 99mTc phosphate bone scans, they identify nonperfused tissue by 10 days after injury and surgically remove necrotic tissue. The remaining nonvascularized and nonviable, yet non-necrotic and noninfected, tissue is salvaged by early coverage with well-vascularized tissue. Theoretically, if nonvascularized tissue has not undergone autolysis and is not infected, it should behave like a composite graft. Preliminary reports are promising, because with better imaging, more accurate prediction of viable tissue is possible. Anecdotal reports suggest that there may be increased risk for infection when complex reconstructions are undertaken at an early stage.70
AMPUTATION Surgery should usually be delayed unless there is evidence of overwhelming sepsis.1 Because there is rarely a rush, a suitably experienced multidisciplinary surgical team familiar with performing a range of amputations should undertake the procedure(s). Careful preoperative planning involving the relevant medical, surgical, physiotherapy, and occupational therapy teams should take place.69,72 The level and type of tissue excised during the amputation will be determined by the specific injury or injuries. Vascular surgeons are usually the most experienced in lower limb minor and major amputations, resulting from their experience with diabetic feet. Plastic or hand surgeons usually have the most upper limb experience; however, these skill bases vary from hospital to hospital.
Recently, increased use of the Internet to access expert advice has been driven by patients and clinicians with more limited experience in treatment of frostbite, permitting a virtual opinion from anywhere in the world.71 The United Kingdom–based service can be accessed via the Diploma in Mountain Medicine or the British Mountaineering Council website: http://www. thebmc.co.uk/Category.aspx?category=19. The service is run by diploma faculty members and being increasingly used by climbers and physicians worldwide, often to obtain a second opinion or to seek specialized advice. It is also possible to follow up patients in a “virtual clinic,” reviewing recent digital images and discussing management options by phone or via e-mail69 (see Figures 8-18 to 8-21). Digital images have been used to assess wound healing in conjunction with HBO therapy.44
Long-Term Sequelae of Frostbite Until 1957, little was recorded about the long-term sequelae of frostbite injuries. Blair and colleagues11 studied 100 veterans of the Korean conflict 4 years after their injuries. In order of decreasing frequency, the victims reported excessive sweating, pain, coldness, numbness, abnormal skin color, and joint stiffness. The investigators noted frequent asymptomatic abnormalities of the nails, including ridges and inward curving of the edges. In general, the degree of long-term disability was related to the severity of the original injury. Symptoms were worse in cold than in warm weather. This is attributed to the fact that vessels do not react as well to stress.163 Previously injured blood vessels do not constrict when exposed to cold as effectively as do normal vessels, and they do not dilate as effectively when vasoconstriction is blocked. Hyperhidrosis is probably both a cause and result of frostbite. Hyperhidrosis suggests the presence of an abnormal sympathetic nervous response induced by cold injury and is abolished by sympathetic denervation. Sensitivity to cold and predisposition to recurrent cold injury should suggest hyperhidrosis. Blanching and pain on subsequent cold exposure may be a nuisance or may be dramatic enough to suggest a diagnosis of Raynaud’s phenomenon (see Figure 8-12). Almost without exception, after sympathetic interruption, a painful, shiny, cyanotic, and sweaty limb becomes warm, dry, and useful.161,162 Schoning160 examined the changes in the sweat glands of Hanford miniature swine after experimental frostbite injury to determine the etiology of hyperhidrosis. She noted that severe sweat gland changes were of two types: degeneration with necrosis and squamous metaplasia. Clearly, if hypohidrosis was a sequel to frostbite injury, morphologically normal and active sweat glands would be an expected 197
CHAPTER 8 Frostbite
Following amputation, primary skin cover is usually preferred. The temptation to preserve bone length by accepting closure by secondary intention or skin grafting needs to be balanced against the problems associated with a dysfunctional neuropathic weight-bearing stump. Split grafts grafted directly onto bone tend to ulcerate as a result of shear forces on insensate grafted skin as soon as the patient mobilizes and becomes weight bearing, and a delayed revision then becomes necessary. Inappropriate attempts at preserving long bone length also restricts use of modern “intelligent” prosthetic limbs; preoperative consultation with the rehabilitation/prosthetic team is strongly advised. The patellar tendon–bearing orthosis technique was originally designed to support body weight for treatment of the below-knee segment that is structurally inadequate or causes severe pain.154,174 The technique allows unloading of the leg at the below-knee level while retaining full knee movement. It is beneficial in treatment of plantar neuropathic ulcers of the feet, allowing the patient to mobilize while minimizing further damage from vertical and horizontal shear forces. Using this approach, with early bedside interventions as part of an integrated approach (including aggressive vascular/endovascular surgery), the major lower limb amputation rate and length of stay have both been significantly reduced.79
PART 2 COLD AND HEAT
finding. One can conclude that hyperhidrosis lacks histologic documentation. A beneficial effect of open cervicothoracic sympathectomy for postfrostbite sequelae in 48 patients has been described.80 The minimally invasive endoscopic transthoracic sympathectomy approach reduces surgical trauma, allows more rapid recovery (Figure 8-25), and may have a limited role in late persisting palmar hyperhidrosis. Iontophoresis may be of benefit in plantar hyperhidrosis. The late abnormalities of change in skin color, including depigmentation of dark skin and an appearance resembling erythrocyanosis in light skin, are most likely the result of ischemia.11 Similarly, the nail abnormality is comparable with that seen with ischemia. Usually, neither of these sequelae requires treatment. Late symptoms of joint stiffness and pain on motion are relatively common and are undoubtedly related to the underlying scars and mechanical problems occasioned by the variety of amputations. “Punched-out” defects in subchondral bone of involved limbs have been noted. These localized areas of bone resorption generally appear within 5 to 10 months after injury and may heal spontaneously. Vascular occlusion is the probable cause of these lesions. Such bone involvement in close proximity to joint surfaces may help to explain joint symptoms. The effects of frostbite on premature closure of epiphyses in the growing hand have recently been reemphasized.191 Extent of premature closure has been correlated with severity of frostbite and noted in partial-thickness injuries. In the digits, premature closure is more frequent from a distal to proximal direction (distal interphalangeal greater than proximal interphalangeal greater than metacarpophalangeal). The thumb has been less often involved. In only 2% of cases does partial epiphyseal closure cause angular deformity. Cold-induced neuropathy may play an important role in the long-term sequelae of cold sensitivity after local cold injury. An alteration in somatosensory function was found that was more pronounced in lower limb injuries.4 Changes in nerve conduction
velocity measurements may provide objective findings in coldinjured patients and in those with few or no conspicuous clinical signs. Tissue that has recovered from frostbite is more susceptible to further injury. This needs to be recognized when advising individuals about a return to environments where they may be at risk. Preventive measures remain the mainstay of primary and secondary treatment.69 Malignant transformation of old frostbite scars is a rare but well-recognized condition with reports dating back to 1930.175 They are sometimes described as Marjolin’s ulcer,180 but more usually as squamous carcinomas.39 One of the largest series of patients found that the tumors tended to be low grade and unlikely to metastasize; the physicians advocated surgical excision.153
Prediction of Individuals at Risk Recent experimental techniques have been studied to predict which individuals are susceptible to frostbite injury. Predicting those at risk would be helpful to assess risk for people planning to work or travel to high altitude or into extreme cold and may be particularly valuable to military recruiting and planning. It would also be particularly helpful when trying to advise those who have sustained a previous cold injury. RIF finger skin temperature response, determined in a simple laboratory test, may be related to the risk for cold injuries during operations in the field.29 The reproducibility of the time course of CIVD suggests this methodology may be of value for further studies examining the mechanism of the response.126 Kamikomaki77 proposed that a case of frostbite in a climber with ACE DD allele was caused by genetic propensity for vasoconstriction. Perhaps we will see the evolution of testing for genetic predisposition to frostbite as a screening tool in the future. Thermography is an easy, noninvasive method for monitoring thermal changes after experimental frostbite, but its clinical value is as yet unresolved.37,75,158 Laser Doppler techniques have been used to assess efficacy of HBO treatment of frostbite. The number of visible nutritive capillaries in frostbitten areas was shown to increase.41
Prevention
A
In 1950, Herzog67 and Lachenal made a successful lightweight bid without oxygen for the summit of Annapurna, the first 8000-m (26,247-foot) peak to be climbed. Herzog lost his gloves near the summit, and the summit team spent a night out in a crevasse. Both climbers suffered severe frostbite to their hands and feet. In a heroic retreat, Dr. Jacques Oudot first gave intra-arterial vasodilators and then performed field amputations without anesthetic. Eleven of the 210 deaths on Mt Everest between 1921 and 2006 were attributable to hypothermia,42 and a significant proportion of climbers attempting to climb to extreme altitude develop frostbite,47 suggesting that climbing above 8000 m (26,247 feet) carries significant risk for permanent cold injury (see Figure 8-7, online).
STRATEGY TO PREVENT FROSTBITE
B FIGURE 8-25 A, One of the two 3-mm thoracoscopic port insertions into the axilla for a right endoscopic transthoracic sympathectomy (ETS) performed under general anesthesia; B, view of right sympathetic chain during ETS. (Courtesy Christopher H.E. Imray, MD.)
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Prevention of frostbite is the key to safe and successful travel and work in cold environments. General prevention strategies are summarized in Box 8-3. Sound preparticipation education, selection of proper clothing, optimal nutrition, and hydration are all keys to a good outcome. Washburn’s recommendations,189 originally published in 1962, remain as relevant as ever: • Dress to maintain general body warmth. In cold, windy weather, the face, head, and neck must be protected, because enormous amounts of body heat can be lost through these parts. • Eat plenty of appetizing food to produce maximal output of body heat. Diet in cold weather at low altitude should tend toward fats, with carbohydrates intermediate and proteins least important. As altitude increases above 3048 m (10,000 feet), carbohydrates become most important and proteins remain least. • Do not climb under extreme weather conditions, particularly at high altitudes on exposed terrain, or get too early
Good experience is the base of core survival skills • Wear protective clothing—layers, loose, heat insulating • Avoid constriction of body parts with clothing • Stay dry • Wear wind protection • Hands: • Wear mittens instead of gloves • Use chemical hand warmers • Feet: • Avoid tight-fitting boots • Wear suitably warm boots such as triple-layer extremealtitude boots • Use electric-heated insoles • Ensure adequate nutrition • Maintain hydration • Take aspirin (if not contraindicated) • Use supplemental oxygen at extreme altitude
a start in cold weather. The configuration of a mountain can help the climber find maximal shelter and solar warmth. • Avoid tight, snug-fitting clothing, particularly on the hands and feet. Socks and boots should fit closely, with no points of tightness or pressure. In putting on socks and boots, a person should carefully eliminate all wrinkles in socks. Old matted insoles are to be avoided. • Avoid perspiration under conditions of extreme cold; wear adequately ventilated clothing. If perspiring, remove some clothing or slow down. • Keep the feet and hands dry. Even with vapor-barrier boots, socks must not become too wet. All types of boots must be worn with great care during periods of inactivity, especially after exercise has resulted in damp socks or insoles. Wet socks in any type of boot soften the feet and make the skin more tender, greatly lowering resistance to cold and simultaneously increasing the danger of other foot injuries, such as blistering. Extra socks and insoles should always be carried. Light, smooth, dry, and clean socks should be worn next to the skin, followed by one or two heavier outer pairs. • Wear mittens instead of gloves in extreme cold, although gloves can be worn for short intervals when great manual dexterity is required for specialized work such as photography or surveying. In these situations, a mitten should be worn on one hand and a glove temporarily on the other. If bare-finger dexterity is required, silk or rayon gloves should be worn, or metal parts that must be touched frequently should be covered with adhesive tape. Occasionally, the thumbs should be pulled into the fists and held in the palms of the mittens to regain the warmth of the entire hand. • Be careful while loading cameras, taking pictures, or handling stoves and fuel. The freezing point of gasoline (−57° C [−70.6° F]) and its rapid rate of evaporation make it very dangerous. Metal objects should never be touched with bare hands in extreme cold, or in moderate cold if the hands are moist. • Mitten shells and gloves worn in extreme cold should be made of soft, flexible, dry-tanned deerskin, or moose, elk, or caribou hide. Horsehide is less favorable because it dries stiffly after wetting. Removable mitten inserts or glove linings should be of soft wool. • Mittens should be tied together on a string hung around the neck or tied to the ends of parka sleeves. Oiled or greased leather gloves, boots, or clothing should never be used in cold weather operations. • Keep toenails and fingernails trimmed. • Hands, face, and feet should not be washed too thoroughly or too frequently under rough weather conditions. Tough, weather-beaten face and hands resist frostbite most effectively.
• Wind and high altitude should always be approached with respect. They can produce dramatic results when combined with cold. Exercise should not be too strenuous in extreme cold, particularly at high altitude, where undue exertion results in panting or very deep breathing. Cold inspired air will chill the whole body and under extreme conditions may damage lung tissue and cause internal hemorrhage. • When a person becomes thoroughly chilled, it takes several hours of warmth and rest to return to normal, regardless of superficial feelings of comfort. A person recovering from an emergency cold situation should not venture out into extreme cold too soon. • Avoid tobacco or alcohol at high altitudes and under conditions of frostbite danger. • A person who is frostbitten or otherwise injured in the field must remain calm. Panic or fear results in perspiration, which evaporates and causes further chilling. • Tetanus immunity should be current.
CHEMICAL OR OTHER WARMERS The well-equipped sojourner at extreme altitude or in cold environs should have a wide selection of gloves and mittens, including spares (Figure 8-26, online). In addition to protective clothing and insulation, external heat sources are advisable. A recent paper by Sands and co-workers157 assessed the efficacy of commercially available disposable chemical hand and foot warmers. They found that there were variations between the devices, but a strong relationship between the mass of the devices and the duration of their heat production. Although concern has been expressed as to whether the chemical hand warmers (Figure 8-27, online) function at the low levels of oxygen found at extreme altitude, anecdotally they function well.70 Electric foot warmers are probably more useful in extreme cold and high altitude (Figure 8-28) than are chemical foot warmers, where removing boots to insert warmers may be not only impractical, but unwise. New lithium batteries opened for summit day are probably superior to rechargeable units. Chemical warmers also occupy a significant volume, resulting in pressure points that can either overheat and burn or lead to blistering.70
Potential Future Developments PREVENTIVE STRATEGIES Over the past decade, there has been substantial improvement in available equipment; in part this is caused by increased numbers of climbers attempting 8000-m (26,247-foot) peaks. Consequently there is considerable financial incentive for developing state-of-the-art equipment. Current 8000-m boots are rated down to −50° to −60°C (−58° to −76° F) (see Figure 8-28). As new technologies, such as “intelligent fabrics” or temperatureresponsive fibers, are developed, numerous outdoor applications are likely to occur. Newer insulating materials have already given rise to significantly better boots, gloves, and mittens (see Figures 8-26 to 8-28). Climbing equipment has also improved. For example, newer step-in crampons greatly reduce the time involved in fitting the crampons and the likelihood of having to adjust them while climbing, both of which substantially reduce the risk for cold exposure.
Possible Future Treatments TRANSCATHETER ARTERIAL THROMBOLYSIS A recent case report study describes successful use of a combination of endoluminal approaches in a patient with frostbite affecting both hands. Upper extremity and hand angiography performed within 16 hours of the frostbite injury demonstrated thrombotic occlusive disease and vasospasm. Bilateral brachial artery catheters were placed and a papaverine infusion initiated, followed by intra-arterial t-PA thrombolysis.155 In a second case report, a 16-year-old boy was treated for hypothermia and concomitant 199
CHAPTER 8 Frostbite
BOX 8-3 Strategies for Prevention of Frostbite
PART 2 COLD AND HEAT
A
B
FIGURE 8-28 Triple-layer, 8000-m mountaineering boots (A) rated to −55° C (−67° F) and electric boot warmers (B) used on a frostbite-free summit day on Mt Everest. (Courtesy Christopher H.E. Imray, MD.)
frostbite of the right foot and both hands.165 The patient was rewarmed and then treated with selective angiography and an intra-arterial vasodilator (nitroglycerin), followed by intra-arterial t-PA thrombolysis, which resulted in salvage of the limbs, but loss of the right great toe (Figures 8-29 to 8-32). “A Proposed Screening and Treatment Tool for the Use of Thrombolysis in Cases of Frostbite” was included in the case report (see Table 8-5).
TIMING OF INTRA-ARTERIAL THROMBOLYSIS FOR FROSTBITE Current opinion suggests that t-PA for acute frostbite may be beneficial if it can be started within 24 hours of the initial injury. However, there is considerable evidence from both the treatment of acute coronary syndrome21 and treatment of acute stroke82 that there is a variable window of opportunity for successful t-PA treatment. The timing of intervention for frostbite is yet to be
determined, but longer delays are likely to be associated with poor outcomes36 and are more likely to require secondary interventions such as fasciotomies for reperfusion injuries, or subsequent amputations.70
ULTRASOUND-ACCELERATED THROMBOLYSIS In vitro work has shown ultrasound accelerates transport of recombinant t-PA into clots.46 Ultrasound is believed to reversibly loosen fibrin strands and reduce their diameter, exposing more individual strands, increasing thrombus permeability, and exposing more plasminogen receptor sites for binding.15 More rapid and complete thrombolysis has been reported with the use of this technique than with standard catheter-directed thrombolysis. A study has suggested percutaneous ultrasound-accelerated thrombolysis is more effective at clearing clots than is catheterdirected thrombolysis in patients with acute massive pulmonary embolism.97
A A
B
B FIGURE 8-29 Early appearance of hands. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)
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FIGURE 8-30 Initial angiographic images of the hands of the patient in Figure 8-29. After the infusion of vasodilators, diagnostic angiographic images of the hands show relatively preserved perfusion of the thumbs and ring fingers, but abrupt termination of the proper digital arteries of each of the remaining fingers at the midphalangeal level. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)
A FIGURE 8-32 Appearance of right hand of the patient in Figures 8-29 to 8-31 at approximately 30 days. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)
VACUUM-ASSISTED CLOSURE THERAPY
B FIGURE 8-31 Repeat images of the hands of the patient in Figures 8-29 and 8-30 after 24 hours of intra-arterial catheter-directed thrombolytic therapy with tissue plasminogen activator show markedly improved perfusion at all levels. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)
ANTIPLATELET AGENTS There have been significant advances in the understanding, management, and outcomes of patients with acute coronary syndrome via introduction of IV antiplatelet agents, such as glycoprotein IIb/IIIa inhibitors. Inhibiting platelet aggregation is a vital link in optimizing outcome.141 In a pilot study, outcomes in unstable symptomatic carotid patients appeared to be improved using a glycoprotein IIb/IIIa inhibitor.182 There is likely to be a role in frostbite treatment for use of combination oral (aspirin and clopidogrel) and/or IV antiplatelet agents to improve vessel patency after t-PA clearance of thrombus.
TUMOR NECROSIS FACTOR-α There is evidence for the role of tumor necrosis factor-α–induced reactive oxygen species in endothelial dysfunction during reperfusion injury.49 Investigation into the effects of inhibition of phosphodiesterase type 4 and tumor necrosis factor-α on local and remote injuries following ischemia and reperfusion injury has suggested it may be possible to modify the processes.170 This particular approach might offer improved outcome in early frostbite.
Vacuum-assisted closure therapy has been shown to be beneficial in accelerating wound healing in partial diabetic foot amputations.2 This therapy can be used in community and specialty hospitals, and in many tertiary care hospitals it is being administered through specialist tissue viability nurses. There has been a recent anecdotal report of a good outcome with frostbite.139
FROSTBITE THROMBOLYSIS REGISTRY AND THE INTERNET One of the persisting characteristics of frostbite research is the lack of good evidence to support newer treatments. An international frostbite thrombolysis registry would allow pooling of data, accelerating the learning process.
Conclusion Although still potentially a disastrous injury associated with a high morbidity rate, frostbite can now be treated more effectively to ensure tissue loss is minimized and functional outcome maximized. With adequate preventative measures, the risk for frostbite injury can be reduced. Research progress is likely to be slow because injuries tend to be variable and unpredictable and presentation is often significantly delayed, making subjects difficult to standardize for comparison in treatment groups. A good animal model for basic research is lacking, and apart from the military, there is little likelihood of achieving significant funding for research programs.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 9
Polar Medicine BETTY CARLISLE, LESLEY J. OGDEN, IAN DAVIS, AND KENNETH V. ISERSON
Like much of wilderness medicine, polar medicine’s identity derives to a large extent from its setting. Polar, however, can be defined in several different ways. Geographically, the Arctic and Antarctic circles, at latitudes 66 degrees, 33 minutes north and south, delimit areas in which the sun does not rise or set on at least 1 day of the year. A more functional definition is the 10°
isotherm, which joins those areas in which the average temperature in the warmest month of the year is 10° C (50° F); this correlates roughly with the tree line. For medical purposes, the definition of polar is more complex. Although climate and geography are clearly important, the salient features of polar medicine are logistic and experiential. Unlike
For online-only figures, please go to www.expertconsult.com
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PART 2 COLD AND HEAT
high-altitude medicine or hyperbaric medicine, for example, polar medicine is not unified by an underlying pathophysiology. High-altitude medicine is a medical field because of the environment’s effect on the human organism, but polar medicine is largely medical practice within this setting. Medical practice in isolated settings is paradigmatic of wilderness medicine: the patient population is essentially, if not literally, a small demographic island. A provisional definition of polar medicine, then, could be “the practice of medicine in isolated settings within an extreme cold environment.” It is the cold, remoteness, hostility, and unforgiving nature of the environment in which humans struggle to survive, let alone work, that make medicine in polar areas, and in particular Antarctica, so challenging.66
The Distinction Between Arctic and Antarctic Medicine Although the polar regions share the predominant attributes of cold, dark, isolation, and severe weather, they display many important contrasts. The Arctic has been described as a frozen sea nearly surrounded by land, whereas Antarctica is a land and ice mass circumscribed by ocean. The moderating effect of the North Polar waters compared with the elevation (2835 m [9301 feet]) of the South Polar plateau accounts for the roughly 40° C (72° F) differences in wintertime low temperatures. On a plot of temperature versus humidity, the polar plateau is more similar to Mars than to the rest of the earth. The flora and fauna are unique to each area. The Arctic has an abundance of land- and sea-based animals as well as migratory birds and plant life. On the other hand, the Antarctic has no permanent land-based animals, although there are migratory birds, as well as a rich marine life and limited plant life. The differences in population patterns mark an important north–south disjunction in polar studies in general and in polar medicine in particular. The northern polar or frigid areas above 66° latitude comprise a frozen sea that is surrounded by eight countries, each with its unique set of populations and medical care services. The countries of the Arctic are Canada, Finland, Greenland (Denmark), Iceland, Norway, Russia, Sweden, and the United States. Together, they make up approximately 8% of the earth’s surface. Human population is scattered throughout the Arctic, with several relatively large urban areas, but for the most part the Arctic is sparsely populated, totaling less than 1% of the world’s population.124 The overall estimated population of the Arctic as defined by the Antarctic Monitoring and Assessment Programme (AMAP) is approximately 4 million; indigenous peoples make up 10% of that population, and constitute the majority of the total population in Greenland and in sparsely settled areas of northern Alaska and Canada.62,123 Within the Arctic, there are 8 major indigenous peoples and more than 30 minority groups. Some of these peoples have separate governments, languages, and socioeconomic possibilities. There are no indigenous peoples in Antarctica, which is regulated by the Antarctic Treaty, with 12 original and currently a total of 47 signatory countries.4 This complex treaty helps delineate the relationships of the countries that are active in Antarctica and how the continent is to be best preserved and used for peaceful purposes. Seven countries claim territorial rights.4 Of the 79 stations in Antarctica, 39 are operated year-round.22 The total population living in Antarctica, all seasonal, now exceeds 4400 persons in the summer and well over 1100 in the winter.18 In the Arctic, there are two overlapping but distinct spectra of medical problems—those of indigenous Arctic people and those of visitors and immigrants to the polar region. Many of the medical problems among the Inuit, Sami, Chukchi, Nenet, and other northern groups are those of populations making the often Faustian demographic and cultural transition to a Western industrialized society. Thus medical practice among these groups is similar to that among many other displaced indigenous populations. In a sense, the current illnesses and health risks of the indigenous Arctic populations are the results of contamination from distant sources and too much contact with other cultures.14 In contrast, medical problems in Antarctica among the usually 202
young and fit scientific, commercial, tourist, and expedition support personnel are often related to trauma and the environment and thus fall more appropriately under the purview of travel or expedition medicine. Furthermore, tourist cruise ships often bring older adults, whose complex medical problems can create logistic dilemmas. It makes sense to focus not only on the health of elite visitors to these remote areas but also on the health of the local population and the effects caused by visitors.
Importance of Polar Medicine INCREASES IN TOURISM AND EXPEDITIONS The combined geographic polar regions cover about one-sixth of the earth’s surface, and their territory in the imagination has been enlarged by several remarkable expeditions and recent popular magazine articles and books on polar tourism. In the past decade, there has been a veritable explosion of tourist activities in both the Arctic and the Antarctic. Despite or because of the forbidding environment, tourism of various sorts is increasing.77 The Arctic is a trendy destination. An estimated 1.5 million tourists visit the Arctic each year, up from 1 million in the prior decade.122 In 1980, it was estimated that a total of 31,000 paying tourists, adventurers, or guests of national scientific expeditions had ever visited Antarctica, but its increasing lure has led to explosive growth. According to International Association of Antarctica Tour Operators (IAATO) statistics, more than 62,000 tourist, staff, and crew visited Antarctica by air or ship in 2009. Since 1989, tourists have visited approximately 200 sites, including 20 research stations in the Antarctic Peninsula region, the most common site for tourists. About 50 of these sites have received more than 100 visitors in any one season, and about the same number have been visited only once. Most visits are to one of 35 sites. Fewer than 10 sites receive around 10,000 visitors each season. The British Antarctic Survey (BAS) monitors Port Lockroy and maintains an ongoing program on the effects the 10,000 visitors per year have on wildlife and ecology of the area.49 Although the bulk of tourists visit aboard cruise ships, there is an increasing number of overland participants who engage in camping, kayaking, diving, skydiving, mountaineering, Arctic or Antarctic traverses, polar challenges, and adventure tourism.50,77 Concerns about the dramatic increase in tourism and its effect on the ecosystem have led to a movement to limit the total number of tourist visits per year. The World Wildlife Fund and the United Nations have proposed guidelines to developing ecofriendly tourism in the Arctic. The guidelines cover its impact on the environment as well as on local populations. In April 2009 the consultative countries of the Antarctic Treaty endorsed a proposal to limit the size of cruise ships and the number of tourists who can go ashore at any one time and to eventually make it binding to all parties.122 This increasing number of visitors and expeditioners has created interest in polar medicine, in particular as it relates to land-based and extreme expeditions. Wilderness medicine courses specific to polar medicine are now offered. Tourist vessels generally carry a physician and sometimes a nurse. Although facilities vary in level of care, all have preparations for the most frequently encountered medical problems. Most illnesses are upper respiratory infections, gastrointestinal (GI) problems, motion sickness, and mild bruises or strains. As might be expected given the ages of many visitors, an occasional cardiac event or serious fracture occurs. The occasional expeditioner who needs rescue or assistance from a scientific station uses scarce resources.23,77 One peculiar phenomenon is that when patients and medical/rescue/evacuation resources are from different countries, a complex flurry of high-level diplomatic interchange must often occur before help can be rendered. Perhaps the most notable tourist fatalities were associated with the ill-fated skydiving venture at the South Pole, which resulted in the death of three of the four participants,45 and the Air New Zealand flight that crashed into Mt Erebus with the death of all 257 people aboard.83 Hazards are inherent in any expedition and may well be the attraction for some participants. To be allowed to participate in risky activities, some tourists may fail to declare serious medical
GEOPOLITICAL CONCERNS The interests of governments in polar regions have not lagged behind those of tourists. Political and territorial concerns have been important in both polar regions. With increasing exploration of mineral and oil reserves and fishing potential, migrating humans will continue to bring medical problems with them. Although the Antarctic Treaty of 1959 prohibits territorial or commercial claims, seven nations have made sectoral claims on the continent. Some of these claims overlap and in the future may lead to a less-thanpeaceful resolution. Yet in early 2010, Australia failed to legally pursue Japan for ramming and sinking an antiwhaling boat in Antarctic waters supposedly governed by Australia. The most common reason given was that Australia feared that the International Court of Justice would nullify all territorial claims to and national governance over parts of the continent. Concern about the environmental impact of increasing human activity in polar regions seems to be tempering the pace of development, but as national resources diminish, the Antarctic may come under increasing pressure to open up to extraction, similar to the situation in the Arctic.
INCREASES IN RESEARCH ACTIVITIES Scientific research has been a part of polar exploration throughout this century. There are scientific and medical journals devoted to the polar regions, and thousands of articles are indexed each year in the Antarctic Bibliography (http://www.coldregions.org/ antinfo.htm). The International Journal of Circumpolar Health (http://ijch.fi/Issues.htm) is a richer source for health issues in polar regions. Antarctic research continues to expand. All the continent’s permanent stations are primarily there to support research. The biggest study is the IceCube project at the South Pole station, which uses a series of downward-looking detectors spread over a square kilometer to look for traces of the notoriously elusive neutrinos, invisible particles churned out by nuclear reactions. The detectors seek particles that have already passed through the earth. The South Pole also hosts two large telescopes. Another huge project involving multiple countries is ice core drilling, designed to catalog climate changes of tens of thousands of years. Other scientific endeavors include marine biology and ocean dynamics research; atmospheric and climatologic research, including air cleanliness monitoring and ice sheet movements; medical research (primarily at Japanese and Chinese stations)80; biologic research (ecosystems, penguins, seals, bacteria, lichen); seismic monitoring; aerial and sea floor mapping with unmanned vehicles in the harsh environment; paleontology; meteorite searches; and demonstrations of alternative power in extreme circumstances (e.g., wind generators at New Zealand’s Scott Base). Some observers have discerned a north–south split, perceiving research in Antarctica as having more of a political motivation and that in the Arctic as being more practical. For both scientific and political reasons, an important part of scientific research in polar regions concerns environmental issues. The remoteness of these regions enhances their value as benchmarks for studies of pollution. Indeed, several worrisome facts have been revealed about the contamination of formerly pristine wilderness, such as
widespread radioactive contamination, the prolonged effective half-life of radioactive fallout deposits,115,125 and increased chemical contamination, particularly in animals high on the food chain, with persistent organic compounds, heavy metals, and other contaminants affecting the environment and food supply.68,125 Widening of the ozone hole carries implications of increased ultraviolet (UV) radiation. As occupational and environmental health issues draw more attention, this aspect of polar medicine assumes greater importance.27,28
Brief History of Human Habitation in Polar Regions A perspective on the contrasts between Arctic and Antarctic medicine may be sharpened by a brief summary of human habitation in polar areas. Humans are known to have inhabited Arctic regions for at least 4500 years. Anthropologists have uncovered evidence for several waves of population migration from Siberia through northern Canada to Greenland. Each of these migrations was probably linked to climatic conditions, and each resulted in a distinct set of cultures. The general pattern was of a nomadic life with population densities of approximately one person per 400 km2 (154.4 square miles).52,118 In more recent times, this longestablished and remarkable adaptation to a hostile environment has been disturbed. The pace of cultural change increased dramatically during the second half of the 19th century, when the whaling industry moved into Hudson Bay, leading to sustained contact between Europeans and the Inuit. In the early part of the 20th century, religious missions, trading company posts, government stations, church missions, and eventually medical clinics and schools began to encourage permanent settlements, roughly quadrupling the population density.52 In some areas, such as Eurasia, large industrial and mining cities arose. This change in population distribution has at times led to conflict between indigenous and European cultures, and it has had significant environmental and medical consequences.126 The known history of human exploration of Antarctica, unlike that of the Arctic, is quite recent. Recorded sightings of the continent date only to around 1800, and “winter-over” sojourns did not occur for another century. Waves of settlement can also be observed to have occurred in Antarctica; there was sealing in the early 19th century and whaling in the early 20th, and there has been scientific exploration since the mid-20th century.118 The heroic era of Antarctic exploration occupied the early years of the 20th century, with exploits such as the highly publicized race for the South Pole between Roald Amundsen and Robert Scott in 1911, the extraordinary survival of the crew of the 1914 Endurance expedition, led by Ernest Shackleton,61 and the heroic survival of Douglas Mawson, an Australian geologist who wintered alone after his other expedition members perished.72 Perhaps because of these and other dramatic events, and perhaps because of the absence of an indigenous population and a scarcity of easily exploited resources, human activities in the Antarctic have retained a somewhat more expeditionary flavor than in the Arctic. This has helped shape the contrasts in medical practice between the northern and southern polar regions.
Arctic Medical Problems EFFECTS OF CULTURAL AND DEMOGRAPHIC TRANSITION The Arctic is not a homogeneous region. Although the population is only approximately 4 million, it is very diverse, with few features in common except the latitude of residence and hours of daylight. Medical problems among indigenous populations in the Arctic, approximately 10% of the total population, are characteristic of displaced aboriginal people elsewhere in the world. There is a wide range of interrelated factors, including demographics; the social, economic, and physical environments; personal health practices; and availability of good-quality and culturally appropriate health care services.12,53 Although increased contact with industrialized cultures has brought benefits, it has also brought many problems. Some of the benefits include 203
CHAPTER 9 Polar Medicine
problems that later precipitate emergency medical evacuation. Thus one real concern is increased risk taking and the consequences thereof, or the dilemma between what is reasonable and what is foolhardy. From a medical perspective, making a risk assessment is multifactorial and differs for people, places, and goals. Hazards of an evacuation need to be assessed for both the patient and rescuers. Setting guidelines and anticipating needs in pre-event preparation are the keys to successful evacuation.46 Because of the occasional tourist in need of expeditious medical evacuation, IAATO and other governmental groups have suggested requiring insurance to defray the costs associated with these evacuations. There is also discussion of the ethical versus medicolegal implications of whether to render aid. The overriding issue should be care of the patient. Polar Challenges and expeditions are discussed later (see Medical Aspects of Arctic Racing).
PART 2 COLD AND HEAT
greatly improved life expectancy, largely due to a decrease in morbidity and mortality from infectious diseases and diseases of childhood (prevented by vaccines). Nevertheless, in indigenous Arctic peoples of the United States, Canada, and Greenland, infant mortality is higher and life expectancy is lower when compared with Arctic dwellers in Nordic countries.98 For many years, health care has lagged behind national norms in the Canadian Arctic, with infant mortality 2 to 3.5 times the national average.113 Age-adjusted death rates are also telling, with 8.4 per 1000 Northern Canadian people, compared with 5.8 per 1000 for the Canadian national average; 14.3 per 1000 in Greenland and up to 29.2 per 1000 in parts of Russia. Other striking statistics reveal a suicide rate in Nunavik six times that of the southern provinces of Canada,60,119 and an unintentional accidental death rate three to four times higher than the national average. Tuberculosis has decreased but is still unacceptably prevalent at 47 versus 7.1 per 100,000 persons. Diabetes mellitus has increased to 5% of the population of 30- to 39-year-olds, compared with 1% in the general Canadian population. In a population in which dental caries were previously almost unknown, the need for restorative dental work is up to 60%. Widely prevalent alcoholism and tobacco use greatly contribute to these problems.10,42,113 As the Arctic environment and indigenous Arctic populations make the cultural and demographic transitions to a Western industrialized way of life, the spectrum of medical problems has shifted. Changing social patterns have resulted in disturbing trends: increasing numbers of young adolescent mothers, rising prevalence of gonorrhea and syphilis among Greenlanders, and concerns about other transmissible diseases, such as viral hepatitis and acquired immunodeficiency syndrome (AIDS).76,130 Changes from the traditional diet and lifestyle have led to increased obesity, diabetes, cardiovascular disease, and mental health problems, including depression, binge drinking, alcoholism, and higher suicide rate.12,113,119
ENVIRONMENTAL AND OCCUPATIONAL HEALTH PROBLEMS Transboundary pollutants, primarily from Eurasia and the North American continent, have made deep and lasting changes.10 The Arctic, once viewed as pristine, is now considered a pollutant sink. Even so, promising new data reflect that strict environ mental control (e.g., bans/restrictions on uses and emissions of persistent organic pollutants [POPs]) is working.123 The nuclear accident at Chernobyl in April 1986 led to cesium-134 and cesium-137 levels in reindeer meat 50 to 100 times those considered safe, forcing destruction of the Sami reindeer herds. During that same time, lake fishing and berry picking were curtailed because of contamination.37,126 Fortunately, research 20 years since this accident demonstrates thriving flora and fauna even in the most contaminated areas, demonstrating a rebounding environment. Nevertheless, the young people exposed to the nuclear accident have shown an impressive increase in thyroid cancers, and those exposed to the highest doses of radiation show an increase in leukemias, solid cancers, and circulatory system diseases.114 Industrial emissions from neighboring regions, including an estimated 100 million tons of sulfur dioxide, have led to the “Arctic haze” phenomenon, a gradual whitening of the historically deep-blue Arctic sky.37 Environmental impacts have had direct health consequences.10,42 During the last 500 years, industrial pollution has led to a sevenfold increase in lead levels in human tissues in the Arctic.37 Another survey found blood mercury levels above the normative limit in over 10% of Sami reindeer herders in northern Finland. In North Greenland, a study revealed that in 84% of human mothers, blood mercury levels were above the World Health Organization provisional limit.39 Oceans, rivers, and lakes reveal contamination and concentration of heavy metals in fish.126 Further contamination of the food chain with long-lasting POPs, including polychlorinated biphenyls (PCBs) and many organic pesticides, is increasingly identified.28,126 Long-term consequences of environmental pollutants on the health of the Arctic dwellers continue to be studied.27,28 Recent work suggests that the endocrine-disrupting effects of PCBs may have changed the normal ratio of male-to-female births from 1.05 to 1.02 in the past 30 204
years.12 It has been documented that the concentrations of PCBs in breast milk are seven times higher in the Arctic than in Quebec.113 As previously noted, fallout from radioactive testing has caused river pollution, and other environmental degradations have affected the food chain, such that it is estimated that an increase in certain cancers has been noted in both animals and humans.132 Fear of the effect of pollutants has caused many to abandon or significantly limit their consumption of traditional foods (e.g., marine mammals, fish, terrestrial mammals, and birds). Unfortunately, this can have negative nutritional effects, such as obesity, diabetes, and increased cardiovascular disease, and in some instances relative malnutrition.38 Tragically, POPs, even in low concentrations, have been shown to cause increased risk for diabetes, so both consumption of traditional foods and changes in diet to processed foods have contributed to the increased rate of diabetes in these regions.123 In some areas, consumption of traditional marine foods has led to blood levels of mercury exceeding current recommendations. Local health departments have to weigh overall nutritional benefits of traditional land and marine food sources against the potential longterm risks of neuropsychological and other potential health problems, particularly in newborns and infants.68 Fortunately, new trends show human exposure to pollutants in the Arctic is decreasing. For example, the number of Arctic childbearing-age women with excessive levels of PCBs, mercury, and lead is decreasing. This is believed to be due to dietary changes and increased awareness of the problem. However, new research is demonstrating many additional chemicals, some newly developed, that have the potential to collect in the Arctic food chain, so ongoing research, identification of these chemicals, and regulation of them are essential to continue improving the health of indigenous peoples.123 Nontoxicologic factors also make important contributions to Arctic morbidity and mortality. Accidents are more prevalent in the Arctic. In younger (up to age 35) Inuit groups, injuries account for approximately one-third of all deaths.15 It is striking that Alaska’s occupational death rate is three to four times that of the U.S. national average deaths per 100,000 workers, but this is markedly improved from five times the national average in the 1990s.85 With establishment of the Alaska surveillance system in 1991, there has been a 50% reduction in work-related deaths, including a significant reduction in commercial fishing deaths and very sharp decline in helicopter logging–related deaths.21 These data reflect in part the inherently hazardous working conditions and occupations and possible demographic biases of a young population. Other factors, however, may play a role. Because aircraft are a predominant mode of transportation in polar regions, it is not surprising that Alaska accounted for greater than one-third of all air crashes in the United States and 20% of the fatalities from 1990 to 2008.84 Nonscheduled or commuter plane (less than 30 seats) flights, commonly used in isolated areas, pose a risk for fatal crash six times that of scheduled airline flights, a figure not surprising given the often extremely challenging flying conditions (terrain, weather, and isolated landing sites with limited navigational aids and operator error). In recent years, the pilot occupational fatality rate has fallen from 298 to 148 per 100,000 (less than twice the rate for all U.S. pilots), felt to be due largely to increased awareness and proactive intervention in the industry.84 Overall, the mortality rate for Alaska natives is 939 per 100,000 per year as compared with the overall U.S. rate of 698.9 per 100,000 per year.123
PSYCHOSOCIAL HEALTH PROBLEMS With social disruption and increased environmental and occupational health risks, psychological problems in the Arctic have achieved greater visibility in recent years. For a variety of reasons, stress seems to be higher in winter. One survey of over 7000 adults living north of the Arctic Circle found a prevalence of midwinter mental distress of 14% in men and 19% in women.40 Most other studies suggest that this figure may be low. One study among Inuit found that 22%, or one in five, experience depression during the winter months, and 7% appeared to have seasonal affective disorder (SAD).36 Cultural stress, erosion of traditional lifestyles, and substance abuse are all contributory
CURRENT AND FUTURE TRENDS In summary, indigenous populations of the Arctic show lower life expectancy, higher rates of infectious diseases, higher infant mortality, and higher rates of injuries and suicides when compared with norms in their respective countries.123 Fortunately, there are encouraging signs related to Arctic health care. The incidence of low birth weight, 5.5% in the central Canadian Arctic, has decreased, although it is still higher than that among non-Arctic dwellers.12 Tuberculosis, which incapacitated up to 20% of the Canadian Inuit by 1950, has largely been brought under control, although the rate of occurrence is still as much as 10 times the national average.15 Trends in environmental and occupational health problems show increased monitoring, intervention, and improvement. Unfortunately, the age-adjusted incidence of diabetes mellitus is dramatically rising among First Nations populations.25 An important development in recent years has been the institution of trauma registries to track and target significant causes of morbidity and mortality. Recent research emphasizes that injury prevention is not solely a function of safer design of equipment but is a complex interplay of environment, activity, and people, notably including personal risk-taking behavior. If current trends continue toward greater economic independence and education of Arctic peoples, such potentially modifiable adverse health behaviors may recede in importance in coming years.58,59
Antarctic Medical Practice Medical practice, problems, and their study in the Antarctic are somewhat different from those in the Arctic. Extreme isolation makes Antarctic medicine unique. Because of the remoteness, it may not be possible to medically evacuate (medevac) a patient for weeks or even months. It might be easier to medevac from the international space station than from some of the more remote Antarctic stations.35 In general, the population is adult and is physically and mentally healthy, although at least the U.S. Antarctic Program grants health waivers to some individuals with certain chronic diseases so that they can visit or work for a limited time. Winter-over personnel, including those spending a year or more at a time in Antarctica, are required to pass medical screening that varies in intensity with the various national programs. Most stations only house adults. There are two exceptions: Chile and Argentina have families living at their principal bases and have even had children born on them. All stations have some form of medical care, usually a station physician. The more temporary camps have varied medical support, ranging from firstaid wilderness responders to paramedics or midlevel providers with limited medical supplies. In general, the permanent yearround bases have more sophisticated facilities, with radiograph, laboratory, surgical, and dental provisions and a reasonably
well-stocked pharmacy for expected emergencies. There is at least one physician and sometimes nurses and ancillary medical personnel.
MEDICAL STATIONS IN ANTARCTICA Medical facilities in the Antarctic polar regions can be conveniently divided into permanent and expeditionary facilities. As a result of community expectations and long-term commitment to research in Antarctica, a notable shift from an expeditionary to an operational attitude has occurred in many of the Antarctic programs. What type of physician is needed? To paraphrase Grant, the physician cannot be too specialized in approach; broad knowledge and a wide range of practical skills are necessary to provide good Antarctic medical care.35 Specialization in emergency medicine or the equivalent seems to be a suitable choice, especially to deal with emergencies. In nearly all bases, there is no room for the luxury of anesthetists and surgeons, dermatologists, and psychiatrists. These roles reside within the same person. However, modern communication, including video teleconferencing (VTC), help the polar physician be less isolated from advice, counsel, and guidance. For a significant proportion of the Antarctic population, it is still extremely difficult and costly to evacuate patients.35 The following is a description of the personnel and facilities in the U.S. Antarctic Program; other nations maintain similar facilities. McMurdo Station (MCM) has the largest population— around 200 in the winter and 1200 in the summer. Whereas the winter MCM and South Pole populations are isolated, their summer populations constantly have an influx of rotating personnel that bring new diseases. In the summer season, the medical component is staffed with two physicians, a physician’s assistant or nurse practitioner, an Air Force flight surgeon, a dentist, a radiograph technician, a laboratory technician, and a physical therapist. In the winter, the staff is composed of one physician, a physician’s assistant, and a physical therapist. All are cross trained on site. (Other large national stations provide necessary additional training in advance.) In addition, MCM has a full fire department with paramedics who respond to emergencies on station. The South Pole population peaks at 250-plus in summers and reaches a nadir of around 50 in the winter. There is one physician, a physician’s assistant or nurse practitioner, and a volunteer trauma team trained on station. Palmer Station is the smallest, with a population of 45 in the summer and a low of 10 to 20 persons in the winter. There is one physician, and volunteers are trained on site to provide assistance. How well these volunteers can function was demonstrated in 2009 when the station’s physician developed a peritonsillar abscess. She had one of the station emergency medical technicians needle drain and then incise it under topical and local anesthesia. She then used VTC and an intraoral camera to consult with an otolaryngologist based in the United States. She improved within a few days.26 The Australian stations have one physician. Before deployment, there is a 2-week training course for two of the crew in operating-theater nursing skills and for two persons in anesthesia assisting. The predeployment training has proved very valuable, as was clearly demonstrated in the case of a scientist who fell into a crevasse and suffered serious injuries, including internal bleeding, that required on-site surgery (Figure 9-1).102 All permanent U.S. medical facilities have digital radiograph and ultrasound capabilities, laboratory equipment for blood chemistries and cardiac enzymes, and the capability to perform immunologic testing for β-hemolytic Streptococcus, infectious mononucleosis, and influenza A, as well as common resuscitative equipment, including Life Pak 12 and Zoll monitor/defibrillators, portable ventilators, and crash carts similar to those in most emergency departments. The pharmacies are well stocked and cover a broad range of potential medical problems. There is no blood storage, but in the event of significant bleeding, a “walking blood bank” (walkin donor system) is activated. To facilitate this process, all winterover and most summer personnel are blood typed and screened for hepatitis B, C, and human immunodeficiency virus (HIV). After a series of acute cholelithiasis cases, South Pole winter-over personnel are now screened with ultrasound for gallbladder 205
CHAPTER 9 Polar Medicine
factors.12 Studies investigating scientific staff at Arctic research stations are relatively uncommon, but they show patterns of sleep disturbances, depression, and alcohol use reminiscent of those in Antarctic stations. The double apparent risk factors of high latitude and displaced indigenous populations have made alcohol abuse and concomitant violence a serious problem in the Arctic. In Greenland, one in three Inuit dies a violent death, and roughly 25,000 adults consume 28 million cans of beer a year, one of the highest per capita consumptions of alcohol in the world. Prevalence of “binge drinking” among Arctic peoples ranges from 12% to 39%, with male rates being greater than female rates. Fetal alcohol syndrome is 13% higher in Alaska than in the continental United States.12 One study compared alcohol consumption by the Greenland Inuit with nonindigenous local inhabitants and found that alcohol consumption was less among the Inuit. However, other studies found the reverse.60 Accidents are the leading cause of death in the Arctic, and one-third of these are estimated to be alcohol related. In the Canadian Arctic, alcohol consumption is one and a half times the national average, and Inuit and Indians between 15 and 24 years of age have a suicide rate up to 11 times the national average. In some communities, for boys and men ages 15 to 29, suicides are the most common form of injury leading to death.60,82
PART 2 COLD AND HEAT
FIGURE 9-2 Historic midwinter rescue at the South Pole. Twin Otter aircraft flown by pilots from Canadian Kenn Borek Air Service.
FIGURE 9-1 Trauma and rescue teams are frequently composed of volunteers and at least one experienced, trained individual. This rescuer is practicing for possible extrication of a victim from a crevasse. (Courtesy Betty Carlisle.)
disease. The Australian physician undergoes prophylactic appendectomy. Otherwise, the experience has been that early antibiotic therapy can abort an acute appendicitis attack, allowing the appendix to be removed electively at a later time. The South Pole does not have 24-hour satellite coverage, but year-round stations have facilities for telemedicine, including live camera, still photos, fax, and digital radiography for transmission and consultation via satellite and the Internet. VTC, used for many years in Antarctica by multiple programs,35 came of age at the South Pole in 2002 with a midwinter repair of a patellar tendon rupture. The tendon was surgically reattached by the base physician under the direction of consultants at major medical centers via live video and voice connection. Various physicians at Antarctic stations are also able to consult with colleagues via VTC, such as with the South Pole medical staff’s successful management of a severely hypotensive tourist in 2009 with VTC input from MCM clinicians. In addition, telemedicine has been used for diagnosis and consultation in the treatment of a wide variety of ailments, including acute cholecystitis, ophthalmologic lesions, pancreatitis, pericarditis, fracture treatment, psychological consultations, radiologic reports, and many other situations. Telemedicine has improved the quality and availability of sophisticated care in these and other remote, hostile environments. Medevacs are frequently dangerous and costly. Summer is the only season during which some stations can be reached for an evacuation. Winter evacuations are infrequent, very dangerous, and costly. Logistically it may be 2 or more weeks before a rescue can take place, and for some stations it may not even be possible. A historic medical evacuation from the South Pole was undertaken in the winter of 2001 with the first successful landing of a twin Otter aircraft in full darkness at a temperature of −68.9° C (−92° F) (Figure 9-2). This event, while fraught with danger, has opened new possibilities and has been repeated.16,19 To further increase the ability to provide medical assistance, even during the winter months, the U.S. Air Force recently proved their capability of landing C-17 aircraft at MCM using night-vision goggles and made successful air drops of critical equipment at the South Pole. Certainly, though, prevention through careful screening of candidates and increased use of telemedicine as a way to avoid medevacs still remains the ultimate goal. To reduce the number of medical crises and need for urgent medical evacuations, all participants must pass a “physical qualification test.” Medical clearance criteria are used as a screening tool. To establish appropriate guidelines, evidence-based criteria from the medical literature, historical data of the Antarctic 206
Program, and guidelines from other programs, such as the National Aeronautics and Space Administration (NASA), the Peace Corps, and the Navy, that have activities in remote areas were used. What appears to be lacking is screening for body mass index and alcoholism. However, up to 30% of all medical evacuations (both emergent and urgent) have been for trauma— that is, they were not related to the evaluation criteria. Of emergent and urgent evacuations, 10% were for GI and 8% for cardiovascular reasons (Figure 9-3). Considering only truly emergent medical evacuations, 28% were for cardiovascular and 28% were for GI reasons (Table 9-1). Figure 9-4, online is a chart showing the number of medevacs from MCM and the South Pole station.
SOMATIC HEALTH PROBLEMS Many of the primarily somatic health problems in Antarctica have to do with cold, altitude, and trauma and are thoroughly covered in the chapters on those topics. In a midwinter setting where a tossed mug of coffee freezes before the liquid hits the ground, the dangers of frostbite are clear. Anyone gasping for breath after climbing the six flights of stairs with 92 steps from the tunnel to the living area of the South Pole’s elevated station, or who has lost 5 kg (11 lb) in the first 2 weeks merely from resting Pregnancy Ophthalmic 1% 0% Vascular Diabetes 3% Pulmonary 1% 4% Neurological 2% Genitourinary 4% Infections 2% Dental 7% Anxiety/ depression 5%
Injuries 42%
Tissue mass/ tumor 6% Cardiovascular 8%
Gastrointestinal 10%
Altitude related 5%
FIGURE 9-3 Evacuations for medical reasons, with percentages of 5-year totals (1998-2003). (From Mahar H [Safety and Health Officer, OPP/NSF]: Medical clearance criteria: Revalidation study. Personal communication, 2003.)
Reason for Evacuation Injury Tissue mass/tumor Cardiovascular Genitourinary Gastrointestinal Altitude related Pulmonary Vascular TOTALS
1998-1999
1999-2000
2000-2001
2001-2002
2002-2003
5 Year Total
Percent of 5-Year Total
1 — — — 1 — — 1 3
1 1 1 — — — — — 3
— — — 1 — — — — 1
— — 1 — 3 — — — 4
1 — 3 — 1 1 1 — 7
3 1 5 1 5 1 1 1 18
17 6 28 6 28 6 6 6 —
From Mahar H (Safety and Health Officer, OPP/NSF): Medical clearance criteria: Revalidation study. Personal communication, 2003.
tachycardia and tachypnea, can appreciate the physiologic stresses of rapid ascent to an equivalent of 3200 m (10,499 feet). Likewise, the dangers of UV exposure at altitude with an ozone hole and snow surface reflectance of 80% to 90% can become painfully evident to the unwary visitor.20,112 Cold-Related Problems Cold is a dominant factor in polar medicine. It can be a source of humor, such as the infamous “300 Degree Club” at the South Pole. Membership requires sprinting, while somewhat less than completely clothed, from a 93.3° C (200° F) sauna to the Pole outside at an ambient temperature of −73.3° C (−100° F) or lower. Similarly, the quintessential polar first-aid story involves creative solutions to the problem of finding warm fluids,2 but it would be reckless to forget the ever-present danger of such a hostile environment. Windchill commonly drops the effective temperature far below −73° C (−100° F). It has been estimated that under the most severe winter conditions, an inactive person in full polar clothing could undergo a life-threatening drop in core temperature in only 20 minutes. Airplane refueling crews and others working with liquids at polar ambient temperatures are constantly reminded that even a small splash can mean instant frostbite.31 Rescue and treatment are complicated by the additional need for both victim and rescuer to avoid hypothermia and frostbite.52,54 Disorientation and confusion from hypothermia, clumsiness from bulky clothing, and degraded performance characteristics of equipment and intravenous (IV) fluids can complicate otherwise straightforward procedures. A recent case report describes almost immediate freezing of fluid in IV lines and shattering of the plastic IV tubing despite vigorous attempts to warm them.54 Simple devices commonly used in warmer settings, such as air splints and pneumatic antishock garments, would be similarly unusable. In more sophisticated equipment, batteries rapidly fail, unwinterized mechanical moving parts seize up, and metal objects become dangerous sources of frostbite. Clothing, not normally considered a medical topic, assumes special importance in the polar environment (Figure 9-5).73,100 Although the clothing used for many polar research programs in the summer seems adequate, a strong argument can be made for specialized winter gear, possibly adapted from the space program, that would allow relatively delicate manipulation of scientific equipment while offering protection from the cold. In fact, at temperatures below those of most military specifications, material properties of equipment, including plastic electrical insulation, create unexpected hazards, such as splitting of insulation and other plastics, and extreme rigidity of cables and hoses such that they cannot be used. Fortunately, the importance of ergonomic issues in the design of machinery and clothing for polar conditions is receiving increased attention.44,128 There is new research on use of personal heaters, which are particularly effective for extreme cold and for sedentary work in the cold.106 Phase-change material can store latent heat and then release it during periods of low activity.100 These newer materials will allow thinner gloves with high thermal protection to be worn for work in the cold that requires dexterity, and they will be particularly effective for persons whose efforts alternate between heavy work that can produce sweating and light work with associated cooling (Figure 9-6, online). In addition, as phase-change material clothing becomes readily available, clothing will be lighter and less bulky,
particularly advantageous when doing intricate work in the cold as well as alternating active with sedentary work in the cold. Altitude Illnesses Altitude illness can be a major issue at many Antarctic stations, camps, and research locations, including the South Pole, Vostok, and Mt Erebus. A literature-based approach to preventing altitude illness with the least possible adverse outcomes over the season was to administer acetazolamide (Diamox) 250 mg twice per day starting 24 hours before altitude exposure. Participants voluntarily took this medication for an additional 3 days of exposure. If the individual still had symptoms, such as observed periodic breathing or headache, the dose would be increased to 3 times a day. Dexamethasone (Decadron) 4 mg twice a day beginning the day of ascent was used as a alternative for persons who had experienced serious side effects or allergic reactions, who had an allergy to sulfa-containing medications, or who had no notice before having to ascend to high altitude. This was also continued for 3 days at altitude. After 3 days at altitude, the body’s own compensatory mechanisms have had time to adjust to the new environment, and the medication is no longer needed. Because medication use was voluntary, complications seen from not taking it included high-altitude pulmonary edema requiring use of a Gamow bag before urgent evacuation, relative hypoxemia, and decreased work tolerance. Complications from taking acetazolamide included dehydration and electrolyte abnormalities in patients who were already ill or had severe underlying
FIGURE 9-5 Clothing is an important topic in polar medicine. A researcher prepares to leave the station for an extended time at −56.7° C (−70° F). The total weight of his clothes is 11.5 kg (25.4 lb). Notice the multiple layers for each area of the body. (Courtesy Stephen Warren.)
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TABLE 9-1 Emergent Evacuations
PART 2 COLD AND HEAT
diseases.51 Please see Chapter 1 for current recommendations for prophylaxis and treatment of high-altitude related illnesses. Nutritional Studies Nutrition occupies a key niche throughout the history of polar expeditions. Early expeditions in both polar regions provided several examples of nutritional illnesses, including scurvy and possible hypervitaminosis A and lead poisoning. More sophisticated nutritional analyses have been possible during recent expeditions,112,116 and advances continue to be made in development of lightweight but nutritionally dense rations. When participants in endurance events are well trained, it is possible to compete without loss of lean body mass.70 Although many prolonged unsupported expeditions include an element of malnutrition or even starvation, protein synthesis is still active.116,117 During a Canadian-Soviet transpolar ski trek, participants skiing approximately 20 km/day (12.4 miles/day) at a speed of about 3.5 km/hr (2.2 miles/hr) while carrying 37- to 45-kg (81.6to 99.2-lb) packs showed increased strength, decreased body fat, and increased high-density lipoprotein cholesterol. A paradoxical drop in aerobic power was noticed, perhaps because of intensive pretraining and conditioning, as well as increased efficiency of skiing as the trip progressed. More recently in a nonsupported, two-man, 86-day trans-Greenland trip, well-trained and experienced skiers eating an adequate caloric diet had little if any significant impairment. Their average energy intake in rugged terrain was 28 to 34 kJ/day (6688 to 8121 cal/day) and in level terrain 14 to 16 kJ/day (3344 to 3822 cal/day).31 Although applicability of these figures to more sedentary polar sojourners is probably limited, work is being done to alter the diets of more sedentary expeditions to improve the lipid profile of participants.71 Better availability of common foods and fresh fruits and vegetables during the summer, and frozen foods in the winter at the permanent stations allow participants to choose a healthier diet. However, frequent fried and high-fat food intake leads to elevation of lipid profiles and the associated increase in cardiovascular risks. Some studies have demonstrated that it is possible to make simple and acceptable changes in food preparation that have a significant impact on lowering cardiovascular risk factors of winter-over personnel.6,71 An area that has received increased attention involves the possibility that the prolonged low dose of sunlight may have longterm effects on bone metabolism and immune and cardiovascular systems. One study showed a decrease in the 25-hydroxy metabolite of vitamin D (25OHD) as UV radiation ceased. However, the active metabolite 1,25-dihydroxyvitamin D (1,25[OH]2D) did not show such variation.101 A few studies have demonstrated significant decreases in serum vitamin D as measured by 1,25(OH)2D and associated increases in serum osteocalcin during the dark period, possibly indicating bone remodeling.133 Another study in which low doses of vitamin D were given showed increased bone mass in lumbar vertebrae and leg bones, but no bone mass increase in the pelvis or upper extremities. This was felt to be the result of vigorous activity over the winter. The study also showed a decrease in serum calcium and 25OHD levels during the winter.86 A study was undertaken in the 2003-2004 Antarctic summer and followed 53 Australian expeditioners for 2 years. It showed that they became vitamin D deficient after just a few months; after 12 months, this began to result in loss of bone density. Further study is planned to identify the minimal dose of supplementation needed to prevent deficiency and whether these expeditioners have greater risk for developing osteoporosis in later life.55 Because many participants return for successive winters, further studies are needed to delineate possible long-term effects of bone mass after redeployment. Infection and Epidemiology With particular reference to the space station analogy, a number of studies have taken advantage of the physical isolation of Antarctic stations as a natural laboratory for infectious disease epidemiology. Because microorganisms are believed not to survive the extreme cold long enough to be carried in by winds, midwinter respiratory tract infection outbreaks in the absence of outside contacts have suggested that such organisms could persist in clothing or other fomites.97 208
Despite a widely reported leukopenia, decrease in cell-mediated immunity, and decreases in salivary IgA and IgM during the isolation of wintering over, it is not clear whether persons emerging from Antarctic stations are more susceptible to infection,30 or whether the changes in immunity are related to the stress associated with a winter over. Circadian Rhythms, Endocrine Studies, and Sleep Research Pioneering studies of Natani and colleagues79 and Shurley and co-workers on sleep electroencephalograms at the old South Pole station demonstrated clear patterns of sleep disturbances and “free cycling” of the sleep–activity cycle. Some of these findings have been extended in more recent studies. For example, among four subjects at a small winter-over camp, summer sleep cycles synchronized within the group and with clock time. During 126 days of sunless winter, rhythms free cycled in all four people and then resynchronized with reappearance of the sun.57 The degree of synchrony versus free cycling appears to depend on a number of factors, notably zeitgeber strength (an environmental agent or event that provides the cue for setting or resetting a biologic clock—that is, activities, social contacts, and the most important zeitgeber in nature, light).32 Studies in Indian stations also confirm continuing sleep pattern changes.13 A number of studies have examined the effect of prolonged polar residence on diurnal variations in the level of melatonin. Its important role in free radical scavenging and sleep regulation is beginning to be elucidated.56 Melatonin has been studied as a chronobiotic and is used as a supplement to treat circadian rhythm disorders.5,109 Of the various studies using melatonin to treat sleep disorders, including delayed sleep phase and for night-shift workers, most have only small numbers of participants. Although the initial studies are promising, more research needs to be done. It appears that exogenous melatonin can be used effectively for most persons. The short-term side effects (headache, nausea, and drowsiness) are few. There are no longterm studies. Use of blue-enriched white light in the workplace improved alertness, performance, and sleep quality, as well as daily resetting of the melatonin cycle.29,75,109 Other endocrine fluctuations also appear to be correlated with the length of the day.122 Some endocrine studies have examined the effects of prolonged residence in polar regions with a longer than diurnal time constant. Twenty-four-hour urinary excretion of catecholamines increases in the cold, but social stresses appear to overwhelm climatic determinants of catecholamine metabolism, correlating with increases in diastolic blood pressure and pulse during the year.41 A more consistent pattern of elevated thyroid-stimulating hormone (TSH), decreased free thyroid hormones, and increased triiodothyronine (T3) clearance after several months has been demonstrated. It has been suggested that rapid clearance of T3 is caused by the cold. A pattern of increased pituitary release of TSH in response to IV thyrotropin-releasing hormone and increased serum clearance of orally administered T3 has been identified and dubbed the “polar T3 syndrome.”24 The full clinical significance of these findings remains unclear, but it appears that the T3 may well be related to the winter-over syndrome (see later).87,95 Several studies that used thyroxine supplementation noted improvement in midwinter cognitive function, mood, and vigor.102,105,127 Environmental Health Issues Because of Antarctica’s isolation, it seems a particularly disturbing site for litter and pollution. As in the Arctic, events such as the early problems with a nuclear reactor at MCM (since removed) and the 1989 oil spill from the Bahia Paraiso near Palmer Station, and studies by groups such as Greenpeace, have focused attention on environmental health risks in the Antarctic.78,125 Environmental inspections at a broad range of Antarctic stations have raised concern about toxic effluents and heavy-metal residues, as well as about radioisotopes used for research. To address these issues, a number of countries have begun to implement more responsible waste-management and water-monitoring policies and are taking corrective actions. Most have active recycling programs in place, and many cleanups are in progress or have been completed. Currently, most stations, including all U.S.
Occupational Health and Injury Prevention Rigorous studies of risk are important for injury prevention. Unfortunately, they are complex and often bedeviled by challenges, including controversial data, multiple variables, and biases. For example, for purposes of occupational epidemiology, it may ultimately prove useful to stratify the Antarctic sojourner population into groups such as sport expeditions, military, commercial, and scientific, but the health behaviors of these groups overlap, and few studies have gone beyond aggregate descriptive statistics. There is no current system for archiving these data, except by individual programs or organizations; therefore much of the data is not available for review. There were plans to address this issue at the Council of Managers of National Antarctic Programs (COMNAP) at the planning meeting for the International Polar Year of 2007-2008.9 Unfortunately, because of funding issues, this has not been done.33 Even from these broad statistics, some figures emerge that may be useful cognitive anchors. There were 16 fatalities from 1947 to 1999 in the Australian Antarctic Program, but only 1 fatality in the past decade. Among 3500 scientists and support personnel (2000 person-years), there were 4 medical deaths, 2 myocardial infarctions, 1 case of appendicitis, 1 perforated gastric ulcer, and 1 cerebral hemorrhage. The remainder of the events were accidents involving falls, head injuries, hypothermia, drowning, crush injury, and burns.65,67 There have been 60 deaths in the U.S. Antarctic Program since 1946.1,69 These can be ranked by cause: aviation, 61%; vehicles, 11%; ships, 7%; recreational, 7%; station/industrial, 5%; field activities, 5%; and other, 4%.69 Although it is difficult to adhere to standard occupational safety practices when in a remote location, new guidelines and serious efforts in some of the programs have led to improved worker and participant safety. A review of data for the Australian National Antarctic Research Expedition (ANARE) 2002-2003 season listed the following reasons for medical consultation: medical (e.g., upper respiratory, GI), 39%; injuries (sprains, strains, dermatologic, lacerations, fractures), 27%; follow-up visits, 24%; and preventive (immunizations, midyear examinations, wellness programs), 10%.17 For the 2004-2005 season, Antarctica New Zealand (ANZ) reported the following: musculoskeletal, 42%; medical (e.g., upper respiratory infections, GI), 22%; other injuries, 20%; dermatologic, 15%; and preventive, dental, and other, 8%.99 Usually, most visits are related to injuries, and the next most frequent medical clinic visits are attributable to upper respiratory infections. Environmental problems include dry skin and fissures, particularly on fingertips as a result of cold and very dry conditions. Cyanoacrylate glue hastens healing of disabling fingertip and heel fissures.7 Coldinduced urticaria, frostnip, and frostbite are frequently underreported, except for moderate to severe cases. Small nasal bleeds occur frequently, but they rarely require treatment beyond instruction to use petrolatum or antibiotic/antiseptic ointment once or twice a day to protect the delicate nasal epithelium, which easily becomes dehydrated or can suffer frostnip. Although the bulk of care is limited to routine visits, the pathologic conditions encountered even among this carefully screened population have included myocardial infarctions, massive GI bleeds, unreported Crohn’s disease, bowel obstructions, acute cholelithiasis with pancreatitis, pulmonary emboli, massive head injuries, fractures, crush injuries, newly diagnosed schizophrenia, and cancer. Fire Safety In light of the extreme cold, it is somewhat counterintuitive that fire is a major concern and significant danger at all Antarctic stations. This surprising assessment rests on a number of factors. Cold temperatures severely limit the utility of water for fire suppression. Firefighting equipment may become inoperative in extreme cold, and frequent high winds can fan fires. The extremely low absolute humidity in many polar regions results in an even lower relative
humidity when outside air is warmed in station dwellings. This in turn leads to increased static electricity and dryness of combustibles, already at risk from frequent use of space heaters. Finally, alternative food, shelter, and fuel are limited. Elaborate predeployment training, frequent on-site drills, and keen awareness of potential fire hazards have correlated with a satisfactory fire safety record to date, but this good fortune cannot be taken for granted. One of the most life-threatening events was the explosion and fire at Vostok in 1982, leaving the station basically without power or adequate heat. Only one person died, however there were several injuries, and the winter crew had to endure 8 months without a power plant to supply heat.103 In 2001, the BAS Rothera Station lost its new Bonner Lab building when an electrical short started a fire. No one was injured, but with 50- to 70-knot winds, little could be done to save the station.11 Although fire-suppression systems are built into the newer buildings, a historic A-frame building at New Zealand’s Scott Base burned down in May 2009 and, much more seriously, a two-story building at Russia’s Progress Station burned down in October 2008, killing one person and seriously injuring two others. Because the building contained their radio equipment, they could not contact the outside world for 4 days after the event. In Antarctica, fire is an ever-present threat. Tourist Safety Polar regions are imbued with a sense of the exotic, conjuring up “images of hardship, personal valor, danger, adventure, and of course, the hero.”111 As transportation increasingly opens up previously inaccessible areas, this image attracts growing tourist traffic and, with it, hot debate from both legal and environmental viewpoints. The essential medicolegal issue is the extent of governmental organizations’ responsibility for medical care of participants in nongovernmental activities, whether scientific, political, or commercial. Although this discussion started much earlier, it is still ongoing.77 When a tourist group requires aid beyond its own capabilities, whose responsibility is it? To what extent should a research station with limited medical supplies be required to divert some of those supplies to an individual who presumably bears responsibility for planning his or her own medical coverage? By default, stations provide what assistance they can, although they often try to bill tourist companies and their insurance agencies for costs involved in patient treatment or transport. The Antarctic Treaty Consultative Meeting XXXI provided attendees with a list of guidelines recommended before trips to Antarctica, including travel insurance, contingency plans and other necessary equipment.3 Air Safety As in the Arctic, reliance on aircraft for transportation has highlighted the critical importance of air safety. The worst Antarctic air accident was the crash of an Air New Zealand tourist “flightseeing” DC-10 on Mt Erebus in November 1979.83 This accident killed all 257 people aboard and temporarily ended such flights, although IAATO records indicate that overflights are now happening with new guidelines in place. There have been 35 airrelated fatalities in the U.S. Antarctic Program since 1946 from crashes related to either fixed-wing or rotor aircraft.69,111 A skiequipped LC-130 Hercules crashed at the remote D-59 camp in 1971 (Figure 9-7). Fortunately, none of the 10 crew members aboard was injured, but during a salvage operation in 1987, another LC-130 bringing supplies to D-59 crashed nearby, killing two and injuring nine. More recently, a helicopter crash occurred in the dry valleys; both the pilot and passenger were seriously injured. After a weather delay, they were extricated and evacuated to New Zealand for definitive care.17,81 The review of literature for air crashes in Antarctica is exhaustive. With better weather prediction and increased safety standards, the accident profile is improving.
PSYCHOSOCIAL HEALTH PROBLEMS As the U.S. Polar Manual explained in 1965, “No psychiatric case ever got better in the cold.”43 For many, polar living arrangements and psychosocial issues may be more important than the strictly medical or environmental factors. Psychiatric problems are 209
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stations, discharge raw sewage. Proposals are in place to find a way to ameliorate the contamination from raw sewage that is discharged into the sea, and/or into large bubble holes in the ice for the inland stations. The BAS Rothera Station installed a sewage treatment plant with significant improvement in the nearshore marine environment.47,48,74
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Judicious use of monitoring can help identify persons who may need intervention before an accident happens.
FIGURE 9-7 LC-130 Hercules partially stuck in a hidden crevasse, demonstrating the inherent hazards of working in Antarctica. (Courtesy National Science Foundation photo archive.)
mentioned even in reports of early expeditions, and almost any participant in expeditions will recognize Thor Heyerdahl’s observation: “The most insidious danger on any expedition where men have to rub shoulders for weeks is a mental sickness that might be called ‘expedition fever’—a psychological condition that makes even the most peaceful person irritable, angry, furious, absolutely desperate because his perceptive capacity gradually shrinks until he sees only his companions’ faults while their good qualities are no longer recorded by his grey matter.”121 Most psychological problems, primarily sleep disturbances, are minor and temporary. Many disturbances are more related to the social environment than to the physical environment.89,108 Appropriate lighting or changes in photo periodicity (the duration of daylight and darkness in a 24-hour period) help improve mood and sleep.91,129 In addition to appropriate exercise facilities, opportunities for quality mental stimulation and frequent contact with friends and family via the Internet and telephone can help maintain stability. Except for insomnia, which is perhaps endemic, the incidence of psychiatric problems is lower than expected in the overall population. Many nations use formal and informal psychological screening, especially for participants planning to winter over in Antarctica. How well the screens function is debatable. A British study showed that an extensive psychological screening examination weeded out many participants with problems with “defensivehostility” and “emotion-focused coping.” Simple interviews did not identify these problems.34 Alcohol Abuse Adjustment to psychosocial stresses in polar communities depends on a complex array of sociocultural factors. One coping mechanism is alcohol use. As in many isolated communities at high latitudes, alcohol use can disrupt or lubricate social interactions. In the U.S. Antarctic Program, summer support-staff members are not infrequently terminated for alcohol abuse, and both summer and winter-over staff are occasionally prohibited from purchasing alcohol. In some instances, interventions with group support are found to be very effective. At many Antarctic stations, alcohol is easily available and may be subsidized. In some stations, rations can be excessive or nonexistent. Observations are that at least 50% of recreational injuries are alcohol related. Recommendations have called for routine monitoring of alcohol levels of anyone involved in an accident111 or even prohibition of alcohol at Antarctic stations. However, as with prohibition in other countries, this might create more problems than it might solve. 210
Psychoneuroimmunology Psychological stress at research stations may arise from several sources. One is the environment itself; environmental severity has been found to be an independent predictor of hostility and anxiety after wintering over.90 Perhaps more important is the perception of the environment. Newcomers to the South Pole station are usually observed wearing a full 12-kg (26.5-lb) polar outfit at −20° C (−4° F) for several weeks after arrival. By midwinter, the same individuals think little of walking short distances in only workout shorts and a T-shirt at −60° (−76° F). Stress can also result from disjunction between a person’s original motivation for joining the program and the realities of life in the station—that is, the sociocultural environment. This may be the greatest determinant of difficulties.90 Studies suggest that people who go to Antarctic stations to seek thrills or to challenge themselves often have more difficulty sustaining their motivation and performance than those who go to accomplish a scientific mission or even those primarily motivated to earn money. In general, older individuals who are somewhat introverted are able to set work goals and work toward them, and persons who have broadly defined hobby interests seem to cope better with the social isolation and dynamics of wintering over. One study found that members with low social coherence reported significantly more depression, anxiety, and anger than did individuals belonging to expeditions with high social cohesion.88,130 Small-Group Dynamics In addition to external climate and internal motivational factors, stress can arise from interpersonal interactions. Although there are many exceptions, participants in the Antarctic program often speak of a tendency for personnel to form cliques or microcultures. People may cluster according to ordinary personal chemistry, along lines of OAE (Old Antarctic Explorer) versus novice, winter-over versus summer status, or according to scientific, civilian, or military affiliation. With time, such social clusters can be a source of support or of friction. In an attempt to unify the core group, winter-overs participate in a mini–Outward Bound type of group bonding experience before deployment. Social isolation is an important factor in polar communities, although this isolation has been lessened by modern communications and transportation. A number of studies have drawn parallels between group processes in polar stations and those in other isolated and confined environments, such as submarines or in space. As space travel becomes a reality, studies on group selection, leadership style, and interaction between the isolated group and headquarters take on urgency.35,63,93,131 Collaborative efforts are being made between many stations and space agencies, in particular the European Space Agency (ESA) and the NASA program.108 Cross-cultural and cross-gender issues by research groups are currently being studied at the international station, Concordia, particularly as an analog for long-distance space missions. Whereas in some areas cross-gender differences increase difficulties, in others they are beneficial. Further studies on rigorous selection criteria and training before deployment will avoid the problems that have occurred with sexual harassment. It is felt that the positive effect of better communication, less rude behavior, and increased supportive environment outweigh the negative effect. Other stations have already gone through this process.63,108 Winter-Over Syndrome Stressors such as those mentioned previously can result in what has been termed the winter-over syndrome. The historically oftmentioned “Big Eye” or “20-foot stare in a 10-foot room” seems to be less common now, perhaps because the stations are increasingly comfortable and have stimulating environments. But the constellation of depression, hostility, sleep disturbances, and impaired cognition still seems to be both common and underreported.94,95,105 The winter-over syndrome is not a static condition but a time- and individual-dependent process. At the South Pole research station, for example, winter-over staff characteristically
Seasonal Affective Disorder A probable contributor to and confounder of the winter-over syndrome is the apparently fairly consistent exacerbation of stress and depression under conditions of winter or night, leading to seasonal affective disorder (SAD). Subsyndromal SAD (S-SAD) is perhaps a better definition of what is experienced by many who winter over in the dark latitudes.92 Further studies indicate that S-SAD may be part of the T3 syndrome.95 Correlations with melatonin levels have been shown to be associated with the frequent sleep disturbances at higher latitudes, both with advanced or delayed phases, and with increased latency.5,129 In some studies, melatonin’s chronobiotic properties are used to resynchronize the individual’s sleep.5 Other studies have demonstrated the effectiveness of light therapy in helping resynchronize the body.129 SAD may be no more prevalent in Antarctica than at lower latitudes; some of the depressive symptoms may well be the result of social isolation or related to seasonal changes.96 Beneficial Effects of Isolation An interesting point is that isolation may have positive as well as negative effects.96 Isolation is not synonymous with loneliness and depression, as Amundsen reported from his sojourn at Framheim. In fact, a subset of “professional isolates” may actually prefer polar stations to “normal” society.120 In some cases, reentry and adaptation to the rest of the world can take up to 6 months. The positive effect of isolation may be reflected in a study of somatic complaints, published in 1992, that compared Navy volunteers who qualified for winter duty in Antarctica and wintered over, with those who were physically qualified but were assigned elsewhere because of the limited number of winter assignments. Those who spent the winter in Antarctica had fewer illnesses and hospitalizations after the winter-over period. These volunteers were followed an average of 5.4 years after the winter period. It was also noted that the complex psychophysiologic symptoms experienced during the winter-over period were probably adaptive coping mechanisms. Coping led to a process of negotiation leading to compromise, which frequently led to finding new strategies or resources that could be used for subsequent stressful experiences. Newer studies confirm the salutogenic effect of completing a long-term contract in an isolated environment.88,96 Screening and Selection Based on the preceding findings, several attempts have been made to refine the selection and screening processes for successful polar and space sojourners. It is not surprising that previous successful polar experience seems to be among the best predictors of subsequent high performance. Biographic data, peer ratings, psychometric testing, and interviews all seem helpful in selection, although each has weaknesses and inconsistencies. Recent studies have suggested that team climate significantly related to the perception of good leadership.110 More research needs to be done to explore the characteristics and behaviors that constitute effective leadership, in order to guide selection of crew and leader.14,110 Early studies led to the tripartite “ability, stability, compatibility” criteria for successful participation in the Antarctic programs.34 This simple but useful scheme recognizes that technical skill, emotional equilibrium, and interpersonal skills all play important roles in an individual’s performance and internal satisfaction. It would be desirable to improve measurement and predictive usefulness of these factors; such studies remain at the active frontier of Antarctic research.34
Overview and Future Developments A point made early in this chapter was the challenge inherent in meaningfully synthesizing Arctic and Antarctic medicine. Reflection on some of the issues raised previously suggests several common areas of linkage and directions for future work.
ISSUES OF METHODOLOGY AND MEDICAL EPISTEMOLOGY The state of knowledge about the human factors involved in living in the Antarctic is still rudimentary, although renewed interest by NASA and the ESA in Antarctica as a space analog has led to increased research funding and should lead to better information. Studies in polar settings are often handicapped by extremely difficult research conditions and may never achieve the statistical power and validity expected of counterparts in more forgiving climes. Commonly encountered methodologic problems include, most notably, small sample sizes, unknown effect sizes, measurement of proxy variables, and multiple confounders.
FOURTH WORLD MEDICAL DECISION MAKING Polar medical lore is replete with stories like that of the physician of the sixth Soviet Antarctic Expedition at Novolazarevskaya Station, who performed an appendectomy on himself in April 1961 with assistance from the station mechanic.107 Although the basic principles of emergency medicine, epidemiology, occupational health, psychology, and other disciplines still apply in polar settings, the spectrum of health problems and some important aspects of their management are undoubtedly skewed. However, with newer and improved technical communication modalities and transportation, delivery of advanced care in the polar latitudes has improved, and many lessons learned in Antarctica are applicable to space exploration and settlement. Fourth World medicine requires distillation of medical practice into a compact yet comprehensive package that is sufficiently robust to travel well. Novel constraints and the inherently unpredictable nature of a hostile environment further stretch the usual, already-tentative rules and thresholds of medical decision making. Perhaps to a greater extent than in most settings, prevention and preparation are paramount in polar medicine. As might be imagined, cold and its effects on both humans and equipment exacerbate the risks from even minor mishaps, altitude impairs tissue oxygenation and wound healing, and bulky clothing restricts dexterity and vision. Isolation from medical facilities exerts a multiplier effect on these risks. Victim extrication and resuscitation that would be routine in most urban or suburban settings present overwhelming challenges in polar settings.102 With lives at stake, arguments have been made for planning for worst-case scenarios rather than only for likely situations.111 On the other hand, a realistic balance point on the cost-versusutility curve, based on estimated risks, must be set for each situation. Given existing fiscal and logistic constraints, preventive measures should take priority over higher-cost options.8 A recurrent medical issue in polar stations involves contingency planning and the optimal level of inventory. This question applies equally to drugs, equipment, training, and personnel and is faced immediately by any incoming physician. “Just in time” principles of inventory management are not likely to be appropriate.8,111 Combined improvements in communications systems, the Internet, and the powerful tool of telemedicine with its many modalities have transformed what was once an extremely isolated practice of medicine. The advantages of rapid access to organized databases and remote consultations for radiology and other specialties via video are realities. Telemedicine is in place and functioning in many northern Arctic regions. The Australian, British, Italian, and United States Antarctic Programs and many others have been using it successfully for a number of years.35,56,64,104 Physiologic, psychological, and occupational health data can be monitored or retrieved, ultimately linking geography and information flow and allowing nearly real-time consultation and guidance from multiple specialists. These promising tools 211
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report a recognizable pattern of fluctuating activity and mood. There is often a mixture of relief, pride, and fearful anticipation as the last LC-130 flight departs in mid-February, followed by a period of frenetic activity to beat inventory deadlines, file resupply orders, launch projects, and prepare the station for winter. As work and recreation routines develop, mood generally drops with the setting sun. A rise in mood occurs toward sunrise but is followed with anticipation, increase in anxiety, and stress as the time of the arrival of the first return flight draws near. Studies at the Australian stations of Mawson and Macquarie Island suggest that the influx of new staff at station opening may actually be associated with increased depression.
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are real solutions to the problems of isolation faced by earlier physicians.
Medical Aspects of Arctic Racing In the spring of 2003, the first-ever Polar Challenge race, from Resolute Bay in northern Canada to the Magnetic North Pole (1996 position), took place, with Dr. Ian Davis as senior medical officer. The Polar Challenge is run annually as an ultra-extreme endurance race covering 580 km (360 miles) in temperatures down to −48° C (−54.4° F) with windchill −54.4° (−65.9° F). Teams of two or three persons race the distance on foot and skis, pulling pulks, which are small sleds weighing up to 80 kg (176 lb) attached to the skier. Teams pass through two manned checkpoints during the race. The medical needs of the competitors and support staff are unique in such a challenging and harsh environment. Provision of medical care has been perfected and refined over the preceding 7 years.
THE MEDICAL TEAM Before the start of the race, and after consultation with local hospitals, an emergency evacuation plan is written for extrication of racers to the most appropriate trauma/emergency medical facility, depending on the type of injury. At each checkpoint, a physician is available to provide treatment and consultation to the racers. A more experienced polar physician forms part of the mobile medical team (contacted via satellite pager), which also includes a navigator and a local Inuit guide/mechanic. This team is placed strategically on the ice for the duration of the race. It responds to any medical event either by snowmobile or on foot, with full air evacuation support on standby at all times. The race physicians carry an extensive range of equipment and drugs (Box 9-1) designed to handle any eventuality in this environment. This kit is refined annually after each postrace injury debriefing.
PRERACE SELECTION AND TRAINING Competitors for the race range in ability from experienced and very well trained Arctic travelers to complete novices. Ages so far have ranged from 20 to 65 years with a mix of two-thirds men and one-third women, totaling 80 racers in 7 years. All are offered the same training program (Box 9-2). If required, experts are available for extra tutoring specifically tailored to individual needs. When they join the race, competitors are sent a standard medical questionnaire that is used as a tool for excluding
BOX 9-2 Training Program for Polar Challenge
Competitors
In the 6 months before the race, training is carried out in three locations: the United Kingdom (UK), Austria, and northern Canada. UK Training • Fitness training • Navigation • Firearms • Polar bear training • Medical training for cold-weather injury avoidance and treatment Austrian Training • Polar clothing and equipment • Pulk packing (small sleds for gear, attached to skier by a flexible harness) • Arctic food • Stove use • GPS navigation • Medical training for cold-weather injuries • Firearms • Ski technique and tent craft • Cold-water immersion exercise Northern Canada Training • Cold-weather injuries • Communications • Safety • Evacuation • Firearms • Polar bears • Navigation • Mini 3-day expedition (fully guided) to start line of race
medically unsuitable applicants. Conditions such as cardiac disease and insulin-dependent diabetes would prove very difficult to treat in such a remote and hostile environment. The practicalities of racing with such conditions are discussed in detail with applicants, and then a decision is made as to whether they will take part in the event. Through a process of reflective practice, the training program has been refined, with the result that the current program achieved a 98% competitor completion rate.
BOX 9-1 Physician’s Medical Bag Drugs Multiples of the drugs found in the competitors’ medical bags, plus the following physician-use-only drugs: • Ketamine, 100 mg/mL, 10-mL vials • Morphine, 10 mg/mL, 1-mL vials • Midazolam, 5 mg/mL, 2-mL vials • Flumazenil, 0.1 mcg/mL, 5-mL vials • Adrenaline, 1 in 1000 (1 mg/mL), 1-mL vials • Hydrocortisone, 100 mg/mL, 1-mL vials • Prednisolone, 5-mg tablets • Salbutamol, 90 mcg per metered inhalation • Metoclopramide, 10 mg/mL, 1-mL vials • Lidocaine 1%, 10 mg/mL, 10-mL vials • Oxybuprocaine hydrochloride eye drops, 0.4% • Norethisterone, 5-mg tablets • Dexamethasone drops for ears Medical Equipment • Trauma kit, including chest tube • Suture kit • Urinary catheter kit • Airway kit, including bag valve mask
212
TEAM MEDICAL TRAINING Each team is required to carry a prepacked medical bag. The bags and their contents are identical for all teams. Constructed of lightweight yet tough material, they have two outer pockets and internal color-coded pouches, whose contents are listed in Box 9-3. Each bag contains a color-coded contents list with instructions for use. This makes giving advice over the sate llite telephone much easier, reducing the likelihood of error. Each race physician knows which drugs are in which color-coded pouch and so can instruct racers accordingly. The external pouches contain emergency dressings and wound and blister treatments. Before the race, competitors are given both group and individual instructions on the contents of the medical pack and their use. They receive lectures on cold-weather injuries and how to avoid them, as well as instructions on what to do in a crisis. The medical packs can be individualized if racers have specific medical needs.
ARCTIC RACING INJURIES ENCOUNTERED TO DATE Frostnip in varying degrees has been seen in most competitors during the race, regardless of their previous cold-weather experience. It has affected mainly the extremities, such as the nose,
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BOX 9-3 Polar Challenge Medical Advice Sheet 2005 Suspected fractures or serious trauma or illness—tent up and call for help Painkillers • Begin with regular simple pain relief. Use acetaminophen (paracetamol), 500 mg, 1 to 2 tablets, maximum of 8/day. • If needed, add acetaminophen with codeine (paracetamol [325 mg] plus codeine [30 mg]), maximum of 4/day. • For increased pain relief, take an antinflammatory (do not take if have stomach ulcers or asthma). Try either (but not together in the same 24 hours) diclofenac (50-mg tablets, 3/day), or piroxicam (20-mg tablets, 1 per day). Take with food. • For headache, try the above. If this does not work, take 2 aspirin (325 mg) plus 1 metoclopramide tablet (10 mg) repeated twice a day. If headache is increasingly severe, contact the physician.
FIGURE 9-8 Frostnip ear. (Courtesy Ian Davis.)
Antibiotics • If worried about infection, call physician, giving the site of the infection and symptoms. We will then advise. • If your communications break down, take Augmentin (500 mg) for any suspected infection. Take 1 tablet, 3/day for 1 week. Do not take Augmentin if allergic to penicillin. If you have an allergy to penicillin, take azithromycin (500 mg, 1 tablet per day for 5 days). Eyes • Any problems with eyes, please try contacting physician first. Otherwise, chloramphenicol eye drops is a good general antibiotic for eyes. If your eyes generally become very sore/red and watery, you may have snowblindness, so call for advice. Gut • Diarrhea—Take Imodium (2 mg, 1 tablet after each explosion!!). • Heartburn—Try Gaviscon. If this doesn’t work, take 1 lansoprazole (Zoton), 30 mg, fast-tab per day. • Constipation—Drink lots of fluids and take senna, 25 mg, 2 tablets at night. • Abdominal pain—Contact physician.
A
Allergy • Piriton (chlorpheniramine maleate 4 mg) 1 tablet 3/day. Nausea and Vomiting • Metoclopramide tablets (10 mg, 1 tablet 3/day). Skin • Any general rashes (groin, etc.)—Apply clobetasone 0.05% cream (Trimovate, green tube) twice a day. • Injuries to finger tips and burns—Use silver sulfadiazine 1.0% (Flamazine) cream twice a day. Cold Sores • Acyclovir 5.0% cream, apply 5 times a day over affected area. Blisters • Try using DuoDerm (hydrocolloid dressing), which can be cut to size. Leave at least a 2-cm margin of the dressing around the blister. Leave on for 3 days before changing it. It is normal while the DuoDerm is on the skin to accumulate a blob of fluid buildup over the affected area. General Wound Care • Lacerations—Depending on size, use either MedLogic skin protectant (similar to Steri-Strips) with glue, or just glue on its own (octyl cyanoacrylate [Dermabond, LiquiBand]). • Larger wounds—Apply direct pressure with a dressing, and call for advice.
ears, and fingertips (Figure 9-8). All cases were treated by rewarming and diligent future protection. The number of frostnip injuries decreased after a team buddy system was instituted, which led to rapid prediction of impending injury and timely avoidance.
B FIGURE 9-10 A, Frostbitten fingers. B, After recovery from frostbite. (Courtesy Ian Davis.)
Frostbite was seen in six competitors, five of whom had finger injuries (Figure 9-9, online). All the fingers made a complete recovery largely as a result of early detection and rapid evacuation of affected competitors from the race to a rewarming and treatment facility. One case of fingertip frostbite was caused by a fuel spill onto the fingertips, which caused rapid freezing and subsequent injury. This competitor was a highly experienced Arctic traveler and was therefore allowed to continue, subsequently making a full recovery during the race (Figure 9-10). The final case of frostbite was more unusual, affecting a competitor’s penis (Figure 9-11). After urinating, he forgot to close the zipper correctly on his wind suit. After walking into a headwind with a windchill factor of −80° C (−112° F) for an hour, he discovered his foreskin to be frozen. Rapid evacuation prevented further damage and, after a circumcision on his return to the United Kingdom, he made a complete recovery both in sensation and function. During the event, this competitor could easily have gone into urinary retention and would have been catheterized accordingly, making it essential to carry such equipment in the physician’s medical kit. Musculoskeletal injuries, most commonly of the lower back, shoulders, knees, and wrists (related to cross-country skiing and pulk pulling), were seen in most of the competitors. They were 213
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FIGURE 9-11 Frostbitten foreskin. (Courtesy Ian Davis.)
all treated with appropriate analgesia and advice from both the mobile and static medical teams. This enabled most competitors to finish, with only 5% of the total having to withdraw for this reason. The most serious musculoskeletal injury was a dislocated shoulder, which was relocated by a teammate using a slow Kocher’s method. The race physician talked him through this maneuver over the satellite telephone. This competitor went on to finish the race. Snowblindness was seen in 4% of racers (Figure 9-12, A). Diagnosis in the field was achieved with the aid of fluorescein stain, and the eyes were treated with topical local anesthetics, antibiotics, oral analgesia, rest, and eye patches (Figure 9-12, B). All affected racers went on to complete the race. Dermatologic problems, including sweat rashes, were seen mainly in the groins of male racers. All were treated successfully using appropriate topical creams. All the female racers (and none of the male racers) developed a cold-induced urticarial rash isolated to the anterior surfaces of the thighs (Figure 9-13). This was treated with oral antihistamines
A
FIGURE 9-13 Cold-induced rash. (Courtesy Ian Davis.)
and topical corticosteroids but was difficult to cure, taking days to weeks to resolve in a warmer environment after the race. Steps are being taken to design clothing for female competitors to prevent this from happening in the future. Blisters were seen in 30% of competitors. All were treated effectively using DuoDerm hydrocolloid dressings. This type of dressing is extremely adherent and can be cut to any shape and applied for up to 5 days. Extra adherence at the edges of these dressings on high-friction areas like the heels can be obtained by using zinc oxide tape. Trench foot was reported in two competitors at a late stage in the race (Figure 9-14). Both were treated after completion of the race. Diligent foot care during the race would have helped prevent this injury. Respiratory disease was seen once in a hypothermic competitor who collapsed during a storm with a severe case of asthma. The victim was unable to speak in complete sentences and was so cold that he had stopped shivering. He was rewarmed in a prewarmed tent and treated with inhaled salbutamol and IV corticosteroids, followed by oral corticosteroids and oral antibiotics, with air evacuation as soon as there was a weather window. The competitor made a full recovery. Fatigue and hypothermia affected all racers to varying degrees. Despite consuming 7000 cal and drinking 4 L per day, most competitors are likely to lose 10% of their body weight. Training is given to all the teams on how to treat a teammate with severe fatigue and hypothermia. Only two competitors have withdrawn for such reasons (Figure 9-15, online). GI problems were mainly diarrhea, which was treated with loperamide and adequate hydration. Constipation, anticipated in the medical packs with senna tablets, has not yet been a problem. Psychological problems, such as fear of polar bear attack or of becoming lost or injured, have led to at least one person pulling out of the race. Lacerations and split skin were seen in some competitors; the lacerations were minor. All victims were treated very successfully
B FIGURE 9-12 A, Snowblindness. B, Eye patches. (Courtesy Ian Davis.)
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FIGURE 9-14 Trench foot. (Courtesy Ian Davis.)
using tissue glues (octyl cyanoacrylate tissue adhesive). This proved much more effective than did teaching competitors suturing techniques. Other potential injuries that are anticipated include major trauma from polar bear attack or firearms injury; burns, both minor (from stoves) and major (from tent fires); carbon monoxide poisoning; long-bone fractures; medical emergencies (e.g., anaphylaxis, cardiac problems, infection, and pneumothorax); surgical emergencies (e.g., abdominal sepsis from appendicitis); dental problems; and problems unique to female racers, including vaginal candidiasis, menstrual problems, and urinary tract infections.
THE USE OF FROZEN MEDICATIONS The medical literature is relatively sparse on this topic.31 One of the authors has rewarmed frozen fluorescein stain, oxybuprocaine hydrochloride 0.4%, ophthalmic local anesthetic, corticosteroid creams, antifungal creams, inhaled salbutamol, and IV
hydrocortisone, all of which worked normally after rewarming. All forms of tablet medications warmed from frozen have also been fine after rewarming. A study from the BAS found that most medications remained stable, even after multiple freeze-thaw cycles. The exception was hydrocortisone cream, although the investigator also recommended against subjecting eye medications to temperature extremes. Medical devices, such as IV cannulas, worked normally after rewarming, as did all forms of tape and dressings. Frozen IV fluids expanded when frozen, perforated the bags, and thus leaked when rewarmed. Acknowledgments. Special thanks to Kenneth H Willer, MLS, Manager—Library Services, Samaritan Health Services, Corvallis, Ore,
[email protected].
REFERENCES Complete references used in this text are available online at www. expertconsult.com.
CHAPTER 10
Pathophysiology of Heat-Related Illnesses LISA R. LEON AND ROBERT W. KENEFICK*
Heat illnesses are best viewed as existing along a continuum, transitioning from the mild conditions of heat cramps and heat exhaustion to the life-threatening condition of heatstroke. Environmental heat exposure is one of the most deadly natural hazards in the United States, with approximately 200 heatstroke deaths per year. Although the majority of heatstroke deaths are observed in vulnerable populations during annual heat waves, young fit individuals may also succumb to heatstroke while engaging in strenuous activities such as athletic competitions, military operations, or occupational tasks. Multiorgan system failure is the ultimate cause of heatstroke death, and there is a complex interplay among the physiologic and environmental factors that compromise an individuals’ ability to adequately respond to heat stress. The pathophysiology of heatstroke is thought to be caused by a systemic inflammatory response that occurs in response to endotoxin leakage from the gut, but there remains limited understanding of the mechanisms that mediate morbidity and mortality. This chapter provides an overview of the pathophysiologic responses that are observed in patients and experimental animal models at the time of heatstroke collapse and during long-term recovery. A brief discussion is provided on current clinical heatstroke treatments and promising avenues of research that may aid in the development of more effective interventions and/or treatments to prevent this debilitating illness.
Heat Stress and Thermoregulation FOUR AVENUES OF HEAT EXCHANGE Mammals and other homeotherms are capable of maintaining body temperature within a fairly narrow range (approximately *Approved for public release: Distribution is unlimited. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Army or the Department of Defense. Any citations of commercial organizations and trade names in this report do not constitute an official Department of the Army endorsement of approval of the products or services of these organizations.
35° to 41° C [95° to 105.8° F]) despite large fluctuations in environmental temperature. Environmental variables that have the largest impact on heat exchange are temperature; humidity; radiation from the air, water, or land; and air or water motion.88 To maintain stable body temperature, organisms rely on four avenues of heat exchange: conduction, convection, radiation, and evaporation. Dry heat exchange is achieved by conduction, convection, and radiation. The effectiveness of these mechanisms depends on differences between the skin and environmental temperatures. That is, dry heat loss occurs when skin temperature exceeds that of the environment, and dry heat gain occurs when environmental temperature exceeds that of the body. Conduction occurs when the body surface is in direct contact with a solid object and depends on the thermal conductivity of the object and the amount of surface area in contact with the object. Conduction is typically an ineffective mechanism of heat exchange because of behavioral adjustments that minimize contact with an object. For example, the wearing of shoes is an effective behavioral adjustment that minimizes conduction of heat from a hot surface (e.g., desert sand to the foot). Within the body, conductive heat transfer occurs between tissues that are in direct contact with one another, but is limited by poor conductivity of the tissues. For example, subcutaneous fat has approximately 60% lower conductivity than does the dermis and impedes conductive heat loss.332 Convection is a mechanism of dry heat transfer that occurs as air or water moves over the skin surface. The windchill index is an example of the convective cooling effect of wind velocity. The rate of convective heat transfer depends on the temperature gradient between the body and environment, thermal currents, bodily movements, and areas of the body surface that are exposed to the environment, which can vary dramatically with different clothing ensembles. Within the body, convective heat transfer occurs between blood vessels and tissues and is most efficient at the capillary beds, which are thin-walled and provide a large surface area for heat exchange. Radiative heat transfer is electromagnetic energy that is exchanged between the body and surrounding environmental objects and is independent of air velocity or temperature. It is effective even
For online-only figures, please go to www.expertconsult.com
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when air temperature is below that of the body. All objects within our environment absorb and emit thermal radiation, but clothing can reduce radiant heat that impinges on the skin from various environmental sources. Evaporation represents a major avenue of heat loss when environmental temperatures are equal to or above skin temperature or when body temperature is increased by vigorous physical activity. In humans, evaporative cooling is achieved as sweat is vaporized and removes heat from the skin surface, with approximately 580 kcal of heat lost per each liter of evaporated sweat.94 The most important environmental variables affecting evaporative cooling are ambient humidity and wind velocity. Sweat is converted to water vapor and readily evaporates from the skin in dry air with wind, whereas the conversion of sweat to water vapor is limited in still or moist air. If sweat accumulates and fails to evaporate, sweat secretion is inhibited and the cooling benefit is negated. Small mammals, such as rodents, do not possess sweat glands but achieve evaporative cooling by grooming nonfurred and highly vascularized skin surfaces, such as the ears, paw pads, and tail, with saliva that evaporates in a manner similar to that of sweat in humans.104,294
BODY TEMPERATURE CONTROL Regulation of a relatively constant internal temperature is critical for normal physiologic functioning of tissues and cells because membrane fluidity, electrical conductance, and enzyme functions are most efficient within a narrow temperature range. By convention, thermal physiologists describe body temperature control with a two-compartment model that consists of an internal core (i.e., viscera and brain) and an outer shell (i.e., subcutaneous fat and skin) (Figure 10-1).70 The skin is the final barrier between the body and the environment and functions as a conductive pathway for heat transfer to the environment, while also serving as the primary site to sense changes in environmental temperature. Skin temperature
37° C
36° C
37° C
Core
32° C
Core
Shell 28° C
34° C
31° C
Cold
Warm
FIGURE 10-1 Distribution of temperatures within the human body into core and shell during exposure to cold and warm environments. The temperatures of the surface and thickness of the shell depend on the environmental temperature: the shell is thicker in the cold and thinner in the heat. (From Elizondo RS: Human adaptation to hot environments. In Rhoades RA, Pflanger RG, editors: Human physiology, ed 3, Philadelphia, 1996, Saunders. Reprinted with permission of Brooks/Cole, a division of Thomson Learning. http://www.thomsonrights.com.)
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may fluctuate because of changes in environmental temperature, relative humidity, wind velocity, and radiation. Heat-transfer mechanisms are evoked in response to changes in body heat storage (S), which depends on metabolic rate, work, and the four avenues of heat exchange, as follows: S = M − (W) − (E) − (C) − (K) − (R) where M is metabolic rate, W is work, and E, C, K, and R are evaporative, convective, conductive, and radiant heat transfer, respectively.132 The impact of the four avenues of heat exchange on total body storage depends on a variety of organismal (e.g., age, gender, adiposity), environmental (e.g., humidity, wind velocity), and occupational (e.g., protective clothing, work intensity) variables. Under conditions in which heat production and/ or heat gain exceeds heat loss, such as during exercise or heat exposure, positive heat storage occurs and body temperature increases. When heat loss exceeds heat production and/or heat gain, such as during prolonged cold exposure, negative heat storage occurs and body temperature decreases.88 Endothermic animals use both autonomic and behavioral thermoeffector mechanisms to regulate body temperature. Autonomic thermoeffector responses are often referred to as “involuntary” and include sweating, vasodilation, vasoconstriction, piloerection (furred mammals), and shivering and nonshivering thermogenesis (brown fat heat production). Behavioral thermoeffector mechanisms are considered “voluntary” and include clothing changes, use of heat or air conditioning systems, huddling or use of blankets, fan cooling, and seeking of shade or shelter. Rather than working independently of one another, autonomic and behavioral thermoeffector mechanisms typically function in concert to maintain temperature control. For example, evaporative cooling in rodents requires autonomic stimulation of salivation and behavioral spreading of saliva onto nonfurred surfaces.104,294 Many large species in the wild use natural water sources to facilitate cooling. Elephants spray water onto their skin surface, and hippopotamuses and other species are often observed near or in watering holes. Water is a more effective medium to facilitate convective heat transfer than air, because of its high heat-transfer coefficient (approximately 25 times greater than air),305 even if the water temperature is tepid. However, voluntary suppression of behavioral mechanisms of cooling in humans can increase the risk for thermal injury. This is illustrated by older adults who refuse to use air conditioning systems or leave their residences during heat waves, or highly motivated athletes and military personnel who voluntarily dehydrate and/ or sustain a high rate of work in hot weather. Regulation of body temperature is best conceptualized as a negative-feedback system consisting of sensors, integrators, and effectors. In vertebrates, neurons in the skin, spinal cord, and abdomen sense thermal stimuli and convert those signals to action potentials that are transmitted by afferent sensory neurons to the preoptic area of the anterior hypothalamus (POAH). The POAH is considered the main central nervous system (CNS) site for thermoregulatory control because it receives and integrates synaptic afferent inputs and evokes corrective autonomic and behavioral thermoeffector responses for body temperature regulation.28 A diagrammatic representation of this negative-feedback loop is shown in Figure 10-2. The concept of a temperature set point was developed as a theoretical framework to examine regulated and unregulated changes in body temperature.19 The temperature set point is analogous to a thermostat that controls a mechanical heating device; under homeostatic conditions, body temperature is approximately equal and oscillates around the temperature set point. Environmental perturbations, such as heat and exercise, cause body temperature to deviate from the set-point temperature as heat gain and/or production exceeds heat loss and the organism becomes hyperthermic (body temperature is greater than the set-point temperature). During prolonged cold exposure, heat loss exceeds heat gain and/or production and the organism becomes hypothermic (body temperature is less than the set-point temperature) (Figure 10-3). Regulated increases and decreases in the temperature set point are referred to as fever and regulated hypothermia (also called anapyrexia), respectively, and are protective immune
Exercise
↑ Temperature Heat gain/production > heat loss ∆S>0 Thermal receptors (skin, spinal cord, abdomen) Sensory afferent signals Preoptic anterior hypothalamus (POAH) Thermoregulatory Integration Center Motor efferent signals Behavioral and autonomic thermoeffectors Heat loss > heat gain/production
thought to protect against injury and inflammation by reducing production of harmful enzymatic end products that compromise tissue function under conditions of low oxygen supply. In bumblebees, infected worker bees spend significantly more time in cooler temperatures outside of the nest than healthy worker bees; this cold-seeking behavior is associated with increased survival from parasitic infection.118,213 Mice inoculated with influenza virus also show cold-seeking behavior and develop regulated hypothermia, which is associated with improved infection outcome.153 Other environmental insults that induce regulated hypothermia in small rodents include hypoglycemia,34,98 hypoxia,194,252 hemorrhage,119 dehydration,129 infection,153,176,264 and heatstroke.173,174 Mechanisms of Heat Dissipation During Thermal Stress Cardiovascular mechanisms have evolved to shunt warm blood from the body core to the skin surface and increase heat loss during thermal stress. Arteriovenous anastomoses (AVAs) are collateral connections between adjacent blood vessels that increase the volume of blood that is delivered to a particular tissue. Mean skin blood flow can vary approximately 10-fold in humans depending on the thermal environment. The hands and feet are concentrated with AVAs that serve as effective areas for dry heat loss. The nonfurred surfaces of small rodents, such as the ears, tail, and paw pads, also have an abundance of AVAs and a large surface area to facilitate convective heat transfer.92,99 During exercise heat
↓ Total body heat storage FIGURE 10-2 Diagrammatic representation of the negative feedback pathway regulating core temperature in homeotherms. Climatic heat stress and exercise (metabolic work) cause heat gain/heat production to exceed heat loss (ΔS > 0) and increase body temperature above baseline. The increase in total body heat storage is sensed by thermal receptors in the skin, spinal cord, and abdomen, which transmit action potentials via sensory afferent nerves to the preoptic area of the anterior hypothalamus (POAH). The POAH receives and integrates synaptic afferent inputs and evokes corrective behavioral (e.g., fanning, removal of clothing) and autonomic (e.g., vasodilation, sweating) thermoeffector responses to decrease total body heat storage and return body temperature to baseline. Solid line indicates stimulatory pathway; dashed line indicates inhibitory pathway.
responses to infection, inflammation, or trauma. Fever is defined as a regulated increase in the temperature set point and is actively established and defended by heat-producing (e.g., shivering and nonshivering thermogenesis) and heat-conserving (e.g., peripheral vasoconstriction, huddling to reduce exposed body surface area) thermoeffectors (see Figure 10-3).132 An individual is considered normothermic once fever is established and body temperature oscillates around the new elevated temperature set point (see Figure 10-3). The highly regulated nature of fever was first suggested by Liebermeister in the 1800s when it was observed that individuals actively reestablished an elevation in body temperature following experimental warming or cooling.180,286 Fever is a protective immune response used by invertebrates, fish, amphibians, reptiles, and mammals to survive infection or injury.* The protective effects of fever are mediated by increased mobility and activity of white blood cells,218,313 increased production of interferon (IFN; antiviral and antibacterial agent) antibodies,64 and reduced plasma iron concentrations, the effects of all of which inhibit the growth of pathogens.89,156 In mammals, inhibition of fever using antipyretic drugs (e.g., aspirin) increases mortality from bacterial and viral infections, which speaks to the importance of fever as an immune response.126,315 Many species also develop regulated hypothermia to survive severe environmental insults. Regulated hypothermia is elicited in response to a decrease in the temperature set point and is actively established and defended by behavioral and autonomic heat-loss mechanisms.132 The Q10 effect states that each 10° C (18° F) change in body temperature is associated with a twofold to threefold change in enzymatic reaction rates. Based on this relationship, a regulated decrease in body temperature is *References 32, 54, 154, 216, 256, 316.
HYPERTHERMIA
HP = HL
HG/HP >HL
HL >HG/HP
HP = H L
Tset Tc
Heat stress, exercise FEVER
HP = HL HC/HP >HL
HP = HL
HL >HC/HP
Tset Tc
Infection, inflammation
FIGURE 10-3 The theoretic concept of core temperature (Tc) changes mediated by a change in the temperature set point (Tset). Hyperthermia represents an increase in Tc in the absence of a change in Tset. In response to climatic heat stress, exercise, or the combination of these factors, heat gain (HG) and/or heat production (HP) exceed heat loss (HL) and Tc rises above Tset as the organism becomes hyperthermic. In response to removal from the heat, cooling, or cessation of exercise, HL exceeds HG/HP and Tc returns to baseline. Fever is defined as a regulated increase in body temperature that is actively established and defended by behavioral and autonomic thermoeffector responses that increase heat conservation (HC) and/or HG and decrease HL to increase Tc to a new elevated level. The rising phase of fever is associated with shivering (increases HP) and the donning of blankets (increases HC). The individual feels “cold” until a new elevated level of Tc is attained. Note that while fever is maintained, Tc oscillates around Tset and the individual is considered normothermic with HP = HL. Once fever breaks, HL exceeds HC/HP as the individual sweats, removes clothing, and so forth, to return Tc to the baseline level.
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Heat stress
PART 2 COLD AND HEAT
stress, increased blood flow to the skin surface is accompanied by sweat secretion. The density, secretion rate, and activation threshold of regional sweat glands determine the volume of sweat loss at a body site. In humans, the back and chest have the highest sweat rates for a given body temperature change, whereas only approximately 25% of total sweat is produced by the lower limbs.217 Additional factors affecting sweat rate include clothing characteristics, environmental conditions, and rate of metabolic heat production. Panting is an effective method of evaporative heat dissipation in large animals, such as birds, dogs, sheep, and rabbits, and occurs at a resonant ventilation frequency that requires minimal energy expenditure.107,257,329 Humans and rodents do not pant per se, but breathing frequency and minute volume increase during severe heat exposure to facilitate evaporative cooling from the respiratory surfaces. In humans, the contribution of respiratory evaporative cooling is small compared with that of skin evaporative cooling (Figure 10-4).
DEHYDRATION AND ELECTROLYTE IMBALANCE Water requirements during heat exposure are primarily determined by a person’s sweat losses. Water depletion dehydration develops when the rate of water replacement is not adequate, which can be a result of a mismatch between fluid intake and sweat loss, lack of water availability, or use of diuretic medications. Sweat rates may range from 0.3 to approximately 3 L/hr during athletic or occupational activities, depending on the environmental conditions and type, duration, and intensity of work.47,143 If high sweat rates are maintained without adequate replenishment of lost water, this can cause electrolyte imbalances that impede the efficiency of autonomic mechanisms of thermoregulatory control. For example, hyperosmolarity alters heat responsiveness of warm-sensitive neurons in the POAH and limits the effectiveness of evaporative heat loss.121,219,276 Severe hypernatremic dehydration is associated with brain edema, intracranial hemorrhage, hemorrhagic infarcts, and permanent brain damage (Figure 10-5, online).214 Severe reductions in electrolytes can have a profound impact on heatstroke outcome. Symptomatic hyponatremia (decreased serum sodium concentration) is a relatively rare condition, but it has been observed in marathon runners and military recruits during training exercises as a consequence of overconsumption of hypotonic fluids with inadequate replacement of sodium losses.210,230 Intracellular swelling is a severe consequence of hyponatremia that may cause CNS dysfunction. Hypokalemia (decreased serum potassium concentration) may be caused by overproduction of aldosterone, excessive sweating, or respiratory alkalosis. Any cause of overproduction of urine (polyuria) potentially causes urinary potassium loss.323 Potassium is a potent vasodilator of blood vessels to the skeletal and cardiac muscles, so excessive loss of this electrolyte can have detrimental effects, such as decreased sweat volume, cardiovascular instability, and reductions in muscle blood flow that predispose to skeletal muscle injury (i.e., rhabdomyolysis).158,279
Heat Illnesses Heat illnesses are best viewed as existing along a continuum that transitions from the mild conditions of heat cramps and heat exhaustion to more serious conditions of heat injury and heatstroke (Table 10-1). Heat cramps are typically brief but can cause agonizing pain in the skeletal muscles of the limbs and trunk. Cramps may be recurrent but are typically confined to the skeletal muscles that are involved in vigorous exercise in the heat. Skeletal muscle spasms in the extremities may be sporadic, but they are painful and develop most frequently in persons who are not acclimatized to physical exertion. However, heat cramps may also occur in fit athletes who are salt depleted. Heat cramps do not predispose to more serious heat illness and are not associated with com plications beyond muscle soreness. The cause of heat cramps is not fully understood, but cramps are thought to occur in response to increased intracellular calcium release that stimulates actin– myosin filaments and muscle contraction. Current treatments 218
A
B
C FIGURE 10-4 Infrared images of various surface regions. The brighter the color, the warmer the surface temperature. A, Female runner after 45 minutes of exercise in a 23° C (73.4° F) environment. Note that the palms of the hands and the face are substantially warmer than the rest of the body surface. B, Two polar bears. Note that only the snout, eyes, ears, and footpads are noticeably different from the surroundings. C, Sled dog relaxing shortly after completing the 17.7-km (11mile) ceremonial starting leg of the 2005 Iditarod Trail Sled Dog Race. The course of the Iditarod is greater than 1850.7 km (1150 miles) from Anchorage to Nome, Alaska. Ambient conditions were 0° C (32° F) with a lightly overcast sky and no wind. The infrared shot shows that the dog’s entire snout is white, meaning it is the hottest part of the body surface. The armpits and ears also are warmer. Maybe that is why dogs love to roll around in the snow, face first, on a warm day. (A and B from Grahn D, Heller HC: The physiology of mammalian temperature homeostasis, TraumaCare 14:52, 2004, with permission; C courtesy D. Grahn, photo by Matthew Grahn.)
Condition
Symptoms
Management
Heat cramps Heat rash (miliaria rubra) Heat exhaustion
Brief, painful skeletal muscle spasms Blocked eccrine sweat glands
Rest; replacement of electrolytes; avoid salt tablets Cool, dry affected skin area; topical corticosteroids, aspirin Move supine individual to cool, shaded environment, and elevate legs; loosen or remove clothing, and actively cool skin; administer oral fluids Ensure an open airway, and move to a cool environment. Immediately cool to <39° C (102.2° F) using ice packs, water bath, wetting with water and continuous fanning; IV fluid administration; reestablish normal CNS function; avoid antipyretics or drugs with liver toxicity
Heatstroke
Mild to moderate illness with inability to sustain cardiac output; moderate (>38.5° C [101.3° F]) to high (>40° C [104° F]) body temperature; often accompanied by dehydration Profound CNS abnormalities (agitation, delirium, stupor, coma) with severe hyperthermia (>40° C [104° F])
Data from Bouchama A, Knochel JP: Heat stroke. N Engl J Med 346:1978, 2002; and Winkenwerder W, Sawka MN: Disorders due to heat and cold. In Goldman L, Ausiello DA, Arend W, et al, editors: Cecil textbook of medicine, ed 23, Philadelphia, 2007, Saunders, pp 763-767. CNS, Central nervous system; IV, intravenous.
include rest and replacement of electrolytes with fluids or salted food. Salt tablets should be avoided because they can cause gastrointestinal irritation and may stimulate excess potassium loss in the distal tubules of the kidneys. Heat exhaustion (also referred to as heat prostration or heat collapse) is a mild to moderate form of heat illness that is associated with moderate (>38.5° C [101.3° F]) to high (>40° C [104° F]) elevations in core temperature and an inability to sustain cardiac output.335 The signs and symptoms of heat exhaustion include fatigue, dizziness, headache, nausea, vomiting, malaise, hypotension, and tachycardia with potential for collapse. Heat exhaustion can occur with or without exercise in hot environments and may progress to a moderately severe condition without associated organ damage. Heat exhaustion is often observed in older adults as a result of medications (e.g., diuretics), inadequate water intake that leads to dehydration, or preexisting cardiovascular insufficiency that predisposes to collapse. Treatment should consist of placing the individual in a recumbent position in a cool environment to normalize blood pressure. Oral fluid ingestion with electrolytes is often adequate for recovery; intravenous (IV) fluid administration may be warranted in severely dehydrated individuals. Heat injury is a moderate to severe condition characterized by tissue (e.g., skeletal muscle) or organ (e.g., gut, kidney, spleen, liver) damage and hyperthermia (core temperature usually, but not always >40° C [104° F]).335 Heat injury may progress to heatstroke if the patient is not rapidly cooled. Heatstroke is life threatening, with the patient presenting with profound CNS abnormalities, such as delirium, agitation, stupor, seizures, or coma and severe hyperthermia (core temperature typically, but not always >40° C [104° F]).335 Reliance on a specific core temperature value for clinical diagnosis of heatstroke is ill advised, because there is wide interindividual variability in documented cases. One of the main reasons for a lack of clinical treatments for heatstroke is the complicated nature of the syndrome, because there are different classifications based on etiology and pathophysiologic mechanisms of injury. Classic (also known as passive) heatstroke occurs at rest in vulnerable individuals, such as infants and older adults. Several intrinsic factors may predispose infants to heatstroke death. These include increased surface area–to–body mass ratio (accelerates heat gain), limited effective mechanisms of thermoregulation (e.g., suppressed behavioral adjustments), increased risk for dehydration (e.g., lack of water availability), and preexisting respiratory infections. Many older individuals have preexisting conditions, such as mental illness, prescription drug use (e.g., diuretics, anticholinergics), or infections that predispose to passive heatstroke (Box 10-1).6,56,312 Exertional heatstroke (EHS) has a different etiology than classic heatstroke and affects young healthy populations that perform strenuous physical activity or work in temperate or hot weather. During exercise, approximately 80% of expended energy is released as heat that must be dissipated from the body to avoid hyperthermia. Military and athletic populations are composed of young, healthy individuals who are highly motivated to perform strenuous physical activity in hot weather, which increases the risk for EHS. A recent epidemiologic study identified a variety of factors
that predispose to EHS, including gender (women greater than men), geographic region of origin (northern greater than southern states), preexisting illness, and race or ethnicity (whites greater than blacks).40 Unfortunately, exercise induces physiologic responses similar to those of heat stress, such that teasing apart the influence of these two factors in EHS is difficult.
Heatstroke Epidemiology and Risk Factors The ability to perform strenuous work in a hot environment is inversely related to the heat stress level, which can be assessed BOX 10-1 Predisposing Risk Factors for Serious Heat
Illness
Environmental Factors High ambient temperature High humidity Lack of air movement Trees and shrubbery Access to air conditioning Lack of shelter Heat wave (3 or more days of temperatures >32.2° C [90° F]) Individual Factors Age (small children, older adults) Obesity Poor physical fitness level Lack of acclimatization Dehydration Drug Use Diuretics Anticholinergics (e.g., atropine) β-blockers (e.g., propranolol) Antihistamines Amphetamines (e.g., Ecstasy) Ergogenic aids (e.g., ephedra) Antidepressants Alcohol consumption Compromised Health Status Viral infection (e.g., pneumonia, mononucleosis) Inflammation (e.g., fever) Skin disorders (e.g., miliaria rubra, burns) Cardiovascular disease Diabetes mellitus Malignant hyperthermia Sickle cell trait Data from references 6, 58, 196, 318, and 340.
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CHAPTER 10 Pathophysiology of Heat-Related Illnesses
TABLE 10-1 Heat Illness Symptoms and Management
PART 2 COLD AND HEAT
using the wet bulb globe temperature (WBGT) index. The WBGT for indoor or outdoor environments is determined in the following manner: Indoor WBGT = 0.7 Tw + 0.3 Tamb Outdoor WBGT = 0.7 Tw + 0.2 Tbg + 0.1 Tamb where Tw is the natural wet bulb temperature, Tbg is the black globe temperature, and Tamb is the dry bulb temperature. Tbg determines the radiant heat load with a specialized thermometer that is surrounded by a 6-inch–diameter blackened sphere. The WBGT is the most widely used index to determine safe limits of physical activity and establish strategies to minimize the incidence of heat illness during military, athletic, or occupational tasks. The WBGT index does not take into consideration different clothing ensembles or exercise intensities, so the most practical and safe application of this measurement requires adjustment for these factors. Heat waves are defined as three or more consecutive days during which the environmental temperature exceeds 32.2° C (90° F).41 In the summer of 2003, Europe experienced 22,000 to 45,000 heat-related deaths during a 2-week period in which the average temperature was 3.5° C (6.3° F) above normal.189,273 The European continent has experienced an increase in minimum daily temperatures over the last 30 years, and this trend will likely increase if average global temperatures continue to rise. A 1.4° to 5.8° C (2.5° to 10.4° F) increase in minimum daily temperatures in Europe is predicted over the next century.131,337 Most prediction models suggest that heat waves in the future will be more severe and longer in duration. Predictions based on climate variability data from the 1995 Chicago and 2003 Europe heat waves suggest that by 2090, heat waves in these cities will be 25% to 31% more frequent and last 3 to 4 days longer.203 Another prediction model suggests a 253% increase in annual heatstroke deaths in the United Kingdom by 2050.61 The impact of climate change is not equally distributed across the globe because of regional variability in thermal tolerance that influences the incidence of heatstroke mortality. A study of 11 U.S. cities showed that threshold temperatures for heatstroke mortality are higher in warmer southern cities than in cooler northern cities.53 A comparison of temperature–mortality relationships in southern Finland, southeastern New England, and North Carolina indicated that lower temperature thresholds in cooler climates are coupled with steeper temperature–mortality relationships.62 Similarly, the upper safety limits of environmental temperatures in the Netherlands, London, and Taiwan are 16.5°, 19°, and 29° C (61.7°, 66.2°, 84.2° F), respectively.192 A case study of 15 Marine recruits who collapsed from heatstroke during training exercises in South Carolina showed that 73% previously resided in northern states and that 60% of cases occurred during the second week of training during the hottest summer months.232 From 1980 to 2002, the highest EHS incidence in military recruits was in nonacclimatized individuals from northern, cold-climate states who were enlisted for less than 12 months.40 During July, many regions of the world have a WBGT index that is greater than 29° C (84.2° F), and military training often occurs in environments with a WBGT index that is greater than 35° C (95° F). During peacetime exercises, approximately 25% of fatal military EHS cases occur during the hottest summer months in recruits who have been in training camp less than approximately 2 weeks.192 Individuals from northern states are expected to be less acclimatized to hot, humid summer conditions than are those from southern states. Heat acclimatization improves thermotolerance but requires several days to weeks of exposure to similar heat stress and exercise conditions to be fully effective. This likely accounts for hot days early in the summer showing a greater impact on heatstroke morbidity and mortality than those cases occurring later in the training process, after the protective effects of heat acclimatization have been realized.105 Humanity’s impact on the landscape in conjunction with increased production of greenhouse gases may be creating the largest climate change. Urban heat islands are created in cities when vegetation is removed and blacktop roads and concrete buildings are erected. Temperatures may be 30° to 40° C (54° to 72° F) higher on asphalt roads and roof tops compared with 220
those of the surrounding air.85 Since 1978 urban sprawl has accounted for an increase in city temperatures in southeastern Asia of approximately 0.05° C (0.09° F) per decade.343 Across the entire land mass of the United States, the surface temperature has increased approximately 0.27° C (0.49° F) per century because of changes in the land cover arising from agricultural and urban development.139 Concrete and asphalt surfaces cool slowly during the nighttime when air temperature decreases, and this increase in urban heat storage magnifies the intensity of heat exposure experienced by individuals living in concrete urban structures.49,165 Several social factors predispose older adults to heatstroke mortality, including living alone, inability or unwillingness to leave one’s home, residing on the top floor of buildings (heat rises), and annual income of less than $10,000.221 Most heat wave early warning systems emphasize use of air-conditioning systems, but availability and use of the units are limited by socioeconomic status because they are expensive to operate.56,221 A working air conditioner was the strongest protective factor against mortality during the 1999 heat wave in Chicago; fan cooling did not afford protection.221 High mortality rates were recorded in Chicago despite extensive programs to educate high-risk populations, such as advising older adults to seek cool shelters or use air-conditioning systems. Approximately 10,000 elders died during the France heat wave of 2003 primarily because of lack of air-conditioning units in residences and hospitals.63,312 In 2005, Hurricane Katrina ravaged the U.S. Gulf Coast, and electrical failures caused high heatstroke mortality of older adults confined to residences, retirement homes, and hospitals because local temperatures exceeded 43° C (109.4° F). Increases in the average human lifespan, global climate change, and use of medications that compromise cardiovascular adjustments to heat stress will necessitate increased reliance on artificial cooling systems and educational programs to prevent heatstroke deaths in vulnerable populations, such as older adults. The high death toll of older adults because of excessive heat per se may be small compared with that caused by aggravation of a preexisting illness. Heat stress refers to environmental and metabolic conditions that increase body temperature; heat strain refers to the physiologic consequences of heat stress. Heat strain imposes large cardiovascular demands on the body. Blood flow is shunted from the viscera to the skin surface to dissipate excess heat to the environment, making cardiovascular fitness a more important factor than age in determining an individual’s susceptibility to heatstroke. Austin and Berry10 examined 100 cases of heatstroke during three summer heat waves in St. Louis and found cardiovascular illness in 84% of patients. Levine181 found heatstroke deaths to be associated with arteriosclerotic heart disease (72%) and hypertension (12%). Cardiac deficiency impedes heat loss and compromises the ability to maintain cardiac output during prolonged heat exposure, leading to circulatory collapse and death. Older individuals may have impaired baroreceptor reflex modulation, lower sweat rates, longer time to onset of sweating, and diminished sympathetic nerve discharge, all of which increase the risk for heatstroke morbidity and mortality.130,144,291 Minson and colleagues210 demonstrated that during heat exposure, older men relied on a higher percentage of their cardiac chronotropic reserve compared with younger men. Preexisting infection or inflammation may compromise an individual’s ability to appropriately respond to heat stress and can be a complicating factor, regardless of age. Fifty-seven percent of heatstroke patients more than 65 years old had evidence of infection upon clinical admission during a Chicago heat wave in 1995.56,157 In Singapore, a young EHS victim had been ill for 3 days before heatstroke collapse.43 It has been proposed that acute illness or inflammation can cause transient susceptibility to heatstroke in young, fit individuals who exercise in the heat. For example, idiosyncratic episodes of hyperthermia were associated with acute cellulitis and gastroenteritis in soldiers exercising in the heat.39,146 Four male Marine recruits presented with viral illness (mononucleosis, pneumonia) before collapse from exertional heat illness (EHI) during training exercises associated with “the Crucible” at Parris Island, South Carolina.289 Peripheral blood mononuclear cells (PBMCs) from these recruits expressed higher levels of IFN-inducible genes than did those
SKIN DISORDERS The skin is the largest organ of the body and an important area for effective heat exchange with the environment. A number of skin disorders can adversely affect temperature control and increase susceptibility to heat illness. Miliaria rubra (also known as prickly heat, sweat rash, or heat rash) occurs when sweat gland ducts become blocked with dead skin cells or bacteria (e.g., Staphylococcus epidermidis). The obstruction causes eccrine secretions of the sweat glands to accumulate in the ducts or leak into the deeper layers of the epidermis, causing a local inflammatory reaction associated with redness and blisterlike lesions. Individuals with miliaria rubra are at increased risk for heat illness when a large area of the skin is affected. If heat illness is expected, the affected area of the skin should be cooled and dried to control infection, and topical corticosteroids or aspirin may be effective in reducing swelling and irritation. Sunburn can impair sweating and cause fever, which increase the risk for heat illness. If the sunburn covers more than 5% of the body, heat exposure should be avoided until the skin has healed. Sunburn is a preventable disorder with the use of sun-blocking lotions, protective clothing, and shelter from sun exposure.
Pathophysiology of Heatstroke The pathophysiologic responses to heatstroke range from those conditions that are experienced immediately following collapse to long-term changes that persist for several weeks, months, or years following hospital treatment and release. Currently more is known about the immediate heatstroke responses because clinical records document symptoms during hospital treatment. However, clinical and experimental research has seen a shift within the past decade toward a focus on understanding the pathophysiologic responses that mediate long-term injury. It is now believed that the long-term pathophysiologic responses to heatstroke are caused by a systemic inflammatory response syndrome (SIRS) that ensues following heat-induced damage to the gut and other organs.24 Following damage to the epithelial membrane of the gut, endotoxin that is normally confined to the lumen of this organ is able to leak into the systemic circulation and elicit immune responses that cause tissue injury. The thermoregulatory, immune, coagulation, and tissue injury responses that ensue during the long-term progression of heatstroke closely resemble those observed during clinical sepsis and are likely mediated by similar cellular mechanisms. Clinical records have provided an extensive database of the immediate consequences of heatstroke, whereas the majority of knowledge regarding the pathophysiologic mechanisms of heat-induced SIRS has been obtained from experimental animal studies. Although there are several gaps in our knowledge of the specific factors that predispose to multiorgan system failure, this is an exciting area of research that is expected to progress at a rapid rate because of continued advancements in experimental and genetic technologies. Figure 10-6 provides an overview of the current understanding of the pathophysiologic responses that are thought to initiate and mediate heat-induced SIRS, which will be discussed in detail here.
BODY TEMPERATURE RESPONSES At the time of heatstroke collapse, the severity of hyperthermia varies widely between individuals, with reported core temperature values ranging from approximately 41° C (105.8° F) to 47° C (116.6° F).* During a summer heat wave in St. Louis in the 1950s, the core temperature of 100 heatstroke patients ranged from 38.5° to 44° C (101.3° to 111.2° F), with 10% of mortalities occurring below 41.1° C (106° F).10 In some instances, individuals may tolerate hyperthermia without adverse side effects. During a competitive marathon race in California, a 26-year-old man maintained a rectal temperature of 41.9° C (107.4° F) for approximately 45 minutes without clinical signs of heat illness.197 However, there are several reports of athletic, military, and occupational workers with core temperatures below 41.9° C (107.4° F) who were hospitalized, experienced permanent CNS impairment, or died from EHS (Table 10-2). Hypothermia and fever are core temperature responses that are often observed in patients and experimental animal models during heatstroke recovery. Hypothermia is not a universal heatstroke recovery response in humans but has been anecdotally observed following aggressive cooling treatment. Hypothermia manifests as a rapid undershoot of body temperature below 37° C (98.6° F) and is thought to represent a loss of thermoregulatory control following heat-induced damage to the POAH. However, evidence in support of this hypothesis is lacking because autopsy reports and experimental animal studies have failed to detect histologic damage to the POAH despite extensive damage in other organs.174,192 Because hypothermia is not observed in all heatstroke patients, it continues to be regarded as a pathologic recovery response. In experimental animals, hypothermia is a natural heatstroke recovery response that is associated with behavioral and autonomic thermoeffector responses that support a decrease in core temperature. Mud puppies are ectothermic species that rely on behavioral adjustments, such as the selection of different microclimates, to control body temperature. Mud puppies heat shocked to approximately 34° C (93.2° F) *References 26, 42, 109, 112, 188, 289.
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CHAPTER 10 Pathophysiology of Heat-Related Illnesses
from controls who participated in the training event but did not collapse.289 High plasma levels of IFN-α and IFN–γ mediate flulike symptoms during viral infection and are often associated with EHI/EHS.24,289 In rats, exposure to lipopolysaccharide (LPS), a cell wall component of gram-negative bacteria, exacerbated inflammation, coagulation, and multiorgan system dysfunction from heat exposure.182 Taken together, these findings suggest that a preexisting inflammatory state compromises an individual’s ability to respond to heat stress with appropriate thermoregulatory or immune responses to prevent collapse or multiorgan system failure and death. The annual Muslim pilgrimage to Mecca (i.e., the Hajj) is associated with high heatstroke incidence each year and provides many lessons regarding etiologic factors that increase susceptibility. The Hajj takes place in the hot desert environment of Saudi Arabia during the extreme weather months of May to September, when temperatures range from 38° to 50° C (100.4° to 122° F).151 Hot weather combined with physical exertion (first day consists of a 3.5-km [2.2-mile] jog), heavy clothing that is traditional to the region (limits heat dissipation), and an older population (approximately 50 years is an advanced age for this region) predispose many individuals to heatstroke. Clothing has a significant impact on Muslim women because they are required to wear darker clothing that covers a larger surface area of the body than does clothing worn by men.114 Medical conditions, such as diabetes, cardiovascular abnormalities, or parasitic diseases, are common.151 Heatstroke is a major concern, but heat exhaustion with water or salt depletion is also prevalent. Overcrowding and congestion impose large demands on sanitation services, as exemplified in the 1980s, when approximately 2 million people participated in the Hajj. Advances in modern technologies, such as more rapid transport to the area, will likely introduce additional factors (e.g., lack of acclimatization, increased greenhouse gas production, increased congestion) to this already complex situation. Protective clothing is a significant predisposing factor to EHS during athletic (heavy uniforms), military (chemical protective clothing), or occupational activities (e.g., pesticide application, firefighting, and race car driving). Protective clothing often consists of multiple layers that insulate anatomic sites from heat exchange, including the skin and head.251 The wearing of protective clothing during strenuous work can quickly result in a dangerous elevation in body temperature. Fifty-one cases of EHI were observed in military trainees in San Antonio, Texas, during participation in a 9.3-km (5.8-mile) march in full battle dress uniform and boots.285 Lack of acclimatization to athletic uniforms and high environmental temperatures results in the majority of cases of EHS in athletes occurring on the second or third day of exposure to hot weather before these individuals are acclimatized to the uniforms and environmental temperatures.97,260
PART 2 COLD AND HEAT
Climatic heat stress and exercise
Heat strain
Cardiovascular responses Gut constricts
Skin dilates
Heat cytotoxicity (Intestine, kidney, spleen, endothelium) HSPs
Ischemia ↑ Gut epithelial membrane permeability Increased tight junction permeability
Systemic inflammatory response syndrome (fever, DIC, rhabdomyolysis, tissue injury) Anergy (Th1 > Th2 response)
Endotoxin
Innate immune system TLR4
Multi-organ system failure
Cytokines
Adaptive immune system FIGURE 10-6 Summary of heatstroke pathophysiologic responses that culminate in multiorgan system failure. An increase in heat strain stimulates a reflexive increase in cutaneous blood flow and decrease in splanchnic blood flow to facilitate heat dissipation to the environment. Gut ischemia causes increased epithelial membrane permeability and leakage of endotoxin into the systemic and portal circulation. Toll-like receptors (e.g., TLR4) detect pattern-associated molecular patterns on the cell membrane of endotoxin and stimulate proinflammatory and antiinflammatory cytokine production. Heat is toxic to several organs and stimulates secretion of heat shock proteins (HSPs) that interact with cytokines and other proteins to mediate the systemic inflammatory response syndrome (SIRS) of the host. Peripheral and central nervous system actions of cytokines and other mediators of SIRS are thought to mediate many of the adverse consequences of the heatstroke syndrome that lead to multiorgan system failure and death. DIC, Disseminated intravascular coagulation.
behaviorally selected a cooler microclimate and maintained a significantly lower body temperature than did nonheated controls during 3 days of recovery.130 This study did not determine the impact of hypothermia on survival, but the association of decreased body temperature with the selection of cool microclimates indicated that this was a regulated response to a decrease in the temperature set point. Small rodents, such as mice, rats, and guinea pigs, showed reductions greater than 1.0° C (1.8° F) in body temperature that were associated with improved survival following passive heatstroke. In mice, hypothermia was associated with an approximately 35% decrease in metabolic heat production and the behavioral selection of microclimates that precisely regulated the depth and duration of this response.174 Exposure of mice to warm ambient temperatures that prevented heat-induced hypothermia caused increased intestinal damage and mortality.173,333 Hypothermia likely provides protection against heat-induced tissue injury in a manner similar to that shown for protection against other extreme environmental insults based on the temperature coefficient (Q10) effect. A common heatstroke recovery response observed in patients and animal models is recurrent fever during the days and weeks of recovery.9,10,173,192,204 In mice, fever was observed within a day after passive heatstroke collapse and associated with an approximately 20% increase in metabolic heat production and increased plasma levels of the proinflammatory cytokine interleukin (IL)6.154,172,174 IL-6 is an important regulator of fever during infection and inflammation and may regulate fever during heatstroke recovery.172 In patients, fever is reestablished following clinical cooling.192 This is reminiscent of Liebermeister’s experimental observations of the recurrence of fever following experimental cooling of the POAH of rats.180,192 In experimental animal models, the inability to recover from hypothermia and develop fever is associated with increased mortality, suggesting that fever may be important for the resolution of infection.173 However, in a case report of human heatstroke, fever was associated with poor outcome. An amateur long-distance runner was hospitalized for 10 days after collapsing from EHS during a 9.7-km (6-mile) footrace.204 Moderate fever (>38° C [100.4° F]) was evident during the first 4 days of hospitalization, but on the tenth day the patient experienced convulsions and a rapid increase of body temperature to 41° C (105.8° F). Rapid cooling and aspirin were ineffective in reducing body temperature, and the patient died.204 The inability of aspirin to inhibit the rapid rise in body temperature suggests that this was not a true fever response, but rather a pathologic response to increased metabolic heat production induced by the convulsions. It is important to recognize that there is an optimal temperature range above which the protective
TABLE 10-2 Clinical Characteristics of Exertional Heat Illness Cases Activity Military Training Army (aviation) Army (basic) Army (basic) Army (Singapore) Marine Corps Marine Corps Marine Corps NBC Athletic Events 6-Mile run Marathon run Marathon run Hajj rituals Migrant farming Firefighter training
Body Temperature ° C (° F)
Age (Years)
Length of Hospitalization
>39.0 (102.2) 40-41.1 (104-106) 41.1 (106) 40-42 (104-107.6)† <38.9-40.0 (102-104) 39-42.5 (102.2-108.5)†‡ 41.1 (106) 41.3 (106.3)
18-59 18-41 20 18-29 17-30 17-19 NR 25
10 min 24 hr to 12 d 5d 45 min to 99 hr None >1 d ≤12 hr 12 d
CNS dysfunction207,* Death192 Recovery233 Death43 Recovery106 Recovery289 Hospitalization106 Recovery51
39.2 (102.6)§ 40.7 (105.3)‡ 41.9 (107.4) <42 (107.6) ≥42 (107.6) 43.9 (111) 42.2 (108) 42.6 (108.7)
29 Late 30s 26 32-80 NR NR 44 22
10 d 5d None NR NR NR None 9d
Death204 Recovery261 Recovery197 Ataxia, infarction, death341 Death341 Recovery341 Death220 Death219
CNS, Central nervous system; NR, not reported; NBC, nuclear, biological, and chemical protective clothing. *CNS dysfunction includes agitation, confusion, disorientation, delirium, poor memory, convulsions, and/or coma. † Indicates patient cohorts with documented prodromal illness before heatstroke collapse. ‡ Body temperature measured several minutes after collapse or cooling. § Patient temperature increased to 41° C (105.8° F) on day 10 of hospitalization before death.
222
Outcome
TABLE 10-3 Toll-Like Receptors of the Innate
IMMUNE RESPONSES
Toll-Like Receptor
Ligand
Cell/Tissue Types
TLR1
Triacyl lipopeptide
TLR2
Lipopolysaccharide Peptidoglycan Lipoteichoic acid Measles virus Human cytomegalovirus Hepatitis C virus Zymosan Necrotic cells Viral double-stranded RNA
Monocytes, macrophages, DCs, polymorphonuclear leukocytes, B and T cells, NK cells Monocytes, granulocytes Brain, heart, lung, spleen
During heat stress, blood flow to the skin is increased to facilitate heat loss to the environment and reduce the rate of total body heat storage. Increased skin blood flow is accompanied by a fall in splanchnic (i.e., visceral organ) blood flow as a compensatory mechanism to sustain blood pressure. Endotoxin is normally confined to the gut lumen by tight junctions of the epithelial membrane, but these junctions can become “leaky” following prolonged reductions in blood flow that cause ischemic stress.108,164 There are several lines of evidence that support the hypothesis that endotoxin leakage from the gut lumen into the systemic circulation is the initiating stimulus for heat-induced SIRS. First, systemic injection of LPS into experimental animals induces symptoms similar to those observed in heatstroke, including hyperthermia, hypothermia, fever, hypotension, cytokine production, coagulation, and tissue injury.175,268 Second, increased portal or systemic endotoxin levels are observed in heatstroke patients and animal models. In primates, circulating endotoxin was detected at rectal temperatures above 41.5° C (106.7° F) with a precipitous increase at approximately 43.0° C (109.4° F).90 Splanchnic blood flow shows an initial decrease at 40° C (104° F); the liver, which is an important clearance organ for endotoxin, shows damage at body temperatures of approximately 42° to 43° C (107.6° to 109.4° F).* In a young athlete with a body temperature of 40.6° C (105.1° F) on the second day of football practice, high circulating levels of endotoxin were associated with hemorrhagic necrosis of the liver.97 In heatstroke patients, endotoxin was detected at approximately 42.1° C (107.8° F) and remained elevated despite cooling.26 Third, rats rendered endotoxin tolerant following the systemic injection of LPS are protected from heatstroke mortality.66,67 The protective effect of endotoxin tolerance is related to enhanced stimulation of the liver reticuloendothelial system (RES), which is composed of monocytes, macrophages, and Kupffer cells that are important for endotoxin clearance.66,67 RES stimulation reduced and RES blockade increased mortality of heat-stressed rats.67 Fourth, antibiotic therapy protects against heatstroke in several species. In dogs, antibiotics reduced gut flora levels and improved 18-hour survival rates by more than threefold when provided before heat exposure.37 In rabbits with heatstroke, hyperthermia and endotoxemia were reduced following oral antibiotics.36 Anti-LPS hyperimmune serum reversed the heatstroke mortality rates of primates and returned plasma LPS levels to baseline, but it was ineffective at the highest body temperature of 43.8° C (110.8° F), indicating that hyperthermia can cause irreversible organ damage and death.91 Heat-induced SIRS is initiated by the innate and adaptive immune systems, which interact to sense the presence of endotoxin and orchestrate an immunologic response. The innate immune system comprises monocytes, macrophages, and neutrophils that use pattern recognition receptors (PRRs) on their cell surfaces to recognize pattern-associated molecular patterns (PAMPs) on the cell surface of endotoxin and other invading pathogens.137 Toll-like receptors (TLRs) are a class of PRRs that have been widely studied in the immune response to infection.208,314 Ten mammalian TLRs have been identified, and the specific pathogenic ligands that activate these PRRs are known (Table 10-3). TLR4 is the principal receptor for LPS that stimulates gene transcription factors, such as NF-κB, to increase the synthesis of a variety of immune modulators in response to endotoxin. Endotoxin infection (i.e., sepsis) is associated with increased expression of TLR4 on circulating human PBMCs, as well as on mouse liver and spleen macrophages.307,308 In the 1960s, a spontaneous mutation in the TLR4 gene was discovered in C3H/HeJ mice, which has been an important animal model to determine the role of TLR4 in endotoxin responsiveness. C3H/HeJ mice show a diminished response to bacterial infection, but increased mortality from SIRS, because of an inability to respond appropriately *References 29, 30, 43, 108, 147, 225.
Immune System
TLR3
TLR4
TLR5
Lipopolysaccharide Fibrinogen Heat shock proteins High mobility group box 1 Flagellated bacteria
TLR6
Diacyl lipopeptide
TLR7
Single-stranded RNA
TLR8
Single-stranded RNA
TLR9
CpG DNA
TLR10
Unknown
DCs, T cells, NK cells, monocytes, granulocytes Placenta, pancreas B cells, DCs, monocytes, macrophages, granulocytes, T cells Spleen Monocytes Ovary, prostate B cells, monocytes Thymus, spleen, lung Monocytes, B cells, DCs Lung, placenta, spleen, lymph node, tonsil Monocytes Lung, placenta, spleen, lymph node, bone marrow, PBLs B cells, DCs Spleen, lymph node, bone marrow, PBLs B cells Spleen, lymph node, thymus, tonsil
Data from Medvedev AE, Sabroe I, Hasday JD, et al: Tolerance to microbial TLR ligands: Molecular mechanisms and relevance to disease, J Endotoxin Res 12:133, 2006; and Tsujimoto H, Ono S, Efron PA, et al: Role of Toll-like receptors in the development of sepsis, Shock 29:315, 2008. CpG, Deoxycytidylate-phosphate-deoxyguanylate; DC, dendritic cell; DNA, deoxyribonucleic acid; NK, natural killer; PBL, peripheral blood leukocyte; RNA, ribonucleic acid.
to endotoxin and induce the full complement of immune responses.103 Inability to respond to antigens is known as anergy and is a proposed mechanism that predisposes to increased risk and mortality from bacterial infection.117 Given that TLR4 mutations exist in humans, this may be one (of several) genetic factors that predispose to mortality associated with heat-induced SIRS, although the association of mortality with TLR4 polymorphisms remains controversial.5,75 C3H/HeJ mice have not been tested for their resistance to heatstroke morbidity/mortality but are a useful experimental model to determine the roles of TLR4 and anergy in this syndrome. Specificity of immune responses is provided by B and T cells of the adaptive immune system. These cells respond to antigens by secreting cytokines, which are intercellular immune signals that elicit proinflammatory (Th1 type) and antiinflammatory (Th2 type) actions during the progression of SIRS. The actions of cytokines depend on the nature of the danger signal, the target cells with which they interact, and the cytokine “milieu” in which they function. Th1 and Th2 cytokines function in a negative feedback pathway to regulate each other’s production and maintain a delicate balance of inflammatory reactions. Anergy is thought to be a consequence of inadequate Th2 cytokine production late in SIRS. For example, increased patient mortality from peritonitis is associated with the inability to mount a Th2 cytokine response.117 223
CHAPTER 10 Pathophysiology of Heat-Related Illnesses
effects of fever are no longer realized because of the toxic effect of high body temperature on cell function.155
PART 2 COLD AND HEAT
Alarmins are endogenous PAMPs that are released from stressed or injured tissues and initiate restoration of homeostasis following an infectious or inflammatory insult.17 High mobility group box 1 (HMGB1) is a highly conserved nuclear protein that functions as an alarmin following release from necrotic (but not apoptotic) cells.272 Necrosis is the premature death of cells in a tissue or organ in response to external factors, such as pathogens and toxins. Because necrosis is detrimental to the host, it is associated with an inflammatory response. Apoptosis refers to genetically programmed cell death that does not elicit an inflammatory response, because apoptosis is beneficial to the host. Release of HMGB1 from necrotic cells stimulates Th1 cytokine production late in the sepsis syndrome and is a purported mediator of lethality; this shift in the balance of cytokines from a Th2 to Th1 phenotype is a potential mechanism of sepsis lethality. In human PBMCs, HMGB1 interacts with TLR2 and TLR4 to enhance Th1 cytokine production in synergy with LPS.124 Elevated serum HMGB1 levels are observed 8 to 32 hours following LPS injection in mice. Anti-HMGB1 antibodies did not protect against LPSinduced mortality unless the antibodies were provided 12 and 36 hours after LPS exposure.324 The delayed kinetics of HMGB1 and the association of elevated serum levels of this protein with poor outcome in sepsis patients suggest that HMGB1 detection late in SIRS may be a sensitive clinical marker of disease severity.115,297,324
Extrinsic pathway TISSUE INJURY
Intrinsic pathway CONTACT ACTIVATION
Tissue Factor (TF)
Factor VII
Factor VIIa
Factor XIIa Factor XIa Factor IXa
Factor XII Factor XI
Factor IX
VIIIa
Factor V
Factor Xa Factor Va
Anticoagulation Protein C
Factor X
Protein S
Activated protein C (APC) Prothrombin
Thrombin
Factor VIIIa
Fibrinogen
Fibrin
Factor VIII
Clot
COAGULATION Disseminated intravascular coagulation (DIC) is a common clinical symptom of heatstroke and manifests in two different forms (Figure 10-7). Microvascular thrombosis is a form of DIC characterized by fibrin deposition and/or platelet aggregation that occludes arterioles and capillaries and predisposes to multiorgan system dysfunction.177 Microvascular thrombosis is commonly observed in response to sepsis or trauma. DIC associated with consumptive coagulation is characterized by excessive blood loss when platelets and coagulation proteins are consumed faster than they are produced.8,12 Hemorrhagic complications in heatstroke victims include prolonged bleeding from venipuncture sites or other areas (e.g., gums), which can have a fatal outcome.148 The primary event that initiates coagulation in heatstroke patients is thermal injury to the vascular endothelium.21,24,215 In vitro studies have shown the ability of heat (43° to 44° C [109.4° to 111.2° F]) to directly activate platelet aggregation and cause irreversible hyperaggregation despite cooling.87,333 Cancer patients treated with whole-body hyperthermia (41.8° C [107.2° F] for 2 hours) showed decreased fibrinogen and plasminogen at body temperatures as low as 39° C (102.2° F), alterations in factor VII activity at 41.8° C (107.2° F), and decreased platelet concentrations from the time of maximum body temperature through 18 hours of recovery.295 Several proteins, including HMGB1, IL-1, tumor necrosis factor (TNF), and activated protein C (APC), affect the coagulation, anticoagulation, and fibrinolytic pathways. In rats, HMGB1 in combination with thrombin caused excess fibrin deposition in glomeruli, prolonged clotting times, and increased sepsis mortality compared with thrombin alone.133 The effect of HMGB1 protein was demonstrated in vitro to be caused by inhibition of the APC pathway and stimulation of tissue factor expression on monocytes.133 Cytokines stimulate microvascular thrombosis by interacting with neutrophils, macrophages, platelets, and endothelium to increase expression of intracellular adhesion molecules. Increased expression of cell adhesion molecules, neutrophil adhesion, and release of reactive oxygen species caused endothelial activation and injury.201,330 APC is an important component of the anticoagulation pathway that inactivates factors Va and VIIIa to inhibit fibrin clot formation. In septic patients, reduced APC production was associated with increased risk of mortality from systemic inflammation and DIC.78,179 In addition to its anticoagulation properties, APC possessed antiinflammatory and antiapoptotic properties that protected against experimental sepsis and heatstroke.44,302 Typical clinical measures of coagulation include prothrombin time (PT), activated partial thromboplastin time (aPTT), and 224
Plasminogen activator Inhibitor 1
Fibrinolysis Plasminogen tPA
Plasmin
Fibrin degradation products
FIGURE 10-7 Pathways of disseminated intravascular coagulation (DIC). The coagulation cascade is stimulated by the extrinsic pathway (also known as the tissue factor [TF] pathway) and the intrinsic pathway (also known as the contact activation pathway). Both pathways represent a series of enzymatic reactions that result in formation of a fibrin clot. Fibrinolysis represents the pathway by which the fibrin clot is resorbed through the actions of plasmin. The major physiologic anticoagulant is protein C, which is activated by protein S and inactivates factors Va and VIIIa to inhibit clot formation. Lipopolysaccharide, interleukin-1, and tumor necrosis factor affect DIC by stimulating TF formation and inhibiting the inactivation of factors Va and VIIIa, which prolong clot formation.
fibrinogen. PT in combination with aPTT assesses the time for plasma clot formation to occur in response to exogenous tissue factor and is a sensitive measure of responsiveness of the coagulation pathway. The reference range for PT is approximately 12 to 15 seconds and may be prolonged severalfold in heatstroke patients. The aPTT normally ranges from approximately 30 to 40 seconds and is used clinically to monitor treatment effects of anticoagulants, such as heparin. Fibrinogen is an acute phase protein synthesized by the liver that is normally in the range of 2 to 4 g/L. Low fibrinogen levels indicate liver damage or DIC, whereas elevated levels are a clinical sign of systemic inflammation. DIC can be difficult to diagnose, but low fibrinogen levels with prolonged PT or aPTT are strong clinical indicators in critically ill patients.
TISSUE INJURY Multiorgan system failure is the ultimate cause of heatstroke mortality and is a consequence of SIRS, which ensues following heat-induced damage to the gut and other tissues.24 A variety of noninfectious and infectious clinical conditions are associated with SIRS, and similar physiologic mechanisms are thought to mediate the pathogenesis of these conditions (Box 10-2). The term sepsis refers to SIRS associated with the presence of infection. Much of the understanding of pathophysiologic mechanisms mediating heat-induced SIRS has been obtained from sepsis studies. Provided here is an overview of the responses that constitute heat-induced SIRS and current understanding of
Illness
Clinical Neurologic symptoms (fatigue, weakness, confusion, stupor, coma, dizziness, delirium) Tachycardia Nausea, vomiting, diarrhea Headache Hypotension Oliguria, multiorgan system failure Hyperventilation Shock Laboratory Metabolic acidosis Elevated hematocrit Elevated blood urea nitrogen (BUN), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) Elevated lactate Disseminated intravascular coagulation Elevated cytokines Circulating endotoxin
the pathophysiologic mechanisms that mediate the adverse events of this syndrome. The severity of heatstroke is primarily related to the extent of damage to the brain, liver, and kidneys and is clinically identified by elevations in serum biomarkers, such as creatine kinase (CK), blood urea nitrogen (BUN), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). CK is released from muscle and is a marker of skeletal muscle injury (also known as rhabdomyolysis), myocardial infarction, muscular dystrophy, and acute renal failure.1,274,322 BUN is a measure of the amount of nitrogen in the blood in the form of urea, which is secreted by the liver and removed from the blood by the kidneys. A high BUN concentration is typically regarded as an indication of impaired renal function, although BUN levels may be altered by conditions unrelated to heat illness, including malnutrition, highprotein diets, burns, fever, and pregnancy.1,267 AST is released by the liver and skeletal muscle and may be a clinical sign of congestive heart failure, viral hepatitis, mononucleosis, or muscle injury. ALT is released by the liver, red blood cells, cardiac muscle, skeletal muscle, kidneys, and brain tissue. AST and ALT are common clinical markers of liver function in heatstroke patients despite multiple tissue sources of these enzymes and occasional false-negative results that complicate interpretation. Unfortunately, all of these biomarkers are released by a variety of tissues and altered by heat-exhaustive exercise, so they do not always provide a precise measure of the extent of tissue injury.95,102,283 The extent and time course of organ injury vary widely between individuals. Tissue injury manifests as primary and/or secondary multiorgan dysfunction, depending on whether heat toxicity alone or in combination with SIRS causes cellular damage.4,192 Gut epithelial barrier disruption is an example of primary organ dysfunction that is evident at the time of heatstroke collapse. Hyperthermia degrades epithelial membrane integrity and causes microhemorrhages, dilation of the central lacteals of the microvilli, and blood clots within the stomach and small intestine (Figure 10-8).27,108,172 It is often difficult to determine if organ injury is caused by primary or secondary factors.* For example, protein clumping in kidney tubular epithelial cells may be a consequence of heat toxicity, elevated myoglobin levels, or DIC.† A conscious mouse model has shown that kidney damage is present within approximately 2 hours following heatstroke collapse and remains elevated through approximately 24 hours of recovery.172 In heatstroke patients, acute renal failure is a nearly universal finding that is accompanied *References 21, 56, 97, 171, 172, 192. † Reference 27, 43, 97, 147, 172, 188, 249, 323.
by decrements in function within 24 hours of admission to the intensive care unit.244 In patients that survive more than 24 hours, severe hypotension, dehydration, BUN, and oliguria are associated with tubular necrosis or intertubular edema.192 Primary changes in the spleen are even less well understood, but cytoplasmic protein clumping is thought to be a consequence of this organ being “simply cooked and coagulated.”43,172 CNS dysfunction is a hallmark of heatstroke that is dominant early in the disorder. Patients are often confused, delirious, combatant, or comatose at the time of clinical presentation. Hyperthermia with exercise is also associated with reduced cerebral blood flow, which may account for these CNS abnormalities.228 Despite rapid treatment, approximately 30% of heatstroke survivors experience permanent decrements in neurologic function.6,24,56 CNS dysfunction is often associated with cerebral edema and microhemorrhages at autopsy in heatstroke patients.* The blood–brain barrier (BBB) is a semipermeable membrane that allows selective entry of substances (e.g., glucose) into the brain while blocking the entry of other substances (e.g., bacteria). Hyperthermia increases BBB permeability in experimental animal models, which permits leakage of proteins and pathogens from the systemic circulation into the brain. Computed tomography (CT) scans have been used to examine CNS changes in heatstroke patients. In the 1995 Chicago heat wave, atrophy, infarcts of the cerebellum, and edema were evident in older adult victims. CT scans also revealed severe loss of gray-white matter discrimination (GWMD), which was associated with headache, coma, absence of normal reflexive responses, and multiorgan dysfunction.299 Loss of GWMD is a consequence of increased brain water content, which is in line with occurrence of edema in heatstroke victims. If GWMD provides an early, sensitive measure of brain injury, it will be a powerful prognostic indicator of outcome for heatstroke patients. EHS is often associated with rhabdomyolysis, which is a form of skeletal muscle injury caused by the leakage of muscle cell contents into the circulation or extracellular fluid. Myoglobin released from damaged muscle cells is filtered and metabolized by the kidneys. When severe muscle damage occurs, the renal *References 48, 140, 192, 281, 282, 284, 299.
15 min
30 min
45 min
60 min
FIGURE 10-8 Effect of heating on villus structure. Representative light micrographs of rat small intestinal tissue over a 60-minute course at 41.5° to 42° C (106.7° to 107.6° F). Note the generally normalappearing villi at 15 minutes (slight subepithelial space at the villous tips), compared with initial sloughing of epithelia from villous tips at 30 minutes, massive lifting of epithelial lining at top and sides of villi at 45 minutes, and completely denuded villi at 60 minutes. Bars represent 100 µm. (From Lambert GP, Gisolfi CV, Berg DJ, et al: Selected contribution: Hyperthermia-induced intestinal permeability and the role of oxidative and nitrosative stress, J Appl Physiol 92:1750, 2002, with permission.)
225
CHAPTER 10 Pathophysiology of Heat-Related Illnesses
BOX 10-2 Predisposing Risk Factors for Serious Heat
PART 2 COLD AND HEAT
threshold for filtration of myoglobin is exceeded, and this protein appears in the urine in a reddish brown color.86 Myoglobin is toxic to nephrons and causes overproduction of uric acid, which precipitates in the kidney tubules to cause acute renal failure, coagulopathy, and death if not rapidly detected and treated.11,86,185,242,323 Not all cases of rhabdomyolysis are associated with myoglobinuria; many patients can be asymptomatic. Clinical markers of rhabdomyolysis include elevated myoglobin, CK, aldolase, lactate dehydrogenase, ALT, and AST, which are influenced by a variety of factors (type, intensity, and duration of exercise; gender; temperature; altitude) and released by more than one organ or tissue.50,205,263 If a clinical diagnosis of rhabdomyolysis is confirmed, immediate medical attention is imperative because approximately 50% mortality rates from acute renal failure have been documented for this condition. Liver failure is one of the most common causes of morbidity and mortality in patients during the later stages of recovery. The time course of liver damage differs from that of the other organs and often does not peak until approximately 24 to 48 hours after heat exposure. For example, liver damage consisting of centrilobular degeneration and necrosis with parenchymal damage was only evident in EHS patients that survived more than 30 hours.192 In addition, enhanced breakdown of fat or an inability of the mitochondria to use fat results in heatstroke-associated fatty liver changes.43 Disturbances in plasma glucose homeostasis are a sign of liver damage that may cause hyperglycemia or hypoglycemia as a result of dysfunction of phosphoenolpyruvate carboxykinase, which is a regulatory enzyme of the liver’s gluconeogenic pathway.21,171,172 Liver dysfunction may also contribute to increased circulating endotoxin levels because of the important bacterialclearance function of this organ.30,225 Unfortunately, many heatstroke patients require liver transplantation. Use of antipyretic drugs, such as acetaminophen (Tylenol), has been associated with hepatic failure.93,113,114,269,319 Many patients are released from the hospital following several days or weeks of treatment and continue to experience organ dysfunction during the ensuing years of recovery. Following the 2003 heat wave in France, mortality rates increased from 58% at day 28 of hospitalization (mean hospital stay was 24 days) to 71% mortality by the second year of recovery.6 An epidemiologic study of military EHS patients showed an approximately twofold increased risk for death from cardiovascular, kidney, and liver disease within 30 years of hospitalization.321 Several of the clinical responses (hyperthermia, dehydration, kidney and liver damage) occurring during progression or shortly after heatstroke collapse are clinically recognized and treated. However, those occurring during the months and years following hospitalization are underreported. The mechanisms responsible for long-term decrements in organ function remain poorly understood.
of cytokine neutralization in altering heatstroke mortality in animal models. Peripheral injection of IL-1β, IL-2, IL-6, IL-10, TNF-α, and platelet-activating factor into experimental animals replicates the pathophysiologic responses observed in heatstroke, including hyperthermia, hypothermia, fever, increased vascular permeability, DIC, and death.* Simultaneous injection of multiple cytokines (e.g., IL-1 and TNF) is most effective in mimicking heatstroke symptoms and has shed light on cytokine interactions in vivo that orchestrate SIRS. Increased circulating levels of IL-1α, IL-1β, IL-1 receptor antagonist (IL-1ra, a naturally occurring antagonist of IL-1), IL-6, soluble IL-6 receptor (sIL-6R), IL-8, IL-10, IL-12, IFN-γ, TNF-α, and soluble TNF receptor (sTNFR) concentrations are commonly observed at the time of heatstroke collapse or shortly after cooling.† Sustained high IL-6 levels during cooling correlate with heatstroke severity, tissue injury, and death, whereas high circulating IL-8 levels are implicated in leukocyte activation and coagulation in EHS patients.23,125 The reciprocal regulation of IL-12 and IL-10 production suggests complex interactions in heat-induced SIRS, but the function of these cytokines has not been clearly delineated. As previously mentioned, high IFN-inducible gene expression and IFN-γ levels are clinical measures of viral or intracellular bacterial infection and are evident in EHS patients with preexisting infections.289 The failure of clinical and animal studies to correlate cytokine production with specific heatstroke responses is probably caused by the short half-lives of these proteins, local tissue concentrations exceeding those in the circulation, or the presence of soluble cytokine receptors that mask detection or alter cytokine action(s).‡ For example, the sTNFR inhibits the actions of TNF and is often higher in heatstroke survivors than nonsurvivors, suggesting that TNF may mediate lethality.109 On the other hand, the sIL-6R may potentiate endogenous IL-6 effects by increasing the concentration of available IL-6 signaling receptors on cell membranes (known as a trans-signaling effect) or reduce IL-6 signaling through competitive binding with IL-6 receptors that are already present on the cell membrane (Figure 10-9). Although cytokines are known to interact with one another, their soluble receptors, and other endogenous stress hormones (e.g., glucocorticoids) during SIRS, it remains unknown how these interactions in vivo affect heatstroke outcome. Taken together, results from the few antagonism/neutralization studies that have been conducted to date indicate that high levels of cytokines may be detrimental for heatstroke recovery, but baseline (permissive) actions of some cytokines (e.g., IL-6, TNF, or proteins affected by their actions) appear to be essential for survival.170 Clearly, more research is required in this area to determine the multitude of cytokine actions in heat-induced SIRS and determine the protective versus detrimental effects of the proteins on multiorgan system function.
CYTOKINES
HEAT SHOCK PROTEINS
Cytokines are a class of intercellular protein messengers released from macrophages, T and B cells, endothelial cells, astrocytes, and other cell types that mediate inflammatory reactions to disease and injury.46,141,195,280,309 Cytokine-inducing stimuli include bacterial and viral infection,65,243 psychological stress,191,234 heat stress,* wholebody hyperthermia,222 and exercise.38,209,224,298 The defining characteristics of cytokines include a lack of constitutive production, the ability to regulate each other’s production, and overlapping actions that depend on the target cell type and cytokine milieu in which they function. Cytokines act over short distances and time spans (half-life is generally less than 60 minutes) and are usually present at low concentrations in the circulation. Cytokines bind reversibly to high-affinity cell-surface receptors and stimulate intracellular signaling pathways (e.g., NF-κB) that alter the transcription of genes involved in immune responses. There are several lines of evidence that link cytokines with symptoms of heat-induced SIRS. These include induction of heatstroke symptoms by cytokine injection in experimental animal models, association of increased circulating cytokine levels with heatstroke morbidity/mortality, and effectiveness
Heat shock proteins (HSPs) are molecular chaperones that prevent misfolding and aggregation of cellular proteins during exposure to stressful stimuli.76,111,134,184 HSPs are found in organisms ranging from bacteria to humans. Their chaperoning activities protect against environmental (heavy metals, heat stress), physiologic (cell differentiation, protein translation), and pathologic (infections, ischemia/reperfusion) stimuli that cause cellular damage.134,160,184 HSPs were originally discovered in Drosophila melanogaster, when puffs associated with novel protein synthesis appeared on the giant chromosomes of the salivary glands in response to heat stress.259,303 It was later discovered that heat denaturation of mature proteins inside the cell was the cellular signal that increased protein synthesis in response to heat stress in Drosophila.120 HSPs are grouped into families according to their molecular mass, cellular localization, and function (Table 10-4). HSP 27 (also referred to as sHSP) is a constitutively expressed cytosolic and nuclear protein with cytoskeletal stabilization and
*References 20, 27, 36, 116, 172, 181.
226
*References 154, 162, 168, 169, 235, 237, 277, 306. † References 20, 26, 27, 109, 112, 172. ‡ References 2, 20, 23, 26, 109, 112, 159, 275.
IL-6
sIL-6R IL-6 IL-6R
IL-6 gp130
gp130
sIL-6R
Signal
Classic signaling
antiapoptotic functions.7,167,241 HSP 60 exists in the mitochondria and cytosol, is released from PBMCs on LPS stimulation, and functions as a “danger” signal for the innate immune system. HSPs interact with PAMPs, such as TLRs, to stimulate monocytes, macrophages, and dendritic cells to produce cytokines.35,226 The HSP 70 family has been extensively studied for protective function(s) against thermal stress,142,340 ischemia/ reperfusion,196,248,293 tissue injury,33 glucose deprivation,334 and sepsis.166,317 HSP 70s function in concert with other molecular chaperones, such as HSP 90 and HSP 110, to facilitate LPS and antitumor responses.127 HSP gene expression is mediated primarily at the level of gene transcription by a family of heat shock transcription factors (HSFs) that interact with the heat shock regulatory element (HSE) in the promoter region of genes. HSF-1 is the major stress responsive element in mammalian cells that is activated by febrile-range temperatures.318,338 HSF-1 interacts with HSEs on cytokine genes to alter transcription and confer protection against endotoxin and TABLE 10-4 Heat Shock Protein Structure and
Function
Family
Function
Attributes
HSP 27 (sHSP)
Antiapoptotic
Constitutively expressed Cytosolic and nuclear Mitochondria and cytosol
HSP 60
Cytoskeletal stabilization Protein refolding Prevents aggregation of denatured proteins Immune responses
HSP 70 family HSP 72 HSP 73 (HSC 70)
Thermotolerance Molecular chaperone
HSP 75 HSP 78 (GRP 79, Bip)
Molecular chaperone Cytoprotection
HSP 90 family: HSP 90 GRP 96
HSP 110/104
Glucocorticoid receptor functioning Glucose regulation Molecular chaperone Tumor antigen presentation
Highly inducible Constitutively expressed Mitochondrial Endoplasmic reticulum Cytosolic and nuclear Endoplasmic reticulum Cytosolic
Data from Hartl FU, Hayer-Hartl M: Molecular chaperones in the cytosol: From nascent chain to folded protein, Science 295:1852, 2002; and Kregel KC: Heat shock proteins: Modifying factors in physiological stress responses and acquired thermotolerance, J Appl Physiol 92:2177, 2002. Bip, Binding protein; GRP, glucose regulated protein-78; HSC, heat shock cognate; HSP, heat shock protein.
gp130
Signal
Trans-signaling
other infectious/inflammatory stimuli. In gene-transfected human PBMCs, inhibition of TNF-α, IL-1β, IL-10, and IL-12 in response to LPS was specific to HSPs 70 overexpression.59 A lack of effect of HSP 70 on IL-6 gene transcription may be an indirect mechanism of protection, because IL-6 functions in a regulatory feedback loop to inhibit IL-1 and TNF production, which are Th1 cytokines with potent proinflammatory activities.59,71,73,325 In murine macrophages, HSP 70 inhibited IL-12 (Th1) and stimulated IL-10 (Th2) production in response to LPS.325 The shift from Th1 to Th2 cytokine production may be a mechanism by which HSP 70 protects against bacterial infection. Heat strain is a consequence of the time and intensity of heat exposure. These factors interact in vivo to influence the magnitude and kinetics of HSP expression. In human PBMCs, maximal expression of intracellular HSPs 70 was observed between 4 and 6 hours after a brief heat shock (43° C [109.4° F] for 20 minutes).288 Increased expression of HSPs 10, 20, 40, 60, 70, 90, and 110 was observed in PBMCs from EHS patients or following exposure to hypoxia in vitro.287,289 Anatomic differences in the magnitude and kinetics of in vivo expression have also been observed, with HSP 70 expression occurring within 1 hour in the brain, lungs, and skin and delayed until 6 hours after heat exposure in the liver of rats.18 In mice, liver expression of HSP 70 showed a progressive increase from approximately 6 to 24 hours following collapse from passive heatstroke.171 In rats, a high rate of passive heating (0.175° C [0.315° F]/min) induced greater HSP 70 expression in the liver, small intestine, and kidneys than did a lower rate of heating (0.05° C [0.09° F]/min), despite attaining the same maximum body temperature (42° C [107.6° F]).80 Differences in tissue blood flow and metabolic activity likely account for regional differences in HSP expression during passive and exertional heat exposure. Thermotolerance is the term used to describe the noninheritable, transient resistance to a lethal heat stress that is acquired following previous exposure to a nonlethal level of heat stress. Increased HSP 70 expression is a mechanism of thermotolerance that protects against heat-induced increases in epithelial permeability. A unique in vitro model system consisting of highresistance Madin-Darby canine kidney (MDCK) epithelial cell monolayers was developed to examine the relationship between HSP 70 expression and changes in epithelial integrity with heat exposure. Following heat stress to 38.3° C (100.9° F), MDCK monolayers showed an increase in permeability that was reversible with cooling.212 If the monolayers were preexposed to a conditioning heat stress of 42° C (107.6° F) for 90 minutes, subsequent exposure to a higher temperature of 39.4° C (102.9° F) was required to increase monolayer permeability.21 The association of a thermotolerant state with increased HSP 70 expression suggests that HSPs shift the temperature threshold upward to prevent heat-induced disruptions in epithelial permeability.212 Follow-up studies showed that HSPs interact with proteins in the tight junctions of the epithelium to regulate permeability. Occludin is a plasma-membrane protein located at tight junctions that was increased, along with HSPs 27, 40, 70, and 90, in intestinal 227
CHAPTER 10 Pathophysiology of Heat-Related Illnesses
FIGURE 10-9 IL-6 receptor signaling pathways. Classic signaling involves binding of IL-6 to the membrane bound IL-6 receptor (IL-6R), which stimulates an interaction between the IL-6:IL-6R complex and the membrane-bound glycoprotein 130 (gp130) to initiate intracellular signaling. Trans-signaling occurs when the extracellular domain of the membrane-bound IL-6R is proteolytically cleaved, leading to generation of the soluble IL-6R (sIL-6R) that binds IL-6. The IL-6:sIL-6R complex can stimulate cells that only express gp130 (i.e., do not normally possess the transmembrane IL-6R) to transmit an intracellular signal. Cells that express gp130 only would not be able to respond to IL-6 in the absence of sIL-6R.
PART 2 COLD AND HEAT
epithelial monolayer (Caco-2) cells exposed to 39° or 41° C (102.2° or 105.8° F).60 Treatment of Caco-2 cells with quercetin (an inhibitor of HSF-1) inhibited HSPs and occludin expression and reversed the thermotolerant state of these cells.60 These studies demonstrate a complex interaction between HSPs and tight-junction proteins for modulation of epithelial barrier function during thermal stress. It is interesting to speculate that differences in HSP expression profiles may be a sensitive marker of heat stress susceptibility among different populations. During the life of an organism, there is an accumulation of protein damage caused by continual oxidant and free radical activity within cells. The lifespan of Drosophila was extended by heat shock treatment or the addition of HSP 70 gene copies, suggesting that increased protein chaperonin activity may protect against aging.148,301 In rats, aging was associated with a significant reduction in liver HSP expression following passive heat exposure, which was associated with greater liver damage compared with that observed in young rats.161,342 Older animals do not appear to have a global inability to express HSP, because exertional heat stress can induce expression profiles similar to those of mature rats.161 Rather, aging is associated with a reduction in the threshold for HSP stimulation.161 Similarly, Fargnoli and co-workers74 showed that global reduction in protein synthesis was not responsible for decreased HSP induction in aged lung fibroblasts. Alzheimer’s disease is thought to be a consequence of decreased HSP function that results in increased deposition of abnormally folded proteins.211 It is anticipated that screening for altered HSP titers will help to identify individuals with reduced thermotolerance caused by aging, infection, or other conditions that may predispose to heatstroke.150
Heatstroke Treatments (See Chapter 11) Current heatstroke therapies fall into two categories: supportive therapies directed at the immediate clinical symptoms and therapies directed at the causative mechanisms of injury. The primary objectives of clinical heatstroke treatments are to reduce body temperature as rapidly as possible, reestablish normal CNS function, and stabilize peripheral multiorgan system function. Supportive therapies consist of rapid cooling and IV fluid administration for restoration of normal blood pressure and tissue perfusion, whereas advanced therapies are directed at the coagulation and inflammatory disturbances that cause organ failure. Despite these efforts, heatstroke morbidity and mortality rates remain quite high, and multiorgan system dysfunction continues to claim the lives of heatstroke victims during ensuing years of recovery.6,321 This section discusses conventional clinical treatments of heatstroke, as well as innovative treatment strategies targeted at SIRS to mitigate injury and death.
possibility of peripheral vasoconstriction with cooling, the skin may be massaged to stimulate increases in cutaneous blood flow. Regardless of the treatment strategy, current medical doctrine dictates that heatstroke patients are cooled as rapidly as possible until normal CNS function is reestablished. Dantrolene and nonsteroidal antiinflammatory drugs (NSAIDs) have been tested for their effects on body cooling, but neither class of drugs has shown efficacy for protection against heatstroke. Dantrolene is a calcium-lowering agent that protects against hyperthermia by lowering intracellular calcium concentrations in skeletal muscle to decrease muscle tone. Dantrolene is effective for the treatment of malignant hyperthermia (MH), which is a genetic mutation that predisposes to involuntary muscle contractions and rigidity following exposure to general anesthetics or muscle-depolarizing agents. Dantrolene has been considered as a treatment for heatstroke, but animal and human heatstroke studies have failed to validate its use for this condition. In a study of heatstroke patients, dantrolene decreased the required cooling time by approximately 20 minutes but had no effect on recovery. Similarly, a randomized, double-blind, placebo-controlled trial of Hajj heatstroke patients failed to show a cooling advantage of dantrolene over traditional cooling methods.22,43 MH is distinct from exertional or passive heatstroke, so it is not surprising that this drug does not protect equally against these diverse conditions. (MH is discussed in detail later in this chapter.) NSAIDs have been considered as therapeutics based on their potent antiinflammatory and antipyretic effects. The action(s) of classic NSAIDs, such as, aspirin, ibuprofen, and acetaminophen, are attributed primarily to blockade of the cyclooxygenase (COX) pathway of eicosanoid metabolism (Figure 10-10). Prostaglandins are synthesized by the COX pathway in response to a variety of stimuli (e.g., bacterial infection, heat shock) and regulate a multitude of physiologic responses, including fever, inflammation, and cytokine production. During fever, prostaglandins are released in response to proinflammatory cytokines (e.g., IL-1, IL-6) and stimulate an increase in the temperature set point to induce fever.292 Inhibition of prostaglandin production by NSAIDs is the primary mechanism for the antipyretic (i.e., fever-reducing) actions of these drugs. However, hyperthermia in response to heat exposure is not caused by an increase in the temperature set point but by an unregulated increase in body temperature that occurs when heat gain exceeds heat loss in an absence of a change in the temperature set point. Rather than providing a beneficial effect, NSAIDs are contraindicated as a treatment for heatstroke because of the potential toxic effects of these drugs on liver function and a lack of clinical and/or experimental data to support their use. For example, pretreatment with sodium salicylate was without effect on skin
COOLING Rapid cooling is considered the single most important treatment for protection against permanent CNS damage and death from heatstroke. To facilitate cooling, the individual should be placed into a supine position and as many clothes as possible removed to expose a large surface area of the body to facilitate heat transfer. If the individual is comatose, he or she should be placed onto his or her side to ensure an open airway. Conventional methods of cooling include cold or ice water immersion, packing ice around the body, sponging with (or without) fanning, or use of a hypothermia blanket. The goal of all cooling methods is to rapidly decrease and maintain body temperature below 39° C (102.2° F) and to prevent rebound hyperthermia. The use of an ice bath or ice packs on the skin surface has met with some resistance because it is thought that cooling of the skin will elicit peripheral vasoconstriction and shivering, which can increase heat production and counteract the cooling effect. This was shown in an experimental study in which young, fit test subjects were heat stressed to 40° C (104° F) and experienced shivering and cold sensations during immersion in cold water.339 Because the threshold for activation of shivering is increased in heatstroke patients, the risk for cold or ice water immersion eliciting such a response and compromising the benefits of cooling is unlikely. However, to minimize the 228
Cell membrane NSAIDs Acetaminophen Salicylic acid Ibuprofen
Liver toxicity
Phospholipids PLA2
Arachidonic acid (AA)
COX Prostaglandins Thromboxanes Fever Platelet aggregation Vasomotor changes Inhibit IL-1, IL-2
LOX Leukotrienes Leukocyte aggregation Vascular permeability Induce IFNγ, IL-1, IL-2
FIGURE 10-10 Eicosanoid metabolism is initiated when cell membrane phospholipids are converted to arachidonic acid (AA) by the enzymatic actions of phospholipase A2 (PLA2). Cyclooxygenase (COX) converts AA to prostaglandins and thromboxanes, whereas the lipooxygenase (LOX) pathway is responsible for the production of leukotrienes. Nonsteroidal antiinflammatory drugs (NSAIDs) block the action of COX enzymes with potential toxic effects on the liver. IFNγ, Interferon-γ; IL-1, interleukin-1; IL-2, interleukin-2.
FLUID RESUSCITATION (See Chapter 70) One of the first lines of defense against permanent tissue damage is treatment with resuscitation fluids. The objective of IV fluid administration is to restore intravascular volume and rehydrate the interstitium to stabilize cardiovascular functioning, improve tissue perfusion, and maintain immune function. The resuscitation fluid needs to be safe, efficacious, inexpensive, easy to transport for use in military or athletic settings, and have the capability to restore tissue oxygen perfusion and minimize cellular/tissue injury. Blood provides oxygen-carrying capacity and volume, but supply is limited and there is a risk for allergic or infectious reactions, difficulties with crossmatching, and potential for high hemoglobin levels to increase blood viscosity and reduce nutrient flow to the tissues.255,258 Balanced salt solutions, such as saline and lactated Ringer’s, have a long shelf life and are inexpensive and in unlimited supply with a minimal risk for disease transmission. However, they are able to freely cross semipermeable capillary membranes, which increases the risk for tissue edema and makes frequent transfusions necessary to maintain adequate plasma volume.110,145,304 Tissue edema increases the distance from blood vessels to tissue mitochondria and limits oxygen delivery to the tissues. There is a greater risk for edema in heatstroke patients because of increases in capillary permeability and lack of muscle movement that limits the flow of lymph following collapse. To minimize the adverse consequences of balanced salt solutions, these fluids may be replaced with colloid solutions. Natural colloids, such as albumin, possess antioxidant properties that reduce tissue injury during times of oxidant stress but carry a risk for infection.84,328 Dextran is an artificial colloid that was in use after World War II until adverse hemostatic effects restricted its use to specific clinical conditions, such as deep vein thrombosis and pulmonary embolism.15,55 Hydroxyethyl starch (HES) is a blood plasma substitute that exerts high colloidal pressure to stimulate movement of fluid from the interstitial space into the blood vessel lumen for plasma volume expansion.239,336,344 Smallvolume treatment with HES protected against heatstroke mortality in rats, but use of HES in other heatstroke animal models and humans has not been validated.187 Because of severe dehydration and acute renal failure with heatstroke, fluid shifts from the interstitial fluid into the vessel lumen may mean HES will not be well tolerated in severe heatstroke patients.
ANTICOAGULANTS Anticoagulants (e.g., heparin, aspirin) have been examined for heatstroke protection, with mixed results. Heparin therapy has been associated with positive heatstroke outcome in patients, although it is difficult to dissociate the direct effects of this therapy from other clinical treatments.245,290 The mechanisms of heat-induced DIC may include prostaglandin synthesis, because aspirin has shown protection against platelet hyperaggregation in vitro and in animal models. In human volunteers, ingestion of aspirin 12 to15 hours before blood sampling or heat exposure of cells was effective in inhibiting platelet hyperaggregation.87 However, aspirin was ineffective if provided after heat exposure, even though complete inhibition of the arachidonic acid pathway was achieved.87 The ability of aspirin to protect guinea pigs from DIC induced by Staphylococcus aureus suggests that similar activities function in vivo to control platelet reactivity.227 However,
there is currently insufficient evidence to support the use of aspirin as a preventive measure in heatstroke patients. Given the hormonal and metabolic alterations that accompany heatstroke, including dehydration, increased catecholamine levels, hypoxia, and others, the mechanisms responsible for DIC extend beyond those mediated by prostaglandins alone. Furthermore, aspirin and other antiinflammatory drugs can cause liver damage if consumed in large quantities, as previously mentioned. Recombinant APC is an effective antiinflammatory drug for the treatment of sepsis and may also hold promise as a treatment for heatstroke patients. APC efficacy appears to depend on a variety of patient conditions, including age (most effective in patients over 50 years of age), extent of organ dysfunction (benefit not apparent if failure of only one organ), and the presence of shock at the time of infusion, which improves its efficacy.327 In rat heatstroke models, the efficacy of APC depends on the time of treatment. A single dose of recombinant human APC provided at the onset of heatstroke inhibited inflammation and coagulopathy, prevented organ failure, and improved survival; however, if treatment was delayed for 40 minutes following the onset of heatstroke, there was no beneficial effect on survival time.45 The efficacy of APC was less obvious in a baboon heatstroke model. Infusion for 12 hours following heatstroke onset attenuated plasma IL-6, thrombomodulin, and procoagulant components but had no effect on mortality.25 APC is the first biologic agent approved in the United States for the treatment of severe sepsis on account of two decades of research in this area,327 but there is insufficient evidence to justify the use of this treatment in heatstroke patients.
ANTICYTOKINE THERAPIES As previously described, attenuations in splanchnic blood flow during heatstroke contribute to increased gut permeability and a rise in circulating endotoxin. This series of events is hypothesized to stimulate elevations in plasma cytokine levels that have been implicated in the adverse consequences of SIRS. Based on these findings, the question arises: Do anticytokine therapies represent an efficacious treatment strategy for heatstroke? There have been no controlled studies examining the efficacy of anticytokine therapies on patient outcome with heatstroke. However, clinical sepsis trials indicate that potential protective effects of anticytokine therapies need to be viewed with cautious optimism. Sepsis patients display high circulating IL-1 levels that correlate with morbidity and mortality, but IL-1ra treatment has been unsuccessful in reducing mortality.236,253 A comparison of 12 randomized, double-blind multicenter trials of more than 6200 sepsis patients showed no significant benefit of antiendotoxin antibodies, ibuprofen, plasminogen-activating factor receptor antagonist, anti-TNF monoclonal antibody, or IL-1ra on all-cause mortality.57 There are several explanations for negative results from anticytokine therapies, including the possibility that the mediator has no pathophysiologic role in the response, the agent failed to neutralize the protein (because of a lack of biologic activity, competition by other mediators, inadequate anatomic distribution), compensatory increase of other mediator(s) with similar activities, administration too early or late in the course of disease, too-short therapy duration, or the need for combination therapy.198 Kinetic studies have shown the half-life of IL-1ra to be approx imately 20 minutes, and phase III clinical trials showed that circulating IL-1β levels at the time of clinical treatment were undetectable in 95% of the patient population.77,246 Exposure to anticytokine therapies before sepsis onset is thought to be desirable (but practically infeasible), although this may suppress shifts in Th1/Th2 immune responses that are important for the resolution of infection. On the other hand, anticytokine therapies given too late in sepsis progression may shift the Th1/Th2 milieu in an unpredictable manner or have no effect because of the overwhelming nature of the septic event.100 The transient nature of cytokine production and/or clearance and lack of correlation between serum levels and disease severity further complicate treatment scenarios. Given the short half-life of TNF-α (approximately 6 to 7 minutes)16 and biphasic clearance patterns of IL-1β and IL-6 (rapid disappearance in the first 3 minutes followed by an attenuated clearance over the next 1 to 4 hours),152 the narrow 229
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temperature and pulse rate but significantly increased the rate of body temperature rise and potentiated hyperthermia in men walking in a hot environment.135 As previously mentioned, the use of antipyretic drugs, such as acetaminophen, has been anecdotally associated with the need for liver transplantation.93,113,114,269,319 Recurrent hyperthermia is a common heatstroke recovery response that is thought to be a true fever and a prostaglandinmediated response to endotoxin leakage and cytokine stimulation. Whether the effects of NSAIDs on cytokine expression or body temperature will protect or exacerbate heatstroke sequelae in vivo is unknown but is an important area of investigation, given the high use of NSAIDs as over-the-counter medications for pain and/or fever relief in our society.
PART 2 COLD AND HEAT
protective window in which anticytokine therapies may be effective is a difficult obstacle to overcome. Interleukin-10 is a potent antiinflammatory cytokine that suppresses production of several proinflammatory cytokines, including IL-1β, IL-6, and TNF-α, and is an important negative feedback loop during infection/disease.101,311 Few, if any, studies have investigated the efficacy of IL-10 treatment for heatstroke recovery, although the cytokine has been commonly used in the treatment of multiple autoimmune diseases, including rheumatoid arthritis, Crohn’s disease, multiple sclerosis, and sepsis.31,229 As with other cytokines, the timing of IL-10 administration must be carefully considered. IL-10 decreases IFN-γ production by natural killer and Th1 cells, which may suppress the clearance of infectious organisms (via IFN-γ).254,320 Consistent with anticytokine therapies, beneficial effects of exogenous IL-10 administration depend on multiple factors, including time of administration, route, and the site to which the cytokine is targeted.229,265 These considerations, along with the immune suppressive and unpredictable nature of IL-10–based therapies, have resulted in diminished enthusiasm for anticytokine therapies for sepsis.
Heatstroke Prevention Heatstroke is currently a more preventable than treatable disease. The most effective preventive measures include acclimatization to the heat, reductions in the duration and extent of physical activity, rescheduling of activities to cooler times of the day, increased consumption of nonalcoholic fluids, and removing vulnerable populations, such as those with preexisting viral or bacterial infections, from the heat stress environment. Fan cooling has not shown protection against heatstroke and is associated with increased thermal discomfort at temperatures higher than 38° C (100.4° F).149
HEAT ACCLIMATIZATION Climatic heat stress and exercise interact synergistically to increase body temperature (core and skin) and cardiovascular strain and to decrease performance in the heat. Heat acclimatization is the within-lifetime changes in an organism (as opposed to evolutionary changes) that protect against these negative effects of heat strain. Heat acclimatization occurs following exposure to the natural environment, whereas heat acclimation develops following exposure to artificial conditions. However, these terms are used interchangeably because they induce similar physiologic adaptations.331 Heat acclimation occurs following repeated bouts of heat exposure that are of sufficient intensity, frequency, duration, and number to elevate core and skin temperature and induce profuse sweating. Heat acclimation may be achieved following exercise or rest in the heat, although the former method is more effective. It is important to note that heat acclimatization is specific to the climate and activity level; therefore, if individuals will be working in a hot, humid climate, heat acclimatization should be conducted under similar conditions (Box 10-3). Although heat acclimation does not require daily exposure to heat and exercise, the rapidity with which biological adaptations are achieved is slower with less frequent exposures. This was shown experimentally in human volunteers in whom heat acclimation was achieved following 10 days of daily heat exposure but required 27 days when the frequency of exposure was reduced to every third day of experimentation (conditions 47° C [116.6° F], 17% relative humidity).74 Continual 24-hour exposures are also not required, because daily 100-minute periods of exposure were adequate to produce heat acclimation in subjects exposed to dry heat.183 However, because of the transient nature of the biologic adaptations, continued heat exposures are required to maintain the acclimated state. Aerobically trained athletes retain heat acclimation benefits longer than do unfit individuals, because they are exposed to high body temperatures during training exercises.240 Improvements in thermal comfort and exercise performance are achieved in heat-acclimated individuals through a variety of physiologic mechanisms, including a lower threshold and higher rate of skin blood flow, reduction in metabolic rate, earlier onset 230
BOX 10-3 Heat Acclimation Strategies Must Mimic Climate of Athletic Event or Occupational Setting and Include Adequate Heat Stress • Heat must be sufficient to cause heavy sweating • Use exercise/rest cycles to intensify or diminish the effect of the heat stress on bodily functions • Include at least 6 to 14 days of adequate heat stress. • Exercise daily for at least 90 minutes Start With Acclimation and Exercise Training • Be flexible in scheduling training • Build confidence • Performance benefits may take longer to achieve than physiologic benefits Methods of Heat Acclimation • Use a climate-controlled room (sauna or heat chamber) or hot weather • Incorporate training by including additional acclimation sessions Days Leading to Athletic Performance or Event • Start slowly, and decrease training duration and intensity; limit heat exposure • Acclimatize in heat of the day • Train in coolest part of the day • Use appropriate work/rest cycles • Be vigilant of salt and fluid needs, especially during the first week of acclimation
and rate of sweating, and improvements in cardiovascular function and fluid balance.271 Figure 10-11, online illustrates the effect of 10 days of heat acclimation on heart rate, core temperature, and mean skin temperature responses of subjects walking on a treadmill in a desert type of environment.70 On the 10th day of acclimation, heart rate was lower by approximately 40 beats/min, and rectal and skin temperatures were reduced approximately 1° C (1.8° F) and 1.5° C (2.7° F), respectively (see Figure 10-11, online).69 Once heat acclimation is achieved, skin vasodilation and sweating are initiated at a lower core temperature threshold, and higher sweat rates can be sustained without the sweat glands becoming “fatigued.”52,81 Whereas an unacclimated individual will secrete sweat with a sodium concentration of approximately 60 mEq/L (or higher), the concentration of secreted sodium from the sweat glands of an acclimated individual is significantly lower at approximately 5 mEq/L.262 This effect of heat acclimation on salt conservation is thought to be caused by increased aldosterone secretion or responsiveness of the sweat glands to this steroid hormone, which is released by the adrenal cortex and increases the resorption of ions and water in the distal tubules and collecting ducts of the kidneys.82,151 Overall improvements in fluid balance with heat acclimation include reduced sweat sodium losses, a better matching of thirst to body water needs, and increased total body water and blood volume.190,270 Provided that fluids are not restricted during physical activities, heat-acclimated individuals will be better able to maintain hydration during exercise and showed a marked reduction in “voluntary” dehydration.13,69,271 Although there is controversy regarding the ability of heat acclimation to alter the maximum temperature that can be tolerated during exercise in the heat,223 individuals who live or train in hot environments may experience reduced incidence of syncope (Figure 10-12).13,96,247 An essential cellular adaptation of heat acclimation is altered expression or reprogramming of genes that encode constitutive and stress-inducible proteins.122 Heat acclimation is associated with down regulation of genes associated with energy metabolism, food intake, mitochondrial energy metabolism, and cellular maintenance processes and upregulation of genes that are linked with immune responsiveness.122 The HSPs are the most extensively studied heat-inducible proteins and show faster
Subjects experiencing syncope
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Days of heat acclimation FIGURE 10-12 Incidence of syncope among 45 subjects who lived in and trained at cool ambient temperatures and could complete a physical training regimen without mishap. Then they were relocated to a hot environment where they carried out the same physical training regimen. (Modified from Bean WB, Eichna LW: Performance in relation to environmental temperature: Reactions of normal young men to stimulated desert environment, Fed Proc 2:144, 1943; and Hubbard RW, Armstrong LE: The heat illness: Biochemical, ultrastructural, and fluid-electrolyte considerations. In Pandolf KB, Sawka MN, Gonzalez RR, editors: Human performance and environmental medicine at terrestrial extremes, Indianapolis, 1988, Benchmark Press, pp 305-359.)
transcriptional response and elevated cellular reserves (HSP 72 specifically) in heat-acclimated versus nonacclimated individuals.122,123,193,200 That is, whereas nonacclimated individuals require de novo HSP 72 synthesis for cellular protection, individuals who reside in hot climates maintain elevated HSP 72 levels.190 The cellular mechanisms of heat acclimation are not fully understood but are thought to involve global and tissue-specific changes in genes involved in thermal responsiveness, DNA repair and synthesis, free radical scavenging, and apoptosis.122
Genetic Polymorphisms Heatstroke susceptibility is influenced by complex interactions between environmental and host genetic factors. Emerging molecular technologies have improved our understanding of the genetic mutations and polymorphisms that may predispose to heat illness or inhibit resolution of SIRS. It is anticipated that the ability to prescreen individuals for genetic polymorphisms that may prevent resolution of SIRS will help in developing more effective therapies to alleviate morbidity/mortality in these individuals.
SINGLE NUCLEOTIDE POLYMORPHISMS Single nucleotide polymorphisms (SNPs) are variations in the nucleotide sequence of DNA that can affect physiologic responses to environmental stimuli. SNPs have been implicated in a variety of diseases, including sepsis, type 1 diabetes, arthritis, inflammatory bowel disease, and rheumatic fever.79,136,250,296 The
MH is a genetic disorder that causes muscle rigidity, hyperthermia, tachycardia, and metabolic acidosis during exposure to volatile anesthetics or depolarizing skeletal muscle relaxants. Exercise, heat stress, and emotional stress also trigger reactions in approximately 5% to 10% of MH patients.58,326 MH reactions are a result of a massive release of calcium from the type 1 ryanodine receptor (RyR1) of the sarcoplasmic reticulum, which overwhelms cellular mechanisms of calcium homeostasis and activates actin–myosin filaments to cause muscle rigidity and hyperthermia.238 RyR1 is the most common mutation in skeletal muscle, but additional isoforms have been identified in B and T cells, thalamus, hippocampus, and heart.163,202,300 Activation of the RyR1 by a variety of pharmacologic compounds, including caffeine, halothane, and the muscle relaxant 4-chloro-m-cresol, has led to the development of an in vitro contracture test of skeletal muscle biopsies to identify MH individuals.266,345 Dantrolene is used to treat MH reactions by lowering intracellular calcium stores, decreasing muscle metabolic activity, and preventing hyperthermia. The use of dantrolene, in combination with improved monitoring standards and early detection using the in vitro contracture test, has helped to reduce mortality rates from greater than 70% to less than 5% in MH patients.186 MH has been identified in several animal species, including dogs,231 boars,278 cats,14 and horses,3 but the most common experimental animal is a porcine MH model that possesses a single mutation in the skeletal muscle RyR1 gene. These animals develop the MH syndrome in response to inhalational anesthetics, exercise, heat, and other stressors.314 Mild exercise exacerbates MH symptoms in response to anesthetics in MH pigs, suggesting that inflammatory mediators released by skeletal muscle may contribute to the MH syndrome.314 MH patients show an approximately fivefold higher expression of IL-1β when stimulated with caffeine and 4-chloro-m-cresol compared with control cells.94 Recent development of a transgenic mouse model that overexpresses the RyR1 receptor has proved useful to study the MH/EHS link and could shed light on the role played in this syndrome by inflammatory cytokine production from skeletal muscle or other organs.69 Association of RyR1 mutations with EHS incidence suggests that screening young, healthy individuals (e.g., athletes, military personnel) for the MH mutation could be a powerful tool to determine heatstroke susceptibility.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
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identification of SNPs in the promoter region of genes suggests that disease susceptibility may be affected by altered transcription of immune determinants of clinical outcome. SNPs have been identified in IL-1, IL-2, TNF, IFNγ, IL-10, IL-1ra, TLR-2, and TLR-4. The risk for death from sepsis is significantly increased in patients with a genetic polymorphism in the TNF-α or TNF-β gene.83 Even for those cytokine polymorphisms located distal to a critical promoter region that do not directly affect gene transcription rates, coinheritance of multiple immune-responsive genes by a process known as linkage disequilibrium can alter immune function. Some TNF-α polymorphisms exist in linkage disequilibrium with HLA haplotypes that encode cell-surface antigens. Coinheritance of these genes may ultimately be responsible for poor sepsis outcome.138,296
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CHAPTER 11
Clinical Management of Heat-Related Illnesses KAREN K. O’BRIEN, LISA R. LEON, AND ROBERT W. KENEFICK
This chapter discusses the clinical manifestations, management, and prevention of heat-related illnesses. The spectrum of injury ranges from milder conditions such as heat cramps to fatal manifestations such as arrhythmias; it involves complications such as rhabdomyolysis and multiorgan dysfunction syndrome, and it may result in death from overwhelming cell necrosis caused by a lethal heat-shock exposure. Exertional heat stroke (EHS) is commonly characterized by development of mental status changes or collapse during physical activity in a warm environment. The severity of heat illness depends on the degree and duration of the elevation in core temperature (Tco). Heat stroke is an extreme medical emergency that can be fatal if it is not treated promptly with rapid cooling. To prevent and minimize complications and save lives, proper prevention, management, and clinical care are essential.
Exertional Heat Illness Dehydration and heat exposure can impair exercise performance and contribute to various illnesses. Exertional heat illnesses are comprised of minor and serious disorders. Minor heat and dehydration-related illnesses include heat cramps, erythromelalgia, and heat syncope. Heat cramps are characterized by intense muscle spasms, typically in the legs, arms, and abdomen. Heat cramps result from fluid and electrolyte deficits and occur most often in persons who have not been fully acclimated to a combination of intense muscular activity and environmental heat. Individuals who are susceptible to heat cramps are often believed to be profuse sweaters who sustain large sweat sodium losses.13,106 Heat syncope (fainting) is characterized by dizziness and weakness during or after prolonged standing or after rapidly standing up from a lying or sitting position during heat exposure. Heat syncope results from blood pooling in the cutaneous and skeletal vasculature, and it occurs most commonly in dehydrated and inactive persons who are not acclimated.93 Erythromelalgia is characterized by pain and swelling in the feet and hands that is triggered by exposure to elevated temperatures.64 Serious illnesses include exertional heat injury (EHI) and EHS. These illnesses have many overlapping diagnostic features; it has been suggested that they exist along a continuum on the severity scale.17 Heat exhaustion is characterized by inability to sustain cardiac output in the presence of moderate (>38.5° C [101° F]) to high (>40° C [104° F]) body temperatures, and is frequently accompanied by hot skin and dehydration. EHI is a moderate to severe illness characterized by injury to an organ (e.g., liver, kidneys, gut, muscle) and that usually (but not always) involves a high Tco of more than 40° C (104° F). EHS is a severe illness that is characterized by central nervous system dysfunction (e.g., confusion, disorientation, impaired judgment) and that is usually accompanied by a Tco of more than 40.5° C (105° F). EHI and EHS can be complicated by cardiac arrhythmia, liver damage, rhabdomyolysis, coagulopathy, fluid and electrolyte imbalances, and kidney failure. Rhabdomyolysis is most often observed with novel and strenuous overexertion. Clinical evidence suggests that dehydration increases the likelihood or severity of acute renal failure associated with rhabdomyolysis.19,91 Among U.S. soldiers who have been hospitalized for serious heat illness, 25% had rhabdomyolysis, and 13% had acute renal failure.22 EHS is usually associated with prolonged exertion in a warm climate; however, in many instances, EHS occurs within the first 2 hours of exercise and not necessarily at high ambient 232
temperatures.17,37 This is because exertion and environmental heat stress during the 72 hours that precede such an event strongly influence the individual’s susceptibility to heat illness.40 Using a Tco of 40.5° C (104.9° F) as a critical temperature to initially diagnose EHS is arbitrary. Mental status changes in an individual who is performing exertion in the heat should be the defining characteristic of heat stroke unless the individual has sustained head trauma. At the stage of collapse, profuse sweating is still likely to be present unless heatstroke develops in an already anhidrotic individual. Dry skin may be evident either in situations in which the climate is very dry and sweat evaporates easily or when heatstroke coincides with a severe degree of dehydration.36 Heat stroke is often categorized as either “classic” or “exertional,” with the former primarily observed in elderly individuals or otherwise sick or compromised populations and the latter in apparently healthy and physically fit persons.
ON-SITE EMERGENCY MEDICAL TREATMENT The early diagnosis of heat illness can be critical to therapeutic success. Early warning signs include flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion.74 If the patient is alert and has no mental status changes, he or she can rest in the shade or indoors, and oral rehydration can be instituted with cold water or an electrolyte-replacement beverage. The concentration of carbohydrates in such a beverage should not exceed 6%; otherwise, gastric emptying and fluid absorption by the intestines may be delayed. Responders should target an intake of 1 to 2 L (0.9 to 1.8 qt) over 1 hour. If the patient does not improve or in fact worsens, he or she should be evaluated by a medical provider. All persons with suspected heat injuries should be observed to ensure that decompensation does not occur. The victim should continue to rest and drink over the next 24 hours. As a general rule, for every pound of weight lost by sweating, 0.5 qt (2 cups or 500 mL) of fluid should be consumed. It may require 36 hours to completely restore lost electrolytes and fluid volume to all body compartments via oral intake. After the acute episode, a medical provider should determine any possible host risk factors for heat illness and review with the victim the signs of heat illness and preventive measures to consider. Any athlete who is performing exercise in warm weather and who develops mental status changes in the absence of trauma should be treated as an EHS victim until proved otherwise.36 EHS is a medical emergency. Rapid reduction of elevated Tco is the cornerstone of EHS management; the duration of hyperthermia may be the primary determinant of outcome.59,100 Cooling should not be delayed so that a temperature measurement can be obtained. Cooling measures should only be minimally delayed for vital resuscitation measures. Nevertheless, it is important to follow the ABCs (airway, breathing, and circulation) of stabilization while cooling efforts are initiated; see Box 11-1 for basic first aid information. Before 1950, the mortality rate with EHS was 40% to 75%.6,35 Long-term survival is directly related to rapid institution of resuscitative measures.49 In the field, the sick individual should be placed in the shade, and any restrictive clothing should be removed. There are multiple ways to cool victims in the field, with cold-water immersion (CWI) being the most effective modality.24,86 In a remote setting, this can be accomplished by using a small children’s pool filled
1. Place the patient in the shade. 2. Assess airway, breathing, and circulation. 3. Initiate cardiopulmonary resuscitation if the patient is pulseless or apneic. 4. Remove any restrictive clothing. 5. Initiate rapid cooling measures. 6. Activate emergency medical services. 7. Measure the patient’s rectal temperature to confirm the diagnosis 8. Evacuate the patient to the nearest medical facility via emergency medical services.
with iced water. The victim should be submerged up to the shoulders and kept under immediate hands-on supervision at all times. Another expedient method in the field is to keep bed sheets soaked in a cooler full of iced water; the victim can then be wrapped in the cold sheets. Particular care should be given to covering the head and to resubmerging the sheets every few minutes to recool them.79 Ice packs can be applied to the groin, axillae, sides of the neck, and head to augment iced-sheet cooling. Cooling should continue until emergency medical services providers arrive. Nonmedical first responders should not attempt to evacuate heat stroke patients themselves, because this may distract from cooling efforts. If CWI or iced sheets are not available, the victim should be kept wet by applying large quantities (20 to 30 L [5.3 to 7.9 gal]) of tap water or water from any source, and the victim’s body should be constantly fanned. Cooling blankets are generally ineffective as a single modality for inducing the rapid lowering of body temperature required for treating heatstroke.
EMERGENCY MEDICAL SERVICES TREATMENT During evacuation, CWI is often not a viable method for treatment. Iced sheets and ice packs can be easily used en route during transport. Many EMS vehicles now carry refrigerated intravenous (IV) fluid to initiate induction of therapeutic hypothermia in cardiovascular emergencies. When used, chilled IV fluid (4° C [39° F]) should be peripherally administered.63 Vascular access should be established without delay by inserting a 12- or 14-gauge IV catheter. Administration of normal saline or lactated Ringer’s solution should be started. Recommendations vary regarding administration rate of fluids. Some clinicians advise a rate of 1200 mL (1.26 qt) over 4 hours,78 whereas others encourage a 2-L (2.11-qt) bolus over the first hour and an additional liter of fluid per hour for the next 3 hours.98 Patients should be placed on a cardiac monitor. Administration of supplemental oxygen may help to meet the victim’s increased metabolic demands, and it may also be used to treat hypoxia that is commonly associated with aspiration, pulmonary hemorrhage, pulmonary infarction, pneumonitis, or pulmonary edema.34,67 A blood glucose determination should be performed, and adults with blood sugar level less than 60 mg/dL should be treated with 1 ampule of 50% IV dextrose solution. Children should be treated with 2 to 4 cc/kg of 25% IV dextrose solution. The use of antipyretics is not effective and may potentially be harmful to heatstroke victims. Aspirin and acetaminophen lower Tco by normalizing the elevated hypothalamic set point that is caused by pyrogens; in heatstroke, the set point is normal, with Tco elevation reflecting a failure of normal cooling mechanisms. Furthermore, acetaminophen may induce additional hepatic damage, and administration of aspirin may aggravate bleeding tendencies. Alcohol sponge baths are inappropriate under any circumstances, because transcutaneous absorption of alcohol may lead to poisoning and coma. In a comatose victim, airway control should be established by inserting a cuffed endotracheal tube. Positive-pressure ventilation is indicated if hypoxia persists despite supplemental oxygen administration.
The victim’s altered mental status may adversely affect the ability of emergency department personnel to obtain a detailed history of precipitating events. Lack of such information may also delay diagnosis. Emergency medical transport personnel should attempt to obtain this history before evacuating the victim and should communicate the information to medical staff. Of particular importance is the duration—and, when available, the maximum degree—of hyperthermia.
HOSPITAL EMERGENCY MEDICAL TREATMENT Patients with suspected heat stroke should be placed in a large treatment room to accommodate the needed number of staff. Patients are often combative and disoriented before reestablishing their baseline mental status. Aggressive cooling measures should continue until mental status returns to normal and Tco is 39° C (102° F).24 After discontinuation of cooling, Tco should be monitored every 5 minutes to ensure that it does not increase. The Tco reported in the field for heatstroke victims may be significantly higher (e.g., 41.1° C [106.9° F]), than those documented in the hospital emergency department (e.g., 37.8° C [100° F]), because Tco may fall during transport to the hospital.99 Documenting only a mild elevation in Tco on arrival does not exclude the diagnosis of heatstroke. Central nervous system (CNS) disturbances (i.e., coma, convulsions, confusion, or agitation) that accompany hyperthermia may also result from CNS infections, sepsis, or other disease processes. Other diagnoses should be considered when the patient does not regain normal mental status when the Tco is normalized in less than 30 minutes. When Tco remains elevated for a longer time, there is a decreased likelihood that mental status will normalize with euthermia.17 Tco can be measured at several anatomic sites, but oral, tympanic, esophageal, and rectal temperatures show regional variations as a result of differences in tissue metabolic activity, local blood supply, and temperature gradients between neighboring tissues. During exercise, active skeletal muscle temperature differs dramatically from that of other areas of the body that are not directly involved in the activity. Oral temperature is considered to be similar to blood temperature as a result of the rich blood supply of the tongue, but it is also influenced by hyperventilation and drinking fluids. Rectal temperature is a highly reliable indicator of body temperature, but it has a slower response rate and gives slightly higher readings than do other sites in the body. The comparison of oral and rectal temperature values in heatstressed underground miners showed a difference of approximately 1° C (2° F), with oral temperatures underestimating rectal values.108 Tympanic temperature responds more rapidly to cooling or heating than does rectal temperature, but it is influenced by changes in the skin temperature of the head and neck.44,68 The ear should be insulated from the environment to prevent cool ambient temperatures (<30° C [86 ° F]) from affecting this measurement. Esophageal temperature is the most accurate and responsive to changes in blood temperature, but its instrumentation is impractical in severely injured or unresponsive patients. If airway control was not previously established and if the patient is still unconscious, a cuffed endotracheal tube should be inserted to protect against aspiration of oral secretions. Supplemental oxygen—and, when hypoxia (PaO2 <55 mm Hg) or hypotension is present, positive-pressure ventilation—should be provided. Overly vigorous fluid resuscitation may precipitate pulmonary edema, so careful monitoring is indicated. Ideally, 1 to 2 L (1.05 to 2.11 qt) of fluid should be administered during the first hour after collapse, and additional fluids should be administered until satisfactory urine output (0.5 cc/kg/hr in an adult and 1.0 cc/ kg/hr in a child) is established.38 Most heatstroke victims arrive with a high cardiac index, low peripheral vascular resistance, and mild right-sided heart failure with elevated central venous pressure. Only moderate fluid replacement is indicated if effective cooling results in vasoconstriction and increased blood pressure. Providers should consider noninvasive intravascular volume monitoring or the minimally invasive monitoring of systolic volume variation and pulse pressure variation. If these methods are not adequate, a Swan-Ganz pulmonary artery catheter may be 233
CHAPTER 11 Clinical Management of Heat-Related Illnesses
BOX 11-1 Basic First Aid for Heat Illnesses
PART 2 COLD AND HEAT
necessary to assess appropriate fluid supplementation. Some victims have a low cardiac index, hypotension, and elevated central venous pressure. These persons have been successfully treated with an isoproterenol drip (1 mg/min).78 Patients with a low cardiac index, low central venous pressure, hypotension, and low pulmonary capillary wedge pressure should receive fluid. Unless the patient has rhabdomyolysis, aggressive fluid hydration is seldom required after initial treatment. Cardiac monitoring should be maintained during at least the first 24 hours of hospitalization. Arrhythmia is most likely to occur during hyperthermia, but it may also occur as a result of electrolyte abnormalities. The use of norepinephrine and other α-adrenergic drugs should be avoided because they cause vasoconstriction, thereby reducing heat exchange through the skin. Anticholinergic drugs that inhibit sweating (e.g., atropine) should also be avoided. Cooling techniques are ineffective when the victim suffers seizures that increase storage of body heat; therefore, convulsions should be controlled. Intravenous benzodiazepines are preferred for their efficacy and renal clearance. Initial dosing is either 4 to 8 mg of IV lorazepam or 10 mg of IV diazepam. If seizures persist for more than 10 minutes after the first dose, an additional 4 mg of lorazepam or 10 mg of diazepam should be administered. As a result of drastic cooling, skin temperature may decrease enough to cause shivering. Administration of 12.5 mg of meperidine via slow IV push103 or of 5 mg of diazepam is effective to suppress shivering and to prevent an additional rise in Tco from metabolic heat production. If CWI is used, the increase in metabolic rate as a result of shivering will be more than offset by the high rate of heat transfer. Therefore the presence of shivering should not be a cause for concern when this method of cooling is used.24,83 Severe muscle cramping may be caused by electrolyte imbalances. Magnesium levels should be obtained. If magnesium levels are low, consideration may be given to the use of 50% IV magnesium sulfate (4 g in 250 mL of 5% dextrose injection at a rate that does not exceed 3 mL per minute).14,15 A Foley catheter should be placed to monitor urine output. Renal damage from myoglobinuria and hyperuricemia can be prevented by promoting renal blood flow by administering IV mannitol (0.25 mg/kg) or furosemide (1 mg/kg).98 If creatine phosphokinase (CPK) levels exceed 100,000 international units, alkalinize the urine of patients with exertional rhabdomyolysis; there is no advantage to alkalinization when levels are lower. Hemodialysis should be reconsidered if anuria, oliguria (<0.5 mL/ kg of urine per hr for >6 hr), uremia, or hyperkalemia develops. Cooling and hydration usually correct acid–base abnormalities; however, serum electrolytes should be monitored and appropriate modifications of IV fluids made. Glucose should be monitored repeatedly, because either hypoglycemia or hyperglycemia may occur after EHS.95 Oral and gastric secretions are evacuated via a nasogastric tube that is connected to continuous low suction. Although antacids, proton pump inhibitors, and histamine-2 blockers have been used to prevent gastrointestinal bleeding, no studies to date demonstrate their efficacy for heatstroke victims. Induced Hypothermia Induced hypothermia is increasingly being used for many neurologic and cardiovascular emergencies, including acute stroke, neonatal hypoxic–ischemic encephalopathy, and after cardiac arrest.9,50,76,94 This therapeutic modality has not been evaluated for effectiveness in individuals with EHS, but may have a role in cooling severe refractory cases of EHS. There may be a role for a period of induced hypothermia after severe EHS. Dantrolene No drug has been found to have a significant effect for reducing Tco. Antipyretics are ineffective, because the thermoregulatory set point is not affected in heatstroke. Furthermore, antipyretics might be harmful, because they cannot be readily metabolized in the heat-affected liver. However, dantrolene has been used quite successfully for the treatment of several hypercatabolic syndromes, such as malignant hyperthermia, neuroleptic malignant syndrome, and other conditions that are characterized by muscular rigidity or spasticity.107,114 Dantrolene stabilizes the 234
calcium (Ca2+)-release channel in muscle cells, thereby reducing the amount of Ca2+ released from cellular calcium stores. This lowers intracellular Ca2+ concentrations, muscle metabolic activity, muscle tone, and thus heat production.27,75 In some studies, dantrolene was claimed to be effective for the treatment of heatstroke, whereas in others it improved neither the rate of cooling nor survival.25,31,66,109 In six patients with rhabdomyolysis, intramuscular Ca2+ concentrations were 11 times higher than in controls, and dantrolene successfully lowered this elevated Ca2+.65 Collectively, the limited data available are at best inconsistent. Despite growing evidence for a possible benefit of dantrolene treatment in patients with heatstroke, justification for its routine use in such cases is not proved, although future clinical trials may change this assessment. Moran and colleagues71 studied dantrolene in a hyperthermic rat model, and found it to be effective as a prophylactic agent in sedentary animals only. Dantrolene induced more rapid cooling by depressing Ca2+ entry into the sarcoplasm; this led to relaxation of peripheral blood vessels with attenuated production of metabolic heat. Dantrolene may also be effective in treating heatstroke by increasing the cooling rate. However, in other animal models, dantrolene was not superior to conventional cooling methods.117 As such, dantrolene is not recommended.
CLINICAL MANIFESTATIONS Clinical manifestations of heatstroke vary, depending on whether the victim suffers from classic heatstroke, which is a common disorder of older adults during heat waves and occurs in the form of epidemics, or EHS,1 which occurs when excess heat generated by muscular exercise exceeds the body’s ability to dissipate it (Table 11-1). Some overlap in presentation may occur; treatment with a medication (e.g., antihypertensive or antipsychotic) that places an older adult at risk for classic heatstroke also places an exercising individual at risk for EHS. The clinical picture of heatstroke usually follows a distinct pattern of events
TABLE 11-1 Comparison of Classic and Exertional
Heatstroke
Characteristics
Classic
Exertional
Age group
Young children and older adults
Health status Concurrent activity Drug use
Chronically ill Sedentary Diuretics, antidepressants, antihypertensives, anticholinergics, and antipsychotics May be absent Usually absent; poor prognosis if present Usually absent Uncommon Uncommon Mildly elevated
Men between the ages of 15 and 45 yr Healthy Strenuous exercise Usually none
Sweating Lactic acidosis Hyperkalemia Hypocalcemia Hypoglycemia Creatine phosphokinase Rhabdomyolysis Hyperuricemia Acute renal failure Disseminated intravascular coagulation Mechanism
Usually present Common Often present Frequent Common Markedly elevated
Unusual Mild <5% of patients Mild
Frequently severe Severe 25-30% of patients Marked; poor prognosis
Poor dissipation of environmental heat
Excessive endogenous heat production and overwhelming heat-loss mechanisms
Modified from Knochel JP, Reed G: Disorders of heat regulation. In Kleeman CR, Maxwell MH, Narin RG, editors: Clinical disorders of fluid and electrolyte metabolism, New York, 1987, McGraw-Hill.
Acute Phase The acute phase of heatstroke is characterized by CNS manifestations. Because brain function is very sensitive to hyperthermia, this phase is present in all heatstroke patients. Early signs of CNS dysfunction are typically cerebellar and include ataxia, poor coordination, and dysarthria.116 Advanced signs of CNS depression include irritability, aggressiveness, stupor, delirium, and coma.2,21,102 Mental status changes usually resolve after return to a normal Tco. After a return to normothermia, persistence of coma is a poor prognostic sign.57,102 Other symptoms include fecal incontinence, flaccidity, and hemiplegia. Cerebellar symptoms may persist beyond the acute phase.69,102,116 Other common disturbances during the acute phase occur in the gastrointestinal and respiratory systems. Gastrointestinal dysfunction, including diarrhea and vomiting, often occurs. However, the latter may reflect translocation of toxic gram-negative bacterial lipopolysaccharide from the lumen of the intestines because of poor splanchnic perfusion as a result of hypotension caused by increased skin blood flow and from CNS impairment.18,41,102 Hyperventilation and elevation of Tco primarily lead to respiratory alkalosis, which in EHS may be masked by metabolic acidosis as a result of increased glycolysis and hyperlacticacidemia.26,74 Hypoxemia may be present in patients with respiratory complications.28,74,105 It should also be noted that oxygen consumption is elevated during hyperthermia, with a 10% to 13% increase for every ° C above euthermia.32 EHS shares many common findings with systemic inflammatory response syndrome (SIRS).17,97 Endotoxemia, hyperthermia, and other risk factors (e.g., preexisting infection) and stressors associated with EHS can trigger this exaggerated inflammatory response. Patients should be assessed for SIRS after admission with the use of the following criteria:16 (1) body temperature of less than 36° C (98.6° F) or of more than 38° C (100.4° F); a heart rate of more than 90 beats per minute, tachypnea, or an arterial partial pressure of carbon dioxide of less than 4.3 kPa (32 mm Hg); and a white blood cell count of less than 4000 cells/ mm3 (4 × 109 cells/L) or of more than 12,000 cells/mm3 (12 × 109 cells/L) or the presence of more than 10% immature neutrophils. When two or more of these criteria are met, SIRS can be diagnosed. The presence of systemic inflammatory response markers during the acute phase predicts the severity of subsequent phases. Hematologic and Enzymatic Phase Hematologic and enzymatic disorders peak 24 to 48 hours after collapse. In the hematologic and enzymatic phase of EHS, hematologic, enzymatic, and other blood parameters are altered. In humans and experimental animals, hyperthermia results in leukocyte activation46 and in changes in lymphocyte subpopulations, both in absolute numbers and in percentages.1 Leukocytes may range from 20 to 30 × 103/mm3 or higher.10,51 In severe cases, leukocyte activation is associated with the systemic activation of coagulation cascades.55 In one study, all fatal cases of EHS involved disturbances in the blood coagulation system.10,101 Prothrombin time, partial thromboplastin time, and the level of fibrin split products increased with a fall in thrombocytes.38 Clotting dysfunction peaked 18 to 36 hours after the acute phase of heatstroke; 2 to 3 days after heatstroke, prothrombin levels fell to 17% to 45% of normal. Depending on the severity of heatstroke, thrombocyte values ranged between 110 × 103/mm3 and 0.100,101 This systemic inflammatory response state resembles gramnegative bacterial sepsis, and it appears that lipopolysaccharide (a cell-wall component of gram-negative bacteria) participates in the pathophysiology of EHS.43 Enzymes One of the prominent and almost pathognomonic characteristics of EHS is the appearance of exceptionally high levels of certain cellular enzymes, which implies cell damage or death. Most patients with EHS show an elevation of serum CPK activity and myoglobinuria, which suggests damage to skeletal muscle.37 CPK values in the range of 103 to 104 international units were
commonly found, with peak values occurring 24 to 48 hours after collapse.30,96 At a Tco of 41.8° to 42.2° C (107.24° to 107.96° F), aspartate aminotransferase and alanine aminotransferase levels rose by factors of 25 and 8, respectively, and bilirubin levels approximately doubled to 1.56 mg/dL.82 These rises in enzyme levels are related to tissue damage, which in turn depends on both Tco and its rates of rise and duration.73 CPK was the most sensitive to increases in Tco, and this was followed by lactate dehydrogenase, which is an index of generalized tissue damage. CPK levels in EHI and EHS typically peak at 24 to 48 hours. Rising values after this point should alert the clinician to the possibility of an occult compartment syndrome. It is not uncommon for a victim of EHI to complain of lower-extremity pain that declares itself as a compartment syndrome. During the 1994 Hajj, 26 heatstroke victims admitted to a heatstroke treatment unit had elevated levels of CPK, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase; these levels remained high after 24 hours. Those who died had higher enzyme levels than did the survivors. Lactate dehydrogenase concentration was useful for distinguishing between those who died and those who had a rapid recovery. The enzymes were better prognostic indicators than were Tco, anion gap, and serum potassium level. Late Phase The late phase of heatstroke manifests 3 to 5 days after collapse, and is characterized by disturbances in renal and hepatic functions. These abnormalities are consistent with multiorgan dysfunction syndrome as a result of SIRS. Acute renal failure is a common complication of severe cases, and occurs in approximately 25% to 30% of patients with EHS patients.60,67,100 Oliguria and anuria are characteristic features. During this phase, urine has been described as being like machine oil, with a high specific gravity.81,84,92,100 Usually present in the urine are red and white cells, hyaline and granular casts, and mild to moderate proteinuria.92 The etiology involves multiple causes,81 but a major one is reduced renal blood flow caused by heat-induced hypotension, hypohydration, and peripheral vasodilation. In addition, direct thermal injury may also lead to widespread renal tissue damage.92 Myoglobinuria and elevated blood viscosity that result from disseminated intravascular coagulation may further contribute to acute oliguric renal failure.84,92,104,111 EHS is usually manifested by increased serum levels of liver enzymes, but acute liver failure has also been reported.115,39 High bilirubin levels, which may last for several days, reflect hepatic dysfunction and hemolysis. In most cases of EHS, liver injury is usually asymptomatic and exhibits reversible elevation in plasma aminotransferase levels.48 Acute liver failure is documented in 5% of patients with EHS.61 Hypophosphatemia (<0.5 mmol/L) at the time of admission may predict occurrence of acute liver failure.39 Despite limited experience and the observation that EHS patients with extensive liver damage may recover spontaneously, orthotopic liver transplantation had been suggested as a potential treatment.12,47,89 Among 16 reported cases of EHS-induced liver failure,45 three patients underwent liver transplantation. In the conservatively managed group, eight patients recovered spontaneously, and five died. Concomitantly, all three patients who received transplantation died. Hadad and co-workers45 concluded that, because of the poor and limited results of liver transplantation after heatstroke, the interpretation of prognostic criteria is crucial before listing a patient for such surgery.
SEQUELAE AND AFTERCARE The combination of the rapid reduction of Tco, control of seizures, proper rehydration, and prompt evacuation to an emergency medical facility results in a 90% to 95% survival rate in heatstroke victims, with morbidity directly related to the duration of hyperthermia.17,97 A poor prognosis is associated with Tco of more than 41° C (105.8° F), prolonged duration of hyperthermia, hyperkalemia, acute renal failure, and elevated serum levels of liver enzymes. Therefore misdiagnosis, early inefficient treatment, and delay in evacuation are the major causes of clinical deterioration. Full recovery without evidence of neurologic impairment has been achieved even after coma of 24 hours’ duration and 235
CHAPTER 11 Clinical Management of Heat-Related Illnesses
with three phases: (1) acute, (2) hematologic or enzymatic, and (3) late.38
PART 2 COLD AND HEAT
subsequent seizures.101 Persistence of coma after return to normothermia is a poor prognostic sign.102 Red blood cell apoptosis (i.e., cell blebbing, asymmetry, and shrinkage) on early peripheral blood smears is a very poor prognostic sign and may indicate extensive cellular necrosis. Neurologic deficits may persist, but usually only last for a limited period of 12 to 24 months and only rarely for longer. CNS dysfunction becomes increasingly severe with prolonged duration of hyperthermia and associated circulatory failure. Nevertheless, coma that persists for up to 24 hours, even with subsequent seizures, is usually followed by complete recovery without evidence of mental or neurologic impairment.2,88 However, chronic disability may prevail for several weeks or months in the forms of cerebellar deficits, hemiparesis, aphasia, and mental deficiency.2,60,88 Only in exceptional cases, when coma persisted for more than 24 hours, did mental and neurologic impairment become chronic and prevail for years. However, in one study of classic heatstroke, 78% of patients had minimal to severe neurologic impairment, such as ataxia or dysathria.30 Long-term EHS victims may have increased mortality from heart, liver, and kidney disease.113
PREVENTION Prevention of heat illness relies on an awareness of host risk factors, altering behavior and physical activity to match these risk factors and environmental conditions, and a requirement for appropriate hydration during physical exercise in the heat. More aggressive educational activity that explains heat illness and its prevention to the public is to be strongly promoted. Primary care physicians should incorporate this information into the anticipatory guidance of routine health assessment. Despite a wealth of medical literature about heat injury, some athletic coaches continue to use physical or psychological methods to force athletes to compete or train under intolerably hot conditions. This practice should be viewed as irresponsible, dangerous, and possibly criminally negligent. The importance of recognizing milder forms of heat illness cannot be overstated. Any time heat injuries occur, coaches and trainers should reassess all athletes and determine what other measures can be implemented to prevent more serious injuries from occurring. Awareness of Host Risk Factors Shapiro and Moran96 studied 82 cases of EHS in Israeli soldiers and concluded that at least one factor that predisposes an individual to heatstroke (e.g., diarrhea, lack of acclimatization, poor fitness) was associated with each case. Correcting those individual risk factors should lead to strategies that can prevent heatstroke. Any underlying condition that causes dehydration or increased heat production or that causes decreased dissipation of heat interferes with normal thermoregulatory mechanisms and predisposes an individual to heat injury. Older individuals are less tolerant to EHI than younger persons, and they are more susceptible to classic heatstroke because of decreased secretory ability of their sweat glands and decreased ability of their cardiovascular systems to increase blood flow to the skin. When healthy young adults exercise strenuously in the heat, EHS may occur despite the absence of host risk factors. Elite and professional athletes, the general public, and the military have widely used ergogenic aids (e.g., the herb ephedra [ma huang]) that contain ephedrine to improve performance and for weight loss. Because ephedra increases metabolic rate, it has caused numerous cases of heat illness and deaths worldwide, and it has been banned. Because there are no clear ergogenic benefits to the use of ephedra alone, use of ephedra-containing substances should be discouraged.80 The ratio of basal metabolic rate to surface area is higher in children than in adults. As a result, a child’s skin temperature is higher for any given Tco. Although the secretory rates of sweat glands are lower in children, children have greater numbers of active sweat glands per area of skin than adults and overall greater sweat rates per unit area.54 Any reduction in the rate of sweating puts children especially at risk. The primary mechanism for heatstroke in young children is hot vehicle entrapment. 236
Between 1998 and 2010, 462 children died from heatstroke as a result of vehicular hyperthermia. The primary means of heat dissipation is production and evaporation of sweat. Any condition that reduces this process places the individual at risk for thermal injury. Poor physical conditioning, fatigue, sleep deprivation, cardiovascular disease, and lack of acclimation all limit the cardiovascular response to heat stress.40,56 Obesity places an individual at risk as a result of reduced cardiac output, the increased energy cost of moving extra mass, increased thermal insulation, and altered distribution of heat-activated sweat glands.72 Older adults and younger individuals show decreased efficiency of thermoregulatory functions and increased risk for heat injury. Several congenital or acquired skin abnormalities affect sweat production and evaporation. Ectodermal dysplasia is the most common form of congenital anhidrosis. Widespread psoriasis, poison ivy, sunburn, scleroderma, miliaria rubra (i.e., “prickly heat,” which is caused by the plugging of sweat ducts with keratin), deep burns, and prior skin grafting may also limit sweat production. Dehydration affects both central thermoregulation and sweating. A mere 2% decrease in body mass through fluid loss produces an increase in heart rate, increase in Tco, and decrease in plasma volume. In an otherwise healthy adult, gastrointestinal infection with vomiting and diarrhea may cause sufficient dehydration to place the individual at risk for EHS. Chronic conditions that may contribute to heat illness include diabetes mellitus, diabetes insipidus, spinal cord injury, eating disorders (especially bulimia), and mental retardation. Alcoholism and illicit drug use are among the 10 major risk factors for heatstroke in the general population.58 An important effect of alcohol consumption is inhibition of antidiuretic hormone secretion, which leads to relative dehydration. Autonomic dysfunction, which is present with many chronic diseases, impairs thermoregulation.52 Despite evidence that hypohydration limits physical performance, voluntary dehydration continues to be routine in certain athletic arenas.5,7,20,110 Wrestlers, jockeys, boxers, and bodybuilders commonly lose 3% to 5% of their body mass 1 to 2 days before competition. In addition to restricting fluid and food, they use other pathogenic weight-control measures, such as self-induced vomiting, laxatives, diuretics, and exposure to heat (e.g., saunas, hot tubs, “sauna suits”). Athletes who are undergoing rapid dehydration are at risk not only for heat injury but also for other serious medical conditions, such as pulmonary embolism.29 Box 11-2 highlights common medications that interfere with thermoregulation. Special attention should be paid to the role of antihistamines in reducing sweating. This class of medications is commonly obtained over the counter, so the general population should be warned about the dangers of exercising in the heat when they are taking antihistamines. Although it has been widely believed that sustaining an episode of heatstroke predisposes the individual to future heat injury, this has been refuted in a recent study of heatstroke victims.8 Ten heatstroke patients were tested for their ability to acclimate to heat; BOX 11-2 Drugs That Interfere With Thermoregulation Drugs That Increase Heat Production • Thyroid hormone • Amphetamines • Tricyclic antidepressants • Lysergic acid diethylamide Drugs That Decrease Thirst • Haloperidol Drugs That Decrease Sweating • Antihistamines • Anticholinergics • Phenothiazines • Benztropine mesylate Data from references 12, 31, 50, 66, 105, and 107.
ADAPTATION TO ENVIRONMENTAL CONDITIONS Appropriate adaptation to hot environmental conditions encompasses many forms of behavior, including modifying clothing, the degree of physical activity, searching for shade, the anticipatory enhancement of physical conditioning, acclimation to heat stress, and paying attention to the level of hydration. Clothing Different regions of the body are not equivalent with regard to sweat production.53 The face and the scalp account for 50% of total sweat production, whereas the lower extremities contribute only 25%. When exercising under conditions of high heat load, maximal sweat evaporation is facilitated by maximal skin exposure. Clothing should be lightweight and absorbent. Although significant improvement has been made in the fabrication of athletic uniforms, the uniforms and protective gear required by certain branches of the military and public safety officers continue to add to the risk of heat injury. Developing protective clothing that permits for more effective heat dissipation is indicated. Uniforms should be modified to decrease the amount of extra protective equipment and head gear needed as much as is safely possible during the first week of training and during times of high heat stress conditions. Activity Behavioral actions can effectively minimize the occurrence of classic heatstroke. Lack of residential air conditioning places indigent persons at risk during heat waves. By sitting in a cool or tepid bath periodically throughout the day, the individual can decrease heat stress and thereby prevent heat injury. The more than 10,000 deaths during the 2003 heat wave in Europe could have been reduced by simple announcements by public health officials of this preventive measure. This type of “heat dumping” activity can also include taking cool showers instead of warm showers. In addition, the forearms and hands can be immersed into water that has been cooled to 10° to 20° C (50° to 68° F) for a period of 10 minutes. This action will achieve a reduction in Tco of 0.7° C (1.3° F) and provide the athlete with sustained capability to train in the heat.42 In addition to forearm and hand immersion in cool or cold water, the concept of cooling the palm by various devices, some of which add vacuum pressure to the palm in addition to cooling, has recently become popular. A comprehensive review23 of cooling rates of various cooling modalities has shown that this methodology is no more effective in lowering body core temperature than limb immersion in tap water (15° C [59° F]). Recent research on these devices has shown that the addition of negative pressure with cooling did not enhance any cooling effect.62 In addition, these devices have been shown to be ineffective in slowing the development of hyperthermia when used between exercise bouts4 and in the improvement of high-intensity, intermittent exercise.112 Cold or ice water has been reported to have a cooling power of 5 to 8 times greater than hand/palm cooling devices.23 Given the low cooling power of these devices, their use in a field or athletic setting, especially for treatment of heat injury or illness, should be questioned. This is also true when viewed in terms of cost vs. limb immersion modalities. Regarding use in a wilderness setting, these devices have additional drawbacks including the need for electrical power via batteries and the added weight of transport. Athletes should be placed in the shade whenever possible during periods of rest and instruction. If shade is not available in areas where warm weather training is routinely conducted, consideration should be given to constructing overhead shelters. If latrines are not easily accessed at training areas, consideration should be given to placing portable latrines nearby to prevent
TABLE 11-2 Determination of Wet Bulb Globe
Temperature Heat Index
Temperature (T, in ° F) Wet bulb T Dry bulb T Black globe T Heat index
Factor
Example
×0.7 ×0.1 ×0.2
78 × 0.7 = 54.6 80 × 0.1 = 8.0 100 × 0.2 = 20.0 82.6
Wet bulb reflects humidity, dry bulb reflects ambient air temperature, and black globe reflects radiant heat load; the heat index is the sum of the three. Alternative equation: Wet bulb globe temperature = (0.567 Tdb) + (0.393 Pa) + 3.94, where Tdb is dry bulb temperature and Pa is water vapor pressure.
voluntary fluid restriction. The authors recommend spacing runners widely apart during group runs to allow for optimal heat dissipation. Modification of physical activity should not be based solely on any individual parameter of ambient temperature (Tamb), relative humidity, or solar radiation, because all of these contribute to heat load. The wet bulb globe temperature (WBGT) is an index of heat stress that incorporates all three factors. This value may be calculated (Table 11-2), or it may be obtained directly from portable digital heat-stress monitors that measure all three parameters simultaneously to compute the WBGT. When heatstress monitors are used, care should be taken to ensure that they are calibrated yearly and that they are not left out in the heat for long periods of time without use. Care should also be taken to ensure that the device measures radiant heat, humidity, air movement, and shaded temperature to calculate WBGT. Devices that measure the heat stress index, relative humidity, and wind speed should not be used to estimate WGBT. Current recommendations from the American College of Sports Medicine for preventing exertional heat illness during workouts and competition are based on the WBGT.3 Most heat injuries occur during cooler WBGT periods as a result of cumulative heat exposure from preceding days. Some clinicians have proposed that heatwarning systems would base their warnings on cumulative heat stress rather than solely on the current WBGT.113 Other clinicians have suggested the use of syndromic surveillance to help alert the public about periods of high heat stress.11 Table 11-3 presents a suggested modification of sports activity that is also based on the WBGT. Although American College of Sports Medicine guidelines for the summer indicate that vigorous physical activity should be scheduled in the morning or evening, individuals should be cautioned that the highest humidity of the
TABLE 11-3 Modification of Sports Activity on the
Basis of Wet Bulb Globe Temperature
Index
Limitation
<10° C (50° F)
There is a low risk for hyperthermia but a possible risk for hypothermia. There is a low risk for heat illness. There is a moderate risk toward the end of the workout. Those at high risk for heat injury should not continue to train; all athletes should practice in shorts and T-shirts during the first week of training. Care should be taken by all athletes to maintain adequate hydration. Unacclimated persons should stop training; all outdoor drills in heavy uniforms should be canceled. Acclimated athletes should exercise caution and continue workouts only at a reduced intensity; they should wear light clothing only. Stop all training.
<18.3° C (65° F) 18.3°-22.8° C (65°-73° F) 22.8°-27.8° C (73°-82° F) 27.8°-28.9° C (82°-84° F) 28.9°-31.1° C (85°-88° F) 31.1°-32.2° C (88°-90° F) ≥32.2° C (90° F)
237
CHAPTER 11 Clinical Management of Heat-Related Illnesses
by definition, the ability to acclimate to heat indicates heat tolerance. Nine of the patients demonstrated heat tolerance within 3 months after the heatstroke episode; the remaining patient acclimated to heat one year after his heat injury. In no case was heat intolerance permanent. Although individuals may show transient heat intolerance after thermal injury, evidence for permanent susceptibility to thermal injury is lacking.
PART 2 COLD AND HEAT
day is usually during early morning. In 1999, Montain and coworkers70 updated the fluid replacement guidelines for warmweather training (see Chapter 70, Table 70-5). It is important to note that compliance with these recommendations does not remove all risk of heat injury. The development of another index of heat stress that provides a better basis for the prevention of EHS is indicated. Rav-Acha and colleagues85 assembled a case series of six fatal cases of EHS in the Israeli Defense Forces and examined the circumstances that led to the deaths. A significant association between the accumulation of predisposing factors and EHS totality was found. In almost all of the fatal cases, seven predisposing factors were noticed: (1) low physical fitness; (2) sleep deprivation; (3) high heat load; (4) high solar radiation; (5) physical exercise unmatched to physical fitness; (6) absence of proper medical triage; and (7) training during the hottest hours. These fatality factors primarily concerned organizational training regulations and not individual factors, which emphasizes the importance of proper guidelines and safety measures in a warm climate—rather than individual characteristics—for preventing EHS fatalities. It follows that a combination of predisposing factors that were already found to impair heat tolerance40 is a strong predictor of a grave prognosis. Dehydration was found in only two of the six cases reported. Conditioning The contribution of cardiovascular conditioning to thermoregulation is discussed in Chapter 4. Ideally, an individual should train under temperate or thermoneutral conditions before exercising in the heat. For the previously sedentary individual, an exercise regimen that incorporates 20 to 30 minutes of aerobic activity 3 to 4 days a week will improve cardiovascular function after 8 weeks. It is important to remember that even physically active individuals may lack physical conditioning relative to a particularly stressful competition or activity. Heat illness in runners commonly occurs when novices exceed their training effort during
238
races or when well-trained athletes increase their pace above normal during long-distance events. Acclimatization During initial exposure to a hot environment, workouts should be moderate in intensity and duration. A gradual increase in the time and intensity of physical exertion over 8 to 10 days should allow for optimal acclimatization.33 Early season high-school heatstroke deaths are most likely to occur during the first 4 days of practice87; children require 10 to 14 days to achieve an appropriate acclimatization response. Acclimatization can be induced by simulating hot environmental conditions indoors. Aerobic activity should be conducted during exposure to the hot environment so that the individual can achieve optimal acclimatization.90 If symptoms of heat illness develop during the acclimation period, all physical activity should be stopped and appropriate interventions begun. Acclimatization is not facilitated by restricting fluid intake; in fact, conscious attention to fluid intake is required to prevent dehydration. As with physical conditioning, there are limits to the degree of protection that acclimatization provides from heat stress. Given a sufficiently hot and humid environment, no one is immune to heat injury.
RESEARCH Areas for future research include improved clarification of when athletes can safely return to play; the role of autonomic nervous system dysfunction in EHS; the benefit of induced hypothermia for EHS treatment; and the role of clonidine, activated protein C, and antibiotics during initial treatment. We extend much appreciation to the previous authors of this chapter, Daniel S. Moran and Stephen L. Gaffin.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 12
Wildland Fires: Dangers and Survival MARTIN E. ALEXANDER, ROBERT W. MUTCH, KATHLEEN MARY DAVIS, AND COLIN M. BUCKS
There can be few natural physical phenomena with the scope and complexity of a forest fire. The fuel that powers it is found in a huge range of sizes, quantities, and arrangements in space. The weather affects the current condition of this fuel array in a bewildering maze of drying and wetting effects, each fuel component responding to a “different drummer.” The combustion process itself, once under way, responds to a complex blend of fuel variation, moisture status, topography, wind speed, and other atmospheric factors. Its frontal intensity varies over an immense range, from tiny flickers easily stepped over, to dense sheets of flame whose fierce radiation keeps the observer at a distance. —VAN WAGNER (1985)
In describing the 13 wildland firefighter fatalities that occurred on the Mann Gulch fire near Helena, Montana, on August 5, 1949, author Norman Maclean275 wrote in his seminal book Young Men and Fire, published in 1992, that “They were still so young they hadn’t learned to count the odds and to sense they might owe the universe a tragedy.” Three years later, Canadian folksinger-songwriter James Keelaghan, inspired by Maclean’s book, paid tribute to the fallen firefighters in a haunting ballad entitled “Cold Missouri Waters.” The Mann Gulch fire has been called “the race that couldn’t be won.”403 Although the crew increased their pace ahead of the fire, the fire accelerated faster than they did until fire and people converged. Miraculously, three people survived the fire. Smoke jumper foreman Wag Dodge ignited an “escape fire” by burning off a patch of cured grass into which he tried to move all of his crew, whereas two others found a route to safety and escaped injury on a nearby rockslide. Many improvements in a firefighter’s odds of surviving an entrapment or burnover encounter with a wildland fire have occurred since 1949. These advances include improved understanding of fire behavior, increased emphasis on fire safety and fire training, and development of personal protective equipment. However, as incidents such as the 14 firefighter fatalities on the 1994 South Canyon fire in Colorado (Figure 12-1) have shown, tragedies continue to occur.170 Norman Maclean’s son, John, would in turn write about this fatal fire 50 years later.271 Grief over lost loved ones can sometimes lead to further tragedies. For example, one of the smoke jumpers killed on the 1949 Mann Gulch fire, Stan Reba, had been married less than one year. His widow grieved for him and never remarried, and then 10 years later took her own life.236,286 Wildland fires are a threat to human life, property, and natural resources in many regions of the world (Figure 12-2). Although the total number of deaths among the general public due to wildland fires in modern times pales in comparison with the death toll and destruction from other natural hazards (e.g., hurricane, tornado, flood, earthquake, tsunami, avalanche)83 and human-made disasters, the fatalities are frequent and devastating.470 There are very few comprehensive summaries of deaths due to wildland fires on a worldwide basis. The compilation of U.S. wildland firefighter fatalities begun in the early 1970s519 is unique.339 Statistics on the number of civilian or wildland firefighter fatalities due to being trapped or overrun by wildland fires on a global basis are unfortunately not kept in any 240
systematic manner.234 It is, however, well known that more than 300 deaths due to bushfire entrapments and/or burnovers occurred in the state of Victoria in Australia alone during the 20th century.248 On Saturday, February 7, 2009, Australia experienced a bushfire disaster of unparalleled portions:473 In the wake of a long drought, and on a day of high temperatures, strong winds and low humidity, bushfires swept through residential and farming communities in Victoria. Some 430,000 hectares [one million acres] of forest and farmland, countless homes and other buildings were burnt, and hundreds of millions of dollars damage were done to economic and community assets. Far more tragically, it was Australia’s worst civil disaster: 173 lives were lost. February 7th 2009 has become Black Saturday, to be (one imagines) seared into the Australian psyche for generations to come. That day, more than 300 fires were reported across the state. Fifteen of these developed into major incidents, with the most extensive damage and loss of life resulting from four fires.138,195,298 A royal commission was established soon afterward to investigate the causes and responses to these fires (http://www. royalcommission.vic.gov.au/). The commission’s final report, issued at the end of July 2010, sets out 67 recommendations for protecting human life, “designed to reflect the shared responsibility that governments, fire agencies, communities, and individuals have for minimizing the prospect of a tragedy of this scale ever happening again.”459 In their report, the commissioners offered a warning: It would be a mistake to treat Black Saturday as a ‘one-off’ event” for “ … the risks associated with bushfires are likely to increase.” Given the occurrence of other major wildland fire disasters involving significant loss of life in recent years—for example, Greece in August 2007525,526and Russia during the 2010 summer fire season—this prediction has global application. This chapter describes the current look at fire as a historical force and discusses fire management policies, the nature and scope of wildland fire hazards, behavior of fires, typical injuries, fatality fire statistics, several fatal fire incidents, and survival techniques. Although the emphasis is on North America, reference is made to other regions of the globe, most notably Australasia and Europe. Wildland fire, like many other disciplines and subjects, has its own unique terminology, so readers may need to consult glossaries.190,300,345
For online-only figures, please go to www.expertconsult.com
FIGURE 12-1 Flame front spreading upslope through Gambel oak (Quercus gambelii) and pinyon (Pinus edulis)–juniper (Juniperus monosperma) fuel complex during the major run of the South Canyon fire in western Colorado on the afternoon of July 6, 1994. Approximately two and a half minutes after this photograph was taken, the first of 14 firefighters was overtaken by the advancing flames that were estimated to have travelled upward of 110 to 165 m/min (360 to 540 ft/min). (Courtesy USDA Forest Service; photo by S. Archuleta.)
Wildland Fire Management and Technology Programs for dealing with the overall spectrum of fire are collectively termed fire management.55 They are based on the concept that fire and the complex interrelated factors that influence fire phenomena can and should be managed. The scientifically sound fire management programs that respond to the needs of people and natural environments must also maintain full respect for the power of fire.55 Since the early 1900s, federal, state, and local fire protection agencies in the United States, for example, have routinely extinguished wildland fires to protect watershed, range, and timber values, as well as human lives and property. The basic methods of fire suppression210,268 have changed very little, although new technologies have gradually come on board (Figure 12-3). However, improvements in fire detection, fire danger rating systems, and fire suppression methods have been developed by fire science laboratories and two equipment development centers maintained by the U.S. Department of Agriculture (USDA) Forest Service, as well other organizations (e.g., state agencies and universities). Patrol planes, some with infrared heat scanners, other fixed-wing aircraft (Figure 12-4), and helicopters (Figure 12-5), can deliver firefighters, equipment, and fire-retarding chemicals or water to the most remote fire. These firefighting resources are organized under an Incident Command System that
FIGURE 12-2 A wildland–urban interface fire in the Amarante region of Portugal on August 5, 2005. Drought conditions contributed to an exceptionally severe fire season in southern Europe during 2005. Twelve firefighters and 10 civilians were killed in Portugal. Eleven firefighters were killed in one separate incident in a nature reserve in the Guadalajara area east of Madrid, Spain, on July 17, 2005. (Courtesy Publico newspaper; photo by Paulo Ricca.)
241
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can easily manage simple to complex operational, logistic, planning, and fiscal functions associated with wildfire suppression actions.113,184,332 Many other countries have followed a somewhat similar path in their evolution with regard to wildland fire suppression and supporting research and development.382-384,387 Modern fire suppression technology, however, cannot indefinitely reduce the area burned by wildfires, as demonstrated, for example, by numerous large fires and major fire seasons in the past 30 years or so in North America: Mack Lake fire in Michigan in 1980; the “Siege of ’87” in California in 1987; Silver Complex in Oregon in 1987; Greater Yellowstone Area fires in 1988; Stanislaus Complex in California in 1989; Foothills fire near Boise, Idaho, in 1992; Garnet fire near Penticton, British Columbia, in 1994; Millers Reach fire in Alaska in 1996; Virginia Hills fire in Alberta in 1998; Florida fires of 1998; Silver Creek fire in British Columbia in 1998; Cerro Grande fire in New Mexico in 2000; Valley Complex in Montana in 2000; Chisholm fire in Alberta in 2001; Biscuit fire in Oregon in 2002; Hayman fire in Colorado in 2002; Rodeo/Chedeski fire in Arizona in 2002; House River fire in Alberta in 2003; “Firestorm 2003” season in British Columbia; and record-setting fire seasons in Alaska and the Yukon Territory in 2004 (Figure 12-6, online), to name a few. Similar incidents have occurred in other regions of the world. The hard lesson learned from these and other fires is that wildfires are inevitable. Several factors have coincided to produce massive forest
PART 3 BURNS, FIRE, AND RADIATION
brome, in the arid regions of the western United States has increased the frequency of fires in desert shrublands.529 Wildland fires can benefit plant and animal communities. Evolutionary development produces plant species well adapted to recurrent fires. Fire tends to recycle ecosystems and maintain diversity.267,523 Thus, there is growing consensus that fire should be returned to many wildland ecosystems where appropriate to perpetuate desirable fire-adapted plant and animal communities and to reduce fuel accumulations.240 A landmark report in 1963 to the National Park Service by the Advisory Board on Wildlife Management259 described how the western slope of the Sierra Nevada had been transformed by fire protection:
A
When the forty-niners poured over the Sierra Nevada into California, those that kept diaries spoke almost to a man of the wide-spaced columns of mature trees that grew on the lower western slope in gigantic magnificence. Today much of the west slope is a dog-hair thicket of young pines, white fir, incense-cedar, and mature brush—a direct function of overprotection from natural ground fires. Not only is this accumulation of fuel dangerous to the giant sequoias and other mature trees, but the animal life is meager, wildflowers are sparse, and, to some at least, the vegetative tangle is depressing, not uplifting. It must also be acknowledged that in some cases, past logging practices contributed to the resulting fuel structure. Nevertheless, the board recommended that the Park Service recognize in management programs the importance of the natural role of fire in shaping plant communities.
WILDLAND FIRE MANAGEMENT POLICIES
B FIGURE 12-3 A helitorch or flying drip torch is a specialized aerial ignition device slung below and activated from a helicopter (A). It dispenses and ignites gelled fuel. The use of a helitorch in wildfire suppression operations can take many forms (e.g., to reduce the intensity, slow, or steer a fire; to remove potentially dangerous fuel concentrations; to widen and strengthen control lines; to expedite mop-up operations). Regardless of its specific purpose, the main objective of this application of “fighting fire with fire” is to speed up or strengthen control actions (B). Aerial backfiring and burning out with a helitorch can be one of the safest, most economic, fastest, and least damaging means of widening control lines and constitutes one of the major innovations in wildland fire suppression technology in the past 30 years. The helitorch is also used in prescribed burning operations. (Courtesy Alberta Sustainable Resource Development and Wildfire Consulting Ltd, Edmonton, Alberta; photos by O. Spencer and W. Bereska.)
mortality, including drought, epidemic levels of insects and diseases,239,319,324 and unnatural accumulations of fuels at the stand level and at a growing landscape scale in some but not necessarily all vegetation types241 as a result of attempted fire exclusion.16,211 This result in the dry forest types of the western United States was foreshadowed by a forester, Harold Weaver,499 in the early 1940s. Many agencies are now using prescribed fire more frequently, deliberately burning under predetermined conditions to reduce accumulations of fuels and to protect human life, property, and other values that are at risk by wildfire.301,320,354 Research has indicated that fires are not categorically bad. In fact, many plant communities in North America are highly flammable during certain periods in their life cycles.81 For example, annual grasses, ponderosa pine, and chaparral plant communities are flammable during almost every dry season. Other communities, such as jack pine or lodgepole pine forests, although fire resistant during much of their life cycle, eventually become fire prone when killed by insects, diseases, and other natural causes. The spread of non-native grasses, such as cheatgrass and red 242
Recent tragedies in the western United States have focused attention on the need to reduce hazardous fuel accumulations.443 The events associated with the 1994 fire season in particular created a renewed awareness and concern among federal land management agencies about wildfire impacts, leading to a combined review of fire policies and programs. The result was enactment
FIGURE 12-4 Specialized fixed-wing aircraft like the amphibious CL-415 “superscooper” are capable of delivering water and chemical fire retardants on or near a wildfire. Although such planes are used in sustained-action situations on isolated sectors of large fires, they are most effective in initial attack operations during the incipient phase of fire growth. In such cases, their primary purpose is to slow down the progress of the fire until such time as ground suppression resources are able to arrive and effect direct containment. Wing-tip vortices are created in the wake of low-flying aircraft. These vortices gradually dissipate as they descend to the ground level. They can cause a sudden, unexpected increase in fire activity as a result of the momentary wind gust. This can pose a threat to anyone located near the fire perimeter. (Photo by T. Nebbs.)
of a new interagency federal wildland fire management policy, which provided a common approach to wildland fire among federal agencies and called for close cooperation with tribal, state, and other jurisdictions.337 The principal points of the 1995 federal wildland fire policies are as follows: • Firefighter and public safety remains the first priority in wildland fire management. Protection of natural and cultural resources and property is the second priority. • Wildland fire, as a critical natural process, must be reintroduced into the ecosystem, accomplished across agency boundaries, and based on the best available science. • Where wildland fire cannot be safely reintroduced because of hazardous fuel accumulations, pretreatment must be considered, particularly in the wildland–urban interface. • Wildland fire management decisions and resource management decisions are connected and based on approved plans. Agencies must be able to choose from the full spectrum of actions—from prompt suppression to allowing fire to have an ecologic function. • All aspects of wildland fire management will involve all partners and have compatible programs, activities, and processes. • The role of federal agencies in the wildland–urban interface includes firefighting, hazardous fuel reduction, cooperative prevention and education, and technical assistance. Ultimately, the primary responsibility rests at the state and local levels. • Structural fire protection in the wildland–urban interface is the responsibility of tribal, state, and local governments.
PRESCRIBED FIRE AND WILDLAND FIRE USE Prescribed fire, the intentional ignition of grass, shrub, or forest fuels for specific purposes according to predetermined conditions, is a recognized land management practice.35,494,508 The objectives of such burning vary: to reduce fire hazards after 243
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
FIGURE 12-5 Several different sizes and models of rotary-wing aircraft or helicopters are used in a wide variety of direct roles as well as support functions in wildland fire suppression, including the dropping of water or fire-retarding chemicals directly on the fire. Helicopters also create wake vortices while in forward motion, just like airplanes, but generally these vortices are much weaker. A more common safety issue with helicopters is the downward induced air flow or rotary downwash. Some downwash effects are unavoidable when helicopters are engaged in direct attack on the fire with water or chemicals. Anyone located near the fire perimeter during such operations could be at risk. Even with a “long line” delivery system operated from a Bell 212 helicopter, as illustrated here on the Anarchist Mountain fire near Osoyoos in southern British Columbia on July 16, 2003, rotary downwash can still be a significant issue. (Courtesy Alberta Sustainable Resource Development.)
• Federal agencies must better educate internal and external audiences about how and why we use and manage wildland fire. The 1995 U.S. federal wildland fire management policy was reviewed and updated in 2001,342 following a particularly severe fire season in the western United States the year before; about 2.8 million hectares (about 7 million acres) were burned over by about 89,000 fires during the 2000 fire season in the United States.479 Results of the 2001 review and update were defined in the “2003 Interagency Strategy for the Implementation of Federal Fire Management Policy.”254 This strategy broadened the scope of fire management to balance fire suppression with management for ecologic benefits and supports the use of the full range of fire management activities to achieve ecosystem stability, including fire use. The 2003 implementation strategy stresses the need to complete or revise fire management plans that are more effectively and directly integrated with other natural resource goals.78 One of the other outgrowths of the 2000 fire season was the National Fire Plan (http://www.fireplan.gov), which calls for the following actions: • Ensuring that necessary firefighting resources and personnel are available to respond to wildland fires that threaten lives and property • Conducting emergency stabilization and rehabilitation activities on landscapes and communities affected by wildland fire • Reducing hazardous fuels (dry brush and trees that have accumulated and increase the likelihood of unusually large fires) in the country’s forests and rangelands • Providing assistance to communities that have been or may be threatened by wildland fire • Committing to the Wildland Fire Leadership Council, an interagency team created to set and maintain high standards for wildland fire management on public lands It is clear from these objectives that one of the major foci of the U.S. National Fire Plan is the human dimension of wildfire (i.e., rural homeowners and communities).235,270 The 2003 implementation strategy was reviewed during a field test in 2008 and resulted in a 2009 policy revision. The revision removed the distinction between wildland fire use and wildfire.254 It provides the highest degree of flexibility ever afforded to managers and facilitates their ability to respond to changing conditions and complexities of a wildfire event. In 2005, the Canadian Council of Forest Ministers signed off on the Canadian Wildland Fire Strategy Declaration,107 which is based on principles of risk management and hazard mitigation. This strategy will strive to strike a balance between public safety, forest protection and health, and fire management expenditures that maintains a strong and effective fire suppression organization, but it also includes innovative hazard mitigation, preparedness, and recovery programs—in other words, a more holistic view of wildland fire envisioned some 40 years ago as land management agencies made the transition from fire control to fire management. This strategy recognizes the need for shared responsibility among the various stakeholders (i.e., property owners, industries, and local, provincial, and federal governments).230 One of the guiding principles of this new declaration was that “public safety—including the safety of firefighters—is paramount.” Fire management policies similar to those of the United States and Canada exist in other parts of the world.191 The Food and Agriculture Organization of the United Nations192 prepared a generic set of fire management guidelines to serve as a basis for developing policies. The Fire Paradox project, a research initiative supported by the European Commission from 2006 to 2010 (http://www.fireparadox.com), examined wildland fire from multiple perspectives as a basis for influencing policies regarding integrated fire management.426
PART 3 BURNS, FIRE, AND RADIATION
logging, expose mineral soil for seedbeds, regulate insects and diseases, perpetuate natural ecosystems, and improve range forage and wildlife habitat.307,500 In some areas managed by the National Park Service, USDA Forest Service, and Bureau of Land Management, naturally ignited fires may be allowed to burn according to approved prescriptions; fire management areas have been established in national parks and wildernesses from the Florida Everglades to the Sierra Nevada in California (Figure 12-7, online). Planned-ignition prescribed fires are also carried out. Similar policies exist in Canadian National Parks.224 Visitors are increasingly aware that wildland fires can be an important part of the natural cycle of an ecosystem and that the future health of parkland may depend in part on today’s managed fires.
Wildland–Urban Interface: New Look of a Historical Problem Just as resource agencies are attempting to provide a more natural role for fire in wildland ecosystems, the general public is increasingly living and seeking recreation in many of these areas. The area where houses and other human-made structures meet or are intermingled with wildland vegetation is regarded as the wildland–urban interface or intermix, although other names have been used (Figure 12-8, online). It is a growing problem from a wildland fire perspective in the United States73,391,467 and many other regions of the world.228 As mentioned earlier, past fire exclusion practices in the United States have allowed abnormal fuel accumulations in some forest types and regions, and this fact has combined with the sacrifice of relatively safe perimeter fire suppression strategies in favor of directly protecting people and their possessions.518 Direct suppression actions within the fire’s perimeter place firefighters at a greater disadvantage from a safety standpoint. The new interagency policy that emphasizes firefighter and public safety as the first priority will result in less effort to save structures in dangerous situations. Thus, what is known of fire behavior and fire survival principles must be readily available to emergency medical personnel, wildland dwellers, and recreationists. In fact, fire protection agencies and others have been making such information more readily available to the general public for some time now,114,162,193,501 although much more needs to be done.17
NATURE OF THE PROBLEM Hot, dry, and windy conditions annually produce high-intensity fires that threaten or burn homes where wildland and urban areas converge (Box 12-1). Can the historical levels of destruction, injury, and fatality be repeated today in the face of modern fire suppression technology? The answer to this question requires an analysis of the conditions that created such high-intensity fire behavior events in the forests of northern Idaho and northwestern Montana during late August 1910 (Figure 12-9, online) in which 85 people (Figure 12-10), including 78 firefighters, were killed.135,179,385,438 The earliest fire incident of note involving a large loss of human life was the series of conflagrations in the Miramichi region of New Brunswick and adjacent areas in Maine in early October 1825, in which at least 160 people139,374 perished.471 This was followed by several fatality fires in the U.S. Lake States region, including the Peshtigo and area fires in eastern Wisconsin in October 1871 (about 1300 fatalities),227,260,510 the Lower Michigan fires of September 1881 (169 fatalities),232 the Hinckley fire in east-central Minnesota in September 1894 (418 fatalities),252 the Baudette fire in northern Minnesota in October 1910 (42 fatalities),374 and the Cloquet fire in Minnesota in October 1918 (538 fatalities).108,232 The western United States experienced other fatality fires, such as in western Washington and Oregon in midSeptember 1902 (38 fatalities).77,296 Canada suffered similar tragedies. For example, the province of Ontario experienced several significant settler-related wildfire fatalities in 1911, 1922, and 1938, including the 1916 “Matheson Holocaust” in which as many as 400 people were killed.53,159,295 In 1908, a forest fire destroyed the city of Fernie, British Columbia. Twenty-two people were reported killed.276 244
Other countries, such as New Zealand299 and France,193 are reported to have suffered similar but varying losses in the 20th century. In Australia, for example, possessing some of the world’s most fire-prone environments,115 71 lives were lost in the state of Victoria on “Black Friday” in January 1939.193,351 On August 1, 1959, 48 people were reported killed by a forest fire northeast of Massif des Aures, Algeria.234 In early September 1963, forest fires swept about 2 million hectares (about 4.9 million acres) in Paraná State in southern Brazil, destroying more than 5000 homes and killing 110 people.434 More than 100 people were killed by extensive forest and savannah fires in Cote D’Ivoire (Republic of Ivory Coast) on the southern coast of western Africa during the 1982-1983 fire season.415 On October 8, 1871, the same day that fire wiped out the town of Peshtigo, Wisconsin, and surrounding communities, the Great Chicago fire devastated urban Chicago.510 Comparative statistics for those two fires highlight the destructive potential of wildland fires. In every way, the Peshtigo conflagration was far worse than the Chicago blaze. The Peshtigo fire covered about 518,000 hectares (about 1,280,000 acres) and killed about 1300 people, whereas 906 hectares (2240 acres) burned and some 200 lives were lost as a result of the Chicago fire.217 The Great Chicago fire is generally acknowledged as the birthplace of modern urban fire prevention. As Lloyd265 notes, “mention the name Peshtigo to most people and all you get is a blank stare. Mention Mrs. O’Leary’s cow to the same person and they will think right away of the Great Chicago fire” and “Some of the same social misconceptions that allowed Peshtigo to be all but forgotten persist today.” So, it is perhaps fitting to consider the following poem entitled “The Peshtigo Calamity:”232 As the years roll along and the ages have sped O’er the charred, blackened bones of the Peshtigo dead, And the story is told by the pen of the sage, In letters immortal on history’s page— No fancy can compass the horror and fright The anguish and woe of that terrible night. The August 1910 wildfires in northern Idaho and Montana had several elements in common with the Peshtigo fires of 1871: many uncontrolled fires burning at one time; prolonged drought, high temperatures, and moderate to strong winds; and mixed conifer and hardwood fuels with slash from logging and land clearing. These large fires occurred primarily in conifer forests north of the 42nd meridian, or roughly across the northern quarter of the contiguous United States.77 One of these critical elements that is not as likely to occur today as formerly is the
FIGURE 12-10 Burned ruins of the foundry in Wallace, Idaho, furnish mute testimony to the destructive force of the 1910 fires. The cottage on the terrace was the only one left standing in that part of town. Of the 85 people reported killed in the “big blowup of 1910,” 78 were firefighters. (Courtesy USDA Forest Service; photo by R.H. McKay.)
D. Blasor-Bernhardt68
B12-1 Tok, Alaska, July 1, 1990, 15 to 30 minutes after the lightning strike that started the Tok fire. (Photo by D. Blasor-Bernhardt.)
July 1, 1990, started out like any other Sunday, but it quickly turned Tok, Alaska, into a near raging inferno. I was working at the Chamber of Commerce Main Street Visitor Centre when an otherwise beautiful day suddenly turned black and foreboding. Blowing in, a huge thundercell hung just southeast of town. I stepped outside just in time to see a long, crooked finger of electricity split from an ominous cloud and drill its way into Earth. Minutes later, where the lightning had hit, a mushroom-shaped cloud began to grow. I grabbed my camera and snapped a few shots. Five days later, and in spite of several thousand firefighters and equipment from all over Alaska, Canada, and the States, Tok was completely under siege and at risk of being cremated. The wind-blown inferno licked greedily at several unoccupied dwellings, then consumed them. East-side residents were evacuated. We, on the west side, were told to pack our things, to be ready to leave, and to await further instructions. Tok was enveloped on two sides by fire—from the eastern and northern directions. My log home was about a mile from the north front of the fire. I stood on the cabin’s sod roof, watching the fire,
when the kids and extended family converged there about the same time, looking to me for instructions. All day, I had the sprinklers and hoses running full blast over the cabins, garage, and surrounding area. By now, the area looked like a swamp. Good. I’d leave them on, even if we evacuated, in the hope that it would help save some of our place from destruction. Smoke stifled each breath. Helicopters screamed back and forth carrying people, equipment, and large buckets of water. There was no fear, no panic, in anyone—just resignation. And there was no way our town would be destroyed. I told the kids to first pack up whatever was closest to their hearts—it didn’t matter how silly an item seemed if that made them feel good. The first thing I placed in my own car was my late husband’s ashes. I couldn’t bear to leave him behind. Next, we would take irreplaceable things: photo albums, mementos. Then down to brass tacks: the necessary things for survival and rebuilding in the event we were burned out. Bombers loaded with retardant flew directly overhead. We were in a war zone—man against fire. The girls loaded their cars with personal items. Mine was loaded with blankets, groceries, and clothing. The boys readied our tandem-axle trailer, loading it with items from the garage— chainsaws, tools, portable generator, water jugs. If the fire drew too near and we had to evacuate, the plan was for the girls and I to load our pets while the boys quickly cut the trees down around the cabins, hopefully providing a bare, wet perimeter between them and the fire. Fully loaded, we assembled in the driveway, ready for word to come. Besides myself, six young adults, a baby, half a dozen dogs, numerous cats, a snake, six vehicles, and a trailer comprised the Bernhardt entourage. We were ready. We waited in the foul air, our eyes smarting from the smoke. An ember hit me on the shoulder, burning a hole though my shirt. Sadly, I turned to look at our homes one last time. Tomorrow they would be gone. Imperceptibly at first, a slight shift in the wind began. I held my breath. “Mom?” my son said. “Yes,” I answered, “but I’m afraid to hope.” The wind, definitely shifting now, was no longer blowing toward us. A sweet, light rain began to fall. While the eight of us stood together, soaking wet in the rain, a trooper came by to tell us the worst was over. In all, the fire burned 109,501 acres (44,314 hectares) at a cost of over $35 million (U.S.), yet not one person had been injured, not one occupied dwelling destroyed, and Tok had been spared by a miracle wind.
From Blasor-Bernhardt D: A town that nearly went … up in smoke, Guide to the Goldfields and Beyond (Harper Street Publishing, Dawson City, Yukon Territory) Summer: 52, 1997.
simultaneous presence of many uncontrolled fires. The effectiveness of modern fire suppression organizations is now able to reach even the most remote wildland locations. High-velocity winds and more than 1600 individual fires contributed to the spread of the fires in 1910; it is unlikely that a multifire situation of that magnitude would occur today.80,115 However, multiple fire starts are still possible owing to human-caused ignitions (e.g., arson, power lines). For example, on October 16, 1991, 92 separate fires occurred in the Spokane region of eastern Washington329 in the space of a few hours under the influence of exceedingly strong winds.31 Prolonged drought, high winds, and flammable fuel types, however, remain significant to the behavior of high-intensity fires. Some of the fires most potentially damaging to human lives and property occur in areas rich in chaparral shrub fuel in southern California. Wilson518 and Phillips372 described the severe 1970 fire season in California, in which official estimates showed that 97% of 1260 fires occurring between September 15 and November 15 were held to less than 121 hectares (300 acres). The other 3% of the fires, fueled by a prolonged drought and fanned by strong Santa Ana winds, produced 14 deaths, destroyed 885 homes, and burned about 243,000 hectares (about 600,000 acres), as chronicled in the 1971 film Countdown to Calamity. Ten years later, the situation recurred over 9550 hectares (23,600 acres) in southern California, the Panorama fire in November 1980, which
resulted in the deaths of 4 people and loss of more than 325 structures.104 On October 20, 1991, a devastating fire “of unprecedented force blew out of control”4 in the hills above Oakland and Berkeley, California. Burning embers carried by high winds from the perimeter of a small fire resulted in a major wildland–urban interface conflagration. The impact on people and their possessions was enormous.4,453 The fire resulted in direct deaths of 25 people, including a police officer and a firefighter, injured 150 others, destroyed 2449 single-family dwellings and 437 apartment and condominium units, burned about 650 hectares (about 1600 acres), and did an estimated $1.5 billion in damage.328 The scenario for disaster included a 5-year drought that had dried out overgrown grass, shrubs, and trees, making them readily ignitable. Other factors included untreated wood shingles, unprotected wooden decks that projected out over steep terrain, low relative humidity, high temperatures, and strong winds that averaged 32 km/hr (20 mph) and gusted up to 56 to 80 km/hr (35 to 50 mph). The area had not experienced any rain for 67 days before the major fire run, although mean monthly maximum temperatures in the 6 months preceding the fire were not appreciably high (i.e., 18° to 23° C, or 64° to 73° F).32 These severe conditions produced a voracious fire that consumed 790 homes in the first hour. Winds lessened to 8 km/hr (5 mph) by the first evening, which assisted with the containment of the fire. 245
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
BOX 12-1 What Is It Like to Experience a Wildland–Urban Interface Fire? A Town That Nearly Went…Up in Smoke by
PART 3 BURNS, FIRE, AND RADIATION
wildfires is the result of a small percentage of fires.446 Thus, on some days, adverse fuel and weather conditions, coupled with an ignition source, will conspire to produce conflagrations that occur in spite of our best fire prevention, detection, and initial attack efforts. Climate change will only exacerbate the situation.188 Recent research involving simulations of evacuations in response to a threatening wildfire has revealed that strategic planning is essential.152-154,163 Communities need to ensure that they are fully prepared well in advance of a threatening wildfire occurrence by developing individual and local government emergency action plans.364 Taylor455 has emphasized that managing the fire risk at the wildland–urban interface is a shared responsibility involving both private citizens and numerous government agencies. Past fire experiences in Australia360,501 have demonstrated that quite often “houses protect people and people protect houses.” Research had demonstrated that a well-prepared house can provide protection from fire and that the presence of people prepared to defend against their home burning down is the most significant factor in determining its survival (Table 12-1). Obviously, zones of defendable space around homes must be established in advance of fires; the young, older adults, and infirm are generally encouraged to leave well ahead of the fire. Communities at risk from wildfires should be encouraged to be responsible for their own safety, because fire service personnel may not be available when burning conditions are severe. The major issue is whether able-bodied residents should stay and defend or “fight” for their homes, or “flee” in the hopes of escaping an advancing fire.516 In the late 1990s, the Tasmania Fire Service had a policy that provided guidance on bushfire safety and evacuation decision making called “Prepare, Stay, and Survive.”205 When there was a threatening wildfire, people were told to go home and assist in the protection of their property. Because human lives and property values are at risk when threatened by wildfires, exemplary cooperation and teamwork are required to ensure adequate safety margins. Team members identified for reducing the loss of life and property include state agencies, local government, the communities, and individuals. The “Stay or Go” policy concerning evacuation was advocated by the Australasian Fire Authorities Council (AFAC)45
Firefighters had the situation under control by the fourth day, but not before they had been given an awful glimpse of the nature of fires in the future. In late October 2003, fires in southern California burned over 300,000 hectares (742,000 acres) in 1 week alone, taking 23 lives and destroying more than 3300 homes.103,242,322 In recent times, wildland fire fatalities among the general public have not been restricted to just California, or the United States for that matter. Four civilians were killed as a result of the massive forest conflagration that converged on the outskirts of Canberra, Australia, in January 2003.3 During the summer of 2003 in Portugal, 21 people lost their lives in 18 different fire incidents.488,493 On January 11, 2005, 9 people (including 4 children and 2 firefighters) perished on the Eyre Peninsula of South Australia as a result of being overrun by an extremely fast-spreading grass fire in what is now referred to as “Black Tuesday” in the state.125,430,437 Mutch and Keller323 give a compelling account of the wildfires that occurred in Texas and Oklahoma during late 2005 and the early part of 2006, in which 19 civilians and 6 firefighters lost their lives. In many parts of the world, but especially in the United States and Canada, the primary response has been to evacuate all people threatened by wildfires.1,136,390 For example, more than 200,000 people were evacuated in Canada between 1980 and 2007 in more than 500 separate incidents67 The pros and cons of evacuation are extensively discussed in Chapter 12 of Webster’s seminal work,501 The Complete Bushfire Saftey Book, entitled “The Decision—Evacuate or Stay? Safety or Suicide?” In this regard, Phil Cheney,119 a renowned Australian bushfire research scientist, feels that “What it comes down to is a civil right to risk your own life to save your house. I personally am in favor of people taking risks in their lives provided that they also bear the responsibility for the consequences.” Some amazing logistic feats have taken place to date without incident using both ground and air transportation. A good example of the latter occurred in early June 1995 as the residents of Fort Norman and Norman Wells in Canada’s Northwest Territories were airlifted to Yellowknife, the territorial capital.160 However, statements later on from the public like “I think they took us away just in time” suggest that this approach is not infinitely infallible. Coupled with this reality is the fact that modern fire records indicate that the vast majority of area burned by
TABLE 12-1 Approximate Probabilities of a House Surviving a Wildland Fire* Scenario Scenario Scenario Scenario
A: Total disregard for any fire safety precautions B: Fire safety precautions taken only in regard to fuels surrounding house C: Fire safety precautions taken only in regard to the house itself D: All reasonable fire safety precautions to and near the house taken Without Persons in Attendance Fire Intensity Class (kW/m)
Scenario
500-1,500
1,500-10,000
With Persons in Attendance Fire Intensity Class (kW/m)
10,000-60,000
Scenario
A 14.4% 1.2% 0.3% B 16.0% 4.9% 1.0% C 26.1% 8.7% 1.9% D 59.1% 28.1% 7.4% kW/m × 0.29 = BTU/sec-ft The following attributes were considered in the above scenarios:
A B C D
500-1500
1500-10,000
10,000-60,000
29.9% 63.6% 76.5% 93.0%
10.3% 32.1% 46.8% 78.2%
2.3% 8.9% 15.3% 42.6%
Scenario House and Surrounding Fuel Conditions
A
B
C
D
Flammable objects nearby (e.g., firewood heap)? Wooden shingle roof? Nonwooden or nontile roof with pitch >10°? External walls made of brick, stone, or concrete? Trees (5+ m high) within 40 m of house?
Yes Yes No No Yes
No Yes No No No
Yes No Yes Yes Yes
No No Yes Yes No
From Alexander ME: Proposed revision of fire danger class criteria for forest and rural areas in New Zealand, ed 2, Christchurch, New Zealand, 2008, Scion Rural Fire Research Group. http://www.scionresearch.com/fire. m × 3.3 = ft. *Based on a logistic regression model as developed from an analysis of 455 houses, which were completely destroyed, threatened, or sustained minor damage by the bushfire that swept through the township of Mount Macedon in Victoria, Australia on the evening of Ash Wednesday (February 16) in 1983.515,517
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*References 87, 89, 221, 225, 266, 464.
where houses are able to survive fires even when fire services personnel are not available. The “team” would consist of the effective partnership between the fire services and home dwellers. The “theme” would comprise the dual strategy of adequate defensible space coupled with the home dweller’s motivation to remain on site as an important factor in suppressing fires initiated by ember attack. In order for this approach to work, rural homeowners must understand that although wildfires can be dangerous, with proper precautions, people can remain with their homes and be an important part of the solution to the wildland– urban interface fire problem. Empowering communities at risk from wildfire to play an active part in their own protection is viewed as a viable long-term strategy to enable safe and harmonious coexistence with fire as an element of nature.117 During the 2000 fire season in western Montana, some individuals took it upon themselves to stay with their homes as flame fronts advanced. They created defensible space, installed sprinkler systems, engaged in fire suppression activities, and provided local intelligence to incoming fire service personnel. No home was lost as people demonstrated responsibility for their personal well-being. A similar “prepare, stay, and defend” action was successfully carried out during the 2003 fire season on the Wedge fire along the North Fork of the Flathead River in western Montana. The property was prepared in advance to be “fire safe,” the homeowner remained with volunteer fire department officials, and the home survived the passage of a high-intensity crown fire (Figure 12-11). Wildland fires that threaten human lives and property are not exclusively located in southern California because the exodus to wildland regions has become a national phenomenon. Fires burned about 81,000 hectares (about 200,000 acres) in Maine in October 1947, killing 16 people;100,172 another area of about 81,000 hectares (about 200,000 acres) burned in New Jersey in April 1963.52 Wildland fire disasters have not always been large
A
B FIGURE 12-11 Homeowners and firefighters (A) successfully prepared, stayed, and defended this rural home in western Montana from a high-intensity flame front (B) associated with the Wedge fire in July 2003. (Courtesy Big Fork Volunteer Fire Department.)
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as a fundamental component of community bushfire safety in Australia.222 Variants to this general theme exist (e.g., “prepare, leave early, or stay and defend”). However, the essence of the approach urges people to make the decision to prepare themselves and their properties to “stay” and defend when a wildfire is likely, or to “go” well before a fire is likely to arrive. Although early evacuation may contribute to increased personal safety, bushfire property losses are likely to increase. Conversely, late evacuation may put people at greater risk than had they stayed in the house as the fire passed around them. An evaluation of this policy is the focus of Project C 6— Evaluation of Stay or Go Policy currently being undertaken by the Australian Bushfire Cooperative Research Centre (http:// www.bushfirecrc.com/research/c61/c61.html), led by co–project leaders John Handmer, RMIT University, and Alan Rhodes, Country Fire Authority of Victoria. Fire management agencies and the public alike will no doubt find the final results of this research project of great interest. Preliminary results emerging from the project generally supported the 2005 AFAC position, while recognizing that implementation issues remained.* However, the fires of February 7, 2009, in Victoria, Australia, and in turn the Royal Commission’s report459 have changed the context for this approach quite significantly. There are a number of emerging issues (e.g., limit of validity), so the policy is most likely to evolve in coming years399in the aftermath of the Black Saturday fires, as evidenced by AFAC’s revised position on bushfire community safety based on emergency risk management principles.49 The 2009 Black Saturday fires have placed an urgent emphasis on the continuing debate over what constitutes the safest strategies for survival in the wildland–urban interface. The Victorian fires led to the creation of a catastrophic, or “Code Red,” level of fire danger. When this category of fire danger is forecast for the next day, it is recommended that people in a high-risk bushfire area leave the night before or in the early morning (http:// www.cfa.vic.gov.au/firesafety/bushfire/danger-warnings.htm). At the next two lower levels (i.e., “Extreme” and “Severe”), it is recommended to stay only if one’s home is well prepared, well constructed, and can be actively defended. Testimony by John Handmer before the 2009 Victorian Bushfires Royal Commission,459 coupled with analyses produced by him and his research team,220 indicate that only a small percentage of homes and property were adequately prepared to be fire resistant. Without preparing a fire-resistant home and property in advance, the only prudent course of action is to evacuate early. This issue of whether to “prepare, stay, and defend” or evacuate early is a subject considered worthy of more open debate and discussion in North America.17,294,325,365,442 Two communities in the United States—Painted Rocks in Montana and Rancho Sante Fe in California—have adopted variations of the original Australian model of “Prepare, Go Early or Stay and Defend.”325 Both communities have had the “Stay and Defend” practice successfully tested by wildfires. Both U.S. communities are carefully monitoring the lessons learned from the 2009 Black Saturday fires to determine if any change is needed in their approach. Meanwhile, Ready, Set, Go! (RSG) was rolled out as a full-scale pilot program by the Ventura County Fire Department and the Orange County Fire Authority for the 2009 fire season in Southern California. Other fire departments, such as Los Angeles County,151 Los Angeles City, San Bernardino County, Riverside County, Santa Barbara County, and Cal Fire, have adopted the basic approach. The RSG approach involves preparing one’s house to withstand a wildfire, preparing one’s family for evacuation, and finally, leaving earlier. The program is now endorsed by the International Association of Fire Chiefs (http://www.iafc.org/displaycommon. cfm?an=1&subarticlenbr=1229). In many regions of the world, people are warned that wildfires are dangerous and that they always need to evacuate. This scare tactic approach reinforces the concepts that wildland fires are always dangerous and that people must leave their homes. Perhaps one solution to dealing with fires in the wildland–urban interface in the future would be to embrace the concept of “A Dream, a Team, and a Theme.”321 The “dream” would be one
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in size. On September 26, 1936, most of the coastal town of Bandon in western Oregon was destroyed, and 11 people were killed by a wildfire that covered probably no more than about 4000 hectares (about 10,000 acres).232 The prevalence of gorse (Figure 12-12), a non-native plant, was considered a key contributing factor to the resulting devastation. More recently, on July 16, 1977, the Pattee Canyon fire in Missoula, Montana, destroyed 6 homes and charred about 500 hectares (about 1200 acres) of
A
B
C FIGURE 12-12 Old man’s gorse (Ulex europaeus) is probably the worst fuel type (A) in the world from the standpoint of wildland fire management for two main reasons. The density of the vegetation and its sharp spines or thorns (B) make it extremely difficult if not nearly impossible to physically engage in any kind of fire suppression activity. Vigorous stands grow outward, crowding out all vegetation and forming a center of fine, dry, dead, elevated fuel. This fuel structure, coupled with the plant’s oil content, readily contribute to the development of high-intensity flame fronts even under relatively mild fire weather conditions (C). Gorse is native to central and western Europe, where it has long been cultivated for hedgerows. It has been introduced to Australia, New Zealand, the west coast of the United States (California, Oregon, and Washington), and southwestern British Columbia. It has also been reported in Costa Rica and the Hawaiian Islands. In the northeastern United States, it has established itself along the Atlantic Coast from Virginia to Massachusetts. (Courtesy Ensis Bushfire Research Group, New Zealand.)
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forests and grasslands in only a few hours.187 Similarly, more than 70 homes were damaged or destroyed by fires in the southern Cape Peninsula region of South Africa that burned about 8000 hectares (about 19,800 acres), during January 16 to 20, 2001.105,486 A whole host of other cases have occurred in North America231 and are steadily accumulating. Fires at the wildland–urban interface are also increasing internationally. For example, the Ash Wednesday fire disaster in southeastern Australia on February 16, 1983, burned about 340,000 hectares (about 840,000 acres) of urban, forested, and pastoral lands in the states of Victoria and South Australia, killing 77 people, injuring some 3500, and destroying more than 2500 homes.57,226,352 Phenomenal fire spread rates in both forests and grasslands occurred,243,393 and flame heights of almost 200 m (650 feet) were observed.454 In May 1987, wildfires in northeastern China409 added a new perspective regarding the devastating impact wildland fires may have on human lives, property, and natural resources. These fires reportedly burned about 1.34 million hectares (about 3.31 million acres), killed 212 people, seriously injured another 226, and left about 56,000 homeless.166 Clearly, it was a disaster of major proportions. These fires resulted from a combination of heavy dry fuels, sustained drought, and strong winds.448 Rates of spread during the major runs reached 20 km/hr (12 mph). Protecting lives and property from wildfires at the wildland–urban interface represents one of the greatest challenges faced by wildfire protection agencies. Large forest fires during the intense El Niño drought conditions of 1997 and 1998 focused public and media attention once again on the need to evaluate public policies and practices in the forestry and nonforestry sectors that directly or indirectly contribute to the impact of wildland fires. The size and damage attributed to these fires were so immense that the Christian Science Monitor termed 1998 “The Year the Earth Caught Fire.” At times, that seemed to be literally true, as smoke palls blanketed large regional areas, disrupted air and sea navigation, and caused serious public health threats.206,389,414,522 At least 60 people were killed in Mexico as a result of the fires,468 and ecosystems that generally are not subjected to fires, such as the Amazon rain forest and the cloud forest of Chiapas, Mexico, sustained considerable damage. A global fire conference sponsored by the Food and Agricultural Organization of the United Nations in October 1998 brought together specialists from 33 countries to review the serious nature of worldwide fires.191 Participants at the conference in Rome concluded that governments needed to enact more sustainable land use policies and practices to reduce the impacts of wildfires on people and natural resources. It is becoming increasingly rare to have a wildland fire situation or incident that does not involve people and their homes. However, people are not fully aware of the fire risks and hazards of living and traveling in or near wildlands.62,214 Risk, in the jargon of the wildland fire specialist, is the probability that a fire will occur. Hazard is the likelihood that a fire, once started, will cause unwanted results. Risk deals with causative agents or ignition sources; hazard deals with the fuel complex.197 The results of two surveys carried out in the western United States during the 1970s indicated a general feeling of overconfidence by most residents toward the potential danger or threat of a wildland fire. Eighty percent of Seeley Lake, Montana, forest residents interviewed thought that the forest fire hazard was low to moderate in their area.196 Seventy-five percent of Colorado residents interviewed thought that the forest fire hazard was low or moderate in mountain subdivisions of their state.233 Forest fire hazards in these two areas were much higher than these public estimates. In a survey of attitudes toward bushfires in the Dandenong Ranges of Victoria, Australia, it was found that people who had experienced bushfires tended to rank their area with a higher rating than did people without such experience.175 However, the survey also revealed that 40% of the people with recent severe bushfire experiences still did not rate bushfires as one of the three most important environmental problems in their area. Dr. Sarah McCaffrey,293 a research social scientist with the USDA Forest Service who has been studying the social dynamics of fire management for nearly a decade, has suggested that the general public is far better informed of the issues dealing with the wildland–urban fire problem interface than was the case during the 1970s and
starts, were unlikely to take all possible steps to safeguard their own properties, and exhibited a negative view of prescribed fire to the extent that it could preclude its use as a risk management tool. There is a growing need for the general public, emergency medical personnel, and fire suppression organizations to be well prepared to deal with wildland fire encounters (Box 12-2). As Reitz and Geissler396 have recently noted, “The old model of individual homeowners and neighborhoods depending solely on government provided firefighting resources is gone. Recent wildland fires have demonstrated that community firefighting resources are easily outpaced when multiple structures are burning simultaneously. The cure is to move most structure protection responsibility to the homeowner and community.” In 2000, 450 residents of Strathcona County, Alberta, Canada, were randomly selected to test which three educational methods would produce the greatest change in homeowner behavior with respect to the wildland–urban interface.444 The study showed that residents could be influenced to change their behaviors when provided with the information materials that enabled them to select between fire-safety alternatives. A recent study evaluated workshops for the adult public featuring experimental learning about wildland fire.363 Participants used hands-on activities to investigate fire behavior and ecology and to assess hazards in the wildland–urban interface. Effectiveness was examined using a pretest, a post-test following the program, and another post-test 30 days later. Participants’ knowledge increased after the workshop, and attitudes and beliefs became more supportive of fire management. The study concluded that hands-on activities can help adults become better informed about wildland fire and more positive about fire management.
BOX 12-2 Recommendations to Reduce Loss of Life and Property in the Wildland–Urban Interface Fire Protection Services • Remember that firefighter and public safety is the first priority in every fire management activity. • Ensure that all personnel receive regular cross-training in fighting wildfires and structural fires. • In urban departments, in particular, recognize the need to extinguish fires in wildland fuels by using thorough mop-up procedures. • Recognize the need for close coordination of response efforts among neighboring departments or agencies. • Develop specific mutual-aid plans for coordinating resources to attack fires in the wildland–urban interface. • Schedule and conduct regular mutual-aid training exercises. • Regularly schedule and conduct fire prevention and fire preparedness education programs for the general public and homeowners. • Conduct an assessment of fire risks, and prepare a strategic plan to reduce these risks. • Work effectively with lawmakers and other government officials to help prevent unsafe residential and business development. Legislators • Examine existing laws, regulations, and standards of other jurisdictions that are applicable locally in mitigating hazards associated with wildland fires. • Adopt National Fire Protection Association (NFPA) guidelines in the form of NFPA 1144, (formerly NFPA 299, 1991 edition) Standard for the Protection of Life and Property From Wildfire.330 The purpose of this standard is to provide criteria for fire agencies, land use planners, architects, developers, and local government for fire-safe development in areas that may be threatened by wildfire. NFPA 1144 provides minimum planning, construction, maintenance, education, and management elements for the protection of life, property, and other values that could be threatened by wildland fire. It is designed to assist local, state, and federal fire agencies in dealing with the escalating challenges presented by the proliferation of
wildland–urban interface communities and the monetary losses of structures in wildland–urban interface areas. These guidelines address the following topics: assessment and planning; access, ingress, egress, and evacuation; fuel modification area; water supply; and residential development design, location, and construction. • Provide strong building regulations that restrict untreated wood shingle roofs and other practices known to decrease the fire safety of a structure in the wildlands. Planners and Developers • Create a map of potential problem areas based on fuel type and known fire behavior. • Evaluate all existing or planned housing developments to determine relative wildland fire protection ratings and advise property owners of conditions and responsibilities. • Ensure that all developments have more than one ingress– egress route. • Offer options for fire-safe buildings. • Provide appropriate firebreaks, fuel breaks, or greenbelts in developments. • Ensure that adequate water supplies exist in developments. • Follow specifications in NFPA 1144 Standard for the Protection of Life and Property From Wildfire.330 Public and Homeowners • Determine the wildfire hazard potential of the immediate area before buying or moving into any home. • Contact federal, state, and local fire services for educational programs and materials regarding fire protection. • Provide a fuel-modified area or defensible space around vulnerable structures to reduce the likelihood of ignition by an advancing wildfire. • Design and build nonflammable homes. • Urge lawmakers to respond with legislative assistance to require appropriate fire safety measures for communities.
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1980s.290,291 She attributes this fundamental change to programs like Firewise, fire safe councils, and media coverage. No doubt the large number of conflagrations in the past 20 years has also contributed to an increased awareness regarding the realities of wildland fire. In more recent surveys carried out in Florida and Minnesota348 of homeowners’ preferences for vegetation and defensible space near their homes, people interviewed recognized the wildfire threat but varied in their perceptions of effective wildfire prevention measures and willingness to take actions to reduce the potential threat to themselves and their homes. Most supported the use of planned fire to reduce fire potential, especially if wildland fire experts who understand the local ecology and fire behavior conducted the prescribed burns. In-depth interviews conducted with homeowners along the northern part of the Colorado Front Range revealed that these people face difficult decisions regarding implementation of wildfire mitigation measures.76 Perceptions of wildfire mitigation options were found to be possibly as important as perceptions of risk in determining likelihood of implementation. These mitigation options were often viewed as tradeoffs between wildfire risk and preferred landscapes. The study participants also reported, however, that one-on-one information sharing with wildland fire experts, as well as increased understanding of the flexibility of mitigation options, encouraged implementation. Personalized contact appears to be a key factor in educating homeowners about the realities of living in a wildland environment.292 Participants in a survey conducted in Michigan521 considered wildland fires as inherently uncontrollable and the resulting damage essentially random. Thus, they only weakly supported investments in fire suppression infrastructure but strongly supported fire prevention programs that reduced the number of fire
PART 3 BURNS, FIRE, AND RADIATION
WILDLAND FIRE LESSONS Recommendations to reduce the loss of life and property in the wildland–urban interface will be useless unless they are implemented at the grassroots level by all stakeholders. An excellent example of a community-based program is one implemented at Incline Village and Crystal Bay in the Lake Tahoe basin.431 The objective of this program is to “reduce the potential for natural resource, property, and human life losses due to wildfire by empowering the communities’ residents with the knowledge to address the hazard, providing the resources necessary to correct the problem, and encouraging the cooperative efforts of appropriate agencies.” The three major components of this defensiblespace program include neighborhood leader volunteers, a slash removal project, and agency coordination. The key to protecting life and property in the wildland–urban interface is property owners’ realization that they have a serious problem and that their actions embody a significant part of the solution. In the Incline Village and Crystal Bay community fire plan, neighborhood leader volunteers are trained in defensible-space techniques and are expected to teach these techniques to their neighbors and to coordinate neighborhood efforts. Such concerted community action will greatly minimize threats from the southern California type of “fires of the future” as discussed earlier. It is also wise to have sensible land development practices, because tragedies arise not only from ignorance of fuels and fire behavior (Figure 12-13) but also from a greater concern for the aesthetics of a home site than for fire safety.331 Several aspects of development detract from fire safety in the wildland–urban interface:137,187 • Lack of access to adequate water sources • Firewood stacked next to houses • Slash (i.e., branches, stumps, logs, and other vegetative residues) piled on home sites or along access roads • Structures built on slopes with unenclosed stilt foundations • Trees and shrubs growing next to structures, under eaves, and among stilt foundations • Roads that are steep, narrow, winding, unmapped, unsigned, unnamed, and bordered by slash or dense vegetation that makes them extremely difficult if not impossible for fire appliances to negotiate • Subdivisions on sites without two or more access roads for simultaneous ingress and egress • Roads and bridges without the grade, design, and width to permit simultaneous evacuation by residents and access by
FIGURE 12-13 This permanent residence, located in west-central Alberta, Canada, is unlikely to survive exposure to even a low-intensity wildland fire, and it would be difficult to stay and defend it for a number of reasons. There is dense forest vegetation immediately adjacent to the structure. Cedar shakes have been used for roofing. This has been shown time and time again to be the “kiss of death” in wildland–urban interface fires (at the time this photo was taken in 1997, the shingles were in such bad shape that they had lichens growing on them). The homeowner also liked to store flammable materials under his deck. (Courtesy Yukon Wildland Fire Management; photo by A.K. Beaver.)
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firefighters and emergency medical personnel and their equipment • Excessive slopes, continuous or heavy fuel situations, structures built in box canyons, and other hazardous situations • Lack of constructed firebreaks and fuel breaks around home sites and in subdivisions • Living fuels that have not been modified by pruning, thinning, landscaping, or other methods to reduce cured vegetation and litter that readily contribute to spot fire development and fire intensity • Homes constructed with flammable building materials (e.g., wooden shake shingles) • Propane tanks exposed to the external environment • Inability to deliver water effectively before and during passage of a fire front around the home property (e.g., lack of proper equipment, such as sprinklers) In a lot of cases, simply cutting the grass and keeping the yard cleaned up will dramatically increase the chances of the house surviving a wildfire.126
WHAT SOME ORGANIZATIONS HAVE TO OFFER The National Disaster Education Coalition is a group of U.S. federal agencies and nonprofit organizations that support common goals in disaster and hazards education. This group worked hard with the nation’s leading social scientists in this area to produce a state-of-the-art guide for public risk education. The group developed a standardized guide327 on hazard safety messages, providing information that all organizations agreed on for national use. The guide covers many different hazards, including wildland fires, as well as general preparedness issues. Firewise Communities is a national mitigation planning pro gram that encourages communities to include land use planning, building codes, landscaping codes, zoning, and fire protection in developing new communities and in retrofitting existing communities.51,376 Firewise Communities is a national initiative designed to reach beyond the fire service and involve homeowners, community leaders, planners, developers, and others in the effort to protect people and property from the dangers of wildland fire. Firewise Communities programs include the Firewise Communities Workshop series, Firewise Communities/USA Recognition Program, and support for fire organizations and community groups. The Firewise Communities program is part of the Wildland–Urban Interface Working Team of the National Wildfire Coordination Group (NWCG), a consortium of wildland fire agencies that includes the USDA Forest Service, Department of Interior, National Association of State Foresters, U.S. Fire Administration, Federal Emergency Management Agency, and National Fire Protection Association. Firewise Communities emphasizes that everyone in every community is responsible for fire protection. Firewise Communities workshops help define responsibilities for a network that includes many partners. The intent is to undertake planning and actions to ensure that people live more compatibly in every neighborhood situation in a wildland fire environment. Toward this end, a website has been developed (http://www.firewise.org), and several publications and books331,428 have been published to assist homeowners living in the wildland–urban interface. A team of scientists from across the United States has been visiting communities to identify the activities they need to undertake to increase their wildfire preparedness and the resources necessary to support these activities. This research is funded by the National Fire Plan and is led by the Social and Economic Dimensions of Ecosystem Management Research Work Unit of the USDA Forest Service’s North Central Research Center. Research partners include the USDA Forest Service’s Pacific Northwest Research Station, University of Minnesota, Southern Oregon University, and University of Florida. Sixteen community preparedness case studies were completed between 2002 and 2004 in a variety of locations throughout the continental United States (jfsp.fortlewis.edu).509,514 Partners in Protection, based out of Alberta, Canada, is a coalition of professionals representing national, provincial, and municipal associations and organizations committed to raising
Fire Behavior URBAN AND WILDLAND FIRE THREATS Safety precautions for wildland firefighting crews are continually upgraded as new knowledge is gained about fire behavior and human behavior. The sites where people were injured or killed by fire are routinely examined284,315,512 afterward to assess fuel conditions, terrain features, probable wind movements at the time of the fire, and actions of firefighters (Figure 12-14). In this regard, author Norman Maclean275 has noted: It is hard to know what to do with all the detail that rises out of fire. It rises out of a fire as thick as smoke and threatens to blot out everything. Some of it is true but doesn’t make any difference. Some of it is just plain wrong. And some doesn’t even exist, except in your mind, as you slowly discover long afterwards. Some of it, though, is true—and makes all the difference. The information gleaned from past wildland firefighter fatalities, as well as data about hazards in the wildland–urban interface, are now included in training programs and safety briefings. In reviewing many past wildland fire tragedies, a sobering observation is that crew members are almost always experienced and well-equipped firefighters, trained to anticipate “blowup” fire
C
B
A FIGURE 12-14 In an attempt to avoid the intense heat of this brush fire in southwestern Colorado, four firefighters took refuge in the fire line, in the foreground at point A. Affected by intense convective and radiant heat and dense smoke, one individual ran into the fire and died at point B. Another individual ran about 300 m (1000 feet) down the ridge, where his body was found at point C. The third fatality was a person who remained at point A; he died a short time after this position was overrun by fire. The only survivor also remained in a prone position at point A with his face pressed to the ground. At one point he reached back and threw dirt on his burning pants legs. The survivor sustained severe burns to the backs of his legs, buttocks, and arms. The deaths of the other three individuals were attributed to asphyxiation. (Courtesy USDA Forest Service.)
conditions (i.e., a temporary escalation in fire behavior). However, when visibility is lowered to 6 m (20 feet), noise levels preclude voice communication, eyes fill with tears, and wind blows debris in all directions, a person’s judgment is badly impaired. For many members of the general public, the first wildland fire they may experience will in all likelihood be a high-intensity conflagration. As Cheney118 notes: The approach of a major fire can appear ominously threatening to those directly in its path, but is often viewed with curiosity and with little concern if it appears that the wind will direct the fire past their properties. Thus, when a combination of circumstances, often associated with a frontal wind passage, exposes residents to a high-intensity fire environment, they are very much unprepared. Their senses are assaulted by sudden darkness, thick blinding and choking smoke, buffeting winds and unexpected calm periods, searing heat and flames which illuminate the smoke-obscured scene and a roaring noise of wind and explosive combustion. In all this activity they observe flames which change from a metre or two to engulfing whole trees. In such a dramatic and emotional situation, many people are apt to invent phenomena (such as, houses exploding, the air burning, fantastic spread rates and the like) to explain the extent of the devastation that confronts them when the smoke clears away. Even for experienced firefighters, previous training can give way to panic-like attacks and poor decision making, leading to actions that can result in serious injury or death.356 This scenario is most evident in urban fires; the pattern of hysteria affecting people trapped in burning buildings is all too familiar to urban firefighters.435 The way fire kills in the urban setting can be compared with wildland fires, as shown here:359 • Heat rises rapidly to upper stories when a fire starts in the basement or on the ground floor. Toxic gases and smoke rise to the ceiling and work their way down to the victim—a vital lesson for families planning protective measures. Smoke poses the double problem of obscuring exit routes and contributing to pulmonary injury and oxygen deprivation. • As the fire consumes oxygen, the ambient oxygen content drops, impairing neuromuscular activity. When the oxygen content drops below 16%, death by asphyxiation will ensue 251
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awareness, providing information, and developing forums with a view to encouraging proactive, community-based initiatives with respect to fires at the wildland–urban interface. Partners in Protection has produced a comprehensive manual with respect to the wildland–urban interface fire problem entitled FireSmart: Protecting Your Community From Wildfire.364 This well-illustrated guide focuses on how individuals and communities can work together to reduce the risk for loss from fires in the wildland– urban interface. It provides practical tools and information for use by residents and by individuals and organizations that operate in the wildland–urban interface. The primary topics are description of interface issues, evaluation of hazards, mitigation strategies and techniques, emergency response for agencies and individuals, training for interface firefighters, community education programs, and regional planning solutions. The manual, available in both book form and CD-ROM, can be viewed online at the Partners in Protection website (http://partnersinprotection. ab.ca) and covers nearly every facet of fire preparations in the wildland–urban interface. In the chapter on communications and public education, for example, several principles are cited for effective communication: • Begin with clear, explicit objectives. • Do not make assumptions about what people know, think, or want done. Take time to find out what people are thinking by using surveys, focus groups, or other research. • Involve all parties that have an interest in the issue. Identify and address the particular interests of different groups. • Identify with your audience. Put yourself in their place, and recognize their emotions. • Take time to coordinate with other organizations or groups. • Choose your spokespeople carefully, and ensure they have the training to communicate your messages effectively. • Practice and test your messages. • Do not either minimize or exaggerate the level of risk. • Promise only what you can do. Do what you promise. • Plan carefully, and evaluate your efforts. Kumagai and colleagues250 also offer some excellent advice with respect to wildland fire education and communication with the general public. Nowadays most local, state, provincial, territorial, and federal fire management agencies have some sort of outreach program related to the wildland–urban interface. For example, the State of Alaska offers teachers both face-to-face wildland fire workshops and an online training course.450 Beginning in 1993, the Country Fire Authority of Victoria, Australia, developed a program called “Community Fireguard,” which assists communities in developing wildfire survival strategies.71
PART 3 BURNS, FIRE, AND RADIATION
unless the victim is promptly evacuated. Asphyxiation, not fire itself, is the leading cause of fire deaths. • Ambient temperatures may rise extremely rapidly from even small fires. Temperatures of 150° C (300° F) will cause rapid loss of consciousness and, along with toxic gases, will severely damage lung tissues. Warning devices may offer the only possibility for survival owing to the rapid onset of debilitating symptoms. Obvious similarities and differences are seen between wildland fires and urban fires: • Smoke, heat, and gases are not as concentrated in wildland situations as in the confined quarters of urban fires. • Flames are not a leading killer in either the urban or wildland situation, although admittedly there is a general lack of autopsies being performed, so this assertion awaits confirmation. • Although oxygen levels may be reduced near wildland fires, there is usually sufficient replenishment of oxygen in the outdoor environment to minimize deprivation. Asphyxiation, however, can also be an important cause of death in wildland fires. • Inhalation of superheated gases poses as serious a threat to life in wildland fires as in urban fires. • Wildland smoke does not contain toxic compounds produced by combustion of plastics and other household materials, but it does impair visibility, contains carbon monoxide, and carries suspended particulates that cause severe physical irritation of the lungs. • Sprinkler systems and automatic early-warning devices to detect smoke or heat may protect people from serious injury or death in the urban environment, but in the wildland environment, people must rely on their experience, senses, knowledge, and skills or ingenuity to provide early warning of an impending threat to life. The general public needs to appreciate that fires occurring under certain fuel, weather, and topographic situations may result in explosive fire growth on an area basis (Figure 12-15, online). The fire that burned through Faro, Yukon, on June 13, 1969, is a good example of this type of behavior.244 The Faro fire, which burned about 15,500 hectares (about 38,300 acres) resulted from a lightning strike that occurred 8 km (5 miles) west of town at 5:04 PM. The fire started to spread fairly quickly in an easterly direction. Fire crews were dispatched from town by vehicle to take suppression action, but little could be done because of crowning activity. By 8:30 PM, the fire had burned through town and was continuing to spread farther east. In other words, the fire had traveled 8 km (5 miles) in less than 3.5 hours. This equates to a rate of spread of around 2.3 km/hr (1.4 mph) or 40 m/min (131 ft/min). This would not be considered an unusual situation in many regions of the North American boreal forest.29,155 How wide would the fire have likely been when it hit the edge of town? A rough rule of thumb is to divide the separation distance by a factor of 2 to 4 based on an assumed wind-driven fire shape.458 The fire would have thus been roughly 2 to 4 km (1.2 to 2.5 miles) wide when it hit the western edge of Faro. Fire Behavior Knowledge: A Wildland Fire Early-Warning System Fire behavior is defined as the manner in which fuel ignites, flame develops, and fire spreads and exhibits other related phenomena as determined by the interaction of fuels, weather, and topography. The science of fire behavior describes and predicts the performance of wildland fires in terms of ignition probabilities, rates of spread, intensity levels, spotting distances and densities, and crowning potentials. To the lay person, a wildland fire can be a perplexing event. As Countryman and Schroeder note:150 A casual observer seeing a forest fire for the first time would probably decide there is little rhyme or reason to the way a fire burns. Its sudden variations in direction of travel, its quick change from a seemingly mild, slow-burning fire to a raging inferno, all seem to add up to erratic behavior without local explanation. Actually a fire behaves in accord with changes in its surroundings—the character and condition of the 252
burnable vegetation, the topography, and the meteorologic factors—that affect fuel flammability, fire intensity, and fire spread. This complex of environmental factors that control the behavior of fire is what we call “fire environment.” Understanding one’s fire environment145 is considered a key factor for safe and effective action in dealing with wildland fires. For example, 4 of the 32 civilians killed in Victoria during the 1983 Ash Wednesday fires in southeastern Australia were caught outside their homes tending to or attempting to herd up livestock,248 apparently unaware of the change in wind direction and speed that accompanied passage of the cold front through their area.393 In such situations in southeastern Australia, the strong prefrontal winds are from the northwest. With the passage of the front, the wind direction changes sharply to the southwest, and winds increase markedly in strength. Had these people understood or been aware of the implications of the cold front passage on fire behavior and received some information on the timing of the change, they may have chosen to stay inside their homes.248 An excellent overview of the fire environment concept has been prepared by the National Wildfire Coordinating Group.336 Experienced firefighters routinely monitor the fire and the fire environment and assess the probable behavior of fires using fire behavior guidelines and experienced judgment based34,54 on current and expected fire weather conditions in relation to local fuel type information, topographic conditions, and moisture levels.85,261,458 This is also referred to as “situational awareness” (i.e., understanding what the fire is doing and what you are doing in relation to the fire and being able to predict where the fire and you will be in the future).377 In the conclusions to their detailed case study report on the 1994 South Canyon fire, USDA Forest Service fire researchers96 noted: None of the findings and observations discussed in this study represent new breakthroughs in wildland fire behavior understanding. Rather, the findings support the need for increased understanding of the relations between the fire environment and fire behavior. We can also conclude that fire managers must continue to monitor and assess both present fire behavior and potential future fire behavior given the possible range of environmental factors. The emergency medical person, backcountry recreationist, and wildland homeowner must also understand certain basic fire behavior principles to provide for adequate personal safety. A cardinal rule in wildland fire suppression is to base all actions on current and expected fire behavior.287,308 Attention to simple principles, indicators, and rules should enable wildland users to anticipate and avoid wildfire threats. Heat, oxygen, and fuel are required in proper combination before ignition and combustion will occur54,201 (Figure 12-16, online). If any one of the three is absent, or if the three elements are out of balance, there will be no fire (Box 12-3). Fire control actions are directed at disrupting one or more elements of this basic fire triangle.14 Physical Principles of Heat Transfer Heat energy is transferred by conduction, convection, radiation, and spotting, but generally only the last three processes are significant in a wildland setting.102 Although conduction through solid objects is important in the burning of individual logs,54 this process does not transfer much heat outward from a flaming front, unless there is a substantial accumulation, such as is found in blowdown.200 Convection, or the movement of hot masses of air, accounts for most of the heat transfer upward from the fire. Convective currents usually move vertically unless a wind or slope generates lateral movement (Figure 12-17). Convection preheats fuels upslope and in shrub and tree canopies, which contributes further to a fire’s spread and the onset of crowning forest fires. Through radiation, heat energy is emitted in direct lines or rays; about 25% of combustion energy is transmitted in this manner. Radiated heat on exposed skin can cause discomfort and severe pain (Figure 12-18), and even death at elevated
Certain universal principles apply to all spreading fires in vegetation, living or dead. These really have nothing to do with biology but are based purely on the physics and chemistry of combustion: 1. There must be sufficient fuel of appropriate size and arrangement in space. 2. This fuel must be of sufficient dryness to support a spreading combustion reaction. 3. There must be an agent of ignition. In practical terms, the primary requirement is a continuous layer of finely divided fuel or minor vegetation on the surface of the ground. This material may be conifer needles, hardwood leaves, grass, lichen, moss, finely divided shrubs, or other minor vegetation. However, it must be present and it must be continuous, or the possibility of spreading fire does not really exist. The second requirement is that the material be dry enough. The maximum moisture content at which fire will spread is hard to specify; for any given fuel or vegetation complex, it will depend on the amount of fuel, its arrangement in space, and the wind speed. Thus, fire spreads poorly or not at all in surface litter of various kinds at moisture contents over 25% or 30% (dry weight basis), whereas fine shrubby fuels or conifer foliage may support fast-spreading fires at moisture contents of 100% or more. The two limiting criteria common to all spreading fires are as follows: 1. The fire must transfer enough heat forward to dry out the unburned fuel and raise it to ignition temperature by the time the flame front arrives. 2. Enough fuel must pass through the moving flame front to produce a continuous solid flame. The behavior of any fire is the result of a complex process that results in a dynamic equilibrium among all elements of mass and energy flowing in and out of the flame zone. However difficult this whole process may be to describe and predict, the above two criteria run like threads through the whole range of fires in vegetation, whether the fuel itself is dead or live. From Van Wagner CE: Fire behaviour in northern conifer forests and shrublands. In Wein RW, MacLean DA, editors: The role of fire in northern circumpolar ecosystems, Chichester, England, 1983, J. Wiley & Sons.
levels.114,142 The amount of radiant heat transferred decreases inversely with the square of the distance from a point source. More radiant heat is emitted from a line of fire than from a point source. Radiant heat travels in straight lines, does not penetrate solid objects, and is easily reflected. It accounts for most of the preheating of surface fuel ahead of the fire front and poses a direct threat to people who are too close to the fire (see Figure 12-17). Most organized fire suppression crews in the United States carry protective fire shelters39,40,368 as part of their personal protective equipment (PPE) (Figure 12-19).369 These aluminized “pup tent” type of structures are intended to protect against radiant heat.99,380 The U.S. Forest Service fire shelter was never designed to mitigate against sustained, direct flame contact.303 Certain materials that fail when in direct contact with flames, such as “emergency space blankets,”193 are also not appropriate for use in wildland fires84 and in fact could cause serious burn injuries. Similarly, “emergency evacuation smoke hoods,” intended for use in urban situations or other human-made environments (e.g., airplanes), have absolutely no application in a wildland fire environment despite manufacturers’ suggestions to the contrary. Spotting is a fire spread or mass transport heat transfer mechanism by which wind currents carry flaming firebrands or glowing embers land beyond the main advancing fire front to start new fires (Figure 12-20). In this manner, fire spread may accelerate very quickly, unexpected new fire starts can occur, and fire intensity and in-draft winds can dramatically increase as spot fires coalesce (Figure 12-21). High-density, short-range spotting up to 100 m (328 ft) is a common feature of many wildfires, especially
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
BOX 12-3 Requirements for Wildland Fire Spread
A Wind
B FIGURE 12-17 Fuels and people upslope (A) or downwind (B) from a fire receive more radiant and convective heat than on the downslope or upwind sides of a spreading fire. (Modified from Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station Paper No. 29, Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Mountain Forest and Range Experiment Station.)
when fine fuels are very dry.37 Low-density, intermediate- to medium-range spotting up to about 1 to 2 km (0.6 to 1.2 miles) is a common occurrence with high-intensity crown fires.29 Longer-range spotting occurs very infrequently in most fuel types. Firebrand material being transported up to 16 km (10 miles) from its source has been reported in North America.38 The native eucalyptus forests of Australia have a notorious reputation when it comes to spotting behavior owing to the bark characteristics of many species, including an authenticated spot fire distance of 30 km (19 miles) or more.269
FIGURE 12-18 Most of the heat felt from a fire is radiant heat, which is largely a function of the height, depth, and angle of the flame front. Wildland firefighters work far enough from the radiating flames to avoid pain to exposed skin (e.g., face and ears). This also limits the amount of radiant heat absorbed through clothing. Wildland firefighters working near an active fire edge with hand tools typically adjust their distance from the flames so that the radiant heat they receive from the fire is little more than that of direct sunlight. (Courtesy British Columbia Forest Service.)
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PART 3 BURNS, FIRE, AND RADIATION
C
A
B
D
FIGURE 12-19 The personal protective equipment for a firefighter includes hard hat and safety goggles, fire-resistant shirt and trousers, leather boots and gloves, and an aluminized fire shelter carried in a waist pouch (A). Firefighters also carry canteens to ensure an adequate water supply in a heat-stressed environment. The fire shelter (B) is deployed (C) by firefighters as a last resort to provide protection from being exposed directly to radiant heat and superheated air (D). (Courtesy USDA Forest Service.)
FUNDAMENTAL WILDLAND FIRE BEHAVIOR CHARACTERISTICS One important aspect of fire behavior that distinguishes urban or structural fires from wildland fires is the latter’s horizontal spread potential. Although urban or structural fires may exhibit some vertical fire spread potential, for practical purposes, they are considered stationary fire sources. Wildland fires on the other hand characteristically involve moving flame fronts, sometimes advancing with astonishing speed (Figure 12-22). Whereas ground or subsurface fires may spread very slowly (about 1 m [3 feet] per hour),507 surface fires in open grown forests can reach rates of about 15 to 25 m/min (50 to 80 ft/min); conversely, surface fires in closed forest types typically spread at 5 to 6 m/
FIGURE 12-20 Fires can easily cross narrow canyons. Fuels and people on the slope opposite a fire in a narrow canyon are subject to intense radiant heat and spot fires from airborne embers. (Modified from Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station Paper No. 29, Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Mountain Forest and Range Experiment Station.)
254
min (16 to 20 ft/min) before the onset of crown combustion. Crowning forest fires generally advance at rates between 30 and 60 m/min (100 to 200 ft/min), occasionally higher.29,155 Grass fires spread at rates up to around 385 m/min (1263 ft/min) or 23 km/ hr (about 14 mph).125,350 It is thus quite possible for forest fires to advance up to 80 km (50 miles) in a single day7,405 and for grass fires to travel correspondingly even farther. The threat to life and property largely depends on a fire’s residence time (Table 12-2). This represents the length of time any object overrun by a fire will be heated by direct flame contact. Coupled with the fire’s rate of spread, the residence time determines the depth of the active or continuous flaming front (Figure 12-23). The length of time that a fire will continue to burn by smoldering combustion depends on the composition, compaction, moisture content, and quantity of fuel present.194 The most basic features of a wildland fire are that (1) it spreads or moves, (2) it consumes or “eats” fuel, and (3) it produces heat energy and light in a visible flaming combustion reaction.6 Byram101 defined fire intensity as the rate of heat energy release per unit time per unit length of fire front, regardless of its depth. Numerically, it is equal to the product of the quantity of fuel consumed in the flaming front, a fire’s rate of fire spread, and a fuel heat combustion value. Flame size is its main visual manifestation. The fastest spreading part of a fire is the head; the back of the fire is the slowest spreading part, with the flanks being intermediate between the two (Figure 12-24). It is for this reason that the fire intensity, flame length, and flame height (see Figure 12-23) are greatest at the front of the fire and least at the rear109 (Figure 12-25). The amount of radiation received from a flame front is determined by the size and geometry (e.g., height, depth, and tilt angle) of the flame front. Radiation levels coupled with residence times determine the nature of burn injuries.84,173 Environmental Factors Influencing Wildland Fire Behavior A wildland fire behaves according to variations in the fire environment (i.e., fuels, weather, and topography). Some of the fire environment factors associated with adverse burning conditions that can signal the potential or onset for severe fire behavior are listed in Box 12-4. These factors or indicators are subject to assessment, measurement, and observation.
B
C
D
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
A
FIGURE 12-21 The occurrence of numerous spot fires is a direct indication that the moisture content of fine fuels has attained a critically dry level and in turn an early warning signal that the potential for extreme fire behavior exists or is imminent. This sequence of photos (A to D) spanned a period of just over 100 seconds taken late in the afternoon of July 9, 2005, near Coimbra, Portugal. The fuel type is a blue gum (Eucalyptus globulus)–maritime pine (Pinus pinaster) stand. (Courtesy Associação para o Desenvolvimento da Aerodinâmica Industrial; photos by M. G. Cruz.)
When a person encounters a wildland fire, the first step should be to review the principles and indicators of fire behavior, sizing up the situation in terms of fuel, weather, topographic factors, and observed fire behavior. After the fire’s probable direction and rate of spread are estimated, travel routes that avoid hazards to human life can be planned (see Figure 12-24). The direction of the main body of smoke is often a good indicator of the direction the fire will take.
Fuel. Because wildland fuels vary so widely in their distribution, their physical characteristics or properties (i.e., moisture content, size and shape, compactness or arrangement, load, horizontal and vertical continuity, chemical content), and their effect on fire behavior, some means of classification is needed for their systematic assessment. Fuels are commonly classified into four groups or strata (Figure 12-26). Some fuel types may exhibit only one or two of the strata (e.g., grasslands, shrublands, and logging slash lack the ladder and crown fuel stratum). An increase in fuel available for combustion affects fire intensity. In other words, the more fuel that is burning, the greater the heat energy released by the fire. As Brown and Davis77 noted:
Flame flashes
Prevailing wind Flame length
Ash FIGURE 12-22 A novel approach to reminding people of the capricious nature of wildland fire spread. This sign is located at Betty’s Bay on the South African coast near Cape Town. The vegetation type is fynbos—a highly flammable Mediterranean shrubland fuel complex.485 (Courtesy CSIR Natural Resources and the Environment, Stellenboch, South Africa; photo by B.W. van Wilgen.)
Flame height
Flame angle
Flame depth
Compact surface layer
FIGURE 12-23 Cross-sectional view of a stylized free-burning fire in a grass fuel bed. (From Cheney P, Sullivan A: Grassfires: Fuel, weather and fire behaviour, ed 2, Collingwood, Victoria, Australia, 2008, CSIRO Publishing.)
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PART 3 BURNS, FIRE, AND RADIATION
TABLE 12-2 Nominal Residence Times for Four Broad Fuel Complexes and Computed Maximum Theoretic Flame
Depths* Associated With Variable Rates of Fire Spread
Rate of Fire Spread
Broad Fuel Complex Grassland Shrubland Forest stand Logging slash
Residence Time
10 m/min (33 ft/ min) Flame Depth
20 m/min (66 ft/ min) Flame Depth
40 m/min (131 ft/ min) Flame Depth
(sec)
(min)
(m)
(ft)
(m)
(ft)
(m)
(ft)
10 20 45 90
0.17 0.33 0.75 1.5
1.7 3.3 7.5 15
5.6 10.9 24.6 49.2
3.4 6.6 15 30
11.2 21.7 49.2 98.4
6.8 13 30 60
22.3 42.7 98.4 196.8
*Numerically equal to residence time multiplied by the rate of fire spread (in compatible units).
The ignition, buildup, and behavior of fire depend on fuels more than any other single factor. It is the fuel that burns, that generates the energy with which the fire fighter must cope, and that largely determines the rate and level of intensity of that energy. Other factors that are important to fire behavior (that is, moisture, wind, etc.) must always be considered in relation to fuels. In short, no fuel, no fire! Certain types of fuel, such as chaparral, pine, and eucalyptus, burn more intensely because their foliage contains flammable oils and resins (see Figure 12-12). The size and arrangement of fuel also influence fire behavior. Small, loosely compacted fuel beds, such as dead grass, long pine needles, and shrubs, burn more rapidly than does tightly compacted fuel. Large fuels burn best when they are arranged so that they are closely spaced, such as logs in a fireplace. Scattered logs with no small or intermediate fuel nearby seldom burn unless they are decomposed. Seasonal changes in the moisture content and live-to-dead ratio (e.g., degree of curing in grasslands) of conifer tree foliage, shrubs, grasses, and other herbaceous plants can result in gradual changes in fuel flammability over the course of a fire season.147,269 Wildland fire research has identified a wind speed threshold in fuel types with a discontinuous, combustible surface layer (e.g., due to the presence of areas of bare, mineral soil).82,86 In these discontinuous fuel types, fire spread is exceedingly limited until a certain or threshold wind speed level is attained, and then
Finger
Head
Left flank
the rate of advance can be quite unexpectedly rapid199 (Figure 12-27, online). This kind of situation could lead a person into a false sense of security regarding fire potential, until unfortunately it is often too late. Various weather phenomena (e.g., wind, hail, snow, ice, and frost) and insect and disease epidemics can drastically elevate the flammability of a fuel complex, creating decidedly new fire safety concerns.33 For example, on July 9, 1999, heavy rains and winds in excess of 145 km/hr (90 mph) blew down about 181,000 hectares (about 447,000 acres) of sub-boreal forest in northeastern Minnesota, resulting in heavy dead and downed woody fuel loads.200 Weather. The greater the wind, the more rapid the spread of fire. Thunderstorm downdrafts and winds associated with dry cold frontal passages can be especially hazardous.125,411 Low relative humidity and high air temperatures decrease the moisture content of fine, dead fuels and thereby increase ignition ease and rate of spread. Prolonged drought makes more medium and heavy fuels available for combustion, leading to increased intensity levels. When fuels reach critically dry levels, fires become very responsive to minor changes in wind and slope. Fires tend to burn more vigorously under unstable atmospheric conditions. The North American continent has been classified into 15 fire climate regions based on geographic and climatic factors411 (Figure 12-28). Major fire seasons, or periods of peak fire activity, can be used to warn emergency medical personnel and wildland users of the most probable times for life-threatening situations. Exceptions occur. For example, rapidly spreading grass and forest fires can occur during the winter months in the northern latitudes, such as happened in southwestern and west-central Alberta on December 14, 1997, under Chinook conditions and
Spot fire
Rear Wind direction
Pocket Finger Right flank Unburned island
FIGURE 12-24 The parts of a fire are described in terms of its left flank, right flank, head, and back or rear. There may also be unburned islands within the fire and spot fires ahead of the fire. The safest travel routes generally involve lateral movement on contours away from the fire’s flank or movement toward the rear of the fire. Moving in front of a head fire should be avoided. The burned area inside the fire’s peri meter can offer a safe haven provided smoldering or glowing combustion levels are low and the flaming perimeter can be safely penetrated by an individual; falling trees or snags and rolling rocks could, however, still pose a hazard. (Modified from Mobley HE, Moore JE, Ashley RC, et al: Planning for initial attack, rev ed, Forestry Report SA-FR-2, Atlanta, Ga, 1979, USDA Forest Service, Southeastern Area State and Private Forestry.)
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FIGURE 12-25 Elliptical fires resulting from multiple, wind-driven, point source ignitions associated with a prescribed burning operation in a southeastern U.S. pine plantation. As indicated by the smoke drift, the winds are blowing roughly from lower right to the upper left. (Courtesy USDA Forest Service; photo by C.W. Adkins.)
Fuel • Continuous fine fuels, especially fully cured (dead) grasses • Large quantities of medium and heavy fuels (e.g., deep duff layers, dead-down logs) • Abundance of bridge or ladder fuels in forest stands (e.g., branches, lichens, suspending needles, flaky or shaggy bark, small conifer trees, tall shrubs extending from ground surface upward) • Tight tree crown spacing in conifer forests • Presence of numerous snags • Significant amounts of dead material in elevated, shrubland fuel complexes • Seasonal changes in vegetation (e.g., frost kill) • Fire, meteorologic or insect and disease impacts (e.g., preheated canopy or crown scorch; snow-, wind-, or icedamaged stands; drought-stressed vegetation; or mountain pine beetle–killed stands) Weather • Extended dry spell • Drought conditions • High air temperatures • Low relative humidity • Moderately strong, sustained winds • Unstable atmosphere (visual indicators include gusty winds, dust devils, good visibility, and smoke rising straight up) • Towering cumulus clouds • High, fast-moving clouds • Battling or shifting winds
no snow cover.213 One of the grass fires advanced 33 km (20.5 miles) in less than 4 hours for a spread rate of around 8 km/hr (about 5 mph), seriously threatening the community of Granum.70 A forest fire near the town of Hinton in west-central Alberta on the same day posed a similar threat. Although the fire season for the southern Pacific coast is shown in Figure 12-28 as June through September, critical fire weather can occur year-round in the most southerly portion. Fire
• Sudden calm • Virga (i.e., a veil of rain beneath a cloud that does not reach the ground) Topography • Steep slopes • South- and southwest-facing slopes in the northern hemisphere • North- and northeast-facing slopes in the southern hemisphere • Gaps or saddles • Chutes, chimneys, and narrow or box canyons Fire Behavior • Many fires that start simultaneously • Fire that smolders over a large area • Rolling and burning pine cones, agaves (a desert plant found in the southwestern United States), logs, hot rocks, and other debris igniting fuel downslope • Frequent spot fires developing and coalescing • Spot fires occurring out ahead of the main fire early on • Individual trees readily candling or torching out • Fire whirls that cause spot fires and contribute to erratic burning • Vigorous surface burning with flame lengths starting to exceed 1 to 2 m (3 to 6 feet) • Sizeable areas of trees or shrubs that begin to readily burn as a “wall of flame” • Black or dark, massive smoke columns with rolling, boiling vertical development • Lateral movement of fire near the base of a steep slope
seasons are most active during spring and fall in the Great Plains, Great Lakes, and North Atlantic regions. The pattern of seasonal fire occurrence in Australia has also been mapped,269 as has the frequency of large fire occurrences.115 Topography. The steeper the slope, the more rapid the spread of fire. Fire usually burns uphill, especially during daylight hours. Changes in topography can cause rapid and violent changes in
Crown fuels
Ladder fuels Surface fuels
Ground fuels Mineral soil
FIGURE 12-26 Profile of a stylized forest stand showing the location and classification of fuel complex strata. Wildland fuels contain energy, stored over extended periods through photosynthetic processes, that is released rapidly, occasionally explosively, in combustion. (Modified from Brown AA, Davis KP: Forest fire: Control and use, ed 2, New York, 1973, McGraw-Hill.)
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CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
BOX 12-4 Early Warning Signals or Indicators Associated With Extreme Fire Behavior Potential
PART 3 BURNS, FIRE, AND RADIATION FIGURE 12-28 Fire climate regions of North America, based on geographic and climatic factors: (1) interior Alaska and the Yukon, (2) north Pacific Coast, (3) south Pacific Coast, (4) Great Basin, (5) northern Rocky Mountains, (6) southern Rocky Mountains, (7) Southwest (including adjacent Mexico), (8) Great Plains, (9) central and northwest Canada, (10) sub-Arctic and tundra, (11) Great Lakes, (12) Central States, (13) North Atlantic, (14) Southern States, and (15) Mexican central plateau. The bar graphs show the monthly and annual precipitation for a representative station in each of the fire climate regions. Months on the map indicate fire seasons. The graph for Decatur, Illinois, obscures the provinces of Newfoundland and Prince Edward Island on the map. (Modified from Schroeder MJ, Buck CC: Fire weather, Agriculture Handbook 360, Washington, DC, 1970, USDA Forest Service.)
fire behavior (Figure 12-29). On steep terrain, rolling firebrands may cause a fire to initially spread downhill, followed by upslope runs. Mountainous terrain can modify wind speed and direction and in turn influence fire behavior in exceedingly complex ways.411 Slope exposure or aspect has a very pronounced diurnal effect on fine-fuel flammability, a fact directly incorporated into the Campbell Prediction System of wildland fire behavior (http:// www.dougsfire.com).106 Extreme Fire Behavior Extreme fire behavior is generally considered a level of fire activity that often precludes any fire suppression action by conventional means.300 It usually involves one more of more of the following characteristics: 258
• High rates of spread and intensity • Active crowning • Prolific spotting • Presence of large fire whirls • Well-established convection column Fires exhibiting such phenomena often behave in an apparent erratic, sometimes dangerous manner. Fire whirls appear frequently in and around wildland fires.144 Most fire whirls are small and short-lived, but occasionally one becomes large and strong enough to do tornado-like damage and cause serious injury, such as occurred at Mt Kuki, Japan in 1977;181 death is also a distinct possibility. Their occurrence is commonly associated with unstable air, moderate winds, and large heat sources created by plentiful and dry fuel
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL FIGURE 12-29 Chutes, chimneys, and box canyons created by sharp ridges provide avenues for intense updrafts (like a fire in a woodstove) and rapid rates of spread. People should avoid being caught above a fire under these topographic conditions. (Modified from Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station Paper No. 29, Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Mountain Forest and Range Experiment Station.)
concentrations (Figure 12-30) or terrain configurations that concentrate the heat from the fire (e.g., lee side of a ridge).207,218 These fire-induced tornado-like whirlwinds can travel up to 2.5 km (1.6 miles) from the main fire441 and can cause considerable damage and even lead to fatalities. On March 7, 1964, a fire whirlwind that formed on the Polo fire near Santa Barbara, California, cut a 1.6-km (1-mile) path, injuring four people, destroying two houses, a barn, and four automobiles, and wrecking a
FIGURE 12-30 Large fire whirl associated with the burning of logging slash debris near Whitecourt, Alberta. (Courtesy University of Alberta; photo by M.Y. Ackerman.)
100-tree avocado orchard.373 The fringe of the fire whirl passed over a fire truck and sucked out the rear window of the vehicle. A firefighter standing on the rear platform of the vehicle was pulled up vertically so that his feet were pointing to the sky while his hands clasped the safety bar. A small piece of plywood was rammed 7.6 cm (3 inches) into an oak tree. Several years of drought combined with a national forest health issue that has produced many dead and dying forests set the stage for extreme fire behavior conditions that threaten people, property, and natural and cultural resources. Protection from these conditions requires understanding of the crown fire process. Crowning involves a fire spreading horizontally as a “wall of flame” from the ground surface up through and above the canopies of trees (Figure 12-31) or tall shrubs. The first views inside a crown fire were documented on videotape during the International Crown Fire Modelling Experiment near Fort Providence in Canada’s Northwest Territories in 1997.457 The onset of
FIGURE 12-31 Experimental crown fire in a northern jack pine (Pinus banksiana) and black spruce (Picea mariana) forest near Fort Providence, Northwest Territories. The average height of flames from crowning forest fires is generally one to one and a half times taller than the tree height. Flame flashes will extend considerably higher into the fire’s convection column. (Courtesy Canadian Forest Service.)
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PART 3 BURNS, FIRE, AND RADIATION
crowning is significant from both a safety and suppression perspective. At a minimum, when a fire crowns, the rate of spread and intensity doubles, and the area burned quadruples.12 Author Norman Maclean274 gives an indication of how crown fires were handled in the early part of the 20th century by the USDA Forest Service: By the time they reached the fire, it had spread all over the map, and had jumped into the crowns of trees, and for a lot of years a prospective ranger taking his exam had said the last word on crown fires … When asked on his examination, “What do you do when a fire crowns?” he had answered, “Get out of the way and pray like hell for rain.” This wisdom seems still valid today. Rothermel402,404 described the conditions that produce a crown fire: 1. Dry fuels 2. Low humidity and high temperatures 3. Heavy accumulations of dead and downed fuels 4. Small trees in the understory, or “ladder fuels” 5. Steep slope 6. Strong winds 7. Unstable atmosphere 8. Continuous crown layer The two most prominent behavior patterns of crown fires are wind driven and plume (or convection) dominated. Each type of crown fire poses a distinct set of threats to people. Free-burning wildland fires are seldom uniform and well behaved, so these descriptions of wind-driven and plume-dominated crown fire behavior may not be readily apparent. The behavior of these types of fires can be expected to change rapidly as environmental, fuel, and topographic conditions change.402 Wind-Driven Crown Fire. A running crown fire can develop when winds increase with increasing elevation above the ground, driving flames from crown to crown (Figure 12-32). Steep slopes can produce the same effect. Spread rates in conifer forests can reach up to 12 km/hr (7.5 mph) for brief periods of time243,427 and are possibly faster in mountainous terrain,402 especially in open forest or nonforested or shrubland fuel types.96,129 A running crown fire is accompanied by showers of firebrands downwind, fire whirls, smoke, and rapid development of a tilted convection column. As long as the wind remains fairly constant from one direction, the flanks of the fire can remain relatively safe. The greatest threat is to people who are immediately at the head, or
downwind side, of the fire, although medium- and long-distance spot fires can also pose an unexpected risk.5,66 Plume-Dominated or Convection-Dominated Crown Fire. An alternative form of crown fire develops with relatively low wind speeds or when wind speed decreases with elevation above the ground. This type of crown fire is referred to as plume dominated or convection dominated because it is characterized by a towering convection column that stands vertically over the fire (Figure 12-33). This type of fire poses a unique threat to people because it can produce spot fires in any direction around its perimeter. It can also spread rapidly as the combustion rate accelerates. One form of a plume-dominated crown fire that can be especially dangerous is when a downburst of wind blows outward near the ground from the bottom of the convective cell. These winds can be extremely strong216 and can greatly accelerate a fire’s spread. This type of wind event occurred during the major run of the Dude fire near Payson, Arizona, on June 26, 1990, when six firefighters were killed.208 Some indicators help signal the onset of a downburst from a plume-dominated crown fire. The surest indicator is the occurrence of precipitation of any amount, even a light sprinkle, or the appearance of virga (evaporating rain) below the base of a cloud formation.402,411 Another indicator is rapid development of a strong convection column above the fire, or nearby thunder cells. A third and very short warning is the calm that develops when the in-draft winds stop before the turnabout and outflow of wind from the cell. This brief period of calm may be accompanied by a humming sound just before the reversing wind flow arrives. If any of these indicators is present, the area should quickly be evacuated and a safe refuge sought. The downburst may also break or uproot trees, creating an additional hazard for people.402 Value of Fire Danger Ratings Forest fire control in the early days before organized protection was relatively simple. As Williams513 explains: One tried to keep wild fires out of the settlements and in the woods where they belonged. There was no planning—fire was fought wherever it could not be avoided. Later, as forest fire control became organized, specific plans for fire control action became an obvious necessity. To form the basis for such plans, a reliable measure of the day-by-day state of forest flammability was needed.
Wind
Heading fire
Backing fire
1
2
3
Ignition point
3
2
1
FIGURE 12-32 Cross-sectional view of a wind-driven crown fire, illustrating the various stages of combustion: preignition (1), ignition and flaming combustion (2), and glowing or smoldering combustion (3). People are most at risk on the downwind side and upper flanks of such a free-burning fire. This type of fire is caused by winds that increase in velocity with increasing elevation above the ground. (Modified from Cottrell WH: The book of fire, ed 2, Missoula, Mont, 2004, Mountain Press Publishing Co.)
260
Died in Tasmanian Fires, February 7, 1967
Location
No. of Deaths
Mustering stock Firefighting Traveling in a vehicle Escaping from and found at some distance from houses Within a few meters of houses In houses
2 11 2 11 10 17
From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7 February 1967, Hobart, Australia, 1967, Government Printer.
FIGURE 12-33 Cross-sectional view of a plume-dominated or convection-dominated crown fire. People are at risk around the complete perimeter of this type of fire because it has the potential to spread intensely or spot in any direction around its perimeter with little or no warning. This form of crown fire develops when wind velocities are relatively low or when velocities decrease with elevation above the ground coupled with critically dry and abundant fuel conditions. The convective plume associated with this type of fire may rise to 7600 to 9100 m (25,000 to 30,000 feet) above the ground. (Modified from Cottrell WH: The book of fire, ed 2, Missoula, Mont, 2004, Mountain Press Publishing Co.)
To help fill that need, full-time research into the systematic measurement of forest flammability or “fire danger” began in the United States and Canada in the 1920s and has continued more or less uninterrupted since that time.22,77 Fire management agencies employ fire danger rating systems to help them gauge ignition and fire behavior potential based on fuel characteristics, past and current weather conditions, and certain topographic variables that encapsulate fire behavior knowledge garnered from research.23,269,456 Such systems have been demonstrated to be of value in accurately predicting fire behavior in the wildland–urban interface.10 In commenting on the historic fatality fires around the turn of the 20th century, Brown and Davis77 pointed out that in general terms, these situations reflected the public’s indifference to forest fires that had persisted for so many years and still lingers on to some degree today. They noted: The Maine fires of 1947 were a sobering reminder in this respect. They occurred at a time when fire danger measurement was well understood and means for mass public dissemination of this information were well developed. Responsible officials were aware of the mounting fire danger. Nonetheless, some fifty fires were reported to have been burning in Maine at the time the major break occurred on October 23. A contributing circumstance was the general feeling that, as it was late October, the fire season was over. Fire danger rating outputs are being applied directly to the task of community fire safety and protection, including early warning or alert systems linked to fire weather forecasts that operate during the fire season, such as those developed for the Northwest Territories, Canada.30 This information is now commonly accessible to the general public on the Internet regarding
countries like the United States (http://www.fs.fed.us/land/wfas), Canada (http://cwfis.cfs.nrcan.gc.ca), New Zealand (http://nrfa. fire.org.nz/fire_weather), the European Union (http://www.effis. jrc.ec.europa.eu), and many other countries (see http://www.fire. uni-freiburg.de). Forecasts of fire weather conditions are by themselves useful; the information can also be used to forecast fire danger indexes and potential fire behavior characteristics.61,156,411 In Australia, television and radio are relied on extensively to alert the public of “total fire ban” days (i.e., extreme fire danger) based on current fine-fuel moisture levels, drought status, and forecasted fire weather conditions.123 Fire danger rating and fire behavior predictions can be used to judge whether evacuations are required or to assist people with preparing for the eventuality of a fire arriving.229 Evacuation routes must be established in advance, and the actual time taken to evacuate to a safe zone needs to be determined in much the same manner as a wildland firefighter uses an escape route to reach a safety zone or an urban dweller evacuates a building fire using preidentified travel routes and exit locations.
Fire-Related Injuries and Fatalities Few would argue that battling wildland fires is physically arduous work that occurs in austere conditions and includes inherent dangers. As a result, injuries and death occur infrequently but regularly. In the United States, statistics for wildland fire–related serious injuries and deaths have been maintained for decades and have provided useful data in developing protocols for safe firefighting practices. The nature of these fatalities can be broadly categorized as deaths directly by fire in burnover or entrapment situations and deaths resulting from fire suppression activities. Most fatalities in wildland fire burnover situations occur on days of extreme fire danger when people are exposed to abnormally high heat stress caused by weather or proximity to fires. Loss of life is dramatically highlighted under extreme burning conditions; however, many more people are injured than are killed by fires. One of Australia’s worst bushfire disasters occurred on February 7, 1967, when 62 people died in Tasmania.288,511 Analysis of the locations and ages of 53 individuals at the time of death are instructive (Tables 12-3 and 12-4). Most people whose bodies were found within or near houses were old, infirm, or physically disabled. More than one-half of the houses vacated by the 11 people who traveled some distance before being killed were not TABLE 12-4 Age Distribution of 53 Persons Who
Died in Tasmanian Fires, February 7, 1967
Age Group (yr) 1-25 26-50 51-75 76-88
No. in Group
Average Age (yr)
1 13 26 13
23 38 64 82
From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7 February 1967, Hobart, Australia, 1967, Government Printer.
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CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
TABLE 12-3 Location of Bodies of 53 Persons Who
PART 3 BURNS, FIRE, AND RADIATION
burned. Most of these victims would probably have survived if they had remained in their homes. Most of the 11 firefighters who died were inexperienced. Many might have survived if they had observed fire behavior and safety rules. Krusel and Petris248 investigated the circumstances surrounding the 32 civilian deaths that occurred during the 1983 Ash Wednesday bushfires in Victoria. As a result, they identified three categories of victims, suggesting ways to address the deficiencies in the manner in which individuals respond to the wildfire threat: • Victims who recognized the real threat to their safety with enough time to save their lives, but chose an ineffective survival strategy • Victims who did not recognize the real threat to their safety in time to implement an effective survival strategy • Victims who were physically incapable of implementing an effective survival strategy. Similar situations have been reported around the world. For example, during the 1993 fire season in the Tarragona Province of eastern Spain, five people were killed trying to escape from their home, built in the woods and surrounded by a fire; four of the victims were older adults and did not dare to flee until it was impossible to escape.487 In 2007, the National Wildfire Coordinating Group published an analysis of 310 wildland firefighter fatalities that occurred in the United States from 1990 to 2006.281 During this 17-year period, burnover situations constituted only the fourth most common cause of death, and the number of these incidents declined during the surveyed years. A total of 64 deaths, or 20.6%, were attributed to burnovers during this time period. By comparison, 72 deaths (23.2%) resulted from aircraft accidents, 71 deaths (22.9%) were caused by vehicle accidents, and 64 wildland firefighters (21.9%) died from heart attacks. The remaining percentages were classified as deaths resulting from falling trees, snags, or rocks (3.9%), other medical causes (2.9%), and miscellaneous causes (4.5%). Thus the top three leading causes of deaths related to wildland firefighting activity were not the result of individuals being burned over or entrapped by a wildland fire, although five firefighters were killed at a single location on the 2006 Esperanza fire in southern California.484 Reports for 2007-2009, in which 49 wildland firefighters died, showed similar trends.283 Interventions are possible to reduce the number of firefighter fatalities associated with aircraft and vehicle accidents, as well as those linked to heart attacks (Box 12-5).279,282 There have been more than 160 wildland fire suppression– related fatalities in Canada during the 70-year period between 1941 and 2010.24 Although the causes for all these firefighter
fatalities are not precisely known, certainly aircraft-related fatalities have been far more common in recent decades compared with earlier years of recordkeeping. It is much more difficult to gather accurate information regarding the incidence of minor to moderate injuries and episodes of illness among wildland firefighters. There are a number of reasons why these statistics do not exist. In general, the field draws individuals with a “can-do” attitude who are willing to work through many hardships that would cause workers in a general workforce to take time off for rest. Secondly, the vast majority of the care happens informally either on the fire lines as work continues or at base camps at temporary, low-level medical facilities where formal records are not maintained. Firefighters will often wait until they leave a fire to seek treatment from a private provider for an ongoing problem, and the injury or illness will not be tracked as a workplace-related incident. In the United States, the Bureau of Land Management has guidelines outlining the nature of burn injuries that require transport to and evaluation at a specialized burn center.237 This protocol largely corresponds to the guidelines of the American Burn Association (http://www.ameriburn.org/). By comparison, other medical protocols are region dependent. Fire suppression crews frequently have one or two medics, usually trained to the Emergency Medical Technician (EMT)-Basic level, among their members. The skill set of these medics depends on whether they are active, professional medical providers when they are not fighting wildland fires or if they maintain the certification solely for the position on the crew. Larger incidents may employ additional medical personnel to survey personnel on the fire lines or at portable medical tents/trailers in the base camp. Midlevel providers, such as paramedics, nurse practitioners, and physician’s assistants, usually staff these facilities. The availability of a medical command physician varies by region in the United States. When a firefighter requires evaluation and care outside the scope of first responders, the patient must be transported from the incident. The nature of the problem dictates if this transport requires specialized care at a trauma or burn center or if the local hospital closest to the incident can provide care. When large fires require hundreds to thousands of personnel, a small local hospital in a rural area may be overburdened by the temporary additional population. Transport protocols are determined on a regional basis and may use ground ambulances or air medical service (via rotary- or fixed-wing aircraft) depending on the nature of the incident and availability of resources.
BOX 12-5 21st-Century Common Denominators for
COMMON DENOMINATORS OF FIRE BEHAVIOR ON FATALITY FIRES
More than 20% of fatalities during wildand firefighting operations continue to concur in burnovers and entrapments. Carl Wilson’s original common denominators519 are just as important in the 21st as they were in the 20th century However, as the major causes of firefighter fatalities shift, it has suggested that additional factors need to be considered: • Firefighters are most likely to die in an aircraft accident. Before every flight, fire managers must ask, “Is this flight essential?” and “Is everyone onboard essential to the mission?” • Firefighters are nearly as likely to die in a motor vehicle accident as in an aircraft accident. Driving too fast for the conditions, failure to wear seat belts, rushing to a fire, and driving home while exhausted from firefighting kills firefighters. • Firefighters can reduce their risk for dying from heart attack on the job by staying fit, maintaining their ideal body weight, and having regular medical checkups. • Unexpected events such as falling snags, rolling rocks, downed power lines, and lightning strikes cause more than 8% of fatalities during wildland firefighting operations. Firefighters and fire managers can reduce fatalities by learning to expect these unexpected events.
A review of wildland firefighter fatality records between 1926 and 1976 shows that 145 men died in 41 fires from fire-induced injuries.339,340,519 Besides the 1949 Mann Gulch and 1990 Dude fires, large losses occurred on the 1933 Griffith Park fire in California (29 deaths and 150 others injured),174 the Blackwater fire in Wyoming in 1937 (15 deaths),75 the Pepper Hill fire in Pennsylvania in 1938 (8 deaths),413 the Hauser Canyon fire in California (11 deaths),110,432 the Rattlesnake fire in California in 1953 (15 deaths),272 the 1956 Inaja fire in California (11 deaths),412,474 the 1966 Loop fire in California (12 deaths),148 and the 1968 Canyon fire in California (8 deaths).149 Wilson’s review519 of people killed by wildfires in areas protected by other federal, state, county, and private agencies indicated 77 fire-induced fatalities in 26 fires during this same time period. The United States is not the only country to have had firefighters killed by entrapments and burnovers. For example, 25 soldiers were killed while involved in wildland firefighting operations near Lisbon, Portugal, on September 6, 1966.234 Australia has experienced a number of firefighter fatality incidents.115,234 For example, on December 2, 1998, five volunteer firefighters were killed near the town of Linton, Victoria, when the tanker they were traveling in was overrun by fire.140 From his analysis of the incidents in the United States during the period 1926 to 1976, Carl Wilson519 identified several common features associated with fatal fires: 1. Most of the incidents occurred on relatively small fires or isolated sectors of larger fires.
Wildland Fire Fatalities
Modified from Mangan R: Wildland firefighter fatalities in the U.S.: 1990-2006, National Fire Equipment System Publication PMS 841, Boise, Idaho, 2007, National Interagency Fire Center, National Wildfire Coordinating Group, Safety and Health Working Team.
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NATURE OF INJURIES AND FATALITIES Fire-related injuries and fatalities are a direct consequence of heat, flames, smoke, critical gas levels, or indirect injuries280,316 (Figure 12-34, online). Injuries and fatalities associated with wildland fires fall into one of five categories: heat (direct thermal injury, inhalation, and heat stress disorders), flames (direct thermal injury and inhalation), smoke (inhalation and mucous membrane irritation), critical gas levels (oxygen, carbon monoxide, and carbon dioxide), and indirect effects (acute and chronic medical disability and trauma). Intense fires that produce very high temperatures generally last for only a short time. The duration of intense heat increases with fuel load, being greater in a forest fire where heavy fuels452
are burning than in a grass125 or shrub fire (see Table 12-2). Temperatures near the ground are lower because radiant heat is offset somewhat by inflow of fresh air and the fact that gases of combustion rise and are carried away by convection.114 Close to the ground, within a few meters of flames reaching up to 11 m (36 feet), air temperatures may be less than 15° C (59° F) above ambient temperature. The breathing of heated air can be tolerated for 30 minutes at 93° C (199° F) and for 3 minutes at 250° C (482° F).269 Death or severe pulmonary injury occurs when these limits are exceeded. Thermal injuries of the respiratory tract frequently contribute to the clinical picture of smoke inhalation. People trapped in a fire may have no choice but to breathe flame or very hot gases. This usually injures the tissues of the upper airway and respiratory tract, most commonly the nose, nasopharynx, mouth, oropharynx, hypopharynx, larynx, and upper trachea. These injuries may result in edema that obstructs the airway and produces asphyxia or that causes tracheitis and mediastinitis. Signs of thermal injury to the airway include thermal injuries to the head, face, and neck; singed facial hair; burns of the nasal, oral, or pharyngeal mucosa; and stridor or dysphonia.312,449,528 Associated with a history of exposure to flame and hot gases in a closed space, these clinical findings strongly suggest the presence of a thermal injury to the airway. With the potential for acute airway obstruction, there is obvious urgency in establishing this diagnosis. Most experts who treat thermal injuries of the tracheobronchial tree advocate early visualization of the vocal cords by laryngoscopy and bronchoscopy.313 Bronchoscopy is a useful predictor of the clinical course and urgency of intensive care unit intervention. In addition, one report shows a significantly greater incidence of pneumonia and late mortality in people with facial burns than in those without them.524 Burns of the lower trachea are rarely reported. In fact, injuries to and beyond the carina are difficult to produce when the trachea is cannulated and hot gases are delivered in the anesthetized dog.310,527 Air has a very low specific heat and is therefore a poor conductor of thermal energy. In addition, the thermal exchange systems of the upper airway are quite efficient. The hot gas or flame is cooled sufficiently in the upper airway so that it does not burn the bronchi or more distal structures. However, although water or steam in the hot gas mixture is probably rare, it is a far more efficient conductor of heat and permits significant thermal injury to the lower trachea and bronchi. A delayed onset (2 to 24 hours after smoke inhalation) of pulmonary edema and adult respiratory distress syndrome is widely reported and should be anticipated. Heat stress169,417 occurs when air temperature, humidity, radiant heat, and poor air movement combine with strenuous work and insulative clothing to raise body temperature beyond safe limits. Sweating cools the body as moisture evaporates. When water lost through sweating is not replaced, physiologic heat controls can deregulate, and body temperature may rise, leading to heat exhaustion or heatstroke (see Chapters 10, 11, and 70). Direct contact with flames causes thermal injury, and death is inevitable with exposure for long periods. Burns may be superficial, partial, or full thickness (see Chapter 13). Immediate death results from hypotension, hyperthermia, respiratory failure, and frank incineration. As mentioned earlier, the common cause of asphyxia in wildland fire is smoke. Danger increases where smoke accumulates because of poor ventilation, as in caves, box canyons, narrow valleys, and gullies. Dense, acrid smoke is particularly irritating to the respiratory system and eyes. Excessive coughing induces pharyngitis and vomiting. Keratitis, conjunctivitis, and chemosis may make it impossible to keep the eyes open. There are concerns about the levels of oxygen, carbon monoxide, and carbon dioxide associated with wildland fires. Critical levels readily occur in a closed space and near burning or smoldering heavy fuels, but the open space associated with wildland fires usually contributes to continual mixing of air. Misconceptions or myths about lack of oxygen or excessive carbon monoxide and carbon dioxide in a wildland fire abound in the popular literature.125 Flaming combustion can be maintained only at oxygen levels that exceed 12%, a level at which life can also be supported.114,269 263
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
2. Most of the fires were innocent in appearance prior to the “flare-ups” or “blow-ups.” In some cases, the fatalities occurred in the mop-up stage. 3. Flare-ups occurred in deceptively light fuels. 4. Fires ran uphill in chimneys, gullies, or on steep slopes. 5. Suppression tools, such as helicopters or air tankers, can adversely modify fire behavior (helicopter and air tanker vortices have been known to cause flare-ups). Many firefighters were surprised to learn that tragedy and near-miss incidents occurred in fairly light fuels, on small fires, or on isolated sectors of large fires, and that the fire behavior was relatively quiet just before the incident, even in the cases involving aircraft.149,161,215 Many have been led to believe that it is the conflagration or large, high-intensity crown fire in timber and heavy brush that traps and kills firefighters. Yet, with some exceptions, most fires were innocent appearing just before the fatal moment. Case studies of wildland firefighter fatality incidents from other regions of the world suggest similar patterns and circumstances—for example, the 25 fatalities at Puerto Madryn, Argentina, on January 21, 1994164; 10 fatalities in the Sabie district of the Mpumalanga Province of South Africa in 1994165; and 5 fatalities associated with three different incidents that occurred in Portugal during the 1999 and 2000 fire seasons.492 Wildland firefighter fatalities have been reported in Italy, Spain, Portugal, and Croatia in the last decade.489,491 Wilson concluded that the hairline difference between fatal fires and near-fatal fires was determined by the individual’s reaction to a suddenly critical situation. Escapes were due to luck, circumstances, advance planning, a person’s ability to avoid panic, or a combination of these factors. Frequently, poor visibility and absence of concise fire information threatened survival opportunities by creating confusion and panic. For many years, Wilson’s findings were summarized in a popular booklet, published initially by the USDA Forest Service and in later years by the National Wildfire Coordinating Group.338 This information has now been incorporated into the 2010 edition of the Incident Response Pocket Guide, published by the National Wildfire Coordinating Group.346 The British Columbia Forest Service found many of the same factors identified by Wilson in their investigation of a number of close calls or near misses that occurred during the 1994 fire season.50 Although there have been few wildland firefighter fatalities in Canada due to entrapments or burnovers,36,463 those that have occurred are also in alignment with Wilson’s findings.60 Most fatality fires are the result of a temporary escalation in fire spread, an increase in flame dimensions, crowning and spotting activity, or the development of large fire whirls, often occurring suddenly and with very little warning. A gentle surface fire will rapidly develop into a high-intensity fire. This could occur, for example, as a result of thunderstorm downdraft winds,125,411 a change in fuel types,50 fire-whirl development upon the fire reaching a ridgeline with an opposing gradient wind,144 or a “slope reversal” (e.g., fire slowly backs down a northerly aspect, crosses the drainage, and then rapidly spreads up the southfacing slope),388 such as documented with time-lapse photography on the 1979 Ship Island fire in central Idaho.336 As the moisture content of dead and live fuels decreases, fires become increasingly more responsive to slight changes in wind strength and slope steepness. Once “critically” dry levels are reached, fire behavior becomes exceedingly unstable.28,85,269
PART 3 BURNS, FIRE, AND RADIATION
With continued in-drafts of air that feed the flames, a fresh source of oxygen is usually present. Even mass fires, in which large tracts of land are burning, rarely reduce oxygen to hazardous levels. Low oxygen levels may occur, however, where there is little air movement, such as in caves or mine shafts (Figure 12-35) or in burned-over land that continues to smoke from smoldering fuels. Concentrations of carbon monoxide exceeding 800 parts per million (ppm) can cause death within hours. Most fires produce small quantities, but atmospheric concentrations rarely reach lethal levels because of air movement. High concentrations appear to be associated with smoldering combustion of heavy fuels, such as fallen trees or slash piles, and carbon monoxide may also collect in low-lying areas or underground shelters (e.g., root cellars).116 Outdoors, the danger lies in continual exposure to low concentrations that can increase blood carboxyhemoglobin levels. Prolonged exposure affects the central nervous system, resulting in headache, impaired judgment, progressive lethargy, decreased vision, and other psychomotor deficits.519 Carbon monoxide levels of 50 ppm were measured close to a prescribed burn in grass.143 In another estimate, concentrations of 30 ppm were found roughly 61 m (200 feet) from the fire front. Studies on the 1974 Deadline and Outlaw forest fires in Idaho showed that firefighters were exposed to levels above the standards proposed by the National Institute of Occupational Safety and Health (35 ppm over an 8-hour period).465 However, more recent measurements of carbon monoxide levels and particulates made on wildfires between 1992 and 1995394 indicate that wildland firefighters are seldom exposed to smoke that exceeds the Occupational Safety and Health Administration’s permissible exposure limits.395 Decreased ambient oxygen may contribute to hypoxia and the overall picture of smoke inhalation (Table 12-5). This mechanism is at least variably operant. When standing gasoline was ignited in a closed bunker, the fire self-extinguished, whereas the ambient oxygen level remained at 14%, a survivable level.310 Injecting burning gasoline or napalm into bunkers produced nearly complete and prolonged exhaustion of ambient oxygen. Conflicting
TABLE 12-5 Human Response to Decreased
Ambient Oxygen at Sea Level
Ambient Oxygen (%)
Human Response
20.9 16-18 12-15
Normal function Decreased stamina and capacity for work Dyspnea with walking; impaired coordination; variable impaired judgment Dyspnea at rest; consciousness preserved; impaired judgment, coordination, and concentration Loss of consciousness; death without prompt reversal Death in 6 to 10 minutes
10-12 6-8 <6
data make it difficult to classify definitively situations in which decreased ambient oxygen and subsequent hypoxia of exposed individuals contribute to the clinical picture of smoke inhalation. Studies in which ambient oxygen was measured by scientists did not show significant depletion at the scene of the fire.209 Few data are available on levels of carbon dioxide around wildland fires. Although it may be produced in large quantities, it apparently never reaches hazardous concentrations, even in severe fire situations.114,269 The quantity of burning fuel and type of topography affect levels of oxygen and toxic gases. Danger is greater in forest fires where heavy fuels burn over long periods of time than in quickmoving grass and shrub fires. Topography has a major influence: caves, box canyons, narrow canyons, gulches, and other terrain features can trap toxic gases or hinder ventilation, thereby preventing an inflow of fresh air. Although most fatalities result from encounters with smoke, flames, and heat, critical gas levels can induce handicaps sufficient to render the victim more vulnerable to other hazards. Whereas respirators285 are not routinely used on wildland fires or on wildland–urban interface fires, they could possibly play a role in the future as a means of protection against airborne toxic materials.
WILDLAND FIRES, AIR TOXINS, AND HUMAN HEALTH
FIGURE 12-35 USDA Forest Service Ranger Ed Pulaski led 42 men and two horses to this mine tunnel near Placer Creek in northern Idaho to seek refuge from the 1910 firestorm. One man failed to get into the tunnel and was burned beyond recognition. All the men in the tunnel were evidently unconscious for a period of time. Five died inside, apparently from suffocation. The remainder of the crew was evacuated to the hospital in Wallace, where all recovered. For a fuller account of this incident, see reference 384. (Courtesy USDA Forest Service; photo by J.B. Halm.)
264
In the United States each year, about 80,000 firefighters are involved with suppression activities on about 70,000 wildland fires that burn an average of more than 0.8 million hectares (2 million acres). In 1988, more than 2 million hectares (5 million acres) of land were burned, with a total combined suppression cost exceeding $600 million. The firefighting effort has another cost that has not been quantified: the effect of smoke on firefighter health and productivity. Over the 4 months of the Greater Yellowstone Area fires, about 40% of the 30,000 medical visits made by wildland firefighters were for respiratory problems. More than 600 firefighters required subsequent medical care. In the Happy Camp area during the Klamath fire complex in California in 1987, ambient concentrations of carbon monoxide measured as high as 54 ppm on a volume basis.497 A better understanding of the long-term effects of wildland fire smoke on people is clearly needed, although “firefighters just keep coming back year after year,” notes Dr. Brian Sharkey,422 a wildland firefighter health and safety specialist with the USDA Forest Service’s Missoula Technology and Development Center (MTDC) who coordinated an 8-year study of the health hazards of smoke on wildland firefighters.418,420 Combustion of wildland fuels produces many by-products in a variety of concentrations, depending on the type of fuel and the nature of the fire characteristics.357 The impact of these byproducts is very difficult to assess. Short-term studies have been inconclusive, and long-term studies are enormously complex and essentially absent from the literature. Completion of a prospective epidemiologic study would be highly informative. The combustion products of concern include these classes of materials: • Particulate matter • Polynuclear aromatic hydrocarbons
“camp crud,” especially late in the fire season, suggest a classic infectious outbreak pattern. Other infectious outbreaks that have spread through the wildland fire community include a series of methicillin-resistant Staphylococcus aureus (MRSA) outbreaks in fire camps during the 2008 and 2009 seasons in the United States.264,482,483 Infectious illness shared among firefighters is likely promoted by a variety of factors, including close working and living proximity, challenged immune conditions resulting from strenuous work and nutritional demands, hygiene conditions dictated to some degree by the environment, and potentially firefighters’ access to seasonal vaccinations. Identifying possible interventions to decrease the burden from infectious illness would be beneficial to improving firefighter wellness and productivity. The epidemiologic data collected for wildland firefighting are very sparse, either for analysis of short-term outbreak situations or long-term health and wellness.
Wildland–Urban Interface Fire Survival Principles and Techniques History has demonstrated repeatedly that individuals simply were not prepared to make correct choices of survival alternatives under stressful situations. At least 437 wildland firefighters were killed in the United States between 1910 and 2009 as a direct result of a burnover or entrapment by a free-burning wildfire.339,281,283 Overconfidence, complacency, ignorance, bad habits, lack of preparation, poor decision making, and a whole host of other human factors quickly lead to improper and unsafe actions during fire emergencies.356,504,519 “Learning from mistakes” in these settings is not a reasonable education strategy because second chances are frequently unavailable in the wildland firefighting profession. The USDA Forest Service organized a task force in 1957 to “study how we might strengthen our ways and means of preventing firefighting fatalities.”309 A major recommendation was to adopt service-wide standard firefighting orders. Ten standard firefighting orders287,308 summarize the fundamental principles of safety on the fire line (Box 12-6). Although these were written for wildland firefighters, they apply to all people working, living,
BOX 12-6 Ten Standard Firefighting Orders Adapted
for the General Public
1. Keep informed of fire weather conditions, changes, and forecasts and how they may affect the area where you are located. 2. Know what the fire is doing at all times through personal observations, communication systems, or scouts. 3. Base all actions on current and expected behavior of the fire. 4. Determine escape routes and plans for everyone at risk, and make certain that everyone understands routes and plans. 5. Post lookouts to watch the fire if you think there is any danger of being trapped, of increased fire activity, or of erratic fire behavior. 6. Be alert, keep calm, think clearly, and act decisively to avoid panic reactions. 7. Maintain prompt and clear communication with your group, firefighting forces, and command and communication centers. 8. Give clear, concise instructions, and be sure that they are understood. 9. Maintain control of the people in your group at all times. 10. Fight fire aggressively, but provide for safety first. (Nonqualified or untrained and improperly dressed or equipped persons should engage in firefighting operations only when it is absolutely necessary to assist injured persons. Wildland firefighting is a physically demanding task and should not be attempted by persons who are not in good physical condition.)
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CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
• Carbon monoxide • Aldehydes • Organic acids • Semivolatile and volatile organic compounds • Free radicals • Ozone • Inorganic fraction of particles Large variances are associated with the development of smoke combustion products and exposure to the materials of concern.497 Ward and colleagues498 indicated that the toxicity of the combination of combustion products depends on the relative concentrations of the individual compounds, as well as the overall concentration and length of exposure. Individual toxicities are associated with many of the compounds found in smoke. The combined toxicity of these substances is not known. A detailed set of studies is being carried out to provide answers so that risk management options can be exercised. One of these studies suggested that wildland firefighters experience a small cross-seasonal decline in pulmonary function and an increase in several respiratory symptoms.407 Eye irritation, nose irritation, and wheezing were associated with recent firefighting. The strenuous work of fighting or escaping a fire magnifies chronic illnesses, age disabilities, exhaustion, and cardiovascular instability. Common trauma is induced by falling trees or limbs, rolling logs or rocks, vehicular accidents, poor visibility, panic, falling asleep in unburned fuels that later ignite, and leaving the safety of buildings and vehicles. Cuts, scrapes, scratches, lacerations, fractures, and eye injuries (foreign particles, smoke irritation, sharp objects) are other common afflictions. Poison oak, poison ivy, stinging insects, and poisonous snakes are additional sources of trauma during wildland fires. To avoid fire-related injuries and fatalities, a person must keep attuned to mental and physical stress levels and be aware of cumulative effects.417 Ignorance of this simple principle is disastrous. Accurate statistics have not been collected to document the frequency and nature of injuries and illnesses over the course of different fire seasons. The common afflictions listed above are inherent to completing strenuous work under adverse conditions. Overall, the infrequency of major traumatic injuries speaks to the success of firefighters’ adhering to established safety protocols. A range of occupational and overuse injuries consistently emerges over the course of the fire season. Blisters and foot problems occur frequently early in the season, especially if offseason fitness has fallen by the wayside. As with other soft-tissue injuries, these can be complicated if not promptly addressed with standard first aid. Muscle strains, back problems, and tendinitis often follow particularly intense work periods. These maladies are best prevented by firefighters’ maintaining off-season fitness regimens to endure the physical rigors of firefighting.264 Research and development carried out by the MTDC of the USDA Forest Service have led to invaluable contributions regarding the health and safety of wildland firefighters, including the following: • Optimal work-rest patterns • Firefighter nutrition and hydration requirements and regimens • Heat stress and uniform/personal protective equipment design • Tool testing to optimize firefighter efficiency • The relationship between firefighter nutrition and immune function These studies have informed U.S. firefighting protocols to improve productivity and firefighter safety.168,419,421,423,424 The informal surveys conducted of wildland firefighter health demonstrate a pattern of increasing respiratory symptoms over the course of the fire season. This pattern has become common enough that firefighters have coined a term—”camp crud”—to describe the range of symptoms shared throughout the camps. The severity and frequency of symptoms can have legitimate safety and productivity consequences. Smoke exposure has been considered as one factor contributing to the frequency of respiratory illness44 and decreased respiratory function over the course of the fire season,198 but there is no consensus on how interventions could be feasibly instituted to reduce smoke exposure in wildland fire suppression. Regular occurrences of the flulike
PART 3 BURNS, FIRE, AND RADIATION
Lookout(s)
Hazard (Fireline hazards such as fire entrapment or falling or rolling objects are inherent in the wildland fire environment)
Communication(s)
X
Escape routes
Firefighters
Route 1
Route 2
Safety zone(s)
FIGURE 12-36 Concept of the LCES wildland fire safety system. (From Gleason P: LCES: The key to safety in the wildland fire environment, Fire Manage Notes 52:9, 1991.)
or traveling near wildland fires and are adapted here to remind emergency medical personnel, wildland homeowners, and recreationists of safety precautions to be taken around wildland fires. Much of this material is summarized in the handy Incident Response Pocket Guide.346
LCES: THE KEY TO SAFE PROCEDURES IN WILDLAND FIRE ENVIRONMENTS LCES stands for lookout(s), communication(s), escape routes, safety zone(s).203 These variables are key components in evaluating the threat posed by fire-line hazards and determining the best course of action (Figure 12-36). Some fire management agencies have added an “A” to LCES, thus LACES, for a variety of meanings—attitude, awareness, and anchor points.251,461 The Australasian Fire Authorities Council has, for example, adopted the LACES wildland fire safety acronym with the proviso that the “A” stands for awareness.46 Most Canadian fire management agencies have taken the “A” in LACES to connote anchor point.460 The importance of an anchor point is quite vividly highlighted in the video A Firefighter’s Return From a Burnover: The Kelly York Story, which details the severe burn injuries received by a volunteer firefighter while attempting to suppress a grass fire in central California during the 1995 fire season.177 As Australian fire management and research pioneers Harry Luke and Alan McArthur269 state in their seminal reference book Bushfires in Australia, fire suppression “must at all times start from an anchor point.” The wildland fire environment’s basic hazards are lightning, volcanoes, falling of fire-weakened trees and snags, rolling rocks and logs, entrapment by free-burning fires, respirable particulates, air toxins, and heat stress. When these hazards exist, there are two options: 1. Do not enter the environment, or 2. Adhere to safe procedures according to LCES. LCES should be viewed from a “systems” point of view, stressing their interdependence. For example, the best safety zone is worthless if the escape route does not offer access at the point of need. People must be familiar with the LCES plan well before it is needed. In addition, the nature of wildland fires dictates that LCES be redefined in pace with changing conditions. The LCES wildland fire safety system is implemented as follows: • Lookout(s): Fixed lookouts or roving lookouts must be where both the hazard and the people can be seen. A lookout is trained to observe the wildland fire environment and to recognize and anticipate changes in fire behavior. 266
When the hazard becomes a potential threat or danger, the lookout relays this information so people can depart for the safety zone. • Communication(s): Communication refers to alerting people to the approaching or pending hazard. Promptness and clarity are essential. • Escape routes: These paths lead from a currently threatened position to an area free from danger. More than one escape route must be available. Escape routes are probably the most elusive component of LCES because they change continuously. Timely access to safety zones is the most important component.63 Research on wildland firefighter travel rates27,56,97,408 suggests that, although civilians could momentarily advance at a rate in excess of what most wildland fires are capable of achieving, even the most fit individuals would not be able to sustain such a pace for more than a few minutes before being burned over by an advancing fire, especially on steep slopes—escaping uphill is thus a very questionable concept, unless a safety zone is known to be very nearby. Furthermore, some fire researchers believe there is a common tendency to overestimate the distance to a fire when observing through the forest, which may lull firefighters into thinking there is more time available for an orderly exit than is actually the case.124 • Safety zone(s): In a safety zone, threatened persons find adequate refuge from danger. The size of the safety zone must be sufficient to provide protection from flames, radiant heat, convective heat, falling trees and snags, and rolling rocks and logs. The necessary size varies with changes in fuels, topography, wind conditions, and fire intensity. The question of whether a previously burned area will serve as a safety zone depends not only on the size of the area but also on the degree of completeness of fuel consumption, both vertically and horizontally.96,366 What constitutes a safety zone varies widely among individuals.440 Based on theoretic consideration for radiation emitted from a “wall of flame” under idealized conditions (e.g., level terrain, steady-state fire conditions),93 it has been suggested, from the standpoint of flame radiation, that a safety zone should be large enough that the distance between the human occupants and flame front be at least four times the maximum expected flame height at the edge of the safety zone95 (Table 12-6). It should be emphasized that in deriving this rule of thumb, several assumptions had to be made that could ultimately limit the usefulness of this simple guide,451 although some field verification has been accomplished.94 Furthermore, both the modeling and resultant TABLE 12-6 Minimum Safety Zone Separation
Distances and Sizes (Circular Shape) in Relation to Flame Height*
Flame Height
Separation Distance
Area†
Meters
Feet
Meters
Feet
Hectares
Acres
2 5 10 20 40 60
6.5 16 33 66 128 262
8 20 40 80 160 240
26 64 132 264 512 1048
0.02 0.13 0.5 2.0 8 18
0.05 0.31 1.2 5.0 20 45
*For a single person on flat topography based on the “four-times-flame-height” rule of thumb for radiant heat only (i.e., no convection) and no allowance for flame impingement or other fire line hazards.93,95 It is assumed that the person is standing upright and is properly clothed, including headgear and gloves. † Assuming the area of a circle is equal to approximately 3.14159 times the square of the separation distance, where the separation distance is deemed to be the radius of a circle. For perspective, a typical North American ice hockey rink is 0.16 hectare (0.39 acre) in size, whereas Canadian and American football fields are about 0.6 hectare (1.5 acre) and 0.4 hectare (1.1 acres) in size, respectively. In turn, the maximum sizes of outdoor soccer and rugby fields would be approximately 0.8 hectare (2.0 acres) and 1.0 hectare (2.5 acres), respectively. A full-size basketball court is about 0.04 hectare (0.1 acre) in size.
EIGHTEEN “WATCH OUT!” SITUATIONS IN THE WILDLAND FIRE ENVIRONMENT The following list of 18 “Watch Out!” situations, adapted from the wildland fire community’s safety guidelines,306,311,429 are of particular relevance to emergency medical personnel and wildland users; each of these situations has come about as a result of one or more wildland firefighter fatalities: 1. You are moving downhill toward a fire, but must be aware that fire can move swiftly and suddenly uphill. Constantly observe fire behavior, fuels, and escape routes, assessing the fire’s potential to run uphill. 2. You are on a hillside where rolling, burning material can ignite fuel from below. When below a fire, watch for burning materials, especially cones and logs, that can roll downhill and ignite a fire beneath you, trapping you between two coalescing fires. 3. Wind begins to blow, increase, or change direction. Wind strongly influences fire behavior, so be prepared to respond to sudden changes. 4. The weather becomes hotter and drier. Fire activity increases, and its behavior changes more rapidly as ambient temperature rises and relative humidity decreases.
5. Dense vegetation with unburned fuel is between you and the fire. The danger in this situation is that unburned fuels can ignite. If the fire is moving away from you, be alert for wind changes or spot fires that may ignite fuels near you. Do not be overconfident if the area has burned once because it can reignite if sufficient fuel remains. 6. You are in an unburned area near the fire where terrain and cover make travel difficult. The combination of fuel and difficult escape makes this dangerous. 7. Travel or work is in an area you have not seen in daylight. Darkness and unfamiliarity are a dangerous combination. 8. You are unfamiliar with local factors influencing fire behavior. When possible, seek information on what to expect from knowledgeable people, especially those from the area. 9. By necessity, you have to make a frontal assault on a fire with tankers. Any encounter with an active line of fire is dangerous because of proximity to intense heat, smoke, and flames, along with limited escape opportunities. 10. Spot fires occur frequently across the fire line. Generally, increased spotting indicates increased fire activity and intensity. The danger is that of entrapment between coalescing fires. 11. The main fire cannot be seen, and you are not in communication with anyone who can see it. If you do not know the location, size, and behavior of the main fire, planning becomes guesswork, which is an unfavorable response. 12. An unclear assignment or confusing instructions have been received. Make sure that all assignments and instructions are fully understood. 13. You are drowsy and feel like resting or sleeping near the fire line in unburned fuel. This may lead to fire entrapment. No one should sleep near a wildland fire. If resting is absolutely necessary, choose a burned area that is safe from rolling material, smoke, reburn, and other dangers or seek a wide area of bare ground or rock. 14. Fire has not been scouted and sized up. 15. Safety zones and escape routes have not been identified. 16. You are uninformed on strategy, tactics, and hazards. 17. No communication link with crew members or supervisors has been established. 18. A line has been constructed without a safe anchor point. Humorous artwork has even been developed to help illustrate or visualize the 10 standard fire orders and 18 “Watch Out!” situations.317
FIFTEEN STRUCTURAL “WATCH OUT!” SITUATIONS FOR THE WILDLAND–URBAN INTERFACE Continuing development creates ever more wildland–urban interface; therefore fires are tending to occur more often in that interface. These 15 structural “Watch Out!” situations have been defined to increase awareness of structural fire dangers:466 1. Access is poor (e.g., narrow roads, twisting, single lane with inadequate turning). 2. Load limits of local bridges are light or unknown; the bridges are narrow. 3. Winds are strong, and erratic fire behavior is occurring. 4. The area contains garages with closed, locked doors. 5. You have an inadequate water supply to attack the fire. 6. Structure windows are black or smoked over. 7. There are septic tanks and leach lines. These are found in most rural situations. 8. A house or structure is burning with puffing rather than steady smoke. 9. Inside and outside construction of structures is wood with shake-shingle roofs. 10. Natural fuels occur within 9 m (30 feet) of the structures. 11. Known or suspected panicked individuals are in the vicinity. 12. Structure windows are bulging, and the roof has not been vented. 13. Additional fuels can be found in open crawl spaces beneath the structures. 267
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
radiation-based guide do not consider flame impingement or horizontal reach into a clearing, fire whirls, or any allowance for convective heat transfer, which will be significant under windy conditions in sloping terrain.125,401 Obviously, further study, including field measurements, and development are warranted (e.g., allowance for convective heating on a slope), which is indeed the case.90 Nevertheless, while acknowledging these limitations, this rule of thumb has been incorporated into existing operational guidelines,346 training course material,463 and computer programs.41 According to Butler and Forthofer,98 additional modeling (e.g., radiation on a sloping surface), subsequent observations, and other field measurements support “four times flame height” for minimum safety zone size, although research is continuing on this matter.91 While serving as the ignition boss during the International Crown Fire Modelling Experiment (ICFME) in the Northwest Territories,18,445 one of the authors (MEA) was able to informally evaluate the Butler and Cohen93,95 safety zone guideline. Based on observations and the experience of being on the backside or upwind edge of all the ICFME experimental crown fires,447,457 the four-times-flame-height rule of thumb seems to be reasonably valid. As Butler and Forthofer98 point out, “It’s important to realize that this should be considered a minimum—meaning that in all cases larger is better.” In using Butler and Cohen’s rule of thumb93,95 for safety zones or in turn Table 12-6, the logical question is: How does one go about estimating flame height in advance of a fire’s occurrence? On the basis of various fire behavior observations and various analyses, we can say with some degree of certainty that the maximum flame heights in grasslands, shrublands, and hardwood stands would vary, depending on the burning conditions, from about 2 to 10 m (7 to 33 feet). Thus a separation of at least 40 m (130 feet) should be adequate in most fuel types that do not contain conifer trees. The average flame height of crown fires in conifer forests is generally 2 to 2.5 times the stand height.447 Any area smaller than a safety zone should be regarded as a possible “survival zone” or site. Unfortunately, no quantitative description of what constitutes a survival zone presently exists. The FPInnovations–Feric Wildland Fire Operations Research Group (http://fire.feric.ca) and the University of Alberta are currently engaged in a project to better define the criteria for survival zones in wildland fires.25,26 Nevertheless, specific case study examples (e.g., 1937 Blackwater fire in Wyoming, 1958 Wandilo fire in South Australia, and 1990 Dude fire in Arizona) suggest that survival is possible in relatively small areas even when exposed to a highly hostile thermal environment provided a person maintains a prone position and uses every possible bit of protection against radiation, convection, and direct flame contact. Movement within the survival zone may also be possible and necessary as the flame front surrounds the site.
PART 3 BURNS, FIRE, AND RADIATION
14. Firefighting is taking place in or near chimney or canyon situations. 15. Elevated fuel or propane tanks are present. These are also known as the “Wildland–Urban Watch Outs!”346
TAKING REFUGE IN VEHICLES, BUILDINGS, AND PROTECTIVE FIRE SHELTERS USED BY WILDLAND FIREFIGHTERS The radiant energy of a fire, although highly intense at a given location, typically lasts for only a short time. Because radiant heat travels in straight lines, does not penetrate solid substances, and is easily reflected, seeking refuge in vehicles, buildings, or protective fire shelters should be viewed as a lifesaving solution. Vehicles Wildland firefighters have survived severe fire storms or the passage of fire fronts by taking refuge in vehicles.278,289,361,362 Sadly, there are reported cases in which civilians would have survived or avoided serious injury had they remained in their vehicles.234,358 Bereska65 has indicated that he and two others were forced to drive a 3 4 -ton Dodge 4 × 4 truck at a moderate speed (25 to 30 km/hr or 16 to 19 mph) through the flame front of a grass fire during a prescribed burning operation carried out in northcentral Alberta in early April 1980. Winds at the time of the incident were light (less than 12 km/hr [7 mph]), and the flames, although high (3 to 4 m [10 to 13 feet]), were not deep (1 to 2 m [3 to 7 feet]). He remembers “it got very hot instantly and as we came out of the flames we opened the windows and appreciated the cool fresh air.” The following three U.S. case histories serve as examples of intense burning situations in which lives were saved because people stayed inside vehicles while the fire front passed by their location:429 • In 1958, a veteran field section fire warden and two young men were fighting forest fires that burned in heavy fuels near the Bass River State Forest in southern New Jersey. A 90-degree wind shift transformed the flank fire into a broad head fire, with the advancing flames reaching up to 12 m (40 feet) in height. The men entered their vehicle, a Dodge W300 Power Wagon, which stood in the middle of a 4-m (13-foot) wide sand road. Simultaneously, the engine and radio failed. The fire warden repeatedly admonished the crewmen, who wished to flee, to stay in the truck. Subsequently, the truck was rocked violently by convection currents and microclimatic changes generated by the flames. The men could neither see nor breathe because of smoke, and the cab began to fill with sparks that ignited the seat. The men stayed with the truck for only 3 or 4 minutes during passage of the head fire, but they indicated later that the interval involved seemed more like 3 or 4 hours. At the first opportunity, all of them left the vehicle on the upwind side and crouched beside it to escape the searing heat and burning seats. The warden proceeded to burn his hand severely while disposing of a flaming gas can located in the truck bed. Although the young men escaped virtually unscathed, the older man suffered lung damage and remained on limited duty for 5 years. He has since recovered completely and subsequently retired. • In a 1962 California Division of Forestry fire in Fresno County, three men, followed by a flank fire that had turned into a head fire, raced back to their truck only a few feet ahead of the flames. The truck would not restart. After the main body of flames passed over the vehicle, the men jumped out to breathe because the truck was burning. Almost completely blinded by smoke and heat, they stumbled headlong into matted fuels, and two received first- and second-degree burns. One man was not burned but had to be treated for smoke inhalation. The truck was a loss. • In 1976 a firefighter died while fighting a grass fire near the town of Buhler in Reno County, Kansas. A flashover occurred from buildup of gases on the lee side of a windbreak. A fire truck was caught in the flashover, and the firefighter working from the back of the vehicle ran and 268
was killed. Although the truck burned, the driver was not seriously hurt. Sitting in a vehicle during a passing fire front is often perilous, but when a person is trapped, it is almost certain doom to attempt escape by running from the fire. The preceding case histories illustrate a few facts that, if remembered, may prevent panic-like reactions: • The engine may stall and not restart. • The vehicle may be rocked by convection currents. • Smoke and sparks may enter the cab. • The interior, engine, or tires may ignite. (Tires exploded during the Crank fire burnover in California in August 1987 involving several wildland fire engines.334 This is obviously unsettling in an already stressful situation that could lead to panic-like reactions.) • Temperatures increase inside the cab because heat is radiated through the windows. • Metal gas tanks and containers rarely explode. • If it is necessary to leave the cab after the fire has passed, keep the vehicle between you and the fire. The type of vehicle determines the amount of protection afforded. Two travelers died in a fire in 1967 in Tasmania, Australia, when they were caught in a canvas-topped vehicle.269 A later fire in Australia led to further research on various vehicles’ protection and the explosiveness of gasoline tanks. In 1969 near Lara, Victoria, Australia, a fast-moving grass fire crossed a fourlane expressway.193,269 Several cars stopped in the confusion of smoke and flames. Seventeen people left the safety of their cars and perished. Six people stayed inside their vehicles and survived, even though one car ignited. Investigations were carried out by the Forest Research Institute (now the Commonwealth Scientific and Industrial Research Organization [CSIRO], Division of Forestry and Forest Products) in Canberra, Australia, to collect accurate data and dispel the misconceptions that make people flee a safe refuge if trapped by fire.114 Cars were placed between two burning piles of logging slash to study a car’s ability to shield against radiation.269 The test was a hotter, longer-duration fire than would normally be encountered in a wildland setting. Car bodies halved the external radiation transmitted at the peak of the fire, but a person inside would have suffered severe burns to bare skin. Although air temperatures inside the car did not reach hazardous levels until well after the peak radiation had passed, smoke from smoldering plastic and rubber materials would have caused discomfort and made the car uninhabitable. In this study, metal gasoline tanks did not explode, whether intact on cars or separated and placed on a burning pile of slash. Apparently, when tanks are sealed, the space above the liquid contains a mixture too deficient in oxygen vapor to support an explosion. Several years ago, Cheney114,116 offered the following general advice for survival when in a car and trapped by fire: • If smoke obstructs visibility, turn on the headlights and drive to the side of the road away from the leading edge of the fire. Try to select an area of sparse vegetation offering the least combustible material. • Attempt to shield your body from radiant heat energy by rolling up the windows and covering up with floor mats or hiding beneath the dashboard. Cover as much skin as possible. • Stay in the vehicle as long as possible. Unruptured gas tanks rarely explode, and vehicles usually take several minutes to ignite. • Grass fires create about 30 seconds (maximum) of flame exposure, and chances for survival in a vehicle are good. Forest fires create higher-intensity flames lasting 3 to 4 minutes (maximum) and lowering chances for survival. Staying in a vehicle improves chances for surviving a forest fire. Remain calm. • A strong, acrid smell usually results from burning paint and plastic materials, caused by small quantities of hydrogen chloride released from breakdown of polyvinyl chloride. Hydrogen chloride is water soluble, and discomfort can be relieved by breathing through a damp cloth. Urine is mostly water and can be used in emergencies.
Buildings The decision to evacuate a house or remain and defend it is not an easy one. Fire services generally prefer that residents evacuate the threatened area so that agencies can concentrate on protecting structures. Authorities also agree that evacuation of older adults and very young, infirm, and fearful people is usually a good idea.248 People should evacuate only if it can be accomplished safely, well in advance of any danger. If not, then it is
BOX 12-7 Guidance for People in a Vehicle During a
Wildland Fire
Advance Preparation • Always carry woolen blankets, leather gloves, and a supply of water in the vehicle. • Dress in suitable nonsynthetic clothing and shoes, including a hat. Encountering Smoke or Flames • If you see a wildland fire in the distance, carefully pull over to the side of the road to assess the situation. If it is safe to do so, turn around and drive to safety. • If you have been trapped by a wildland fire, find a suitable place to park the car and shelter from the fire. Positioning Your Car • Find a clearing away from dense bush and high ground fuel loads. • Where possible, minimize exposure to radiant heat by parking behind a natural barrier, such as a rocky outcrop. • Position the car facing toward the oncoming fire front. • Park the car off the roadway to avoid collisions in poor visibility. • Do not park too close to other vehicles. Inside Your Car • Stay inside your car—it offers the best level of protection from radiant heat as the fire front passes. • Turn headlights and hazard warning lights on to make the car as visible as possible. • Tightly close all windows and doors. • Shut all the air vents, and turn the air conditioning off. • Turn the engine off. • Get down below the window level into the foot wells, and shelter under woolen blankets. • Drink water to minimize the risks of dehydration. As the Fire Front Passes • Stay in the car until the fire front passes and the temperature has dropped outside. • Fuel tanks are unlikely to explode. • As the fire front approaches, the intensity of the heat will increase, along with the amount of smoke and embers. • Smoke gradually gets inside the car, and fumes will be released from the interior of the car. Stay as close to the floor as possible to minimize inhalation, and cover mouth with a moist cloth. • Tires and external plastic body parts may catch on fire. In more extreme cases, the car interior may catch on fire. • Once the fire front has passed and the temperature has dropped, cautiously exit the car. (Be careful—internal parts will be extremely hot.) • Move to a safe area such as a strip of land that has already burned. • Stay covered in woolen blankets, continue to drink water, and await assistance. Modified from Australasian Fire Authorities Council: Guidelines for people in cars during bushfires, East Melbourne, Victoria, Australia, 2008, AFAC.
safer to shelter in place. Several principles should guide the evacuation decision:501 • A fire within sight or smell is a fire that endangers you. • Occupants are often quite effective in preventing their house from burning down. The more they understand the dynamics of fire behavior and have prepared for a fire occurrence, the easier and safer this task will be. • Evacuation when fire is close is too late; evacuation must only be done when it is certain that it is safe to do so. • More people are injured and killed in the open than in houses. • Learn beforehand about community refuges. • Evacuate only to a known safe refuge only when it is safe to do so. Whether people can find refuge in buildings depends on construction materials, house design detail, and proximity of fuels around the structure. If a home is constructed amid flammable vegetation, plans and procedures to safeguard the home and its occupants are essential. A building usually offers protection while the fire passes, even if it ignites during or after the fire’s passage, because it shields against radiant heat and smoke. After the fire passes, it may be necessary to exit if the building is burning. Either attempt to suppress the fire or to move onto burned ground. Numerous wildfire case histories from Australia, starting with the 1939 Black Friday fires in Victoria,258 demonstrate that homes provide safe havens.248,269,358,517 In 1967 in Tasmania, 21 people left their houses as fire approached. All died, and some were within a few meters of the buildings. Many houses did not burn and would have been refuges. When taking refuge in a building, give people useful jobs, such as filling vessels with water, blocking cracks with wet blankets, and tightly closing windows and doors. If possible, assign lookouts to keep watch for spot fires on and within the building throughout the fire event. Before fire approaches the house, plan to have taken the following precautions:257,429 • If you plan to stay, evacuate your pets and livestock and all family members not essential to protecting the home well in advance of the fire’s arrival. • Be properly dressed to survive the fire. Wear long pants and boots, and carry for protection a long-sleeved shirt or jacket made of cotton fabrics or wool. Synthetics should not be worn because they can ignite and melt. Wear a hat that can offer protection against radiation to the face, ears, and neck areas. Wear leather or natural fiber gloves and have a handkerchief handy to shield the face, water to wet it, and safety goggles, if possible. • Remove combustible items from around the house, including lawn and poolside furniture, umbrellas, and tarp coverings. If they catch fire, the added heat could ignite the house. • Ensure that anything that might be tossed around by strong fire-induced winds is secured (e.g., sheet metal, lumber, and plywood). • Ensure that the areas around any external propane tanks are fuel free for a considerable distance. Ensure that the tanks are properly restrained and the pressure relief value is directed away from buildings and access ways. • Close outside attic, eave, and basement vents to eliminate the possibility of sparks blowing into hidden areas within the house. Close window shutters. • Place large plastic trash cans or buckets around the outside of the house and fill them with water. Soak burlap sacks, small rugs, and large rags to use in beating out burning embers or small fires. Inside the house, fill bathtubs, sinks, and other containers with water. Toilet tanks and water heaters are an important water reservoir. • Place garden hoses so that they will reach any place on the house. Use the spray gun type of nozzle, adjusted to spray. Avoid laying the hose over or adjacent to combustible objects. • If you have portable gasoline-powered pumps to take water from a swimming pool or tank, make sure they are operating in place and well protected from nearby combustible elements. 269
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
Subsequent experiences,88 coupled with new research carried out by the Australian Bushfire Cooperative Research Centre,256 have lead to more definitive guidelines (Box 12-7).48
270
Home destruction No
Expected
Not expected
Not expected
Expected
Yes
Yes
No
High-intensity wildfire
PART 3 BURNS, FIRE, AND RADIATION
• Place a ladder against the roof of the house opposite the side of the approaching fire. If you have a combustible roof, wet it down or turn on any roof sprinklers. Turn on any special fire sprinklers installed to add protection. Do not waste water. Waste can drain the entire water system quickly. Where possible, divert water from gutters back into the firefighting supply. • Back your car into the garage, and roll up the car windows. Disconnect the automatic garage door opener (otherwise, in case of power failure, you cannot remove the car). Close all garage doors, and seal them with wet rags where possible. Avoid storing combustible elements in a garage that cannot adequately be sealed from ember attack. • Place valuable papers and mementos inside the car in the garage for later departure following passage of the fire, when it is safe and may become necessary to do so. In addition, place all pets in the car. • Close windows and doors to the house to prevent sparks from blowing inside. Close the damper on the fireplace to prevent smoke and embers from entering the house. Leave the doors inside the house open. This will enable occupants to remain vigilant throughout the exposure. If a room or area in the house ignites and develops beyond the occupants’ ability to contain it, then doors can be closed in the house to manage smoke spread. Begin to plan an exit to the outside, bearing in mind the state of the fire outside the house. The approach should be to retreat to a room with an exit door that opens onto a region with little fuel. Turn on a light in each room to make the house more visible in heavy smoke. Have a backup plan for when the electricity supply fails by having flashlights handy. • Turn off the main gas supply to stoves and furnaces. • If you have time, take down drapes and curtains. Close all Venetian blinds or noncombustible window coverings to reduce the amount of heat radiating into the house. This provides added safety in case the windows give way because of heat or wind. • As the fire front approaches, go inside the house. Stay calm; you are in control of the situation. Continually move around inside the house, monitoring its state and the progress of the fire outside. Avoid spending time in the areas that have only one way of exiting the space. If practical, include monitoring of the roof cavity. Goggles will prove handy in dealing with any smoke that enters the house. • After the fire passes, check the roof immediately. Extinguish any sparks or embers. Then check the attic for hidden burning sparks. If you have a fire, enlist your neighbors to help fight it. For several hours after the fire, recheck for smoke and sparks throughout the house. It is worth noting that research in this area by the Australian Bushfire Cooperative Research Centre is continuing under Project D1—Building and Occupant Protection (http://www.bushfirecrc. com/research/d11/d1123.html) under the leadership of Justin Leonard, CSIRO Sustainable Ecosystems. If a person expects to take refuge in his or her home and in turn survive to ensure its defense, then it is critical that steps are taken to reduce the ignition potential of the structure as much as possible. Recent research on home ignition involving field experiments, coupled with modeling and observations of recent wildland–urban interface fire incidents, has provided valuable new insights into the means of ensuring home survival.130,131,133 The research has shown that the characteristics of the home (e.g., exterior building materials) and in an area referred to as the “home ignition zone” located within 30 to 60 m (100 to 200 feet) of the home (e.g., surface fuel accumulations immediately adjacent to the structure that would be receptive to ignition by airborne firebrands) principally determines its ignition potential and thus its survivability during exposure to a wildland fire (Figure 12-37), videos that summarize this research are available from Firewise Communities.132,185,186 It is quite conceivable, for example, that a home could have little or no natural surface fuel within the immediate vicinity of the dwelling, but because cedar shake shingles were used in the roof construction, it is vulnerable to ignition from airborne embers or firebrands from an approaching wildfire. If such a burning structure is not handled
FIGURE 12-37 Expectations of home destruction as a result of exposure to a wildfire. Home survival is expected if low fire intensities occur (lower right cell) and unexpected if the home is destroyed (lower left cell). Conversely, home survival is not expected if high fire intensities occur (upper left cell) and unexpected if the home survives (upper right cell). (From Cohen JD: Home destruction. In Graham RT, technical editor: Hayman fire case study: Summary, General Technical Report RMRS-GTR-115, Fort Collins, Colo, 2003, USDA Rocky Mountain Research Station.)
soon after ignition, it can contribute to the demise of neighboring houses if left unattended314 or push the limits of fire protection to effectively keep up if too many structures become involved.134 The use of external sprinkler systems on a home141,349,436 should not be viewed as a panacea for a lack of fuel treatment in the home ignition zone and beyond or the use of flammable building materials. There is a perception that sprinklers should be capable of providing thermal protection from a high-intensity wildfire assault when in fact their real value is in preventing ignitions from airborne firebrands,304 direct flame contact, and radiation. The FPInnovations–Feric Wildland Fire Operations Research Group has been engaged in a number of research studies related to the use of sprinkler systems for home and cabin protection since 2002, including outdoor field trials, using simulated structures, involving both prescribed and experimental fires.495,496 According to the group’s leader, Ray Ault,43 he and his colleagues maintain that the greatest use of commercially available Rain Bird types of sprinklers and small portable pumps for individual home structure protection is in applying water in sufficient quantities and locations to inhibit external ignitions from airborne firebrands by an approaching or passing wildfire well in advance. If the presoaking or application of water for wetting down fuels is applied for too long, it can lead to other problems (e.g., flooded basements). Irrigation systems have also been occasionally applied to the task of wildland–urban interface protection. Other more elaborate systems have been devised. For example, the Saskatchewan Fire Management and Forest Protection Branch has successfully adapted and applied operationally a manure drag hose transportation system to the task of creating wet “breaks or belts” in values protection or to facilitate backfiring or burnout operations.249
PROTECTIVE FIRE SHELTERS USED BY WILDLAND FIREFIGHTERS The concept of a protective fire shelter for wildland firefighters described earlier (see Figure 12-19) was originally conceived by Australian bushfire researchers in the late 1950s.245,269 The USDA
States in the mid to late 1960s and became a required PPE item for federal wildland firefighters in 1977. More than 1200 U.S. wildland firefighters have deployed their fire shelters to date (up to and including the 2010 fire season).370 The fire shelter is credited with having saved the lives of more than 320 firefighters and preventing at least 315 serious burn injuries,370 although it is not known with any degree of certainty how many would have actually survived and suffered no burn injuries without the fire shelter. Some personal accounts of fire shelter deployments (Box 12-8) have been published.112,397 Why protective fire shelters work well was demonstrated dramatically on August 29, 1985, when 73 firefighters were forced
BOX 12-8 What Is It Like to Experience a Wildfire Entrapment in a Protective Fire Shelter?
B12-2 Shelter deployment on the Shelley fire, Gila National Forest, June 24, 1989. (Photo by Mark Erickson, copyright 2006.) Mark Erickson, a freelance photographer from Silver City, New Mexico, was unexpectedly involved along with 40 wildland firefighters in a fire shelter deployment associated with the major run of the Shelley fire that took place in the Gila National Forest on June 24, 1989. He recently recounted the experience:182 Dr Bruce Hayward, a biologist from Silver City, and I had been putting together a joint effort about the Gila Wilderness, he doing text and I covering the photography. It was decided that during the fire season that I should get out and get some images of fire because of its importance as ecological process in the area. The Shelley fire was started by lightning on June 16, 1989 but I didn’t visit the fire site until June 23. I initially went out to the Sheep Corral area toward Goose Lake to photograph the slurry bombers dropping fire retardant but decided to return the next day and get on the line. Jim Turner from the Shasta Ranger District in California was assigned to go with me and we headed up to the Snow Creek spike camp being manned by the local National Guard. The troops had a water tender and some miscellaneous stores with which to resupply the firefighters. We left our vehicle at the spike camp and headed down the fireline in a northeasterly direction. The fire had been turned over to a Class I Incident Command Team and an infrared imaging aircraft had been brought in to determine the location of hotspots. There was major concern down the valley near Lake Roberts about the many structures that could conceivably be in the path of the fire if the current fire suppression efforts were to fail. I photographed many of the hotshot crew members as they built fireline and felled snags near the line. It is hot, dirty work, especially when air temperatures are already high and there is little or no humidity.
Working our way along Panther Canyon, we noticed that there was a large column of smoke in the direction from which we had just come. Apparently the fire was heading right for the Snow Creek spike camp where the National Guardsmen were being hurriedly schooled on the use of fire shelters. A slurry bomber went over just as the Sacramento Interagency Hotshot Crew came up the fireline from the south. I took a few photographs of the hotshots with the “blowout” in the background and we turned and headed back toward a deployment zone or area on the fireline. The guardsmen were spared having to deploy as the fire made another turn and started toward us instead. Entering the deployment zone, the crew began to take care of the business of stowing gear such as chainsaws and fuel bottles on the perimeter of the area. Cubitainers of water were brought to the center of the deployment zone and personal gear was laid out. Last minute clearing was taking place as the fire began chugging its way closer to us. Even though there was some “good” black between us and the advancing fire front, the noise created by the crowning was incredible as it got closer to our location. Someone gave the order to deploy the fire shelters and all of us retreated underneath. Located in the center of the deployment zone, I continued to photograph the fire as it crowned around us. Comments from the firefighters about the reverberating sounds created by the fire were prevalent. The winds created by the fire were truly amazing and I was glad that the folks at the Technology and Development Center in Fort Missoula had seen fit to add straps to the fire shelters so that they wouldn’t fly away. Cinders from the fire were making small pin holes in the shelter, resulting in a planetarium effect as the flames surrounded the deployment area. The worst of all was the smoke. Everyone was chattering back and forth checking on their buddies. The duff was really burning when the fire decided to come back on us. We were ordered to move in the opposite direction and ended up laying in the smoldering pine needles. Thank heavens for Nomex as we all ended up with lots of holes in our clothing, but nothing burst into flame. I wish we would have had more time to rake the area before the fire hit our deployment zone. One could really feel the radiant heat from the shelters and I was really glad that we had them. There were many comments about being done on one side and “could we turn over to the other?” The fire finally moved on down the canyon, but we stayed in the shelters for an hour it seems. Finally we stuck our heads out to a smoke-filled environment where it was difficult to see more than 10 feet. I continued to take photographs as I thought folks wouldn’t really believe it if I just told them about this. A few of the crew were having some respiratory problems, but everyone was mobile. The cubitainers had been stripped of their cardboard casings and cases of MREs (meals ready to eat) were burnt to the ground. The handles on the fire tools were history, but the chainsaws and fuel bottles were intact. The deployment zone was still smoldering. I’m amazed how small it felt during the peak period of fire activity. Our shelters were fairly well spent and we tossed them into a pile—an unwise decision if we had had to deploy later again that day—and we headed down to the spike camp. General observation: cool heads keep a situation from escalation.
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CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
Forest Service equipment development center in Missoula, Montana (now the MTDC) initiated research and development of protective fire shelters around the same time as the Australians,475 and this work has continued to this day99,380 with a view to reducing the number of serious burn injuries and fatalities among firefighters who become trapped while fighting wildland fires.39 Shelters designed in the shape of a pup tent protect the firefighter by reflecting radiant heat. Constructed of an aluminum-foil and fiberglass cloth laminate, the shelter reflects about 95% of the radiant heat emanating from a fire. These shelters were never designed for direct flame contact. Fire shelters were first introduced operationally on the wildland fire scene in the United
PART 3 BURNS, FIRE, AND RADIATION
to take refuge in their shelters for about 1.5 hours following passage of a high-intensity, active crown fire that swept over and around their location.8,326,406 The incident took place during the Butte fire in the Salmon National Forest in central Idaho. Observers described the crown fire that overran the firefighters as a standing wall of flame that reached about 60 m (about 200 feet) above the treetops. Within the shelters, firefighters experienced extreme heat for as long as 10 minutes. Shelters were so hot that they could be handled only with gloves. After leaving the shelters, some firefighters showed symptoms of possible carbon monoxide poisoning, including vomiting, disorientation, and difficulty breathing. Emergency medical technicians administered oxygen to several individuals before evacuation from the site after the incident. Five firefighters were hospitalized overnight for heat exhaustion, smoke inhalation, and dehydration. The consensus of those interviewed was that without the shelters, none would have survived.333 It should be emphasized that the fire shelter was intended to be used as a last resort when it became impossible to escape to a safety zone before being overrun by a fire. However, despite the emphasis placed on this basic tenet and extensive training in entrapment avoidance over the years,306,308,335,341,463 the results from a recent study74 suggest a possible link to what has been suspected for many years—that some firefighters are likely to engage in behavior that neutralizes the gain in safety afforded by fire shelters. In other words, fire shelters can lead to additional risk taking410 or what’s called “risk homeostasis.”202 Putnam378 maintains that “you are always better with a fire shelter in an entrapment situation than not.” That is fair enough advice, so it seems. Fire shelters are, after all, relatively light to carry—the current model weighs 1.9 to 2.2 kg (4.2 to 4.8 lb) depending on the size40,367—and a minor inconvenience to carry around. Even when fire shelters become compromised, they still provide some protection. One of the entrapment survivors of the 1990 Dude fire, Dave LaTour, deployed his fire shelter before the arrival of the fire front and stayed under his shelter even after a hole was kicked in it by one of the firefighters who got out of his shelter and attempted to evade the flames.343 This allowed hot gases to enter his shelter. Despite this development, LaTour stayed down on the ground as flat as possible. He did sustain some burn injuries but fully recovered. LaTour was able to mentally concentrate his attention on his family to help him through the ordeal of being burned over by the passage of a highintensity flame front. One of the authors (MEA)11 is of the opinion that the main issue regarding their use, beside not knowing what constitutes an adequate clearing size for a shelter deployment in a particular situation,11,247 is the time taken for their efficient deployment.64 In trying to avoid a wildland fire entrapment or burnover, seconds can mean the difference between life and death.377 Without a regular, formalized training program, carried out under realistic environmental conditions, the precious time taken to deploy a shelter might be better spent attempting to evade the fire’s encroachment on one’s position to reach a safer location.11 The British Columbia Forest Service is the only Canadian fire management agency to have ever formally included protective fire shelters as part of a firefighter’s PPE. In 2005, it undertook an associated risk analysis59 and as a result decided to no longer have its firefighters carry fire shelters,223 relying instead on situational awareness and entrapment avoidance. The Australasian Fire Authorities Council has adopted a similar position on the grounds that fire shelters cannot guarantee firefighter survival and may result in firefighters placing themselves at greater risk in the belief that a fire shelter will protect them.47
EMERGENCY PROCEDURES DURING A WILDLAND FIRE ENTRAPMENT OR BURNOVER The danger of being entrapped or burned over and possibly killed or seriously injured by a wildfire is a very real threat for people living, working, or visiting480 in rural areas subject to wildfires. Arnold “Smoke” Elser,180 an accomplished Montana outfitter, described how he helped guests avoid entrapment by a forest fire in the mid-1960s: 272
The fire began at the bottom of the canyon and proceeded up canyon as fires do. However, the wind currents carried the smoke to the east and not up the drainage to the north; therefore, we received no warning of the fire. The Monture Creek trail goes through some very old mature timber which was not burning as we approached. As my stock, the guests, and I arrived at the fire site and realized that we were in danger, we felt we should fall back and try to flank the fire to the east. Starting back toward this trail, we found a ground fire that made it very hazardous to travel in this direction. Because of my knowledge of the trail and terrain, I knew that our best bet would be to wet down the stock, guests, saddles and outer clothing and try to break through the head of the fire. We successfully did this, receiving only a few minor burns on the horses and the loss of some apparel tied to the backs of the saddles. Some lessons that I learned in this experience were that in handling livestock in a fire situation you must have a very close, firm hand on them. It is also very important that no one panics or shows any excitement, as this alarms the livestock and begins the panic run that is so well known. I found that by talking in very low monotone, keeping the pack stock and saddle stock very close together (head to tail), and moving on a good trail, we were able to come through this fire with virtually no harm. Elser180 had these additional suggestions for wildland recrea tionists: Campers, whether they be livestock-oriented, hikers, or boaters, should know where to camp to provide adequate fire barriers around campsites. All campers should consider at least one, and preferably two, safe escape routes and havens (such as rock piles, rivers, and large green meadows) away from heavy fuel areas. Campers should be alert to canyon air current conditions in critical fire seasons. The safety of many recreationists is threatened by nylon and other synthetic fabrics used in the manufacture of most backpacking equipment. These materials melt upon contact with heat. The very nature of good horse packing equipment is a deterrent to fire; canvas mantles that cover the gear and the canvas pack saddles are easily wet down. Leather items such as chaps, good saddle bags, and western hats [that] can shield against heat blasts all provide important protection for the horse user. Sometimes there may be no chance to easily escape an approaching wildfire. Injuries can be minimized or avoided and possible death adverted by adhering to certain fundamental principles and procedures (Box 12-9). There are, however, four simple concepts that one must try to adhere to at all times:42,114,121,501 • Select an area that will not burn—the bigger the better—or, failing that, with the least amount of combustible material, and one that offers the best microclimate (e.g., depression in the ground). • Use every means possible (e.g., boulders, rock outcrops, large downed logs, trees, snags) to protect yourself from radiant and convective heat emitted by the flames. • Protect your airways from heat at all costs, and try to minimize smoke exposure. • Try to remain as calm as possible. The first requirement will limit the flame dimensions and in turn the potential heat energy from flame radiation. It will also limit the time of exposure, an important factor in thermal injuries. Radiant heat can kill you long before direct flame contact.142,501 The more exposed skin, the greater the likelihood of death. Obviously, the last requirement—to remain as calm as possible—may seem difficult to establish and maintain. The expectation that people will panic (i.e., a sudden uncontrollable fear or alarm leading to unthinking behavior) during an emergency situation such as wildfire entrapment or burnover is very strong. Admittedly, with the benefit of 20/20 hindsight, it is easy to point to some decisions that were not optimal and played a negative role in the outcome of the fire.356 Structural fire researchers feel that most people faced with a fire situation react in a rational manner considering the ambiguity of the initial cues about the fire, their limited knowledge about fire development and
or Burnover
When entrapment or burnover by a wildland fire appears imminent, injuries or death may be avoided by following these basic emergency survival principles and procedures. • Acknowledge the stress you are feeling. Most people are afraid when trapped by fire. Accept this fear as natural, so that clear thinking and intelligent decisions are possible. If fear overwhelms you, judgment is seriously impaired, and survival becomes more a matter of chance than good decision making. • Protect yourself against radiation at all costs. Many victims of forest fires actually die before the flames reach them. Radiated heat quickly causes heatstroke, a state of complete exhaustion. Find shielding to reduce heat rays quickly in an area that will not burn, such as a shallow trench, crevice, large rock, running stream, large pond, vehicle, building, or the shore water of a lake. Do not seek refuge in an elevated water tank. Avoid wells and caves because oxygen may be used up quickly in these restricted places; consider them a last resort. To protect against radiation, cover the head and other exposed skin with clothing or dirt. • Regulate your breathing. Avoid inhaling dense smoke (which can impair both your judgment and eyesight). Keep your face near the ground, where there is usually less smoke. Hold a dampened handkerchief over the nose. Match your breathing with the availability of relatively fresh air. If there is a possibility of breathing superheated air, place a dry, not moist, cloth over the mouth. The lungs can withstand dry heat better than moist heat. • Do not run blindly or needlessly. Unless a clear path of escape is indicated, do not run. Move downhill and away from the flank of the fire at a 45-degree angle where possible. Conserve your strength. If you become exhausted, you are much more prone to heatstroke and may easily overlook a place of safe refuge. • Burn out fuels to create a safety zone if possible. If you are in dead grass or low shrub fuels and the approaching flames are too high to run through, burn out as large an area as possible between you and the fire edge. Step into the burned area and cover as much of your exposed skin as possible. This requires time for fuels to be consumed and may not be effective as a last-ditch effort, nor does this work well in an intense forest fire. • Lie prone on the ground. In a critical situation, lie face-down in an area that will not burn. Your chance of survival if the fire overtakes you is greater in this position than standing upright or kneeling. • Enter the burned area whenever and wherever possible. Particularly in grass, low shrubs, or other low fuels, do not delay if escape means passing through the flame front into the burned area. Move aggressively and parallel to the advancing fire front. Choose a place on the fire’s edge where flames are less than 1 m (3 feet) deep and can be seen through clearly, and where the fuel supply behind the fire has been mostly consumed. Cover exposed skin and take several breaths, then move through the flame front as quickly as possible. If necessary, drop to the ground under the smoke for improved visibility and to obtain fresh air.
fire dynamics, and the restricted time to make a decision and to take action.435 Panic is viewed as being synonymous with a frightened, scared, nervous, or anxious response.435 In actual fact, panic in the form of irrational or crazed behavior (e.g., aimlessly trying to flee) is rare during fires. Social scientists long ago rejected this concept to explain human behavior in urban fires.127,375,435 Instead of panic, what is commonly observed is an increased level of stress. Stress is not panic. As Dr. Guylene Proulx, a human factors specialist with the National Research Council Canada’s structural fire research program, suggests, “This stress is not an abnormal reaction or a negative response; on the contrary, stress is regarded as a necessary state to motivate reaction and action” and that
“Decision-making under stress is often characterized by a narrowing of attention and focusing on a reduced number of options. This explains why training is so important because the person is unlikely to develop new solutions under heightened stress; a well-run decision plan learned and practiced beforehand is easier to apply under stress.” There are four fundamental or basic survival techniques or options (see Box 12-9) available to an individual who is caught out in the “open” and is likely to be entrapped or burned over by a wildfire and is not able to take refuge in a vehicle or building193,269,501 or have a protective fire shelter. These four survival options are as per follows:19,21,416 • Retreat from the fire and reach a safe haven. • Burn out a safety area. • Hunker in place. • Pass through the fire edge into the burned-out area. These four survival options are presented in no particular order of priority. Such factors as the size of the fire, the fire environment, the size and location of safety areas or zones, the prevailing fire behavior, and the location of the person with respect to the head of fire will ultimately dictate which option or options (should the first one of these options selected become compromised) should be selected. Each of these options has its own unique advantages and disadvantages. Survival Option 1: Retreat From the Fire and Reach a Safe Haven When people are under pressure, they fall back on habitual, first-learned, and overlearned responses.504 The natural tendency when a person is threatened by a hazard such as a wildfire is to try and move away from the danger as quickly as possible to a place of safe refuge. If the distance between the fire and safe area is short, the fire’s advance slow, the path to the safe area easily traversed, and the person able bodied, then selection of this survival option is appropriate. Bear in mind that a safe refuge may be very nearby, so one should not avoid the most obvious place even though it may temporarily be uncomfortable to reach owing to smoke or low to moderate radiation levels, for example. In some cases, this might mean just taking a few steps into the “black” or recently burned-over ground. The question of whether a previously burned area will serve as a safety zone will depend not only on the size of the area but also on the degree of completeness of fuel consumption, both vertically and horizontally.96,366 Furthermore, a recently burned-over area may not immediately serve as a safe refuge owing to the burnout time of woody fuels and duff,452 in contrast to grassland fuels in which a person can enter the recently burned area in a matter of a few seconds.125 There are a good many cases in which firefighters have escaped injury and death by being able to outpace or outma neuver a spreading fire.366,463 There have also been many wellpublicized cases or incidents during which attempting to initially outpace and then ultimately outrun an advancing flame front have ended in tragedy, including several incidents already mentioned in this chapter (i.e., 1938 Pepper Hill fire, 1949 Mann Gulch fire, 1953 Rattlesnake fire, 1956 Inaja fire, 1966 Loop fire, 1968 Canyon fire, and 1994 South Canyon fire). Sadly, there are many other examples,398 one of the most recent being the 2003 Cramer fire in central Idaho involving two firefighter fatalities.129 Dr. Ted Putnam,379 a retired wildland fire safety specialist with the USDA Forest Service, considers that many of the abovenoted fatality fires were in fact escapable had better decision making been employed (e.g., dropped tools and packs earlier on to maximize rate of advance, put the fastest pacesetters at the lead, and used fire shelters as shields against radiant and convective heat). Similar incidents involving civilians have also taken place. For example, on November 30, 1957, four members of a group of nine young hikers perished while trying to outrun a bushfire in the Blue Mountains of New South Wales, Australia, as it advanced upslope.193,269 Another incident occurred on August 26, 1995, near the community of São Domingos in the district of Sandtarém, Portugal.490 Three civilians who had been assisting local firefighters in suppression operations eventually ended up being killed while trying to run ahead of the fire when it blew up. A fourth 273
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
BOX 12-9 Surviving a Wildland Fire Entrapment
PART 3 BURNS, FIRE, AND RADIATION
individual received severe burns to his feet, which eventually led to them being amputated, and he died some months later. Simulations carried out by the FPInnovations-Feric Wildland Fire Operations Research Group based on their research on firefighter travel rates,157 coupled with case study information gleaned from the 1949 Mann Gulch and 1994 South Canyon fires,97 clearly indicate that a person is not able to sustain a maximum pace for even a relatively short period of time without being overrun by a rapidly advanced flame front, even on a moderately steep slope.27,56 For example, a fire spreading at 60 m/min (197 ft/min) up a 26% slope would, depending on the fuel type, overrun someone in about 6 to 7.5 minutes or after about 360 to 460 m (1200 to 1500 feet) once the “race” had started. Chandler and colleagues112 state, “In most firefighter fatalities … the unsuccessful strategy has been to try and run away from the fire and continue running until exhaustion or the radiant heat load from the fire front fells the victim and allows the flame front to pass over him or her.” Thus trying to outpace a fire for any significant distance, but especially uphill, is “courting disaster.”269 For this reason, escape routes involving travel upslope should generally not be selected. Survival Option 2: Burn Out a Safety Area Burning out fuels to create an area of safety or to enlarge an existing burned area is a viable survival technique or option in some situations (e.g., light fuels and having sufficient time to implement). As Luke and McArthur269 have noted, “Carrying a box of matches is part of survival planning” (in this regard, a windproof type of matches would be ideal); most wildland firefighters carry fuses, which would be infinitely more reliable and effective than a match. Undoubtedly the most publicized example of this survival strategy being used in modern times occurred on the 1949 Mann Gulch fire, mentioned at the start of this chapter.275,403 However, the technique was known to have been used by American Indians in the early 1800s381,476 and undoubtedly by aboriginals in other parts of the world, as depicted, for example, in the 1989 movie, The Gods Must Be Crazy II. Wag Dodge described his escape fire during his testimony at the board of review investigation into the 1949 Mann Gulch fire as follows: After setting a clump of bunch grass on fire, I made an attempt to start another one, but the match had gone out and upon looking up, I had an area of 100 feet square that was ablaze. I told the man nearest to me that we would wait a few seconds to give it a chance to burn out inside, and then we would cross through the flames into the burned area, where we could make a good stand and our chances of survival were more than even. Interestingly, Dodge’s statement was printed in the letters to the editors section of the September 1949 issue of Life magazine following publication of an article on the Mann Gulch fire entitled “Smokejumpers Suffer Ordeal by Fire” from the previous issue. In that letter, the reader stated, “I am sure that there are many people throughout the country who would appreciate and perhaps benefit sometime by a more detailed account of how Foreman Wagner Dodge, who kept calm and did not become panic-stricken, saved himself.” It has been estimated that Dodge’s escape fire was about 37 m (121 feet) long and 26 m (85 feet) wide at the time that his “island” of survival was engulfed by 3-m (10-foot) tall flames associated with the main fire front.25 Survival Option 3: Hunker in Place When caught in the open, survival may depend on taking advantage of every possible source of cover or protection from radiant and convective heat (e.g., depressions in the ground, large rocks or logs).193 If a cave (see Figure 12-35) or root cellar520 is used as a refuge, it is important to vacate into the open at the earliest opportunity owing to potential problems associated with accumulations of smoke and carbon monoxide. In selecting this option, the importance of staying as flat as possible with one’s nose and mouth pressed down into the ground cannot be overemphasized, because the reduction in radiation received is considerable.26 Lying prone not only 274
minimizes one’s radiation profile, but cooler, denser air will always be present at ground level. In selecting this option, bear in mind the following advice:121 When a fire passes over a point, the air temperature near the ground is higher than the air above it and remains higher for longer. So if someone is sheltering from radiation at ground level, they need to stand up as soon as possible after the fire passes to breathe cool, fresh air. This is most apparent in grass fires where air at ground level is hot and smoky for several minutes whereas at 2 m [6.6 feet] it is cool and breathable within 10 to 15 seconds of the flames passing. Although there have been reported cases of firefighters surviving on large rockslides during a wildfire entrapment or burnover, most notably two smoke jumpers on the 1949 Mann Gulch fire,275,403 there have also been instances in which these apparently safe, fuel-free areas contained enough combustible materials to cause injury or death (e.g., Shephard Mountain fire in western Montana on September 4, 1996). Four firefighters died on a rockslide during the 2001 Thirtymile fire in north-central Washington, due in part to the accumulation of duff and rotting wood lodged in the rock crevices that ignited from airborne firebrands.79,273,478 In selecting this option, maximum use should be made of any clothing or other readily nonburnable material to protect exposed skin. You may have to improvise.477 Synthetics should not be used because they readily melt when exposed to flame radiation. During the 1983 Ash Wednesday fires in Victoria, Australia, two individuals wearing only summer clothing who covered themselves with a synthetic blanket perished, while two other individuals right next to the two victims covered themselves with a wet woolen blanket and survived the burnover.248 A good example of using this option was the Wandilo fire that occurred in an exotic pine plantation near Mount Gambier, South Australia, on April 5, 1958. Eleven firefighters found themselves trapped on a narrow firebreak during a “blowup.”269,289 Eight in the group attempted to run back along the firebreak, but perished after exposure to extreme radiant heat levels and direct flame contact. Of the three who survived, two remained in the cab of their firefighting truck to shelter from the worst of the firestorm and only left this cover when the vehicle was well alight and the fire’s peak intensity had abated. The remaining survivor sheltered in a deep wheel rut in the soft sand of the firebreak with his coat over his face during the peak period of extreme fire behavior. Taking refuge in a natural water body such as a pond, lake, or river must be done with caution, but for other reasons (e.g., swimming ability). For example, in 1986, three firefighters in the province of Quebec, Canada, drowned as a result of being forced to enter a lake with a steep drop-off when their camp location was overrun by fire.13 The risk for hypothermia must also be considered.98 Dion167 described an incident that occurred in westcentral Saskatchewan, Canada, in May 1919 in which 11 Cree Indians perished because they were not able to reach a nearby lake or find deep enough water to avoid radiation burns. Of the 12 who survived the ordeal, 11 “bore the marks of their burns for life.” One adult member of the group “escaped severe burns by staying under the water” as much as was possible. It has been suggested that the minimum depth of water should be 0.45 to 0.6 m (1.5 to 2 feet) deep.344,433 Survival Option 4: Pass Through the Fire Edge Into the Burned-Out Area Luke and McArthur269 have suggested that “running through flames cannot be generally recommended and should certainly not be attempted when flames are more than 1.5 m [5 feet] in height or depth.” Nevertheless, a number of firefighters have done this very thing and survived (e.g., 1991 Tikokino grass fire in New Zealand392). In fact, the five members of the group of young hikers that survived the 1957 bushfire in the Blue Mountains of New South Wales mentioned earlier did so successfully but suffered considerable discomfort. A similar incident occurred on the Warm Springs Indian Reservation in central Oregon in June 1985. Wildland fire behavior analyst Jim Roessler400 has
Convection
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
indicated that those individuals who tried to outrun a grass fire on a moderately steep slope were killed, whereas at least one person who passed through the flame front survived. In contrast, during the blowup of the 1937 Blackwater fire, the “five horsemen” made the decision to move downhill through the advancing flames.75 Three did not make it, no doubt due in part to the heavy fuel conditions. Of the two who did survive, one died later of burn injuries. A group of 41 on another section of the fire rode out the blowup in a ridgeline clearing as the fire progressed upslope; 3 were badly burned and eventually died of their injuries. It has been suggested that a person could theoretically survive passing through flames 3 m (9.8 feet) high and 37 m (121 feet) in depth and still survive.112 It is presumed that the person would be immersed in flames for less than 7.5 seconds and would require ideal running conditions (e.g., good footing, no obstructions) and be properly clothed to withstand the direct flame contact. Although it is reasonable to expect a person to be able to hold his or her breath for this long, the very notion of attempting such a drastic or draconian112 feat seems unimaginable. Nevertheless, it is worth noting that firefighters have lived, albeit while suffering severe burns as a result, by running through high-intensity flame fronts. One of the most notable examples of this involved a prescribed fire (PB-3/79) in heavy logging slash near Geraldton, Ontario, Canada, on August 22, 1979.35,297,318 As a result of a complex set of unforeseen circumstances, eight members of the firing crew found themselves encircled by fire. One member of the party, a local fire technician, realizing that there was no other option except to run through the advancing flame front or face what appeared to be certain death, tried to get seven seasonal employees to follow him. They failed to heed his urgings and were eventually engulfed by the fire, whereas he survived but did suffer serious burn injuries. This outcome is hauntingly reminiscent of the 1949 Mann Gulch fire and Wag Dodge’s escape fire in which 15 firefighters failed to follow his lead and 13 ended up perishing. In this regard, Dr. Karl Weick,505 a renowned professor of organizational behavior and psychology, points out that there is good evidence to support the notion that when people are threatened, their thinking becomes much more rigid and difficult to change. Furthermore, they tend to seek out and talk to only those who are most familiar to them.425 The survival technique or option of moving through the flame front to previously burned ground would logically be most suitable in light, discontinuous fuel types that fail to produce deep, uniform flame fronts, and significant postfrontal smoldering or isolated flaming, such as that afforded by certain grasslands (e.g., heavily grazed areas). Furthermore, if one has the good fortune to take advantage of a lull in the wind, this would lessen the momentary rate of spread and in turn the flame depth (see Table 12-2). An area along the flanks of the fire (see Figure 12-24) would be preferable to the head. One may only have to travel a relatively short distance before reaching previously burned ground that has “cooled” down sufficiently to serve as a safe area. Having reached the burned area, a person would still have to be cognizant of the danger posed by fire-weakened trees and falling snags, hot ash pits and burned-out stump holes, and rolling rocks or logs.263 This would apply to the other survival options as well. It is worth emphasizing that wildland firefighters as well as members of the general public have been killed and seriously burned while engaged in using fire as a land management tool.35,302,441,488,493 Thus the survival principles and options discussed earlier are equally applicable to prescribed fires or controlled burns. Although radiant heat emanating from a wall of flame is generally viewed as the principal killer in wildland fire entrapments and burnovers,142 under certain conditions convective gases or superheated air can have lethal consequences with little or no warning, most notably upslope of a fire source. Under strong winds, a fire’s convection column will not lift away from the surface of a steep slope.125 As slope steepness increases, flames gradually “attach” themselves (Figure 12-38), thereby enhancing fire spread by both direct flame contact and convective heat transfer.401 This is the very reason that fires spread faster
Weak indraft Strong indraft
Flame detached from slope
A
SHALLOW SLOPE
Convection
Indraft Flame attached to slope
B
STEEP SLOPE
FIGURE 12-38 Effect of slope steepness on degree of flame attachment and convective heat transfer for shallow sloping (A) and steep sloping (B) terrains. (Redrawn from Rothermel RC: Fire behavior considerations of aerial ignition. In Mutch RW, technical coordinator: Prescribed fire by aerial ignition: Proceedings of a workshop, Missoula, Mont, 1985, Intermountain Fire Council.)
upslope than on level ground given the same fuel and weather conditions.
Wildland Fires and Human Behavior As discussed earlier, the reality of human behavior in fires is somewhat different from the panic scenario “nourished by the media and movie industry who like to play on strong emotional images.”375 What is regularly observed in urban fire situations is a lethargic response to fire alarms or even the initial cues of a fire (e.g., smoke and visible flame). What has been most troubling to the wildland fire community in recent years is the fact that the same mistakes seem to be made time and time again,170 rather than using “the lessons of the past so we don’t have to keep relearning them the hard way.”340 Since the mid-1990s, there has been a growing recognition among the wildland fire community of the role that human factors play in firefighter fatalities.92,171,377 Morse311 considered the development of a mental “scotoma” among firefighters to be a major contributing factor in many wildland fire fatality incidents, noting, “Scotoma is, literally, a blind spot. In a psychological sense, it is that condition which occurs when a person tends to block out from his or her 275
PART 3 BURNS, FIRE, AND RADIATION
consciousness anything considered not important—or critical—to survival.” In other words, blindness to danger perceived as routine takes hold and blocks out sensitivity to hazardous events or conditions present in the wildland fire environment. The smoke jumpers involved in the 1949 Mann Gulch fire would appear to have suffered from a psychological scotoma or overconfidence.503 By the time they had landed and gathered their gear together, it was nearly 5:00 PM. At the time, “They did not feel the fire threatened them then.”403 Less than an hour later, 12 smoke jumpers and a local firefighter were overrun and killed by the fire. Air temperatures reached a maximum of 36° C (97° F) on the day in question, and in turn, the fully cured grasses were in a critically dry state.403 It was a day of extreme fire danger.15 One of the survivors, Bob Sallee, commented afterwards:403
A
I took a look at the fire and decided it wasn’t bad. It was burning on top of the ridge and I thought it would continue on up the ridge. I thought it probably wouldn’t burn much more that night because it was the end of the burning period (for that day) and it looked like it would have to burn down across a little saddle before it went uphill any more. One crew member was reported to have been taking photographs of the fire less than 10 minutes before the first fatalities occurred.275,403 Similarly, photographs were being taken by firefighters on the line just moments before the 1994 South Canyon fire blowup,96 in which 14 of their fellow firefighters were overrun and killed (see Figure 12-1). Even on the major run of the Thirtymile fire in north-central Washington on July 10, 2001,79,273 the firefighters behaved more as spectators than as potential victims until it was too late for some. A total of 16 people (14 firefighters and 2 civilians) were entrapped and required to deploy protective fire shelters. Four firefighters were killed, and 2 were injured, 1 with severe burns. Earlier during the day in question, the feeling was that the fire was “basically a mop-up show.”79 Some of the firefighters who were overrun by the fire “spent time taking photos or making journal entries” just a half hour before the incident.79 Although wildland firefighters may be subject to a whole host of human failings or other psychological phenomena,129,355,504 openly acknowledging and constantly being aware of the potential for entrapment or a burnover, regardless of the situation, is the initial key step in reducing the risk for injury or death from wildland fires. Complacency may be the most difficult factor to overcome.316 The late Paul Gleason,204 a veteran wildland firefighter and accomplished rock climber, noted that three major causes of climbing accidents are ignorance, casualness, and distractions. Although firefighters are expected to engage a wildfire, civilians are not. Nevertheless, the general public could also become complacent about wildfires and fail to fear the worst, until, unfortunately, it is too late. This may be due in part to a fascination with fire in general (Figure 12-39, online), denial, indifference, or a complete ignorance about free-burning fire behavior. In any case, there is a perception that there is no real sense of urgency until the threat is imminent. As Proulx375 points out, “People are often too cool during fires, ignoring or delaying their response to the initial cues of an actual emergency. Once occupants decide that the situation requires moving to an area of safety, the time left could be minimal.” This is probably best exemplified by an urban fire case study. On May 11, 1985, 56 people burned to death and more than 200 were injured when a rapidly growing fire, caused by a cigarette, engulfed the wooden main grandstand at Valley Parade Stadium in Bradford, England, during a soccer match. Filmed documentation of the fire indicates that the blaze spread the entire 88-m (289-foot) length of the stand in less than 5 minutes—a rate of 18 m/min (59 ft/min). Although people in the immediate vicinity of the developing fire moved toward exits, “Persons in remote sections of the grandstand continued to watch the match, apparently unconcerned about (or perhaps unaware of) the developing fire.”246 One of the seven factors that contributed to the loss of life was “The failure of patrons to perceive the danger of the developing fire in the early stages and begin evacuation.”246 276
B FIGURE 12-40 Fires in fully cured grasslands are very responsive and can attain exceedingly rapid rates of spread. The flank of a grass fire, with a change in wind direction, can quite quickly become the head and catch the unwary off guard. This scene from the multifire situation that occurred in the Spokane, Washington, area on October 16, 1991 (A), reinforces the importance of having well-established escape routes that can be easily navigated (B) to a designated safety zone. (Courtesy Spokane Statesman Review/WorldPictureNews; photos by K. King.)
It is hard sometimes to believe that a wildland fire could become life threatening, especially if it is far away from the observer or small in size and is not burning very vigorously at the time. However, danger is inherent in every wildland fire occurrence, be it a wildfire or a prescribed fire. Some wildland fire situations are simply more hazardous than others and can catch a person or persons off guard (Figure 12-40), possibly leading to severe injuries or even death.54,85 Tom Leuschen262 is an experienced fire manager and wildland fire behavior analyst who worked for many years in north-central Washington, within sight of the area struck in 2001 by the Thirtymile fire. He was involved in the accident investigation and had the following to say about the incident: When I stand at the deployment site and look at their pictures, knowing what I know about the fuels, barriers, and interactions between fires, I honestly do not expect that they will have to shelter either. I am as wrong as they were. Things got very complex as the fires joined at their location. The obvious lesson is that we must prepare for the worst when trapped, regardless of what we may anticipate. They were entrapped at 1634 and deployed at 1724. They had time to get organized. Anyone involved in a wildland fire can become a victim of an entrapment or burnover at any time given the precarious nature of wildland fires and their environmental influences. People need to be constantly mindful or conscious of this fact because, as Weick502,504 says, “safety is not bankable” and it is “an ongoing struggle for alertness.” Plan for and expect the worst every time out. This may be difficult, because a blatant disregard for worst-case scenarios is one of the common, yet least studied, human traits111 (Box 12-10).
Weick’s Book Review of Cerulo’s Never Saw It Coming: Cultural Challenges to Envisioning the Worst*
Karen Cerulo argues that people have a clear preference, culturally shaped, for paying attention to best-case scenarios and casual attention to worst-case scenarios. Whether people render the worst-case invisible or vague or recast the worst case as positivity in disguise, the result is that they are unable to envision the worst case and unprepared to avoid it or deal with it. Thus, the plaintive phrase provides the title of this work, “we never saw it coming.” The reader comes away from this book with a new appreciation of the need for mindful attention, resilient action, and skills of improvisation. With these three resources as part of an action repertoire, we will go a long way toward acknowledging and preparing for worst-case scenarios. *From Weick KE: Book reviews: Never saw it coming: Cultural changes to envisioning the worst, Am J Sociol 113:1762, 2008.
PROPER CLOTHING There are documented cases in which homeowners, who were seemingly prepared to stay and defend their property, have died because they were not properly dressed to do so (e.g., clad only in shorts or a bathing suit and slippers).501 Clothing protects against radiant heat, embers, and sparks, so it is sensible to dress appropriately.141,358 The cover of a recent book on the wildland– urban interface fire situation in southern California219 depicts a lightly clad homeowner on the roof of his house presumably attempting to extinguish sparks or embers with a garden hose as a high-intensity flame front approaches (Figure 12-41). This is a potential recipe for disaster in many respects. This person is not properly attired to stay and defend his property, nor is this the correct approach. Closely woven material is more resistant to radiation and less likely to ignite than is open-weave material. Natural fibers are
best. Wool is more flame resistant than cotton, although cotton can be improved by chemical treatment to retard flammability. As mentioned earlier, synthetic materials are a poor choice because they readily absorb heat or, worse yet, can ignite and melt onto the skin.371 Closely woven materials that provide protection also restrict airflow, so clothes should fit loosely so that they do not interfere with dissipation of body heat. Cotton long johns or undergarments absorb sweat, aid evaporation, and do not melt; however, underwear made of synthetic materials does melt. Wearing excessive layers of clothing generally contributes to heat stress. As little skin as possible should be exposed to fire. Long trousers and a long-sleeved shirt should be worn. For maximum protection, the shirt should be kept buttoned with the sleeves rolled down. Brightly colored (yellow or orange) coveralls or shirts are worn by organized firefighting crews. These colors improve safety and communications because they are visible in smoke, vegetation, and blackened landscapes. Other essential apparel includes a safety helmet (hard hat), gloves (leather or natural fiber), leather work boots, woolen or cotton socks, a warm jacket for night wear, goggles, and a handkerchief. Clothing, backpacks, tents, and other camping equipment made of synthetics should be discarded when a person is close to a fire.
WATER INTAKE Sweating is the primary method for body cooling, although exhaling warm air and inhaling cooler air also decreases body temperature (see Chapter 70). Because the cooling effect of sweat evaporation is essential for thermoregulation, fluids lost during strenuous work must be replaced. In firefighting, water losses of 0.5 L/hr (1 pt/hr) are common, with losses of up to 2 L/hr (2 qt/hr) under extreme conditions.269 Unless water is restored regularly, dehydration may contribute to heat stress disorders, reluctance to work, irritability, poor judgment, and impatience. Thirst is not a good indicator of water requirements during strenuous work, so additional drinking of small quantities of water at regular intervals is recommended. A useful signal of dehydration is dark, scanty urine. An excessive amount of electrolytes may be lost through sweating, leading to nausea, vomiting, and muscle cramps. When meals are missed or unseasoned foods are eaten, electrolyte supplements may be needed to replace lost salts. Sweetened drinks should be used as a source of energy if solid food is not available.
PERSONAL GEAR Some rescue and medical missions take a few days. Therefore it is necessary to be prepared for extended periods and changing conditions in the backcountry (Box 12-11).
HOW TO REPORT A WILDLAND FIRE TO LOCAL FIRE PROTECTION AUTHORITIES
FIGURE 12-41 An inappropriately clad and positioned homeowner attempting to defend his property from ember attack during a wildfire in Rancho Penasquitos, San Diego, California, on August 25, 1995. The fire at the moment appears largely dominated or supported by a plentiful fuel source. However, given the capricious nature of fire and winds, this fire could have easily turned into a more wind-dominated event at any time. Thus this individual could have been incapacitated by a momentary blast of superheated air from the convection or radiant heat produced by the spreading fire. In the absence of any outside assistance, this would then have left him vulnerable to burning by direct flame contact along with his home. Fortunately for this individual, shortly after the photo was taken, an air tanker dropped a load of fire retardant near the advancing flames and effectively nullified the fire’s spread and intensity. (Courtesy California Chaparral Field Institute; photo by R.W. Halsey.)
A caller should be prepared to provide the following information when reporting a fire: • Name of person giving the report • Where the person can be reached immediately • Where the person was at the time the fire was discovered • Location of the fire; orient the fire to prominent landmarks, such as roads, creeks, and mileposts on highways • Description of the fire: color and volume of the smoke, estimated size, and flame characteristics if visible • Whether anyone is fighting the fire at the time of the call The phone number to call varies locally. For example, in Alberta, Canada, the number for reporting wildland fires is 310FIRE or 310-3473 in both the northern and southern halves of the province, even though they have different area codes. In other locations, it may simply be 9-1-1. Rural homeowners should make a point of finding out the number to call before the beginning of fire season. 277
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
BOX 12-10 Envisioning the Worst: An Extract From
PART 3 BURNS, FIRE, AND RADIATION
BOX 12-11 Personal Gear for a Rescue Mission on
a Wildland Fire Incident
• Boots (leather, high-top, lace-up, nonslip soles, extra leather laces) • Socks (cotton or wool, at least two pairs) • Pants (natural fiber, flameproof, loose fitting, hems lower than boot tops) • Belt or suspenders • Shirt (natural fiber, flameproof, loose fitting, long sleeves) • Gloves (natural fiber or leather, extra pair) • Hat (hard hat and possibly a bandanna, stocking cap, or felt hat) • Jacket • Handkerchiefs or scarves • Goggles • Sleeping bag and ground cover • Map • Protective fire shelter • Food • Canteen • Radio (AM radio will receive better in rough terrain; FM is more line-of-sight; emergency personnel should have a two-way radio) • Bolt cutters (carried in vehicles to get through locked gates during escape from flare-ups or in the rescue of trapped people) • Miscellaneous items (mess kit, compass, flashlight, extra batteries, toilet paper, pencil, notepaper, flagging tape, flares, matches (windproof), can opener, washcloth, toiletries, insect repellent, plastic bags, knife, first-aid kit, and lip balm)
PORTABLE FIRE EXTINGUISHERS People should know which extinguisher to select for a specific hazard in the home or recreational vehicle and be trained in its use. When a fire is discovered, first evacuate occupants to safety and promptly report the fire to the appropriate authorities. If the fire is small and poses no direct threat, an extinguisher should be used to fight it. The three major classes of fires are as follows: • Class A fires: fueled by ordinary combustible materials, such as wood, paper, cloth, upholstery, and many plastics • Class B fires: fueled by flammable liquids and gases, such as kitchen greases, paints, oil, and gasoline • Class C fires: fueled by live electrical wires or equipment, such as motors, power tools, and appliances The right type of extinguisher must be used for each class of fire. Water extinguishers control Class A fires by cooling and soaking burning materials. Carbon dioxide or dry chemical extinguishers are used to control class B fires by smothering flames. Multipurpose dry chemical or liquefied gas extinguishers control class A, B, and C fires by a smothering action. Liquefied gas extinguishers also produce a cooling effect. A dry chemical or liquefied gas extinguisher is recommended for recreational vehicles.
BASIC WILDLAND FIRE MATERIALS, TRAINING COURSES, AND OTHER INFORMATION RESOURCES A large number of reference or textbooks on wildland fire suppression currently exist, many of which have been cited or referenced in this chapter. Wildland Fire Fighting for Structural Firefighters is a comprehensive text written specifically for firefighters whose primary focus is fighting structure fires, but who also have wildland and wildland–urban interface responsibilities. 278
This book210 provides an excellent overview on wildland fire behavior, fire apparatus and communications equipment for wildland fires, wildland firefighting tools and PPE, extinguishing agents, wildland incident management, fire suppression methods, wildland and interface fire suppression, firefighter safety and survival, fire prevention and investigation, and fire protection planning. The booklet Planning for Initial Attack published by the USDA Forest Service305 is a handy reference on basic fire behavior and fire suppression principles. Other reference books on the basics of wildland fire suppression exist.268 For a good general reference book on forest fires, see the recent contribution by Omi.353 Managing Fire in the Urban Wildland Interface is the most comprehensive professional guide on the wildland–urban interface fire problem.69 Wildfire magazine, the official publication of the International Association of Wildland Fire, is an excellent source of information on current fire management topics (http://www.iawfonline.org), as is International Forest Fire News (http://www.fire.uni-freiburg. de/iffn/iffn.htm) and Fire Management Today (http://www. fs.fed.us/fire/fmt). Other information that would be valuable to emergency response personnel includes reference materials and materials associated with the Publications Management System (PMS) and “S,” or suppression skills, training courses available through the U.S. National Wildfire Coordinating Group’s National Fire Equipment System (NFES) based at the National Interagency Fire Center in Boise, Idaho.347 These include, for example, “Firefighter Training” (S-130, 2003), “Look Up, Look Down, Look Around” (PMS 427, 1992),335,336 “Lookouts, Communications, Escape Routes and Safety Zones (LCES)” (S-134, 2003), “Fire Operations in the Wildland–Urban Interface” (S-215, 2003), and “Lessons Learned: Fatality Fire Case Studies” (PMS 490, 1998)340,341 The latter course uses nine past fatality fires as a learning tool to help fire line tactical decision makers avoid similar mistakes. It is worth noting that some NFES publications are available online (http://www.nwcg.gov). The WFSTAR (Wildland Fire Safety Training Annual Refresher) website (http://www.nifc.gov/ wfstar/index.htm) is an excellent resource for the latest information on wildland firefighter safety. The Wildland Fire Staff Library (http://www.fireleadership/gov/toolbox/staffride/index. html), developed by the National Wildfire Coordinating Group, is also a highly useful source of information on past firefighter fatality incidents. There are also several CD-ROM–based training courses available on fire line safety,36,463 fire behavior,462 and fire danger rating.439 For additional information on introductory to advanced wildland fire training courses available at the local area, geographic area, and national levels in the United States, visit the Wildland Fire Training website (http://www.nationalfiretraining. net). For national wildland fire training courses in Canada, visit the website of the Canadian Interagency Forest Fire Centre (http://www.ciffc.ca). One of the initiatives of the U.S. National Wildland–Urban Interface Fire Program was a firefighter safety program in the wildland–urban interface series. This training package, which includes three videos, was developed for small community fire departments to address the problems faced by structural and wildland firefighters when fighting fires, especially those threatening structures in the wildland–urban interface.255 Copies can be ordered from Firewise Communities online catalog. The Wildland Fire Lessons Learned Center (http://www. wildfirelessons.net) is a good source for information on nearly all aspects of wildland fire management. An annotated reading list and bibliography on wildland firefighter safety management are available253 on their “My Fire Community” website (http:// www.myfirecommunity.net). The Fire Research Institute library (http://www.fireresearchinstitute.org/), which provides online search capability, is a good source of scientific and technical wildland fire literature.212 Wildfire Today (http://www.wildfiretoday.com) and the Global Fire Monitoring Center (http://www.fire.uni-freiburg.de) are popular websites for the latest news in wildland fire management. Wildland Fire: Home of the Wildland Firefighter (http:// www.wildlandfire.com) is another unique website serving the global wildland fire community.
Fire suppression efforts in the late 1800s and early 1900s were largely ineffective because of limited access, absence of trained firefighting organizations, and lack of a fire detection network. During these times, many residents and numerous firefighters died in wildland fires in the United States and Canada. In the recent past, firefighters were more vulnerable to injuries and fatalities from wildfires than was the general public. Today, with many people living and seeking recreation in wildlands, the odds for serious fire encounters are shifting toward an inexperienced populace. Large property losses and direct injuries are being reported in increasing numbers in the wildland–urban interface. It has now become not a question of “if” a wildfire will come or of it “can’t happen here,” but rather “when and where” the next major wildland–urban interface conflagration will take place (Figure 12-42, online). Emergency medical personnel will probably have increasing exposure to wildland fires in the future and will need to know more about fire-related injuries, fire safety, and fire survival. Many wildland firefighters are in turn feeling compelled to save homes,189 in part as a result of the expectations placed on them by the general public and homeowners in particular, coupled with a culture derived from more than a century of wildland fire suppression.58 Not surprisingly, many wildland firefighter fatalities in recent years have been associated with wildland–urban interface incidents (e.g., the 2003 Cedar fire in southern California).103 Given even the best practices,277 there is an overwhelming need to impress on rural homeowners that no home is worth a firefighter’s life. Although wildland fires have not yet posed a serious threat to backcountry recreationists in the United States to any appreciable degree, the prospect for such confrontations is growing. For example, two recreationists were involved in entrapment and burnover associated with the major run of the 2001 Thirtymile fire178; fire investigators concluded they would probably not have survived, although they did suffer minor injuries, had they not joined up with the firefighters just before (about 14 minutes) their location was overrun.480 Many years of practical experience with wildland fires allow us to conclude the following: • Many indicators point to the fact that financial support and programs that address only emergency responses to wildfires will result in more damaging and expensive wildfire emergencies in the future. Public policies and public education that link sustainable land use practices with emergency preparedness are likely to be most successful in the long run. • Residential shifts to the wildland–urban interface will increase exposures to life-threatening situations. • Expanded use of fire in managing national parks and wilderness areas will increase the likelihood that backcountry recreationists will encounter free-burning fires. • By and large, the general public tends to underestimate existing fire hazards and for the most part is usually not experienced in avoiding wildfire threats. • In some instances, attempted fire exclusion practices have contributed to development of hazardous wildland fuel situations in terms of quantity and continuity, setting the stage for extreme fire behavior in some plant communities. The national ecosystem health issue has compounded this problem by producing vast expanses of dead and dying forests, increasing the threat to people from fast-moving, high-intensity fires. • Knowledge of fire behavior principles and survival guidelines will prepare people to take appropriate preventive measures in threatening situations. The general public must share responsibility with suppression organizations to minimize fire hazards created by humans. Care with fire, proper cleanup of debris, fuel reduction efforts on wildland property, fire-safe construction guidelines, and application of survival skills will minimize fire threats. Such precautions should become as commonplace in the wildland environment as smoke alarms and fire extinguishers have become in urban settings. Every community should undertake, as part of the risk management
process associated with the wildfire threat, an assessment of their fire environment in terms of potential fire behavior. A good example of this type of analysis has been completed for over a hundred communities in northern Saskatchewan, Canada.158 Sadly, major disasters are commonly required for fundamental changes to occur. Disasters do not simply happen.470 They usually involve an “incubation period” that involves “the accumulation of an unnoticed set of events that are at odds with the accepted beliefs about hazards and the norms for their avoidance.”469 Wildland fire suppression agencies will continue to provide fast, safe, and energetic initial attack responses to protect human life, property, and natural resources.14 Many fires will start and burn under environmental conditions that permit their control at a very small size. However, in certain situations (e.g., critically dry fuels or strong winds), some fires9,31,32 will defy control until burning conditions ameliorate. The major runs of the 1985 Palm Coast fire in south Florida2 and the Millers Reach fire that occurred near Anchorage, Alaska, on June 2, 1996,128 are good examples of this kind of fire behavior and associated suppression problems. No radically new concept of fire suppression for stopping the head of a hot, fast-running wildland fire should be anticipated in the future.146 In his book, An Introduction to Fire Dynamics, Drysdale173 points out that “Further major advances in combating wildfire are unlikely to be achieved simply by continued application of the traditional methods. What is required is a more fundamental approach which, can be applied at the design stage … Such an approach requires a detailed understanding of fire behavior.” Strategic fuel management and land use planning could potentially reduce the total number and size of wildfire occurrences, as well as influence their geographic distribution, and thereby mitigate the impacts of too much of the “wrong kind of fire.”386 Science-based-only solutions211 are considered insufficient; effective wildland fire policy must integrate ethics, economics, aesthetics, and values.386 Furthermore, as Cheney118 points out, if we are to encourage people to live safely in the wildland environments, they need to be fully aware of the full potential for fire behavior and what can be done to protect themselves and their assets. He goes on to say that “they must be individually persuaded to recognize what constitutes the fuel for a forest fire and be convinced that, since they own the fuel, they also own the fire it produces and are responsible for the damage they or others nearby incur.” The public and fire management agencies themselves must fully appreciate that fuel management is not a panacea for conflagration mitigation, but rather a prerequisite to aid in successful fire suppression.20,72,122,472 An excellent source of information on fuel management is the USDA Forest Service Fuels Synthesis Project (http://www.fs.fed.us/fire/tech_ transfer/synthesis/synthesis_index).481 After the 1983 Ash Wednesday fires in southeastern Australia, the editor of Australian Forestry commented on what could be learned from studying such wildland fire disasters:176 Advances in technical areas will be of great value. It would be valuable too to make comparable advances in the areas of public policy. People forget, community attitudes change and policies erode. Perhaps one of the greatest challenges, given the realities of southeastern Australia, is to learn how to ensure the permanence of public interest policies where permanence is required. Twenty years later and following the bushfires that engulfed Canberra, Australia, in 2003 (http://www.en.wikipedia.org/ wiki/2003_Canberra_bushfires), Cheney120 offered some advice on this matter: … I believe that there is strong evidence that the policies and institutional arrangements of organizations, both those directly related to fire management and those completely unrelated, will have the result of perpetuating major fire disasters. I also believe that the legal framework in which we’re working is one that [militates against] individuals taking responsibility for their own actions and lifestyle choices. In this country wildfire is inevitable but the impact 279
CHAPTER 12 WILDLAND FIRES: DANGERS AND SURVIVAL
Concluding Remarks
of disastrous fires can be reduced. But this will only be achieved if policies focus on the physics of fire spread and foster a climate of awareness where fuel reduction, from the backyard to beyond, is encouraged and supported by legislation. At the end of the day, though, what can an individual do to improve matters when it comes to living with fire? Kaufmann, Shlisky, and Marchand238 offer some very practical advice: • Get involved in a community-based conservation group working on local landscape restoration projects. • Educate yourself about the role of fire in your local ecosystems. • Provide feedback on agency land management plans. • Consult with regional experts on how to safely reintroduce fire on to your land holding. • Participate in local workshops (e.g., Firewise Communities) to learn how to treat fuels around your home and create defensible space.
Their final suggestion: “Start simply. But start.” Local forestry and fire management agencies are more than willing to offer technical advice and information. Just give them a call to get started today before wildfire comes knocking!183 Acknowledgments. The authors hereby thank the following individuals for their candid comments on various sections of the chapter: M. Ackerman, A. Beaver, K. Brauneis, B. Butler, D. Campbell, P. Cheney, J. Cohen, M. DeGrosky, T. Greer, M. Heathcott, J. Leonard, T. Leuschen, S. McCaffrey, J. McLevin, B. Mottus, P. Murphy, S. Otway, G. Proulx, T. Putnam, D. Quintilio, A. Rhodes, B. Sharkey, R. Smith, D. Thomas, R. Thorburn, K. Weick, and T. Zimmerman. The assistance of the following individuals in the preparation of this chapter is also duly noted: B. Bereska, M. Campbell, M. Cruz, M. Erickson, J. Handmer, T. Petrilli, G. Pearce, and O. Spencer.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 13
Emergency Care of the Burned Victim MICHAEL J. MOSIER AND DAVID M. HEIMBACH
Epidemiology Each year in the United States, approximately 2 million individuals are burned seriously enough to seek the care of a physician, and about 70,000 of these require hospitalization. Fortunately, the number of deaths attributable to burns decreased from 12,000 in 1979 to 4000 in 2009. Although treatment facilities would like to take credit for this decrease, the most likely reason is the widespread use of smoke detectors in both public and private dwellings. It has been estimated that more than 90% of burns are preventable and that most are caused by carelessness or ignorance. During the next few years, the biggest contributions in decreasing burn mortality and morbidity may come not from medical scientists but rather from improved engineering design and more successful programs in teaching burn prevention to the public. Like other forms of trauma, burns frequently affect children and young adults. The hospital expenses and the social costs related to time away from work or school are staggering. Although most burns are limited in extent, a significant burn of the hand or foot may prevent a manual laborer from working for a year or more and in some cases may permanently prevent a return to former activity. The eventual outcome for the burned victim is related to the severity of the injury, individual physical characteristics of the victim, motivation toward rehabilitation, and quality of treatment of the acute burn. Most persons with burns who are seen by physicians visit emergency departments, where judgment in triage, care plan for small burns, and initial management for major burns can influence survival of the victim and eventual cosmetic and functional results. Because most victims are young and about one-third are children, they will live with the consequences of the acute treatment for an average of 50 years. The decisions made at the initial contact with the victim require answers to the algorithm shown in Figure 13-1. This chapter describes first-responder care for major burns and is organized to guide assessment of burn severity and initial 280
management of serious burns, as well as to provide an initial treatment plan for minor burns.
Physiology For burns other than chemical burns, the primary events of injury occur during the time of heat contact. Coagulation necrosis takes place within cells, and denaturation of collagen occurs in the dermis. Either blood vessels are completely destroyed or the endothelium is damaged severely enough to cause clotting, which leads to ischemic necrosis of remaining viable cells. The burn wound is not static. Surrounding the zone of coagulation is a zone of capillary and small vessel stasis. Red cells form into rouleaux, platelet and white cell aggregates form, and the circulation becomes stagnant. Over the next hours or even days, the ultimate fate of the burn wound depends on resolution or progression of this zone of stasis. Cells and tissue stroma release mediators to initiate the inflammatory response. Histamine, serotonin, prostaglandin derivatives, and the complement cascade all have roles. In victims with burns of less than 10% of the total body surface area (TBSA), the actions of these mediators are generally limited to the burn site itself. Capillary permeability increases, neutrophils marginate, and additional inflammatory cells (monocytes, macrophages) are attracted by chemotaxis to the site of injury, initiating the healing process. As burns approach 20% TBSA, the local response becomes systemic. The capillary leak, permitting loss of fluid and protein from the intravascular compartment into the extravascular compartment, becomes generalized. Cardiac output falls as a result of markedly increased peripheral resistance, decreased intravascular fluid volume from the capillary leak, and accompanying increase in blood viscosity. Decreased blood volume and cardiac output, accompanied by an intense sympathetic response, lead to decreased perfusion to the skin and viscera. Decreased flow to the skin can convert the zone of stasis to one of coagulation, increasing the depth of the burn. The capillary leak and depressed cardiac output lead to depressed central nervous system (CNS)
<5% TBSA
>5% TBSA
Superficial or deep but very small
Burn covering >50% of hand or foot
Smoke inhalation without burn Burn ≤20% TBSA Eye involvement
Smoke inhalation with burn Burn >20% TBSA Electrical burn
First aid See MD if not healed in 3-5 days
First aid See MD by day 2
Ground transfer to community hospital
Immediate transfer to burn center
FIGURE 13-1 Algorithm for decision making at the scene. TBSA, Total body surface area.
function, and in extreme cases they result in severe cardiac depression with eventual cardiac failure in healthy patients or in myocardial infarction in patients with preexisting coronary artery disease. The first sign of CNS change is restlessness, followed by lethargy and finally coma. Without adequate resuscitation, burns of 30% TBSA frequently lead to acute renal failure, which in a victim with a severe burn almost invariably leads to a fatal outcome. Cardiovascular changes begin immediately after a burn. The extent of these changes depends primarily on the size of the burn and to a lesser extent on the depth of the burn. Most victims with uncomplicated burns of less than 15% TBSA can undergo oral fluid resuscitation with some salt-containing solution. As the burn extent passes 20% TBSA, massive shifts of fluid and electrolytes occur from the intravascular into the extravascular (extracellular) space. Reversal of the shifts begins during the second postburn day, but normal extracellular volume is not completely restored until 7 to 10 days after the burn. Unless the intravascular volume is depleted, classic hypovolemic shock occurs. An untreated person will die of cardiovascular collapse; if treatment is poor, irreversible acute tubular necrosis and renal failure will develop.
Types of Burns SCALD BURNS In civilian practice, scalds, usually resulting from hot water, are the most common cause of burns. Water at 60° C (140° F) creates a deep partial-thickness or full-thickness burn in 3 seconds. At 68.9° C (156° F), the same burn occurs in 1 second. Freshly brewed coffee from an automatic percolator is generally about 82° C (179.6° F). Boiling water always causes deep burns, and soups and sauces, which are thicker in consistency, remain in contact longer with the skin and often cause deep burns. In general, exposed areas tend to be burned less deeply than areas covered with thin clothing. Clothing retains the heat and keeps the liquid in contact with the skin for a longer time. Immersion scalds are deep and severe burns.18,28,92 Although the water may be cooler than with a spill scald, the duration of contact is longer, and these burns frequently occur in small children or older adult victims with thin skin. Consequently, many states have passed legislation to set home and public hot water heaters to maximum temperatures well below 60° C (140° F). Scald burns from grease or hot oil are generally deep partial thickness or full thickness. Cooking oil and grease, when hot enough to use for cooking, may be in the range of 204.4° C (400° F). Tar and asphalt burns are a special kind of scald. The “mother pot” at the back of the roofing truck maintains tar at a temperature of 204.4° to 260° C (400° to 500° F). Burns caused by tar directly from the mother pot are invariably full thickness. By the time the tar is spread on the roof, its temperature has
FIGURE 13-2 Tar burn of hand. (Courtesy Paul S. Auerbach, MD.)
decreased enough that most of the burns are deep partial thickness (Figure 13-2). Unfortunately, the initial evaluator cannot usually examine these burns because of the adherent tar. The tar should be removed by application of a petroleum-based ointment (such as Vaseline) under a dressing. In the field, mayonnaise may serve this purpose (Figure 13-3). The dressing may be removed and the ointment reapplied every 2 to 4 hours until the tar has dissolved. Only then can the extent of the injury and the depth of the burn be accurately estimated.40,91
FLAME BURNS Flame burns are the next most common burn injuries. Although injuries in house fires have decreased with the advent of smoke detectors, a significant number of burn injuries still result from careless smoking, improper use of flammable liquids, automobile accidents, and clothing ignited from stoves or space heaters. Victims whose bedding or clothes have been on fire rarely escape without some full-thickness burns. Outdoor misadventures result from using cooking stoves fueled by white gasoline, taking lanterns into tents, smoking in a sleeping bag, and starting (or improving) charcoal fires with gasoline or kerosene. Most accelerants, whether gasoline, kerosene, propane, or diesel, behave similarly with ignition temperatures of 210° to 280° C (410° to 536° F) and therefore burn at a high temperature with rapid tissue injury and full-thickness burns.
FLASH BURNS Flash burns are next in frequency. Explosions of natural gas, propane, gasoline, and other flammable liquids cause intense heat for a very brief time. For the most part, unignited clothing protects the skin in flash burns. Flash burns generally have a distribution over all exposed skin, with the deepest areas facing the source of ignition. Flash burns are partial thickness, with the depth dependent on the amount and kind of fuel that explodes. Although such burns generally heal without requiring extensive
FIGURE 13-3 Mayonnaise used to dissolve tar off a hand burn. (Courtesy Paul S. Auerbach, MD.)
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Burn
PART 3 BURNS, FIRE, AND RADIATION
skin grafts, they may be very large and associated with significant thermal damage to the upper airway.
CONTACT BURNS Contact burns result from hot metals, plastic, glass, or hot coals. Such burns are usually limited in extent but are deep. Victims involved in industrial accidents commonly have both severe contact burns and crush injuries, because these accidents often occur from presses or from hot, heavy objects. With the increased use of wood-burning stoves, an increasing number of toddlers are burned each year. The most common injuries are deep burns on the palms because the child falls with hands outstretched against the stove. Contact burns, especially in unconscious persons or those dealing with molten materials, are frequently fourth degree.16,53,80 In the wilderness setting, the most common contact burn is from hot coals, which are often as hot as 537.8° C (1,000° F). Intoxicated campers dance around and then into the campfire, architects of “river saunas” mishandle hot rocks, children fall into fires, and beach walkers may sustain deep burns when coals are buried in sand overnight. Even though the injured areas may be small, they can be deep and devastating when the hiker must walk a considerable distance on burned feet.24
ELECTRICAL BURNS Electrical burns are actually thermal burns from very highintensity heat. As electricity meets the resistance of body tissues, it is converted to heat in direct proportion to the amperage of the current and the electrical resistance of the body parts through which it passes. The smaller the body part through which the electricity passes, the more intense is the heat and the less it is dissipated. Therefore fingers, hands, forearms, feet, and lower legs are frequently totally destroyed, whereas larger-volume areas, such as the trunk, usually dissipate the current enough to prevent extensive damage to the viscera, unless the contact point is on the abdomen or chest. Although cutaneous manifestations may appear limited, massive underlying tissue destruction may be present because muscle, nerves, blood vessels, and bones can be burned beyond recovery.15,33,34,66 Arc burns occur when current takes the most direct path rather than the one of least resistance. These deep and destructive wounds, which may be initiated at extremely high temperature, occur at joints that are in close apposition at the time of injury. Most common are burns of the forearm to the arm when the elbow is flexed, and from the arm to the axilla if the shoulder is adducted when current passes from the upper extremity to the trunk. Electrical burns cause a particular set of other injuries and complications that must be considered during the initial evaluation. As mentioned previously, injuries related to a fall are common. The intense associated muscle contractions may cause fractures of the lumbar vertebrae, humerus, or femur and may dislocate shoulders or hips. Electrical cardiac damage may have symptoms like those of a myocardial contusion or infarction. Alternatively, the conduction system may be deranged. There can be actual rupture of the heart wall or of a papillary muscle, leading to sudden valvular incompetence and refractory cardiac failure. Household current at 110 volts generally either does no damage or induces ventricular fibrillation. Alternating current is more likely to induce fibrillation than is direct current. If no cardiac abnormalities are present when a victim is first seen after shocks of 110 to 220 volts, the likelihood that they will appear later is small. The nervous system is particularly sensitive to electricity. The most severe brain damage occurs when current passes through the head, but spinal cord damage is possible any time current passes from one side of the body to the other.44,48 Myelinproducing cells are susceptible. The devastating effects of transverse myelitis may develop days or weeks after injury. Conduction remains normal through existing myelin, but as the old myelin wears out, it is not replaced and conduction stops. Peripheral nerves are commonly damaged and may demonstrate severe permanent functional impairment.20,30 Every victim with an 282
electrical injury must have a thorough neurologic examination as part of the initial assessment. Myoglobinuria is a frequent accompaniment of severe electrical burns. Disruption of muscle cells releases cell fragments and myoglobin into the circulation to be filtered by the kidneys. If untreated, this can lead to permanent renal failure. Lightning strikes are discussed in Chapter 3, and reviews are available.*
CHEMICAL BURNS Chemical burns, usually caused by strong acids or alkalis, are most often the result of industrial accidents, home use of drain cleaners, assaults, and other improper use of harsh solvents.† In contrast to thermal burns, chemical burns cause progressive damage until the chemicals are inactivated by reaction with the tissue or by dilution by flushing with water. Although individual circumstances vary, acid burns may be more self-limited than are alkali burns. Acid tends to tan the skin (as leather is tanned), creating an impermeable barrier that limits further penetration of the acid. Alkalis combine with cutaneous lipids and saponify the skin until they are neutralized. A full-thickness chemical burn may appear deceptively superficial, appearing as only a mild brownish surface discoloration. The skin may appear intact during the first few days after the burn and then begin to slough spontaneously. Unless the observer can be absolutely certain, chemical burns should be considered deep partial thickness or full thickness until proved otherwise.
Clinical Presentation Cutaneous burns are caused by the application of heat or caustic chemicals to the skin. When heat is applied to the skin, the depth of injury is proportional to the temperature applied, duration of contact, and thickness of the skin. The severity of the burn injury is related to the size of the burn, depth of the burn, and part of the body that is burned.
ESTIMATION OF BURN SIZE Burns are the only quantifiable form of trauma. The single most important feature in predicting mortality, need for specialized care, and the complications expected from the burn is the overall burn size in proportion to the victim’s TBSA. Treatment plans, including initial resuscitation and subsequent nutritional requirements, are derived directly from the size of the burn. A general idea of burn size is provided by the “rule of nines.” Each upper extremity accounts for 9% TBSA, each lower extremity accounts for 18%, the anterior and posterior trunk each account for 18%, the head and neck account for 9%, and the perineum accounts for 1% (Figure 13-4). Although the rule of nines provides a reasonably accurate estimate of burn size, a number of more precise charts have been developed. A diagram of the burn can be drawn on a chart so that a relatively precise calculation of burned area can be made from the accompanying TBSA estimates given. Children less than 4 years old have much larger heads and smaller thighs in proportion to body size than do adults. In an infant, the head accounts for approximately 18% of the TBSA; body proportions do not fully reach adult percentages until adolescence. To further increase accuracy in burn size estimation, especially when burns are in scattered body areas, the observer might calculate the unburned areas on a separate diagram. If the calculations of the unburned areas and the burned areas do not add up to 100%, the observer should begin again with a new diagram to recalculate the burned areas. For smaller burns, an accurate assessment of burn size can be made by using the victim’s hand. The hand amounts to 2.5% TBSA. The dorsal surface accounts for 1%, the palmar surface for 1%, and the vertical surface for 0.5% (including the fingers).
*References 21, 22, 25, 26, 54, 66. † References 23, 35, 59, 62, 73, 76, 82.
9% 9%
9%
18%
1%
9%
9%
9%
A
18% 9% 9% 18% 13.5%
18% 1%
13.5%
18%
9%
B
DEPTH OF BURN An understanding of burn depth requires an understanding of skin anatomy (Figure 13-5). The epidermis, an intensely active layer of epithelial cells under layers of dead keratinized cells, is superficial to the active structural framework of the skin, the dermis. Although metabolically very active, the dermis has no regenerative capacity, and epithelial cells must eventually cover the surface of the dermis before the burn is healed. The skin appendages (hair follicles, sebaceous glands, and sweat glands) all contain an epithelial cell lining, so when the surface epidermis has been killed, epithelial covering must take place from overgrowth of the epithelial cells lining the skin appendages. As these cells reach the surface, they spread laterally to meet their neighbors, creating a new epithelial surface. As the burn extends deeper into the dermis, fewer and fewer appendages remain, and the epithelial remnants must travel farther to produce a new surface covering, sometimes taking many weeks to produce coverage. When the burn extends beyond the deepest layer of
the skin appendages, the wound can heal only by epithelial ingrowth from the edges, by wound contraction, or by surgical transplantation of skin from a different site. The thickness of skin varies both with the age and sex of the individual and with the part of the body considered. Although the thickness of the living epidermis is relatively constant, keratinized epidermal cells may reach a height of 5 mm (0.2 inch) on palms of hands and soles of feet. The thickness of the dermis, on the other hand, may vary from less than 1 mm (0.04 inch) on eyelids and genitalia to more than 5 mm (0.2 inch) on the posterior trunk. Although the proportional thickness of skin in each body area is similar in children, infant skin thickness in each specific area may be less than one-half that of adult skin; the skin does not reach adult thickness until adolescence. Similarly, in patients older than 50 years, dermal atrophy causes all areas of skin to become quite thin. Burns are classified by increasing depth as first degree, superficial partial thickness, deep partial thickness, full thickness, and fourth degree. The following descriptions appear to separate
FIGURE 13-5 Skin anatomy.
Epidermis Dermis Subcutaneous tissue Muscle Bone
First degree Partial thickness Full thickness
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CHAPTER 13 Emergency Care of the Burned Victim
FIGURE 13-4 Rule of nines used for estimating burned surface area. A, Adult. B, Infant.
PART 3 BURNS, FIRE, AND RADIATION
FIGURE 13-7 Deep partial-thickness burn. Note cherry-red color.
scarring, particularly in pigmented individuals and children, becomes inevitable. Full-Thickness Burns FIGURE 13-6 Superficial partial-thickness burn. Note pink color and moist surface.
burns into clearly defined categories, but many burns have a mixture of characteristics that give the observer an imprecise diagnostic ability. Considerable research is under way to devise instruments that will more precisely measure the depth of injury. Much of current burn treatment depends on knowledge of the depth of the burn. First-Degree Burns First-degree burns involve only the epidermis. The prototype is mild sunburn. First-degree burns do not blister. They become erythematous because of dermal vasodilation and are quite painful, both spontaneously and when touched. The erythema and pain subside over 2 to 3 days. By the fourth day, the injured epithelium desquamates in the phenomenon of “peeling.” Superficial Partial-Thickness Burns Superficial partial-thickness burns (Figure 13-6) include the upper layers of dermis and characteristically form blisters with fluid collection at the interface of the epidermis and dermis. Blistering may not occur for some hours after injury. Burns initially thought to be first degree may therefore be diagnosed as superficial partial thickness by day 2. When blisters are removed, the wound is pink and wet, and it is quite painful when contacted by currents of air. The wound is hypersensitive to touch and blanches with pressure, and blood flow to the dermis is increased over that of normal skin. If infection is prevented, superficial partialthickness burns heal spontaneously within 3 weeks without functional impairment. They rarely cause hypertrophic scarring, but in pigmented individuals the healed burns may never completely match the color of the surrounding normal skin. Deep Partial-Thickness Burns Deep partial-thickness burns (Figure 13-7) also blister, but the wound surface is usually a mottled pink and white color immediately after the injury. Alternatively, the burned dermis may be dry, with a cherry red color. The victim complains of discomfort rather than pain. When pressure is applied to the burn, capillary refill returns slowly or may be absent. The wound is often less sensitive to touch than is the surrounding normal skin. By the second day, the wound may be white and is usually fairly dry. If infection is prevented, such burns heal in 3 to 9 weeks but invariably do so with considerable scar formation. Unless active physical therapy is continued throughout the healing process, joint function may be impaired and hypertrophic 284
Full-thickness burns (Figure 13-8) involve all layers of the dermis and can heal only by wound contracture, epithelialization from the wound margin, or skin grafting. Full-thickness burns are classically described as leathery, firm, depressed when compared with the adjoining normal skin, and insensitive to light touch and pinprick. Unfortunately, the difference in depth between a deep partial-thickness burn and a full-thickness burn may be less than 1 mm (0.04 inch). Full-thickness burns are easily misdiagnosed as deep partial-thickness burns, because the two types have many of the same clinical findings. For example, they may be mottled in appearance. They rarely blanch with pressure and may have a dry, white appearance. The burn may be translucent with clotted vessels visible in the depths. Some full-thickness burns, particularly immersion scalds, have a red appearance and can be confused with superficial partial-thickness burns. However, these red, full-thickness burns do not blanch with pressure. Fullthickness burns develop a classic burn eschar. An eschar represents the structurally intact but dead and denatured dermis that, over days to weeks, separates spontaneously from the underlying viable tissue. Fourth-Degree Burns Fourth-degree burns involve not only all layers of the skin but also subcutaneous fat and deeper structures. These burns almost always have a charred appearance. Frequently, only the cause of the burn gives a clue to the amount of underlying tissue destruction.
FIGURE 13-8 Full-thickness burn. Note thick, leathery, white eschar.
CARE AT THE SCENE Flame Burns The first responder must remove the injured person from the source of heat. Because of the potential dangers of smoke inhalation in closed areas, the rescuer in a fire must take extreme caution not to become a victim. Persons with burning clothing should be prevented from running and should be made to lie down to keep flames and smoke away from the face. If water is not immediately available, the flames can be smothered with a coat or blanket. If nothing is available to douse or cover the flames, the victim should be rolled slowly on the ground. Once the burning has stopped, the clothes should be removed; some fabrics will continue to smolder and synthetic fabrics may melt, leaving a hot adherent residue on the victim that will continue the burning process. Scalds and Grease Burns The victim of a scald or grease burn must be removed from the source of heat. Any wet clothing or wrap should be removed, because fabric retains moist heat and may continue to burn skin that is in contact with the hot material. Accidents resulting from cooking indoors with grease are particularly hazardous. The startle response to a grease splatter may cause the victim to drop a pan of grease onto the fire, starting a kitchen fire that can rapidly become a dwelling fire. Airway Once flames are extinguished, primary attention must be directed to the airway. Any person rescued from a closed space or involved in a smoky fire should be considered at risk for smoke inhalation injury. If compressed oxygen is not available, a victim who is coughing independently should be encouraged to continue to do so. If the victim is unconscious or the airway status is in question, the victim should be placed supine and the airway manipulated manually via the chin lift or jaw thrust maneuver. When smoke inhalation is suspected, 100% oxygen should be administered by a tight-fitting mask. If the victim is unconscious and if personnel are trained to insert an endotracheal tube, such a tube should be passed and attached to a source of 100% oxygen. If the airway has to be supported by a tight mask, the rescuers must be aware of the significant danger of aspiration of gastric contents. Air forced into the stomach distends it and causes vomiting. The mask prevents expulsion of the fluid, and the victim rapidly aspirates vomitus into the tracheobronchial tree. No unconscious supine victim should ever be left unattended. Other Injuries and Transport Once an airway is secured, the first responder should quickly assess for other injuries and then transport the victim to the nearest hospital.8,20,66 Victims should be kept flat and warm and should be given nothing by mouth. Aside from establishment of an airway, further resuscitation is unnecessary if the victim will arrive at a hospital within 30 minutes. For transport, the victim should be wrapped in a clean, dry sheet and blanket. Sterility is not required. Cold Application Smaller burns, particularly scalds, may be treated with immediate application of cool water in the hope of limiting the extent of injury. The application of cold water is controversial, but immediate cooling decreases pain, possibly by a decrease in thromboxane production. By the time several minutes have passed, or after arrival in the emergency department, further cooling is not likely to alter the pathologic process. Ice water should not be used except on the smallest burns. Using ice on larger burns can easily induce systemic hypothermia and associated cutaneous vasoconstriction that can extend the thermal damage. Swelling During transport, constricting clothing and jewelry should be removed from burned and distal parts, because local swelling begins almost immediately. Constricting objects increase the
swelling, and removing tight jewelry in the presence of distal edema is time consuming once swelling has occurred. Electrical Burns Electrical burns are particularly dangerous, both to the victim and to the rescuer. If the victim remains in contact with the source of electricity, the rescuer must avoid touching the victim until the current can be turned off or the wires cut with properly insulated wire cutters. Once the victim is removed from the source of current, airway, breathing, and circulation must be checked. Ventricular fibrillation or standstill is a common accompaniment to a major transthoracic current; cardiopulmonary resuscitation should be instituted if carotid or femoral pulses are not palpable. If pulses are present but the victim is apneic, mouth-to-mouth resuscitation alone may be lifesaving. Cardiopulmonary resuscitation should continue until a cardiac monitor can be obtained, which will direct treatment for cardiac standstill or ventricular fibrillation. Once an airway is established and pulses return, a careful search must be made for associated life-threatening injuries. Electrocuted victims frequently fall from heights and may have serious head or neck injuries. The intense tetanic muscle contractions associated with electrocution may fracture vertebrae or cause major joint dislocations. Patients with high-voltage electrical injuries should be treated with spinal precautions and splints if necessary, until fractures can be ruled out. Chemical Burns Whenever possible, chemical burns should be thoroughly flushed with copious amounts of water at the scene of the accident. Chemicals will continue to burn until removed; washing for 5 to 10 minutes under a stream of running water may limit the overall severity of the burn. No thought should be given to searching for a specific neutralizing agent. Delay deepens the burn, and neutralizing agents may cause burns themselves; they frequently generate heat while neutralizing the offending agent, adding a thermal burn to the already potentially serious chemical burn. Hydrofluoric acid is commonly used as a cleaning agent in the petroleum industry or for glass etching. As an acid it causes coagulation necrosis, and the fluoride ion then chelates positively charged ions such as calcium and magnesium, causing an efflux of intracellular calcium, which results in cellular death.65 Fluoride ion is also a metabolic poison that inhibits sodium-potassium adenosine triphosphatase (ATPase), allowing efflux of potassium.55 Hydrofluoric acid burns are classified based on the concentration of the solution according to the National Institutes of Health Division of Industrial Hygiene.94 Concentrations above 50% cause immediate tissue destruction and pain. Concentrations of 20% to 50% create a burn that is apparent within several hours of exposure; exposures with concentrations less than 20% may take as long as 24 hours to become apparent. Systemic symptoms of hypocalcemia or hypomagnesemia are usually absent, although cardiac dysrhythmias may develop and, once present, are difficult to restore to a normal rhythm. QT prolongation is the typical electrocardiogram finding when present. Treatments of hydrofluoric acid exposure are designed to neutralize the fluoride ion and prevent systemic toxicity. Topical calcium gluconate gel (3.5 g of 2.5% calcium gluconate mixed with 5 oz of water-soluble lubricant applied to the wound 4 to 6 times a day for 3 to 4 days) can be used after the wounds are copiously irrigated.57 Pain relief with this approach is often quite rapid. Return of pain is often a sign to repeat the dressing change. Phosphorus can be found in both military and civilian settings. It is an incendiary agent found in hand grenades, artillery shells, fireworks, fertilizers, and some homemade explosives. White phosphorus ignites in the presence of air and burns until the entire agent is oxidized or the oxygen source is removed (such as immersion in water). Treatment should consist of irrigation with large amounts of water, removal of easily identifiable pieces of phosphorus, and moist dressings for transport. Ultraviolet light can be used to identify embedded particles through phosphorescence, allowing for improved removal. Hypocalcemia, hyperphosphatemia, and cardiac arrhythmias have been reported.90 285
CHAPTER 13 Emergency Care of the Burned Victim
Treatment
PART 3 BURNS, FIRE, AND RADIATION
First Aid at the Scene for Smaller Burns Not all burns need immediate medical attention. Burns less than 5% TBSA (excluding deep burns of the face, hands, feet, perineum, or circumferential extremity) can be treated successfully in a wilderness setting if adequate first-aid supplies are available and wound care is performed diligently. Except for the very shallow burn that heals within a few days, most burns should be seen by a physician within 3 to 5 days after injury. Burns should be washed thoroughly with plain soap and water and dried with a clean towel. The water used should be suitable for drinking, but it need not be sterile or bottled. Any obviously dead skin should be peeled off (which may be painful) or trimmed with sharp manicure scissors (usually painless). Large (greater than 2.5 cm [1 inch]), thin, fluid-filled blisters should be drained and the dead skin trimmed to prevent a potential closedspace infection. Deep burns, as from a flame, are firm and leathery, usually do not blister, and do not require immediate debridement. A small tube of silver sulfadiazine cream and tubes of bacitracin or Neosporin antibiotic ointment should be available in the first-aid kit. Either may be used and should be spread lightly over the wound. The wound may then be wrapped in dry, clean gauze, which need not be sterile. Simple dressings (one type of topical cream, plain gauze) are sufficient. Some patients prefer nonadherent dressings, such as Telfa or Adaptic (sometimes known as “greasy gauze”), because they are less likely to stick to the wound during dressing changes. The same effect can be achieved by soaking (with water) a plain gauze dressing that appears stuck to the wound, waiting a few minutes, and then removing the dressing with additional water if necessary. Other dressings (hydrogels, silver-coated dressings, silicone gel sheets, calcium alginate) designed to minimize the frequency of dressing changes and promote healing are available but are not necessary. The authors recommend simple antibiotic ointments such as silver sulfadiazine or bacitracin and plain gauze dressings rather than “specialty” dressings for inclusion in first-aid kits because they are simple, cheaper, and effective. Although patients may prefer one dressing over another for various reasons, no dressing has been shown conclusively to accelerate the healing of burn wounds. As such, the first-aid kit should be stocked with general-use supplies, which are less expensive and easier to replenish. Mobility of the wound area must be actively maintained, and concentrated efforts should be made to avoid dependent positioning, especially when the victim is resting or sleeping. Focal edema in a small burn wound can be painful and alarming and should be prevented with extremity elevation and active rangeof-motion exercises several times a day. Wound care should be performed once a day if the outer dressing remains dry. A wet, sticky outer dressing needs more frequent wound care to keep up with drainage from the wound. If only the outer dressing is dirty, whether soiled from food, dirt, or other substance, it may be changed as often as needed to maintain a clean dressing and aid in patient comfort. For the quickest healing of superficial burns, daily wound care should remove all exudates and crust, both of which significantly retard wound healing. Once a wound has epithelialized or is nearly epithelialized, a moisturizing lotion is recommended to aid in hydration and decrease scarring. Vitamin E, aloe, and oat beta glucan are often used for their antiinflammatory and soothing properties. Melaleuca is a topical antibacterial and antifungal tea tree oil that Australian aboriginal people have used for a variety of medicinal purposes. It is the active ingredient in Burnaid, a popular cream used for superficial partial-thickness burn injuries. When determining the type of dressing to apply to a burn wound, the following considerations are important: • The dressing should cover the entire burned area (an enclosed dressing), leaving no burned skin exposed to air or air currents. • The burn wound surface should stay moist, whereas the unburned skin surrounding the burn should not macerate. • The dressing should be relatively light and not bulky; it should not limit the patient’s ability to actively flex and extend all burned extremities and digits. Frequent flexion 286
FIGURE 13-9 Contact burn from stepping on hot coals. Small, flat blisters do not require debridement.
and extension prevent the burned skin from tightening and thereby assist with pain control and prevention of edema. These principles are far more important than the choice of topical agent to cover the burn. Commonly used topical agents that might be carried in first-aid kits include antiseptic and antibiotic ointments and creams (e.g., bacitracin, Neosporin, Polysporin, double antibiotic ointment, triple antibiotic ointment, silver sulfadiazine) and nonantibacterial ointments (e.g., Aquaphor, Vaseline, A+D ointment). All of these agents are acceptable and the use of a topical antimicrobial is not essential in the early postburn setting. Technique of Burn Wound Debridement. Small intact blisters do not need debridement (Figure 13-9). The blister environment serves as a sterile biologic dressing, preventing desiccation and (usually) pain. The intact blister should be protected from trauma and observed every few hours to ensure that the blister has not popped. If the blister opens, debridement is usually recommended because the leaking blister fluid may lead to crusting that can effectively “seal over” the wound, leading to a closedspace infection (Figure 13-10). Debridement of blisters is essentially painless so long as the blistered skin is cut and not peeled or torn. The burn should be washed with soap and water. Forceps are used to grasp the blistered skin, and small (manicure) scissors can be used to cut off the blister roof (Figure 13-11). Care should be taken to remove as much of the blistered skin as possible, leaving a uniform surface that can then be treated with a topical agent (Figure 13-12). There will be no bleeding during this procedure. To ensure that the procedure will be painless, the body part to be debrided should be stabilized against a solid surface. This prevents motion on the part of the patient, and it optimizes control for the person performing the procedure.
FIGURE 13-10 Contact burn from stepping on hot coals. Leaking blisters that have burst should be debrided (see text).
CHAPTER 13 Emergency Care of the Burned Victim
BOX 13-1 Baxter (Parkland) Formula First 24 Hours—Ringer’s Lactate • 4 mL /kg/% burn in 24 hours One-half in first 8 hours One-half in second 16 hours • Example: 70-kg (154-lb) man with 50% burn 4 mL × 50% × (70 kg) = 14,000 mL in 24 hours 7000 mL in hours 1 to 8 3500 mL in hours 8 to 16 3500 mL in hours 17 to 24
A
Second 24 Hours—Albumin or Plasma at Maintenance • Maintain normal vital signs • Adequate urine output • Example: 70-kg (154-lb) man with 50% burn 250 to 500 mL plasma 2000 to 2500 mL D5W D5W, Dextrose 5% in water.
B FIGURE 13-11 Partial-thickness burn to the dorsal hand from hot oil while cooking at camp. A, Blister is debrided 5 days after the injury. B, Bacitracin ointment is applied. (Courtesy Tim Platt-Mills, MD.)
EMERGENCY DEPARTMENT CARE The primary rule for the emergency physician is to “forget about the burn.” Although a burn is usually readily apparent and is often a dramatic injury, a careful search for other life-threatening injuries must take priority. Only after an overall assessment of the victim’s condition should attention be directed to the specific problem of the burns. Assessment of the nonthermally injured victim is presented in Chapter 21; the following paragraphs consider the specific problems encountered in the victim with burns. Resuscitation Since the 1970s, more than a dozen resuscitation plans have been suggested. The goal of all of them is to complete treatment with a living victim who has normally functioning kidneys and does not have cardiac failure or pulmonary edema. Nearly all of these plans use a combination of colloid and crystalloid solutions, but they vary considerably in the ratio of colloid to crystalloid, timing
FIGURE 13-12 The burn seen in Figure 13-9, after debridement.
of colloid administration, sodium concentration of crystalloid solution, and, to a much lesser extent, total volume of fluid given.* Some require frequent changing of solutions, others require mixing of solutions, and some require careful monitoring of the victim’s electrolytes. Intense controversy rages over which resuscitation plan is best, but this need not concern the physician without a special interest in burn physiology. There is general agreement on a few facts. A victim with very large burns will probably need both colloid and crystalloid. Initially, capillaries are permeable to both crystalloid and colloid solutions. The capillary leak to albumin and other large molecules repairs itself between hours 6 and 24 after injury. The choice of formulas for initial resuscitation is probably of relatively little consequence as long as the rate of fluid administration is modified according to the victim’s changing requirements as the hours pass. Because of its simplicity, ease of administration, and need for little blood chemistry monitoring, the formula developed by Baxter, known as the Baxter formula, or Parkland formula, has been adopted by most experts and recommended officially by the American College of Surgeons Committee on Trauma. According to the Baxter formula, crystalloid is given during the first 24 hours, while the capillaries are still permeable to albumin, and then colloid is given during the second 24 hours, when the capillary leak has presumably sealed. Rapid administration of crystalloid solution results in early expansion of depleted plasma volume, which will return cardiac output toward normal. Once the capillary leak has sealed, colloid (usually in the form of albumin) remains the most effective solution to maintain plasma volume without further increasing edema. The Baxter formula was derived to provide specific replacement of known deficits measured by simultaneous determinations of red blood cell volume, plasma volume, extracellular fluid volume, and cardiac output during burn shock. The first 24-hour and second 24-hour calculations are shown in Box 13-1. The formula calls for the administration of lactated Ringer’s solution, 4 mL/kg body weight per percentage of body surface burned during the first 24 hours after the injury. One-half of this fluid should be given in the first 8 hours and the second one-half during the next 16 hours. Fluid therapy during the second 24 hours consists of the administration of free water in quantity sufficient to maintain a normal serum sodium concentration, as well as plasma (or other colloid) to maintain a normal plasma volume. The adequacy of resuscitation can best be judged by frequent measurements of vital signs, central venous pressure, and urine output and by observation of general mental and physical responses. Despite myriad new monitoring devices, urine output *References 4, 13, 29, 32, 38, 56, 60, 63.
287
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remains one of the most sensitive and reliable assessments of fluid resuscitation. In the absence of myoglobinuria, a urine output of 0.5 mL/kg/hr in adults and 1 mL/kg/hr in children weighing less than 10 kg (22 lb) ensures that renal perfusion is adequate. The victim’s sensorium gives an indication of the state of cerebral perfusion and oxygenation. The victim should be alert and cooperative; confusion and combativeness are signs of inadequate resuscitation or warn of other causes of hypoxia, and supplemental oxygen should be provided in addition to fluid resuscitation. Patients with burns that involve less than 10% TBSA generally do not require fluid resuscitation. They should stay well hydrated but should not be encouraged to force fluids. Patients with burns that involve between 10% and 20% TBSA usually do not require intravenous (IV) fluid resuscitation. They should be encouraged to drink fluids that contain electrolytes (e.g., Gatorade) and should be discouraged from drinking large amounts of water or sodas. Hydration status in these patients should be monitored simply by ensuring that the oral mucous membranes are moist and that urine output is brisk with light-colored urine. Patients with burns that involve more than 20% TBSA should receive IV fluid resuscitation with crystalloid solution until they reach a facility where medical professionals can evaluate the need for other types of fluids. Victims with burns of less than 50% TBSA can usually be resuscitated with a single large-bore peripheral IV line. Because of the high incidence of septic thrombophlebitis, lower extremities should be avoided as IV portals. Upper extremities are preferable, even if the IV line must pass through burned skin. Victims with burns larger than 50% TBSA or who have associated medical problems, are at the extremes of age, or have concomitant smoke inhalation should have additional central venous pressure monitoring. Because of the extremely unstable state of the circulation in victims with burns over 65% TBSA, such victims should be monitored in an intensive care setting where a SwanGanz catheter for measuring pulmonary capillary wedge pressure and cardiac output is available. The presence of myoglobinuria alters the resuscitation plan. Myoglobinuria results from destruction of muscle cells, with release of myoglobin (the red muscle pigment). This is most often a problem when there are associated crush injuries, electrical burns, or extremely deep thermal burns. Characteristic colacolored urine is an indication to increase the amount of fluid given and to establish a diuresis of 70 to 100 mL of urine per hour. An initial bolus of 25 g of mannitol in adults or 0.5 to 1 g/ kg in children with a repeat dose in 15 to 30 minutes should be considered. Escharotomy Careful monitoring of the peripheral circulation is required in victims with circumferential full-thickness burns of the extremities. The edema that forms beneath inelastic eschar increases tissue pressure to a point at which it exceeds lymphatic pressure, thereby further increasing edema. When the edema exceeds venous pressure and eventually approaches arterial pressure, it stops all circulation to the extremity distal to the constricted area. The classic findings of compartment syndrome, usually considered to be pain, paresthesias, pulselessness, and tense swelling, may or may not be present in the burned extremity. Therefore distal pulses should be carefully monitored with Doppler ultrasound. If any of the clinical signs mentioned earlier occur, or if Doppler signals disappear, an escharotomy should be performed immediately. Escharotomy performed in the hospital does not require an anesthetic, because only an insensate full-thickness burn is incised. An incision is made through the eschar into subcutaneous tissue, first along the lateral aspect of the extremity and, if symptoms or signs do not improve, along the medial aspect (Figure 13-13). The incisions need not be as deep as the investing muscle fascia, and bleeding can usually be easily controlled with electrocautery and topical clotting agents. If arrival to the hospital will be within 6 hours, escharotomies should not be done in the field because the victim may bleed to death without proper equipment to control bleeding. 288
FIGURE 13-13 Deep full-thickness flame burns to the bilateral lower extremities and buttocks requiring medial and lateral escharotomies. (Courtesy Michael J. Mosier, MD.)
Circumferential full-thickness burns of the trunk in small children occasionally demand an escharotomy to improve pulmonary function. Chest wall escharotomies are made in the anterior axillary line bilaterally, extending from the clavicle to the costal margin. If the abdomen is involved with the burn, the inferior margins of the escharotomy may be connected transversely (Figure 13-14). Fasciotomies are rarely needed in victims with thermal burns. However, if distal pulses do not return after medial and lateral escharotomies, fasciotomy should be considered. On the other hand, victims with electrical injuries frequently need fasciotomy. Careful monitoring is mandatory for all victims with electrical burns and with burns associated with soft tissue trauma or fractures. In these circumstances, loss of pulses is a strong indication for urgent fasciotomy under general anesthesia in the operating room. The need for escharotomy in the burned hand is somewhat controversial. Fingers burned badly enough to require escharotomy are frequently mummified, and the lack of muscles in the fingers puts less tissue at ischemic risk. Escharotomy done in fingers that may not require it runs the risk of exposing the interphalangeal joints (Figure 13-15), leading to subsequent infection that may ultimately require joint fusion or finger amputation. Both the palmar arch and the digital vessels should be monitored with Doppler ultrasound in any significant hand burn. If the signals disappear over the palmar arch or in the digital vessels, consideration should be given to performing a dorsal interosseous fasciotomy.
FIGURE 13-14 Full-thickness flame burns to the anterior torso and left upper extremity. Escharotomies were performed along the flank, sternum, clavicle, costal margin, and abdomen to release the restricting eschar and allow improved chest and abdominal wall compliance. (Courtesy Michael J. Mosier, MD.)
FIGURE 13-15 Full-thickness flame burns to the right hand with escharotomies in a fan pattern between metacarpals to adequately release pressure from edema formation. (Courtesy Michael J. Mosier, MD.)
Burn Wound Management The burn wound should be cleansed initially with a surgical detergent. All loose, nonviable skin should be gently trimmed. Debridement should be done gently; small doses of IV narcotic are usually sufficient analgesia for this procedure. General anesthesia and operating room debridement should be avoided until resuscitation is complete, unless other surgical procedures are necessary. Once the wound is cleansed, a topical chemotherapeutic agent should be applied. A detailed description of all the agents available is beyond the scope of this chapter, but those most commonly used in the United States and other industrialized countries contain silver sulfadiazine. It comes as a white cream, is soothing to the wound, has a good antimicrobial spectrum, and has almost no systemic absorption or toxicity.6,37,77,85 The victim should be carefully questioned about allergy to sulfa drugs before its use, however, because allergic reactions are encountered in about 3% of patients. These reactions may be manifested clinically as pain after application rather than the soothing feeling that silver sulfadiazine usually provides. If an allergy is suspected by history, a small (10 × 10 cm [4 × 4 inch]) patch of silver sulfadiazine should be applied as a test. The remainder of the wound can be dressed in bacitracin. If no local reaction occurs after 2 to 4 hours, an allergy is unlikely and silver sulfadiazine is the dressing of choice. If an allergy is confirmed, the victim should be referred to a burn center, where the next choice of topical antimicrobial would probably be silver nitrate solution.
OUTPATIENT BURNS The vast majority of victims with burns do not require hospitalization. In many cases, the burn, if merely kept clean, heals spontaneously in less than 3 weeks with acceptable cosmetic results and no functional impairment. Unfortunately, good results in treating superficial minor burns may entice the unwary physician to treat more complex burns by the same methods. For the victim, the consequences of such a mistake can be the need for subsequent hospitalization, joint dysfunction, and hypertrophic scarring that may be difficult to correct, as well as considerable loss of time from work or school. First-Degree Burns Although first-degree burns are very painful, victims rarely seek medical attention unless the burned area is extensive. These victims do not require hospitalization, but control of the pain is extremely important. Aspirin or codeine may be adequate for small injuries, but for large burns, liberal use of a more potent narcotic for 2 to 3 days is indicated. For topical medication, the authors recommend one of the many proprietary compounds containing extracts of the Aloe vera plant in concentrations of at least 60%. Aloe vera has antimicrobial properties and is an effective analgesic.46,74 Anecdotal
Superficial Partial-Thickness Burns Treatment of superficial partial-thickness burns presents little problem. If the wound is kept clean, the victim is kept comfortable, and the joints are kept active, these wounds heal in less than 3 weeks with minimal scarring and no joint impairment. Initially, the wound should be cleansed and debrided as described previously. Small blisters may be left intact. Biochemical analysis of the protein-banding pattern of burn blister fluid, obtained by polyacrylamide gel electrophoresis, has shown it to be similar to that of serum.88 The authors suggest that the fluid is an exudate mainly from the vascular system, that it provides a good environment for the fibroblasts in the damaged site, and that it facilitates the healing process. Larger blisters are difficult to protect, however, and blister fluid is a rich culture medium for bacteria that live in the skin appendages. Therefore large blisters and small blisters in large burns should usually be totally removed with forceps and scissors. In some instances the blister fluid can be aspirated with a large-bore needle, allowing the blistered epidermis to remain on the wound as a biologic dressing. This dead epidermis, however, is fragile, tends to contract, and rarely stays in place except over small areas. After debridement, these wounds can sometimes be managed with one of the newer synthetic dressings that contain elemental silver. There are several on the market (Aquacel Ag, Acticoat, Mepilex Ag) that can be applied and left in place for a week or until the burn is healed at about 2 weeks. However, the most commonly used treatment is wound coverage with silver sulfadiazine and application of a light dressing to promote active range of motion. Some very small burns do not require topical agents. For small facial burns, bacitracin ointment may be a better choice than silver sulfadiazine cream because it is less drying. Pain is managed as for first-degree burns, and the patient usually should return every 2 to 3 days until the wound heals or the patient has demonstrated the ability to manage the wound without supervision. If silver sulfadiazine is used, an appropriate home treatment regimen is to have the patient cleanse the wound once daily with tap water and reapply the topical agent and light dressing. During dressing changes, and as often as possible, all involved joints should be put through a full range of motion. The dressing may be unnecessary while the patient is at home, but the patient should dress the wound before leaving the house. This method is highly successful, but it is inconvenient and fairly painful and requires good patient cooperation. The “exposure” method has little to recommend it. This method involves leaving the wound open, allowing the wound drainage to desiccate and form a scab. Controlled studies in animals have shown that desiccation and crust formation interfere with wound healing. Our experience has also shown that crusts crack over joints, cause considerable discomfort, and can hide infection. Deep Partial-Thickness and Full-Thickness Burns Treatment of deep partial-thickness and full-thickness burns is a matter of grave concern. Full-thickness burns heal only by contraction and epithelialization from the periphery. Epithelium does not begin to migrate until the eschar is removed; the growth rate then is only about 1 mm (0.04 inch)/day. Thus healing of even a small full-thickness burn may involve many weeks of discomfort and disability. Deep partial-thickness burns may take 4 to 8 weeks to heal and then leave an unacceptable scar. If a joint is involved, some loss of joint function is the rule. The authors have adopted a policy of early excision and grafting for such wounds. 289
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evidence suggests that it may decrease subsequent pruritus and peeling. Burns from ultraviolet rays (sunlight, sunlamp) may initially appear to be only epidermal, but the injury may in fact be a superficial partial-thickness burn with blistering apparent only after 12 to 24 hours. Therefore the victim with such a burn should be cautioned about blisters and should be asked to return if they form, because wound management then becomes more important because of the potential for infection and subsequent scarring.
PART 3 BURNS, FIRE, AND RADIATION
Initial outpatient treatment can be followed by elective surgery as soon as it can be scheduled. Small wounds can be treated through day surgery; larger wounds located over dynamically important areas can be closed with only a day or two of hospitalization. Excision and grafting procedures should be done by a surgeon experienced in tangential wound excision. The advantages of this aggressive approach—a pain-free patient with normal joint function, better cosmetic result, and a rapid return to work or school—more than compensate for the brief hospitalization and the very small risk associated with a minor operation. Should the excision and grafting plan be unacceptable to the patient or treating physician, the standard method of daily cleansing and application of silver sulfadiazine cream is used. Most full-thickness burns need grafting at about 3 to 4 weeks after the injury. Deep dermal burns should be seen by the physician frequently during the healing process, and active physical therapy is crucial to ensuring a successful outcome.
REHABILITATION Physicians who regularly care for people with burn injuries recognize that treatment goals extend far beyond healing of the wounds and survival of the victim. The aim is to return victims at least to their preburn functional status physically and to ensure smooth and timely reentry into family and social situations, including work or school. Awareness that recovery from burn injury often depends on a number of nonphysician health care workers is essential. Depending on the severity of the burn and associated social situation, participation is commonly required of nurses, nutritionists, occupational therapists, physical therapists, recreational therapists, social workers, vocational rehabilitation counselors, psychologists, pain management specialists, and clergy. Burn rehabilitation should be initiated by the first physician to see the victim. Once all systemic and wound issues have been addressed, proper positioning of wounded extremities or digits should be assessed by an occupational therapist who has been specially trained in burn management. Splints should be made immediately if deemed appropriate. Range-of-motion exercises should be started on the day of injury, and frequent follow-up by a physical therapist is essential. The best functional outcomes result from meticulous attention to early mobility. Patients almost universally choose not to move a burned body part, and an active ancillary burn staff is essential for satisfactory results. Burn scars require approximately one year to fade, soften, and mature. Physical therapy may be required throughout this time period or longer. Pressure garment therapy may be used in certain cases in an attempt to prevent hypertrophic scars from deve loping. The interested reader is referred to books dealing with acute burn care, reconstructive plastic surgery, and burn rehabilitation.1,7,11
Inhalation Injury Of the nearly 500,000 fire victims admitted to hospitals each year, smoke or thermal damage to the respiratory tree may occur in as many as 30%.68 Carbon monoxide poisoning, smoke poisoning, and thermal injury are three distinctly separate aspects of clinical inhalation injury. Inhalation injury rarely occurs in an outdoor setting.
CARBON MONOXIDE POISONING Pathophysiology Carbon monoxide (CO) is a colorless, odorless, tasteless gas that has an affinity for hemoglobin 200 times greater than that of oxygen. The most simply explained mechanism of action of CO is reversible displacement of oxygen on the hemoglobin molecule. Although worsening hypoxia is important, and the percentage of carboxyhemoglobin (COHb) in the blood represents in large measure the degree of victim hypoxia, this simple mechanism cannot account for all of the experimental and clinical findings seen with exposure to CO. For example, an 290
experimental group of dogs was exchange-transfused with blood containing 80% COHb. They showed no symptoms. In a control group with COHb levels of 80% produced by inhalation of CO, all animals died. Furthermore, the degree of enzyme and muscle impairment may not correlate accurately with the levels of blood COHb.12,17,27,47 In vitro, CO combines reversibly with cardiac muscle myoglobin and heme-containing enzymes, such as cytochrome oxidase (a3).12 Despite its intense affinity, it readily dissociates according to the laws of mass action. The half-life of COHb in humans breathing room air is 4 to 5 hours. In humans breathing 100% oxygen, the half-life is reduced to 45 to 60 minutes.51 In a hyperbaric oxygen chamber at 2 psi, the half-life is 30 minutes, and at 3 atm in a chamber it is reduced to 15 to 20 minutes.87 Clinical Presentation Blood levels of COHb provide a laboratory measure to correlate with associated symptoms of CO poisoning. Levels less than 10% do not cause symptoms, although victims with exercise-induced angina may show decreased exercise tolerance. At levels of 20%, healthy persons complain of headache, nausea, vomiting, and loss of manual dexterity. At 30%, they become confused and lethargic and may show depressed ST segments on an electrocardiogram. In a fire situation, this level may lead to death because the victim loses both the interest and the ability to flee the smoke. At levels between 40% and 60%, the victim lapses into coma, and levels much above 60% are usually fatal. Therapy Victims who have not been unconscious and who have a normal neurologic examination on admission almost always recover completely without treatment beyond administration of 100% oxygen. Victims who remain comatose once COHb levels have returned to normal have a poor prognosis, and in the authors’ experience they rarely awaken. Although enthusiasts for hyperbaric oxygen treatment (HBOT) (see Chapter 76) consider it a standard of care for CO poisoning,2,3,49,58 other physicians are skeptical.75 One controlled study indicated that hyperbaric oxygen made no difference for moderate poisoning, and multiple treatments were no better than a single treatment for victims with severe poisoning.69 Furthermore, when associated with a major burn, transport to a chamber delays definitive care and is associated with numerous complications, including emesis, seizures, eustachian tube occlusion, aspiration, hypocalcemia, agitation requiring restraints or sedation, arterial hypotension, tension pneumothorax, and cardiac arrhythmia or arrest.31,83 The issue of whether, and at what time in the progression of CO poisoning, HBOT may be of value will undoubtedly continue to be studied and debated.
THERMAL AIRWAY INJURY Pathophysiology The term pulmonary burn is a misnomer. True thermal damage to the lower respiratory tract and lung parenchyma is extremely rare unless live steam or exploding gases are inhaled. The air temperature near the ceiling of a burning room may reach 540° C (1004° F) or more, but air has such poor heat-carrying capacity that most of the heat is dissipated in the nasopharynx and upper airway. Heat dissipation in the upper airway, however, may cause significant local thermal injury. Clinical Presentation Victims who have been in explosions (propane, natural gas, or gasoline) and have burns of the hands, face, and upper torso are particularly at risk for pharyngeal edema (Figure 13-16). Therapy Maintenance of the airway is the main concern with potential thermal airway injury. Victims injured in explosions should be examined for oropharyngeal erythema and edema. If these are present, the victim should be intubated for 24 to 72 hours until edema subsides. A simple test to determine if intubation should continue is to see if the victim can breathe around the
endotracheal tube when the cuff is deflated. If so, the airway edema has probably resolved, and extubation should be safe. If doubt exists, extubation should be performed over a fiberoptic bronchoscope or nasogastric tube, which allows easy replacement of the endotracheal tube if necessary. Because this is not a pulmonary parenchymal injury, the purpose of intubation is to protect the airway and not necessarily to assist with ventilation. Ventilator settings should be adjusted accordingly, and vigorous pulmonary toilet should be instituted to prevent the pulmonary problems (atelectasis and pneumonia) commonly seen in intubated victims.
SMOKE POISONING Pathophysiology Some 280 separate toxic products have been identified in wood smoke. Modern petrochemical science has now produced a wealth of plastic materials in homes and automobiles that when burned produce nearly all of these and many other products not yet even characterized.42,64,81,95 Prominent by-products of incomplete combustion are oxides of sulfur, nitrogen, and many aldehydes. One such aldehyde, acrolein, causes severe pulmonary irritation and edema in concentrations as low as 10 ppm. Although the chemical mechanisms of injury may be different with different toxic products, the overall end-organ response is reasonably well defined.* There is immediate loss of bronchial– epithelial cilia and decreased alveolar surfactant. Microatelectasis, and sometimes macroatelectasis, results in and is compounded by mucosal edema in small airways. Wheezing and air hunger are common symptoms at this time. After a few hours, tracheal and bronchial epithelia begin to slough and hemorrhagic tracheobronchitis develops. In severe cases, interstitial edema becomes prominent, resulting in a typical picture of the adult respiratory distress syndrome (ARDS). Pulmonary alveolar macrophages are poisoned, causing severe impairment of chemotaxis, which undoubtedly contributes to the high incidence of late pneumonia seen in victims with associated cutaneous burns. The activated neutrophils release superoxides and free radicals of oxygen, which together with other inflammatory mediators aggravate alveolar–capillary damage, leading to increased interstitial edema and impaired oxygenation. Clinical Presentation Any victim who has been indoors or in an enclosed space with a smoky fire and has a flame burn should be assumed to have smoke poisoning until proved otherwise. The acrid smell of smoke on the victim’s clothes should raise suspicion. Rescuers are often the most important historians and should be carefully questioned. *References 9, 14, 36, 39, 50, 51, 72, 79, 93, 95.
Therapy All victims burned in an enclosed space or having any suggestion of neurologic symptoms should be given 100% oxygen while awaiting measurement of COHb levels. This should be administered through a tight-fitting mask in the field. If the victim demonstrates labored breathing or if a prolonged transport time is anticipated, endotracheal intubation should be performed by trained personnel. Oxygen at 100% can then be administered by ventilator. Mucosal burns of the mouth, nasopharynx, and larynx respond with edema formation and may lead to upper airway obstruction
FIGURE 13-17 View of the proximal airway on bronchoscopy, demonstrating a moderate amount of erythema and carbonaceous debris, consistent with a grade 2 inhalation injury by bronchoscopic criteria. (Courtesy Michael J. Mosier, MD.)
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FIGURE 13-16 Deep full-thickness flame burns to the face and neck with emergent cricothyroidotomy secondary to the inability to perform oropharyngeal intubation. (Courtesy Michael J. Mosier, MD.)
Careful inspection of the mouth and pharynx should be done early. Hoarseness and expiratory wheezes are signs of potentially serious airway edema or smoke poisoning. Copious mucus production and carbonaceous sputum are sure signs, but their absence should not raise false hopes that injury is absent. COHb levels should be obtained; elevated COHb levels or any clinical symptoms of CO poisoning are presumptive evidence of associated smoke poisoning. In very smoky fires, COHb levels of 40% to 50% may be reached after only 2 to 3 minutes of exposure.87 Anyone with suspected smoke poisoning should have a set of arterial blood gases drawn. One of the earliest indicators is an improper ratio of arterial partial pressure of oxygen (PaO2) to fraction of inspired oxygen (FIO2) (the P/F ratio). Normally the ratio is 400 to 500, whereas patients with impending pulmonary problems have a ratio of less than 300 (e.g., a PaO2 of less than 120 mm Hg with an FIO2 of 0.40). A ratio of less than 250 is an indication for vigorous pulmonary therapy and not an indication for merely increasing the inspired oxygen concentration. A number of authorities suggest the routine use of fiberoptic bronchoscopy10,52,71,77 (Figure 13-17). It is inexpensive, quickly performed by an experienced clinician, and useful for accurately assessing edema of the upper airway. Aside from the presence of tracheal erythema, however, it does not materially influence the treatment for smoke poisoning. Therefore, it should be used only when the diagnosis is in doubt or for experimental studies. We have correlated by multivariate analysis a constellation of history, signs, and symptoms with bronchoscopic findings in 100 consecutive patients with suspected smoke inhalation admitted to the University of Washington Burn Center in Seattle. If the patient had the combination of history of closed-space fire, carbonaceous sputum, and a COHb level greater than 10%, there was a 96% correlation with positive bronchoscopy. Presence of two of the above features dropped correlation to 70%, and if only one was present, the correlation dropped to 36%. As discussed previously, upper airway edema was best correlated with an explosion (flash burn) that involved both the face and upper torso. Nearly 50% of such victims had significant upper airway edema and underwent prophylactic airway intubation.
PART 3 BURNS, FIRE, AND RADIATION
at any time during the first 24 hours after the burn. Red or dry mucosa or small mucosal blisters should alert the observer to the possibility of subsequent airway obstruction; they also should raise suspicion that significant smoke inhalation may have occurred. Any victim with burns of the face should have a careful visual inspection of the mouth and pharynx; if abnormalities are found, the larynx should be examined immediately on arrival at the hospital. The presence of significant intraoral and pharyngeal burns is a clear indication for early endotracheal intubation, because the progressive edema may make later emergency intubation extremely hazardous, if not impossible. The mucosal burns themselves are rarely full thickness and can be successfully managed with good oral hygiene. Once inserted, the endotracheal tube should remain in place for 2 to 5 days until the edema subsides. Pulmonary functions early in the course of smoke poisoning are variably affected. Typically, there are decreased lung volume (functional residual capacity) and vital capacity, evidence of obstructive disease with reduction in flow rates, increased dead space, and rapid decrease in compliance. Surprisingly, much of the variability in pulmonary response appears to correlate with severity of the associated cutaneous burn.11 Without associated burns, mortality from smoke poisoning is low, the disease rarely progresses to ARDS, and symptomatic treatment usually leads to complete resolution of symptoms in a few days. In the presence of burns, smoke poisoning appears to approximately double the rate of mortality from burns of any size. Pulmonary symptoms (hypoxia, rales, rhonchi, wheezes) are seldom present on admission but may appear 12 to 48 hours after exposure. In general, the earlier the onset of symptoms, the more severe the disease.86 No standard treatment has evolved to ensure survival after smoke poisoning; each recommended treatment modality is tempered by opinion and the individual experience of the treating physician. In the presence of increasing laryngeal edema, nasotracheal or orotracheal intubation is indicated. A tracheostomy is never an emergency procedure and certainly should be avoided as initial airway management in victims with burns to the face and neck. A soft-cuffed endotracheal tube should be left in place for 3 to 5 days until the generalized oropharyngeal edema subsides. Mild cases of smoke poisoning are treated with highly humidified air, vigorous pulmonary toilet, and bronchodilators as needed. Blood gases are drawn at least every 4 hours, and the P/F ratio is calculated. Worsening symptoms, difficulty in handling secretions, and a falling P/F ratio are all indications for intubation and respiratory assistance with a volume ventilator. If oxygenation is impaired (P/F ratio 250 or less), positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) is initiated and increased by increments of 3 to 5 cm H2O until no further improvement in the P/F ratio occurs or there is evidence of decreased cardiac output. The physician must carefully search for other mechanical causes of poor ventilation (e.g., restricted chest wall motion from full-thickness burns, pneumothorax from high ventilator pressures, or mechanical difficulties with the endotracheal tube). Prophylactic antibiotics have no value in this chemical pneumonitis, and the subsequent burn management and treatment of eventual bacterial pneumonia can be made more difficult by development of resistant organisms if antibiotics are used early. Corticosteroids are commonly used in victims with severe asthma. Clinicians dealing with smoke poisoning often use them for their spasmolytic and antiinflammatory actions. Several authors have studied the use of corticosteroids, but a most convincing study comes from Moylan,61 who showed in a prospective blinded study of patients with smoke poisoning and associated major burns that the rates of mortality and infectious complications were higher in the corticosteroid-treated patients. In patients with associated burns, Robinson and Seward73 found that corticosteroids did not alter the hospital course of patients admitted to the hospital after the MGM Grand and Hilton Hotel fires in Las Vegas in 1981. The decision for hospital admission and need for specialized care rest on the severity of symptoms from the smoke and the presence and magnitude of associated burns. Any victim who 292
shows symptoms of smoke inhalation and has more than trivial burns should be admitted. If the burns are greater than 15% TBSA, the victim should probably be referred to a special care unit. In the absence of burns, admission depends on the severity of symptoms, presence of preexisting medical problems, and social circumstances of the victim. Otherwise healthy victims with mild symptoms (only a few expiratory wheezes, minimal sputum production, COHb level less than 10%, and normal blood gas levels) can be watched for an hour or two and then discharged if they have a place to go and someone to stay with them. Victims with preexisting cardiovascular or pulmonary disease should be admitted for observation if they have any symptoms related to the smoke. Victims with moderate symptoms (generalized wheezing, mild hoarseness, moderate sputum production, COHb levels 5% to 10%, and normal blood gas levels) may be admitted for close observation and treated as for asthma. The patient with severe symptoms (air hunger, severe wheezing, and copious [usually carbonaceous] sputum) requires immediate intubation and ventilatory support in an intensive care unit setting.
Other Considerations Burns are tetanus-prone wounds. The need for tetanus prophylaxis is determined by the victim’s current immunization status. The treating physician should follow the recommendations of the American College of Surgeons. All victims undergoing IV resuscitation should have an indwelling urinary catheter placed for hourly monitoring of urine output. Arterial lines are useful in victims who need frequent assessment of blood gas levels or who will need repeated blood sampling. Necessary laboratory work during the resuscitation phase is relatively minimal. Blood should be drawn for baseline blood chemistries. If major operative procedures, such as fasciotomy or multiple escharotomies, are expected, blood should be sent for type and crossmatching in anticipation of needing several units of whole blood. Determination of blood gas levels is mandatory in any victim with a suspected inhalation injury, and arterial pH measurement is useful as an assessment of the overall treatment of shock. If the Baxter formula is used for resuscitation, frequent electrolyte determinations are not necessary because levels will remain in the normal range. By 48 hours, however, careful monitoring of serum sodium and potassium levels becomes important. High levels of circulating aldosterone result in an increase in renal potassium excretion. Evaporative water loss to varying degrees through eschar dramatically increases the free-water requirements of burned victims. Hemoglobin and hematocrit levels are initially high and remain high or normal until the third or fourth postburn day. Blood glucose level is commonly elevated because of the glycogenolytic effect of elevated catecholamines, gluconeogenetic effect of elevated glucocorticoid and glucagon levels, and relative insulin resistance.41,78,89,96 This well-described “stress diabetes” can become a problem in normal patients if glucose-containing solutions are given during resuscitation, and is frequently a serious problem in patients with preexisting diabetes. All diabetic patients require careful monitoring of blood and urine glucose levels, and most require supplemental insulin during resuscitation. All medications during the shock phase of burn care should be given intravenously. Subcutaneous and intramuscular injections are unreliably absorbed systemically, and their use should be avoided. Pain control is best managed with small IV doses of morphine until pain control is adequate without affecting blood pressure. Before the discovery of penicillin, 30% of burn victims died during the first week after their injury from overwhelming β-hemolytic streptococcal sepsis. The availability of penicillin decreased streptococcal infections but had no influence on mortality or the incidence of bacterial sepsis. Victims then survived the first postburn week only to die of gram-negative penicillinresistant bacterial sepsis during the second or third week after the burn. The advent of effective topical chemotherapeutic agents applied directly to the burn wounds made possible the control of streptococcal infection, obviating the need for prophylactic penicillin. The use of prophylactic antibiotics in outpatient burns
BURN SEVERITY AND CATEGORIZATION Severity of injury is proportionate to the size of the total burn, depth of the burn, age of the victim, and associated medical problems or injuries. Burns have been classified by the American Burn Association and the American College of Surgeons Committee on Trauma into categories of minor, moderate, and severe.5 Moderate burns are defined as partial-thickness burns of 15% to 25% TBSA in adults (10% to 20% in children), full-thickness burns of less than 10% TBSA, and burns that do not involve the eyes, ears, face, hands, feet, or perineum. Because of the significant cosmetic and functional risk, all but very superficial burns of the face, hands, feet, and perineum should be treated by a physician with a special interest in burn care in a facility that is accustomed to dealing with such problems. Major burns, as described previously, most full-thickness burns in infants and older adults, and burns combined with diseases or injuries should also be treated in a specialized facility. Moderate burns can be treated in a community hospital by a knowledgeable physician as long as the other members of the health care team have the resources and knowledge to ensure a good result. Adoption of early excision and grafting or creative use of local tissue rearrangement to achieve early wound closure have made burn care more complex, and an increasing number of victims with small but significant burns are being referred to specialized care facilities to take advantage of these concepts. The criteria for admission to the hospital of victims with minor and moderate burns vary according to physician preference, the victim’s social circumstances, and the ability to provide close follow-up. In some circumstances, superficial burns as large as 15% can be successfully managed on an outpatient basis. In other circumstances, burns as small as 1% may require admission because of the victim’s inability or unwillingness to care for the wound. In general, the threshold for admission of older adults and infants should be low. Any victim (child or adult) who the physician suspects has been abused must be admitted.
TRANSPORT AND TRANSFER PROTOCOLS Once an airway is established and resuscitation is under way, burn victims are eminently suitable for transport.8,19,43 Resuscitation can continue en route, because for the most part patients
remain stable for several days. This was well proved during the Vietnam War, when burn victims were transported from Vietnam to Japan and then from Japan to the military burn center in San Antonio, Texas. The transport was generally accomplished during the first 2 weeks after the burn, with few complications occurring in about 1000 patients transferred. Hospitals without specialized burn care facilities should decide where they will refer patients and work out transfer agreements and treatment protocols with the chosen burn center well in advance of need. If this is done, definitive care can begin at the initial hospital and continue without interruption during transport and at the burn center. In general, transfer should be from physician to physician, and contact should be established between them as soon as the patient arrives at the initial hospital. The mode of transport depends on vehicle availability, local terrain, weather, and the distances involved. For distances of less than 80 km (50 miles), a ground ambulance is usually satisfactory. For distances between 80 and 241 km (50 and 150 miles), many people prefer helicopter transport. It should be noted, however, that monitoring, airway management, and any changes in therapy are more difficult to achieve in a helicopter. All victims transported by air should have a nasogastric tube inserted and be placed on dependent drainage, because nausea and vomiting usually result during the flight. Two large-bore IV lines should be functional in case one stops working. For distances over 241 km (150 miles), fixed-wing aircraft are usually satisfactory. Modern air ambulances are completely equipped flying intensive care units, and the personnel are usually well trained for both critical care and the peculiarities of victim care during the flight (see Chapter 40). The referring physicians must ensure that the victim’s condition is suitable for a long transport and prepare the victim for the flight. The victim’s airway must be secure. At 9144 m (30,000 feet), planes can be pressurized to an altitude of about 1676 m (5500 feet). Although supplemental oxygen can be given in flight, if the victim’s oxygenation is marginal, performing intubation and starting mechanical ventilation before the transport may be preferable. Intubation is difficult en route, so if there is any question of upper airway edema, the victim should be intubated at the referring hospital. Burned victims have difficulty maintaining body temperature, and should be wrapped warmly before transport. Bulky dressings, a blanket, and a Mylar sheet (usually available from the flight team) can help maintain body temperature. In case the victim has any cardiac irregularities, the plane must be equipped with electronic monitoring capability, because noise and vibrations in flight make clinical monitoring difficult. Only after all other assessments are complete should attention be directed to the burn itself. If the victim is to be transferred from the initial hospital to a definitive care center during the first postburn day, personnel at the referring hospital can leave the burn wounds alone, merely calculating the size of the burn for resuscitation, and monitoring pulses distal to circumferential full-thickness burns. The victim can be wrapped in a clean sheet and kept warm until arrival at the definitive care center.
REFERENCES Complete references used in this text are available online at www. expertconsult.com.
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has not been carefully evaluated, so opinion is divided regarding its utility in victims not requiring hospitalization. Stress ulceration of the stomach and duodenum was once a dreaded complication, occurring in nearly 30% of victims with burns. Protection of the gastric mucosa by immediate feeding through a small nasogastric tube or, failing that, decreasing gastric acidity with histamine2 (H2) receptor antagonists, proton pump inhibitors, or coating the gastric mucosa with sucralfate has made stress ulcers rare.45,58,67,70,84 Psychosocial care should begin immediately. The victim and family must be comforted, and a realistic outlook regarding the prognosis of the burns should be given, at least to the victim’s family. In house fires, the victim’s loved ones, pets, and many or all possessions may have been destroyed. If the family is not available, some member of the team, usually the social worker, should find out the extent of the damage in hopes of comforting the victim. If the victim is a child and the circumstances suggest that the burn may have been deliberately inflicted or resulted from negligence, physicians in most states are required by law to report their suspicion of child abuse to local authorities.
CHAPTER 14
Exposure to Radiation From the Sun ANDREW C. KRAKOWSKI AND LEE A. KAPLAN
Sun exposure, sun damage, and sun protection are increasingly the focus of medical, scientific, and public attention. Adverse effects of sunlight overexposure are well documented,84,147 but the relative value and safety of sun-protective strategies are debated. These issues are of particular concern to wilderness enthusiasts, who spend considerable time in the sun. Sun protection against acute phototrauma, especially sunburn, is more easily judged than is protection against chronic phototrauma such as photoaging, cataracts, and photocarcinogenesis. However, these chronic effects are increasingly relevant to modern societies with demographically aging populations. The economic concerns are huge; billions of dollars are spent annually in the cosmetic and medical industries to repair photodamage, photoaging, and skin cancer. Consumer interest in photoprotection is rapidly expanding. With better sunscreens and photoprotective clothing, even more investment in the future will be focused on sun protection.
Solar Radiation ELECTROMAGNETIC SPECTRUM The sun produces a continuous spectrum of electromagnetic radiation (Figure 14-1). The most energetic rays, which are those with wavelengths that are shorter than 10 nm (i.e., cosmic rays, gamma rays, and x-rays), do not appreciably penetrate Earth’s surface. Phototrauma is primarily the result of ultraviolet radiation (UVR). UVR (10 to 400 nm) accounts for about 10% of the incident radiation at Earth’s surface; visible light (400 to 760 nm) accounts for about 50%; and infrared (IR; 760 to 1700 nm) accounts for about 40%.84 UVR has four components. Vacuum UVR (10 to 200 nm) is readily absorbed by air and does not penetrate Earth’s atmos phere. Ultraviolet C (UVC; 200 to 290 nm) is almost entirely absorbed in the stratosphere, which is 15 to 50 km (9.3 to 31.1 miles) above Earth’s surface, and by oxygen and ozone. Manmade sources of UVC (e.g., germicidal lamps, arc-welding devices) are rarely medically relevant. Ultraviolet B (UVB; 290 to 320 nm) is biologically quite active and principally responsible for tanning, burning, and nonmelanoma skin cancer (NMSC) formation.4,147 Beneficial effects of UVB include vitamin D production from a cutaneous precursor, 7-dehydrocholesterol, to form previtamin D3, which is quickly converted to vitamin D3 (cholecalciferol). It is first hydroxylated in the liver into 25-hydroxyvitamin D3 and subsequently in the kidneys into 1,25-dihydroxyvitamin D3; this is the active metabolite, which stimulates calcium absorption from the gut.131 Approximately 90% of 25-hydroxyvitamin D3 is formed in this manner.237 Of the UVR that reaches Earth’s surface, UVB accounts for roughly 10%, whereas ultraviolet A (UVA; 320 to 400 nm) accounts for about 90%, depending on the season and the time of day. UVA is typically subdivided into “near UVA” or UVA II (320 to 340 nm) and “far UVA” or UVA I (340 to 400 nm). Although these subdivisions are somewhat arbitrary, they are based on photobiologic responses. UVA is biologically active, and it contributes to tanning, burning, photoaging, and carcinogenesis. UVA penetrates the skin more deeply than does UVB, with less energy lost in the superficial layers of the stratum corneum and the epidermis. In addition, UVA is the principal trigger for photo-drug reactions. Longer-wavelength visible light and IR may also cause cutaneous phototrauma, albeit rarely. Solar urticaria has been reported to occur with exposure to visible 294
wavelengths. IR alone—as well as in combination with UVR— may produce epidermal and dermal alterations.152
ENVIRONMENTAL INFLUENCES ON UVR EXPOSURE Exposure to UVR is substantially affected by latitude, altitude, season, time of day, solar zenith angle, albedo (reflectivity), clouds, atmospheric pollution, ozone levels, and personal factors, including occupation and personal behaviors.* Most UVR reaches Earth around midday: 80% between 9 AM and 3 PM and 65% between 10 AM and 2 PM.84 UVB peaks at midday, when the sun is at its zenith.179 UVB is absorbed, reflected, and scattered by the atmosphere, and, at midday, it has less atmosphere to traverse. During early morning and late afternoon, when the sun nears the horizon, UVB decreases considerably. Latitude and season have similar effects: peak UVB exposure is approximately 100 times greater in June than in December.179 For each degree of latitude away from the equator, UVB intensity decreases an average of 3%. UVA varies considerably less than UVB with latitude, time of day, and season, as predicted by Rayleigh’s law: Atmospheric light scattering ∝ 1/λ4, where λ is the wavelength. The shorter the wavelength, the greater is the atmospheric scattering, so UVB is scattered much more readily than is UVA. In addition, UVA (but not UVB) is transmitted through window glass, thus allowing for indoor exposure to UVA but not to UVB. UVR may be increased by surface reflection. Surprisingly, water is a relatively poor reflector. UVR at midday penetrates water up to 60 cm (23.6 inches), so submerged skin is not necessarily protected.179 Reflection from water may increase as the sun nears the horizon, but, at that time, there remains little UVB to reflect because of atmospheric attenuation. Ice and snow are considerably better reflectors. Clean snow may reflect up to 85% of UVR,179 which accounts for oddly distributed sunburns in spring skiers. Grass, sand, metal, concrete, salt flats, and other surfaces reflect UVR to varying degrees. The importance of surface reflection was demonstrated in a 2010 study that was conducted in Spain, which showed that a blue-and-white painted canvas beach umbrella with a radius of 0.8 m (2.6 ft) and a height of 1.5 m (4.9 ft) effectively blocked direct UV radiation; however, sensors positioned at the base of that same beach umbrella still measured 34% of the incident horizontal irradiance found “in the open.”297 Clouds may attenuate UVR exposure. Absorption by clouds varies from 10% to 80% but rarely exceeds 40%.147 Polluted clouds, which contain the greatest concentration of hydrocarbons, are the most effective at absorbing UVR. Clouds are more effective at absorbing heat in the form of infrared radiation, occasionally seducing hikers and bathers into excessively lengthy midday exposures. Wind and water augment sunburn. In mice, exposure to wind plus UVR results in more erythema than does exposure to UVR alone.226 In humans, wind may reduce heat perception, thereby encouraging longer exposure. Water increases UVR exposure because moist skin reflects less UVR, thereby resulting in greater *References 181, 198, 102, 205, 228, 293.
For online-only figures, please go to www.expertconsult.com
Does not reach Earth’s surface
Vacuum UVR
UVC
200
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Microwaves
Radiowaves
Reaches Earth’s surface
UVA
UVB UVA II
nm = 10
1011
Hea t
ge
rcin o
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Ultraviolet
103
760
Ligh t
nes Pho toag is ing Pho toto xici Pho toal ty lerg y
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Sun bur n Sun tan Ca
10
Cosmic rays Gamma rays X- rays
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CHAPTER 14 Exposure to Radiation From the Sun
nm = 10–9 m = 10 Å
290
320 340
UVA I 400
FIGURE 14-1 The electromagnetic spectrum.
absorption of UVB. Consequently, swimmers and hikers in humid environments may be at risk for increased UVR absorption.84 Altitude profoundly influences UVB exposure. Until recently, it was generally accepted that UVB exposure rises 4% for each 305-m (1000-foot) rise above sea level. However, Rigel and colleagues247 demonstrated an 8% to 10% increase in UVB for each 305-m (1000-foot) rise above sea level. Beginning at the 3353-m (11,000-foot) summit of a ski run in Vail, Colorado, these investigators measured UVB readings every 152 m (500 feet) as they skied to the base of the run at 2500 m (8200 feet). This study showed that UVB exposure readings in Vail, Colorado (latitude 39 degrees North) at 2591 m (8500 feet) approximated readings made under similar conditions—but 772 miles nearer the equator—at Orlando, Florida (latitude 28 degrees North, elevation 18 m [60 feet]). Snow, wind, and altitude may act simultaneously to greatly augment UVB exposure for skiers and climbers. Singh and coworkers271 reported that 36% of climbers (24 of 67) developed significant sunburns during three consecutive expeditions up to 7000 m (23,400 feet) in the western Himalayas, despite the application of sunscreen. During a year-long study of professional Alpine mountain guides with the use of continuous dosimetry monitoring, Moehrle and colleagues210 confirmed exceedingly high cumulative UVR exposures. These data emphasize the difficulties of providing appropriate UVR protection for high-altitude outdoor enthusiasts.
OZONE DEPLETION AND ULTRAVIOLET RADIATION EXPOSURE Stratospheric ozone, which lies 15 to 50 km (9.3 to 31.1 miles) above Earth’s surface, provides a thin and fragile shield against UVR. The combination of ozone and oxygen absorbs virtually the entire incidence of UVC. Ozone attenuates UVB and modestly reduces UVA II, but it allows the transmission of all UVA I.323 Ozone is continuously created and removed from the stratosphere by natural physicochemical processes that are in turn significantly affected by manmade pollution. Molina and Rowland211 first suggested that chlorofluorocarbons (CFCs) could cause ozone depletion. CFCs are organic chemicals that contain carbon, chlorine, and fluorine that were initially developed during the 1970s as refrigerants. Since then, CFCs have been used in several technologies and industrial processes, including air-conditioning systems, insulation, cleaning solvents, degreasing agents, and metered-dose inhalers. Related compounds known as halons contain bromine, which also depletes stratospheric ozone. Halons arise from seawater, fire extinguishers, and various industrial processes.128 CFCs and halons belong to the group of chemicals known as halocarbons.
The remarkable stability of CFCs allows them to rise into the stratosphere, where, when catalyzed by solar radiation, they release chlorine (Cl−) and chlorine monoxide (ClO−), which in turn degrade ozone. One prominent chemical pathway by which CFCs deplete ozone is as follows:128 Cl − + O3 → ClO− + O2 O3 + UVR → O + O2 ClO− + O → Cl − + O2 Net reaction: 2O3 + UVR → 3O2 Note that Cl− is preserved in this reaction. The half-life of Cl− is approximately 75 years,309 although CFCs may reside in the stratosphere for 50 to 200 years.128 During that time, each Cl− ion may destroy 100,000 molecules of ozone.309 Over Antarctica, additional and augmented ozone-depleting mechanisms may be operative; molecular halogens coat the surface of ice clouds, thereby making them even more reactive and able to degrade ozone.128 Ozone losses were first reported over Antarctica in 198576 by the British Antarctic survey. Ozone showed large declines in the austral springtime (September/October), and it decreased a total of 35% during the springtimes that occurred from 1975 to 1984.128 Ozone depletion is now documented at all latitudes except the equator. This depletion is uneven, with more loss at the poles and less at the middle latitudes.309 There is also a well-documented “waxing and waning” that occurs with the seasons. With the use of its total ozone mapping spectrometer in satellite orbit, the National Aeronautics and Space Administration has documented ozone depletion over continental Europe, North and South America, South Africa, New Zealand, and Australia.169 Significant increases in UVB have been documented, even near the middle latitudes, because of ozone depletion. In Toronto from 1989 to 1993, Kerr and McElroy151 documented surface UVB increases of 35% per year in winter and 7% per year in summer, which corresponded with ozone decreases of 4% per year and 1.8% per year, respectively. Their experimental design allowed for assignment of all of the UVB increase to ozone depletion rather than to cloud coverage or pollution. Similar increases in ground-level UVB that parallel decreases in stratospheric ozone have been documented in Scotland.215 Typically, in the northern hemisphere’s middle latitudes, ozone losses are greater during winter (i.e., about 6% per decade) than during summer (i.e., about 3% per decade).128 Ironically, pollution (e.g., smog, particulates) may mitigate UVR increases by absorbing UVB.309 295
PART 3 BURNS, FIRE, AND RADIATION
The effects of ozone depletion on the biosphere and human skin cancer rates have been estimated. Although these estimates vary, data suggest that, for every 1% decrease in ozone, there is a corresponding 2% increase in the incidence of basal cell carcinoma (BCCa) and 3% increase in the incidence of squamous cell cancer (SCCa).59 Melanoma incidence may increase by 1%.309 However, even if UVB triples near the poles, as is suggested in worst-case scenarios, polar areas will still receive less UVB than current equatorial levels.309 Ozone depletion may have its greatest effects on nonhuman biosystems. Plant and plankton yields may be diminished significantly, causing an uncertain and potentially severe detriment to terrestrial and marine life.323 To prevent ecologic disturbances and to restore ozone levels, international agreements have been negotiated. The Vienna Convention in 1985 and subsequent Montreal Protocol in 1987 were among the first and most notable. The Montreal Protocol, which has now been signed by 184 of the 191 United Nations member nations,299 agreed to limit and then reduce CFC production, which led to a 50% reduction by 1998.128 Three later amendments were made to accelerate progress in response to increasing awareness of ozone depletion in the middle latitudes. The London Amendment in 1990 required the complete phaseout of halocarbon production. The Copenhagen Amendment in 1992 accelerated the timetable for complete phaseout, stopping production in developed countries by 1996 and in undeveloped nations within 10 years; it also extended the protocol to include hydrochlorofluorocarbons. The Vienna Amendment in 1995 revised the phaseout schedule of hydrochlorofluorocarbons.128,273 Although the Montreal Protocol is working—CFC production has been decreased by 90%299—its modest limitations would allow elevated stratospheric chlorine levels through most of the 21st century.128 By contrast, the stricter limitations of the Copenhagen Amendment will result in ozone levels rising again within the first decade of the 21st century.273 Among the remaining sources of CFC production are metered-dose inhalers and cleaning agents for rocket motor manufacturers.128 American factories could produce 53,500 tons of CFCs annually for export until 2005.23 CFC substitutes are more costly, with an estimated 22,000 tons being produced in 1994.23 This led to an international black market in CFCs. A significant portion of this black market is in Freon that is smuggled to automobile air-conditioner rechargers. In 1996, an estimated 10,000 tons of CFCs were smuggled into the United States from Mexico and elsewhere.83 Despite these black-market sources, initial projections suggested that atmos pheric chlorine would begin to fall in this decade, with resultant UVB levels gradually falling by 2050 to levels that were recorded during the 1950s. Unfortunately, recent data suggest that current global warming trends exacerbate ozone depletion and may delay the recovery of the ozone layer.299
Acute Effects of Ultraviolet Radiation on Skin: Sunburn and Tanning The effects of UVR on skin depend primarily on wavelength, length of exposure, intensity of exposure, repetition of exposure, age at time of exposure, site of exposure, and genetic factors of the individual who is exposed. To have a biologic effect, UVR must be absorbed. Absorbing molecules in the skin are known as chromophores, and different wavelengths of UVR are absorbed by different chromophores. Among these are nucleic acids (especially pyrimidine bases), various amino acids in cutaneous proteins, and lipoproteins in cell membranes. These chromophores are at varying depths in the skin, accounting in part for the differing photobiologic responses to UVR. To date, there is only imprecise—but improving—knowledge of how a given photochemical reaction results in a specific biochemical product, thereby leading to an observable clinical change.
ULTRAVIOLET C RADIATION UVC has no appreciable impact on human health, as it is effectively screened from Earth’s surface by stratospheric ozone and 296
oxygen. Even with continued ozone depletion, levels of UVC are not expected to rise. As mentioned, manmade sources of UVC such as germicidal lamps and arc-welding devices have been only rarely associated with cutaneous pathology as might be predicted, because UVC is effectively absorbed by the stratum corneum, which is the outermost cutaneous layer.84
ULTRAVIOLET B RADIATION UVB acutely induces a cutaneous inflammatory response that is at least partially definable clinically, histologically, and biochemically.137 Clinically, erythema or sunburn is the hallmark of acute overexposure to UVB. The action spectrum for erythema peaks with UVB.217 Generally, UVB is considered to be 1000-fold more effective than UVA for induction of erythema. In a human model, 300-nm UVB is 1280-fold more effective at inducing erythema than 360-nm UVA.324 Erythemogenic doses are usually defined as multiples of the minimal erythema dose (MED), which is the lowest dose that elicits perceptible erythema. In a typical fairskinned individual, the MED might range from 15 to 70 mJ/cm2 for UVB and from 20 to 80 J/cm2 for UVA. For example, 1 MED of UVB for a typical fair-skinned individual would require 20 minutes of midsummer exposure in San Diego, whereas 1 MED of UVA would require 2 to 3 hours of exposure. In a day’s time, a person can receive 15 MEDs of UVB but only 2 to 4 MEDs of UVA.200 Consequently, although people are exposed to 10-fold to 100-fold more UVA than UVB, more than 90% of sunlight-induced erythema is attributable to UVB. The erythema action spectrum, which peaks in UVB, is remarkably similar to the absorption spectrum of DNA,217 which suggests that DNA is a principal target chromophore for UVBinduced erythema325 and pyrimidine dimer formation. Supporting this is the finding that pyrimidine dimer yields correlate with erythema.116 Sunburn reflects a local vascular reaction. The causes are multifactorial: DNA damage, prostaglandin activation, cytotoxicity, and other mechanisms are implicated. UVB erythema has its onset 2 to 6 hours after exposure; it peaks at around 12 to 36 hours and fades after 72 to 120 hours.84,137,147 Acute histologic changes that accompany UVB exposure include edema with vasodilation of the upper dermal vasculature137 and endothelial cell swelling, most likely as a result of vasoactive mediators being released.112 Delayed histologic changes include the appearance of sunburn cells in as little as 30 minutes after exposure. These dyskeratotic cells have enlarged nuclei and vacuolated cytoplasm. Initially, sunburn cells are localized in the lower one-half of the epidermis; however, after 24 hours, they are also found in the upper half. These sunburn cells may represent actively cycling and proliferating basal cells that cannot adequately repair UVR-induced DNA lysosomal damage.55 Beginning 1 hour after exposure, stainable Langerhans’ cells (i.e., cutaneous antigenpresenting cells) are reduced by 25%; by 72 hours after exposure, only 10% remain.137 In mice that are exposed to repetitive suberythemogenic doses of UVB, normal numbers of Langerhans’ cells return by 8 days after exposure.137 Vacuolization of melanocytes is seen after 1 hour and returns to normal 4 to 24 hours after exposure.137 Mast cells decrease in number and granularity within 1 hour, returning to normal after 12 to 72 hours.137 By 24 to 48 hours after exposure, there is increased melanin synthesis, epidermal proliferation, and thickening of the stratum corneum. Functionally, the epidermal permeability barrier diminishes after UVB exposure because of the altered kinetics of lamellar-body– containing cells in the exposed epidermis.133 Biochemical changes that accompany sunburn include increased levels of histamine,137 which return to normal within 74 hours. However, histamine is unlikely to be the sole or even the principal mediator of vasodilation and erythema, because antihistamines are ineffective in preventing sunburn. UVR induces increased phospholipase activity, with accompanying increases in prostaglandins (PGs). PGD2, PGE2, PGF, and 12-hydroxyeicosatetraenoic acid are increased in suctioned blister aspirates immediately after UVB exposure, and peak after 18 to 24 hours.137 Topical and intradermal indomethacin, which is a prostaglandin inhibitor, blocks UVB-induced erythema for 24 hours after exposure,275 thus supporting the thesis that
ULTRAVIOLET A RADIATION UVA penetrates more deeply into the skin than does UVB. Whereas 95% of incident UVB is reflected or absorbed by the epidermis, nearly 50% of UVA reaches the dermis.75 UVA contributes modestly to sunburn and may cause clinical erythema. Prolonged daily UVA exposure can approach 125 J/cm2, which significantly exceeds the threshold erythema dose of 20 to 80 J/ cm2.278 Clinically, UVA erythema has an onset within 4 to 6 hours; it peaks after 8 to 12 hours and fades after 24 to 48 hours.137,147 Erythema that results from UVA may have a distinct pathophysiologic mechanism. UVA-induced erythema may be caused by keratinocyte cytotoxicity.137 Histologically, UVA erythema displays more epidermal spongiosis, fewer sunburn cells, and more dermal changes than does UVB-induced erythema, with a denser and deeper mononuclear cell infiltrate and more vascular damage.137
INFRARED RADIATION IR radiation plays a less well-defined role in photodamage. Near-IR preirradiation prevents UVR-induced cytotoxicity,200 which suggests that a possible evolutionary protective mechanism for IR is the daily preparation of skin cells to resist UVRinduced damage. However, no data indicate whether IR protects against UVR’s mutagenic and carcinogenic effects.
SUNBURN TREATMENT Sunburn is self-limited, and its treatment is largely symptomatic, involving local skin care, pain control, and antiinflammatory agents (Box 14-1).15 Studies that have assessed the treatment of sunburn can be divided into those that evaluated the agents used immediately after UV exposure (i.e., before symptoms have manifested) and those that evaluated the agents for the actual treatment of acute sunburn reactions.121 Cool-water soaks or compresses may provide immediate relief, and topical anesthetics are sometimes useful. It is generally preferable to use the nonsensitizing anesthetics menthol,
BOX 14-1 Sunburn Treatments Pain Control Acetylsalicylic acid Nonsteroidal antiinflammatory drugs Skin Care Cool soaks and compresses Nonmedicated moisturizers Topical anesthetics Pramoxine (Prax) lotion Menthol plus camphor (Sarna) anti-itch lotion Anti-itch concentrated lotion (Pramoxine) plus camphor plus calamine (Aveeno) Lidocaine plus camphor (Neutrogena Norwegian Formula) soothing relief moisturizer Steroids Topical (e.g., triamcinolone 0.1% cream applied twice daily when erythema first appears) Systemic
camphor, pramoxine, and lidocaine rather than the potentially sensitizing anesthetics that contain benzocaine and diphenhydra mine. Refrigerating topical anesthetics before application provides added relief. A legion of topical remedies have been suggested anecdotally. These include aloe, baking soda, and oatmeal, but controlled studies are lacking. Topical steroids, with their vasoconstrictive effects, are often considered “first-line” treatment for acute sunburn; however, their efficacy remains controversial. A randomized, double-blind clinical trial of 20 patients with Fitzpatrick skin types I, II, and III compared erythema reactions in areas that were treated with either topical moderate-potency corticosteroid (hydrocortisone-17-butyrate) or high-potency corticosteroid (clobetasol propionate) 30 minutes before and 6 or 23 hours after exposure to UVB (i.e., a bank of TL12 fluorescent tubes); only the areas that had been treated with high-potency corticosteroid 30 minutes before UVB exposure demonstrated clinically significant results.78 Diclofenac gel, which is a topical nonsteroidal antiinflammatory drug, alleviates pain, erythema, and edema for up to 48 hours when it is applied after exposure.152 Oral nonsteroidal antiinflammatory drugs provide analgesia and may reduce sunburn erythema.84 According to a recent Medical Letter, the combined use of topical steroids and oral nonsteroidal antiinflammatory drugs slightly decreases erythema during the first 24 hours if these drugs are administered before exposure or shortly after exposure, before sunburn becomes clinically apparent.238 Few published studies support the value of systemic steroids, but they enjoy considerable anecdotal support. In a metastudy of all published articles related to sunburn treatment from 1966 to 2001, Han and Maibach121 found no therapy to be unequivocally or consistently effective and no consensus for the treatment of sunburn. Moreover, education for acutely sunburned patients is lacking. Warnings regarding skin cancer are rarely given to sunburned patients when they are seen in the emergency department.15
TANNING Tanning, like sunburning, is caused by UVR. Consequently, persons who are seeking a tan risk sunburn. Tanning is biphasic. After sun exposure, there is immediate pigment darkening within minutes, followed by delayed pigment darkening (DPD) in 3 days. Immediate pigment darkening is predominantly the result of the action of UVA on preformed melanin precursors; it occurs in as little as 5 minutes after exposure, peaks in 60 to 90 minutes, and then fades quickly. However, DPD represents new melanin synthesis within melanocytes and the subsequent spread of the richly melanized melanosomes into surrounding keratinocytes. After UVB exposure, DPD is notable by 72 hours, peaks after 5 to 10 days, and then slowly fades. DPD is primarily a response to UVB. Most tanning studies have been performed with erythemal doses of UVR. However, multiple suberythemal exposures to UVA are significantly more melanogenic than is similarly dosed UVB.20 The mechanism of DPD is uncertain, but it is likely to be multifactorial. UVB stimulates tyrosinase release and arachidonic acid metabolites, and it releases α-melanocytestimulating hormone from keratinocytes.7 It also increases the binding affinity of melanocytes for melanocyte-stimulating hormone, thereby resulting in increased melanocyte proliferation, melanization, and arborization.29 UVB increases melanocytes in both exposed and protected human skin,282 which suggests the possibility of a UVR-stimulated circulating factor that promotes melanocyte proliferation.
Chronic Phototrauma NATURAL DEFENSES AND SKIN TYPE Absence of erythema does not preclude cutaneous photoreactions. Chronic exposure to UVR is accompanied by insidious cumulative biologic and clinical changes. Although some of these changes are the result of broadband UVR, UVA and UVB often have distinct and different effects on the epidermis, dermis, extracellular matrix, cytokines, and immune response.311 In response to UVB, the stratum corneum thickens110 and melanin increases; both of these are protective mechanisms to mitigate 297
CHAPTER 14 Exposure to Radiation From the Sun
eicosanoids (PGs and leukotrienes) are significant mediators of UVR-induced inflammation.160 UVB stimulates induction of proinflammatory and mutagenic cytokines: tumor necrosis factor-α and interleukins 6 and 12.133 UVR generates free radicals in the skin that probably contribute to the sunburn reaction193 by causing peroxidative chromosomal, membrane, and protein damage.16 Topical antioxidants may mitigate sunburn when they are applied before but not after exposure. Melatonin16 and vitamin C57 act protectively by scavenging UVR-generated free radicals; however, neither absorbs UVR.
PART 3 BURNS, FIRE, AND RADIATION
BOX 14-2 Skin Types I Always burns; never tans II Often burns; tans minimally III Sometimes burns; tans moderately IV Burns minimally; tans well V Rarely burns; tans deeply; moderately pigmented (brown) VI Never burns; deeply pigmented (black)
further UVB photodamage. The stratum corneum, which is the outermost layer of skin, is composed of flattened anucleate keratinocytes. It reflects, scatters, or absorbs up to 95% of incident UVB, depending largely on its thickness.123 With repeated exposure to UVB, the stratum corneum can increase its thickness up to sixfold.84 As a consequence, the stratum corneum is the main photoprotective factor in whites.110 Repeated UVA exposures may cause some thickening,178 but to a much lesser degree. Consequently, UVA tans are not as photoprotective as are UVB tans. Melanin reflects, scatters, and absorbs throughout the UVR spectrum; it acts as an antioxidant, and it reduces UVR-induced photoproducts.157 Consequently, constitutive (racial) skin color is a principal determinant of an individual’s erythemal response to UVR. Although blacks and whites have similar numbers of melanocytes, these pigment-forming cells are differently melanized and distributed in black and white skin. Increased melanin in blacks can decrease the dermal penetration of UVR up to fivefold53 and increase the MED up to 30-fold. By contrast, tanning is much less protective. After an entire summer of tanning, the MED in whites increased only 2.3-fold.53 Clinically, these racial differences in melanization are reflected in lower rates of burning, photoaging, and skin cancer in blacks. Susceptibility to photodamage is typically defined by six distinct skin types (Box 14-2). Racial pigmentation alone does not account for differences in skin type. Some redheads tan easily, whereas some blacks burn readily. Reporting errors (typically involving the overstating of sun tolerance) are common, thus further complicating the interpretation of skin types.239 Skin type correlates well with MED. Additional factors that influence MED include age and anatomic site. Lower MEDs are recorded in the very young and the very old.147 Differences in stratum corneum thickness and melanocyte concentration may account for body-site–specific differences in MED. For example, the MED of the back is typically less than the MED of the lower leg. Chronic suberythemal UVA exposures also cause photodamage. Repetitive low-dose exposures to UVA result in histologic changes,170,178 including the thickening of the stratum corneum and of the granular and stratified cell layers, decreased elastin, vascular dilation, and inflammation. Aside from the thickened stratum corneum and increased pigmentation, intrinsic mechanisms of photoprotection include antioxidants, such as the glutathione peroxidase-reductase system, that mitigate damage from UVR-induced reactive oxygen species. DNA repair enzymes correct most UVR-induced mutations. Carotenoids stabilize biologic membranes from singlet oxygen attack. Urocanic acid absorbs some of the UVR that penetrates the stratum corneum.58
Chronically sun-exposed sites have fewer Langerhans’ cells. Keratinocytes and fibroblasts from sun-damaged skin have diminished life spans in culture.104 The most notable histologic change with chronic UVB exposure is deposition of thickened amorphous elastic fibers high in the dermis, which is demonstrable in photoexposed white skin by the age of 30 years. In a transgenic mouse model, UVB but not UVA produces this solar elastosis.294 Another mouse model suggests that the action spectrum for “photosagging” peaks in UVA at 340 nm122 and that this action spectrum is remarkably similar to that of the generation of singlet oxygen by the excitation of transurocanic acid. The authors of that study concluded that UVA causes photoaging because of its interaction with transurocanic acid, which releases reactive oxygen species. With photoaging, elastin gene expression appears to be activated, although data are conflicting. Tropoelastin and fibrillin synthesis actually diminish with chronic UVB exposure,310 whereas transcription of other extracellular matrix genes is enhanced. In particular, photoaged skin demonstrates increased matrix metalloproteinases, which are potent mediators of connective tissue damage.80 These arise within hours of UVB exposure and even after suberythemal exposure.79 Interestingly, tretinoin inhibits induction of these UVB-induced proteinases,79,80 perhaps explaining in part its clinical usefulness against photoaging.223,308 Tretinoin also normalizes photoaltered epidermal differentiation and deposits new type I collagen in the upper dermis.115
OCULAR EFFECTS Acute overexposure to UVB may cause photokeratitis (snowblindness), especially in skiers and climbers,326 whereas chronic exposure to UVR may cause or contribute to pterygia, cataracts, and macular degeneration. A full discussion is presented in Chapter 28.
A
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D
PHOTOAGING Long-term repetitive exposures to sunlight result in photoaging.80 This process, known as dermatoheliosis, is distinctive clinically and histologically from chronologic aging; it is not merely accelerated chronoaging. Photoaged skin is characterized by dryness, roughness, mottling, wrinkling, atrophy, and pebbling, and it may be studded with precancers (actinic keratoses) or cancers (Figure 14-2). Most of what we consider “old-looking” skin is in fact the result of photoaging rather than chronoaging. Although age can be estimated from observing sun-exposed sites, it cannot be estimated from photoprotected sites.307 The action spectrum for photoaging includes UVB, UVA, and IR.178 298
FIGURE 14-2 Phototrauma. A, Tan and peeling after sunburn. B to D, Dry, mottled, wrinkled, and pebbled skin with photoaging.
CHAPTER 14 Exposure to Radiation From the Sun
A B
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FIGURE 14-3 A, Actinic keratoses: thin, vague, and scaly papules. B, Basal cell carcinoma: smooth, pearly papule. C, Squamous cell carcinoma: keratotic red and tan papule. D, Melanoma: note the asymmetry, border irregularity, color variegation, and diameter of more than 6 mm (0.24 inch).
SUN AND SKIN CANCER Actinic keratoses (solar keratoses) are considered by many dermatologists to represent in situ dysplasias that result from exposure to solar irradiation. The majority of these lesions are characterized clinically as being 0.3 to 2 cm (0.12 to 0.79 inch) in size, multiple, sharply bordered, irregularly shaped pink papules with adherent scale. It is often easier to appreciate actinic keratoses as “rough spots” via direct palpation than by visual detection alone. A hypertrophic type exists and may lead to cutaneous horn formation, especially on the dorsal surfaces of the hands and the extensor forearms. Actinic keratoses may be tender when rubbed or shaved over with a razor. They are predominantly located in chronically sun-exposed areas. Actinic keratoses tend to be more common in lighter skin, and they typically appear in people who are more than 50 years old, although fair-skinned patients who live in areas of high solar irradiation may develop them much earlier (i.e., at the age of 20 to 40 years). Actinic keratoses may be prevented by sun avoidance and a diet that is low in fats. Treatment strategies range from cryosurgery and topical chemotherapy with 5-fluorouacil or imiquimod to chemical peels, laser resurfacing, and photodynamic therapy. The consideration of skin biopsy is warranted when the lesion is larger than 0.6 cm (0.24 inch), if there is a palpable dermal component, or when the lesion persists despite appropriate therapy. Like precancerous actinic keratoses, true skin cancers (Figure 14-3) are believed by most dermatologists to be overwhelmingly caused by UVR exposure. In particular, UVR is the principal cause of NMSC (i.e., BCCa and SCCa), which is the most common of all cancers. UVR also contributes significantly to melanoma, but it is not a sine qua non. The incidence of skin cancer is staggering. One in five Americans247 and two-thirds of all Australians13 born today will develop skin cancer. In addition, the incidences of both NMSC108 and melanoma continue to increase.246 Three causative factors seem to predominate: • Lifestyle trends, including sun exposure, sunbathing, and tanning bed use
• Aging of the population • Ozone depletion Since the 1890s, epidemiologic evidence has accumulated that links sun exposure with NMSC in humans. The incidence of skin cancer increases with increasing proximity to the equator.54 NMSC has a far greater incidence in whites than in blacks, and occurs primarily on sun-exposed areas. Risk for NMSC increases with increasing sun exposure, and repeated sunburn is an independent risk factor.164 Adopting a sun-protected lifestyle is associated with decreased risk.130 Patients with xeroderma pigmentosum (XP), which involves a deficient ability to repair UVR-induced DNA damage, have a 1000-fold greater risk of developing NMSC, typically at a very early age.160 During the 1920s, laboratory data confirmed that UVR induces and promotes NMSC in mammalian animal models.147,287 UVC and UVB are effective inducers of SCCa in mice.137 Although UVB is primarily implicated, UVA augments UVB-induced carcinogenesis,287 and can be a carcinogen on its own. Development of NMSC in humans is related to the time and intensity of exposure. Sun exposure during childhood and adolescence is more predictive of later BCCa.88 British immigrants to Australia assume the much higher Australian risk of NMSC only if they emigrate before the age of 18 years; after that time, these immigrants retain the lower British risk.189 A separate study suggests that risk decreases after the age of 10 years.163 Gallagher and co-workers88 found that BCCa is associated with sun exposure up to the age of 19 years but that it is not associated with mean annual cumulative summer sun exposure. In this study, risk for BCCa was also associated with fair complexion and freckling. Kricker and colleagues164 suggest that intermittent (rather than continuous) sun exposure in poor tanners is the most important factor in development of BCCa. Clinically, BCCa includes a heterogeneous group of low-grade malignant cutaneous tumors that are characterized by differentiation markers that are usually associated with hair-follicle development. BCCa is the most common cancer in the United States, and, although it can be locally aggressive, it is almost never 299
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FIGURE 14-5 Basal cell carcinoma demonstrating characteristic “rolled” borders and central ulceration.
FIGURE 14-4 Pink, pearly papule with a rolled border and overlying telangiectasias located on the right pectoral area of a 55-year-old surfer from San Diego; biopsy revealed a basal cell carcinoma.
metastatic. These lesions are most commonly found on the head and neck (Figure 14-4), but any part of the body may be involved. Interestingly, in contrast with SCCa, BCCa is relatively uncommon on the dorsal surface of the hand, where solar radiation exposure is high. Several clinical morphologies of BCCa exist, and the diagnosis depends on the astute clinician recognizing the many forms that are taken by this cancer. Nodular BCCa, which comprises the majority of BCCa, may manifest as one or a few small, pearly papules with a central depression and “rolled borders” (Figure 14-5). Telangiectasias may be seen coursing through the lesion; the lesions are usually friable, and they frequently bleed when rubbed with a cotton-tipped swab. Pigmented BCCa is similar to nodular BCCa, but this morphologic type appears brown or black because of the presence of pigment. Cystic BCCa manifests as bluish-grey, dome-shaped cystic papules or nodules that are similar in appearance to hidrocystomas. Morpheaform BCCa manifests as a white sclerotic plaque, usually without the characteristic findings of a pearly, “rolled” border; for this reason, it is often missed or misdiagnosed as a scar. Superficial BCCa, which is the most common pattern seen in patients with human immunodeficiency virus, is another common form of BCCa that favors the trunk and distal extremities; it usually manifests as a superficial, dry, scaly lesion that can resemble patches of slow-growing eczema or psoriasis, although close examination reveals the raised border. Rodent ulcer is a neglected BCCa that has ulcerated; consequently, the “rolled” border of the lesion may not be present or recognizable.
A
SCCa, which is the second most common form of skin cancer, manifests clinically as dull-red, superficial, indurated, welldemarcated plaques that arise on sun-exposed areas such as the face and dorsal surfaces of the hands. Lower-lip lesions may develop with actinic cheilitis; in these cases, a history of repeated sunburns and smoking are predisposing factors. As the lesions grow over the course of months, they become deeply nodular and ulcerate (Figure 14-6, A and B). The ulcer may be hidden by an overlying crust that, when removed, reveals a discrete, indurated, and elevated base. Careful examination of regional lymph nodes is warranted in suspected cases. The rate of metastasis from all skin sites ranges from 0.5% to about 5%; risk factors that can increase this rate include a location that involves the temples, scalp, ear, or lip; recurrence after prior treatment; size and depth of the primary lesion; histologic findings; and host immunosuppression. The relationship of photoexposure and SCCa is distinct and different from that of the sun and BCCa. There is a significantly increased risk of SCCa with chronic occupational exposure, especially during the 10 years before diagnosis.89 Although cumulative lifetime photoexposure and SCCa are not associated, risk factors include periodic recreational exposure, pale complexion, and red hair. Persons who develop SCCa seem to be phenotypically sensitive to UVR, with chronic exposure as adults. Household and office exposure to nonsolar UVR does not increase the risk of BCCa and SCCa.14 In select mouse models, suberythemal UVR has caused SCCa.217 In these models, gradual suberythemal exposures to UVR may actually be more carcinogenic than are erythemal doses.87 This may be relevant to humans, and it may explain why persons without any prior sunburns may develop SCCa.
MELANOMA Melanoma includes a number of different clinicopathologic types. Nodular melanomas are typically smooth, dome-shaped, and
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FIGURE 14-6 Squamous cell carcinoma. A, Neglected squamous cell carcinoma on lateral and posterior shoulder. B, Closer image of the same carcinoma.
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FIGURE 14-7 Melanoma on the posterior helix, which made early selfdetection difficult.
FIGURE 14-8 “Yin-yang”–shaped melanoma on back demonstrating asymmetry, color variegation, and a diameter of more than 6 mm (0.24 inch). The location made early self-detection difficult.
a prior sunburn than are age-matched controls, and they are three times as likely to relate a history of multiple prior sunburns.73 Persons who tan poorly and burn readily are at higher risk for melanoma.180 The distribution of melanomas on the trunk (in both sexes) and the lower legs (in women) is consistent with the hypothesis that intermittent sun exposure is provocative. However, melanomas also arise in sun-protected sites, especially in nonwhite populations, which suggests an additional cause that is separate from sun exposure. A high level of outdoor activity during college is associated with a fourfold risk of later melanoma.72 Servicemen who served in the Pacific theater during World War II have a higher risk of melanoma than do those who served in Europe.39 The incidence of melanoma is increased in indoor workers with higher socioeconomic status, again reflecting the role of intermittent intense sun exposure.149 Fluorescent lights raise some concern,305 but they do not significantly increase melanoma risk, especially when these lights have covers or diffusers.135 Sunburns in childhood may be particularly relevant to the later development of melanoma. Celtic migrants to Australia who arrived before the age of 10 years assume the high melanoma risk of native Australians; migrants who are more than 15 years old on arrival have only one-fourth that risk.255 Europeans who live more than 1 year in a sunny climate have an increased relative risk (i.e., 2.7) of melanoma, and the risk increases substantially (i.e., 4.3) if they arrive before the age of 10 years.10 However, one study suggests that childhood sun exposure contributes a serious risk only if there is subsequent and significant sun exposure as an adult.8 This association of increased melanoma risk with sun exposure during youth may be in part attributable to the effect of sun on the development of melanocytic nevi (moles) in children. Several studies confirm that the number of nevi in children increases with increasing acute and chronic sun exposure.* In Australia, the number of nevi up to the age of 12 years increases with increasing proximity to the equator.150 Increased nevus counts with sun exposure are demonstrable at early ages. In Queensland preschoolers between the ages of 0 and 35 months, increased nevus counts are associated with more time spent outdoors and a history of sunburn.125 These children have the highest number of nevi in the world, and, not surprisingly, Queensland has the highest incidence of melanoma in the world126 at 55.8 per 100,000 for males and 42.9 per 100,000 for females.13,25 The number of nevi is a strong predictor of melanoma risk. Melanoma increases with increasing numbers of benign acquired nevi. In a large European case-controlled study, the most important risk factors for melanoma are the number of nevi and the number of atypical nevi.93 Established nevi may develop histologic changes transiently, thus simulating melanoma *References 37, 92, 93, 125, 126, 302.
301
CHAPTER 14 Exposure to Radiation From the Sun
friable lesions that most commonly occur on sun-exposed areas of the head, neck, and trunk. They are twice as common in men as in women. Lentigo maligna manifests as a tan macule on sundamaged skin, typically among older patients who live in sunny climates; this type of melanoma may darken and spread so slowly that patients are often unaware of changes (Figure 14-7). Superficial spreading melanoma has no known preference for sundamaged skin, and affects adults of all ages. Color variegation (i.e., dark brown, black, red, white, blue) is common with this type of melanoma (Figure 14-8). These lesions may arise de novo or in association with a preexisting nevus; a new papule or nodule may develop as the vertical growth phase develops. Acral lentiginous melanoma, which is the most common type of melanoma in dark-skinned and Asian populations, may begin as a light brown and uniformly pigmented macule or patch that gradually darkens, thickens, and ulcerates with time. Subungual or plantar lesions are often present, and Hutchinson’s sign (i.e., a black discoloration of the proximal nail fold at the end of a hyperpigmented linear streak) portends melanoma in the matrix of the nail. Amelanotic melanoma is difficult to discern clinically, because it lacks pigment and may mimic a benign inflammatory papule or BCCa. Other types include ocular, mucosal, polypoid, desmoplastic, and soft-tissue melanomas. Melanoma has a less well-defined relationship with sun exposure; clearly, however, sun exposure plays a significant role in its development.6 The ultraviolet action spectrum for melanoma remains uncertain, with different results in different animal models. In Monodelphis domestica, a South American marsupial, both UVA and UVB are implicated63; in Xiphophorus (platyfish and swordtails), UVA, UVB, and visible (blue) light are causative63; and in transgenic mice Tyr-SV40E (C57BL/6 strain), UVB is the etiologic waveband.153 In humans with XP, the 1000-fold increased incidence of melanoma strongly supports UVB as a causative agent.161 A unique and elegant laboratory experiment documented that UVB induces melanocytic hyperplasia, atypia, and melanoma in newborn human foreskin xenografts on RAG-1 (immunodeficient) mice.7 Melanoma incidence increases with proximity to the equator in white populations149 in the United States, Australia, and Scandinavia as well as in the nonwhite population of India.167 In the U.S. Surveillance, Epidemiology, and End Results Program from 1992 to 2001, the incidence of melanoma increased with lower latitudes in non-Hispanic whites; no association was noted in Hispanics or blacks.69 In contrast, Hu and co-workers138 noted a positive association of lower latitude and UVR exposure with melanoma in blacks and Hispanics in the United States, although statistical significance was reached for black men only. Intermittent intense exposures pose a particularly high risk for melanoma.71 A meta-analysis of 57 studies published before September 2002 supports a significantly increased risk of melanoma with a history of intermittent sun exposure and sunburn.91 In contrast, there is only a small increased risk for total sun exposure, and there is decreased risk with heavy occupational exposure.73,91 Patients with melanoma are twice as likely to relate a history of
PART 3 BURNS, FIRE, AND RADIATION FIGURE 14-9 Melanoma on the back demonstrating the ABCDEs: asymmetry, border irregularity, color variegation, diameter of more than 6 mm (0.24 inch), and evolving features (i.e., the patient’s wife had noticed that the area at 9 o’clock was “growing out from the rest of it”).
after a single UVR exposure;291 some data suggest that sunburn can induce malignant transformation in benign nevi.47 In the United States, melanoma incidence has increased since records were first kept in the 1930s, rising 121% in the 20 years between 1973 and 1994.117 An estimated 68,130 Americans (29,260 women and 38,870 men) will have developed new cases of invasive cutaneous melanoma in 2010; an additional 46,770 cases of melanoma in situ will have been diagnosed that year as well.143 Today, the lifetime risk of melanoma for a male child born in the United States is 1 in 57; for a female child, the risk is 1 in 81.4 Similarly, large increases in melanoma incidence have been noted in Europe, Australia, and even Japan.149 However, melanoma incidence and death rates show signs of stabilizing and perhaps decreasing for younger cohorts,106,117,149 probably as a result of improved sun-protective behaviors. Significant national efforts have been made to educate and protect populations at risk. In Australia, taxes have been removed from sunscreen sales, hats are typically required for children when they are playing outdoor sports, and artificial shade is increasingly available in public parks. In addition to improved photoprotection, early detection has been widely promoted. The Skin Cancer Foundation encourages monthly self-examinations, with special attention to pigmented lesions that display atypical clinical features, which are the so-called ABCDEs of melanoma:235 asymmetry; border irregularity; color variegation; diameter of more than 6 mm (0.24 inch); and evolving features (Figure 14-9). Nevi with these clinical features, symptomatic nevi, or nevi that bleed should be evaluated by a dermatologist.
MOLECULAR BASIS OF PHOTOCARCINOGENESIS Several photomolecular events are associated with NMSC. UVR causes characteristic photoinsults at sites of adjacent pyrimidines on DNA.36,213,324 UVR photons are absorbed at the 5-5 double bonds, which results in cyclobutane dimers if both bonds open and 6-4 (pyrimidine-pyrimidone) photoproducts if a single bond opens.36 Cyclobutane dimers predominate 3:1, with thymine (T-T) dimers being the most common.160 Suberythemal and erythemal doses of UVR can induce T-T dimers.325 High-performance liquid chromatography can quantitatively measure these UVB photoproducts.42 Such measurements indicate 30-fold interindividual variation in photoproduct yields.42 Resultant UVR-induced mutations have a distinctive signature: two-thirds display cytosine → thymine (C → T) substitutions at dipyrimidine sites, and 10% show CC → TT substitutions.36 These mutations are relatively unique to UVR damage and allow UVR-induced mutations to be distinguished from chemical mutations.36 Data suggest that cyclobutane dimers and 6-4 photoproducts are primarily responsible for the mutagenic171 and carcinogenic160 properties of UVR. Many genes, including genes that are involved 302
in tumor suppression and promotion, may be targets for UVR mutations. Tumor-suppressor genes (TSGs) that are known to play a role in photocarcinogenesis include p53, p16, and PTCH.35,134 A mutation of p53, which is the most common genetic alteration identified in human cancers,134 is found in nearly 50% of all cancers.36,160 Approximately 50% of BCCa, 60% of actinic keratoses, and 90% of SCCa contain p53 mutations.36,328 Although p53 mutations may be found in non–sun-damaged skin at a low frequency, 10−2 to 10−3, mutations are much more common in sun-exposed sites.36 Normal p53 protein is a transcription factor that regulates the cell cycle. DNA damage stimulates p53 protein production, which leads to cell-cycle arrest in G1 (a premitotic phase), thereby allowing time for DNA repair.36 Irreparable damage leads to apoptosis or programmed cell death. Sunburn cells are examples of apoptotic cells.328 Cells with mutated p53 are more resistant to apoptosis with subsequent UVR exposures, which explains why p53 inactivation reduces sunburn cells in irradiated mouse skin.328 Within the p53 gene there are “hot spots:” these are codons where mutations frequently occur.36,43 Most p53 mutations result in a single amino-acid substitution, typically cytosine to thymine (C → T).328 Although normal, wild-type p53 has a short half-life and is generally unstable and unstainable, mutated p53 is significantly more stable and consequently stainable by immunohistochemical techniques.43,247 Both UVA and UVB upregulate p53 expression in human skin.46 After a single UVR exposure to the forearms, p53 protein expression peaks in 24 hours and returns to baseline after 360 hours.119 Mutations in p53 occur as an early initiating event in photocarcinogenesis.160 In actinic keratoses, unique p53 mutations are present throughout the lesion,328 which confirms that they occur before (rather than after) lesion formation. Different actinic keratoses display different p53 mutations, again supporting the role of p53 mutations as initial causative events that are followed by the clonal expansion of mutated cells to form clinically visible lesions of precancerous actinic keratosis.328 Altered p53 provides a survival advantage to mutated cells. In response to chronic UVR, neighboring nonmutated cells become apoptotic and die, thereby allowing space for the further expansion of the mutated clone with ongoing UVR exposure36 and ultimately resulting in development of actinic keratosis or SCCa. However, p53 mutations alone may be insufficient to produce NMSC. Patients with Li-Fraumeni syndrome, who inherit a mutated form of the p53 gene, have increased incidence of sarcomas, adenocarcinomas, and melanomas, but not NMSC.160 Consequently, other factors, such as decreased DNA repair and UVR-induced immunosuppression, must play a permissive role. For example, in patients with XP, there are increased numbers of p53 mutations36 and defective gene repair mechanisms as well as greatly increased numbers of NMSC. DNA repair may also be defective in normal patients who do not have the syndrome who develop BCCa at an early age306 as well as in older adult patients,213 who have a higher incidence of NMSC. Cutaneous lymphomas may also show a higher frequency of UVR signature p53 mutations.197 In mycosis fungoides, these mutations are found in the tumor stage but not the plaque stage,197 which suggests that UVR promotes the clinical progression of this lymphoma. These findings are particularly interesting in the light of epidemiologic data that demonstrate increased incidence of non-Hodgkin’s lymphoma among those who live closer to the equator.1 Other TSGs are less well studied but have increasingly defined roles in photocarcinogenesis. In melanoma, p16 is frequently inactivated139 and increasingly downregulated as melanoma progresses.277 Another TSG, PTCH, which is also located on chromosome 9, is frequently mutated in both familial and sporadic BCCa. Mutations of PTCH are especially notable in patients with XP and multiple BCCa.139 In addition to downregulating TSGs, UVR can activate protooncogenes to form functional oncogenes.139 Included in this group are the proto-oncogenes bcl-2, c-fos, and ras. In response to UVR, the bcl-2 protein is overexpressed, with resultant suppression of apoptosis and consequent permissive expansion of malignant clones. In addition, UVR alters c-fos, thereby disrupting transcription of nuclear proteins that are involved in cell
PHOTOIMMUNOLOGY UVR produces local and systemic immunosuppression.219 Locally, UVB depletes Langerhans’ cells, which are immunocompetent antigen-processing cells, for up to 2 weeks after exposure.208 In addition, UVB functionally alters Langerhans’ cells by interfering with their presentation of antigens to T cells,111 thereby diminishing helper T cell 1 responses (which promote contact hypersensitivity) while preserving helper T cell 2 responses257 (which suppress contact hypersensitivity), thereby effectively converting Langerhans’ cells from immunogenic to tolerogenic. Antigenspecific suppressor T cells arise; their appearance is possibly mediated by the UVR-induced synthesis of interleukin 10 from keratinocytes.257 As a consequence, contact hypersensitivity and mixed lymphocyte reactions are diminished with UVR exposure. This may at least partially explain why UVR-induced skin cancers, which are antigenic, progress to clinical lesions. In mice, this UVR-induced immunosuppression can be transferred with irradiated T lymphocytes.219 Other proposed mediators of UVR-induced immunosuppression include cis-urocanic acid,54 tumor necrosis factor-α, prostaglandins,217 and DNA photoproducts.209 Immunoregulatory failure contributes to formation of skin cancer.165 Skin cancer is often more aggressive and occurs at an earlier age among immunosuppressed patients.74,224 In Australia, 45% of kidney transplant patients develop skin cancer within 11 years, and 70% develop it within 20 years.32 For heart transplant patients in Australia, the incidence of skin cancer is 31% at 5 years and 43% at 10 years; skin cancer accounts for 27% of patient deaths in this group after the fourth post-transplant year.224 In these patients, the ratio of SCCa to BCCa is 3:1, which is the precise opposite of the ratio that is present in nonimmunosuppressed patients. These figures are unusual only because most studies suggest that the risk of skin cancer is higher after heart transplant than after kidney transplant because of higher doses of immunosuppressive drugs with the former. Chronic sun exposure and fair complexion further increase risk of skin cancer in transplant patients,224 possibly as a result of the overexpression of p53.99
Photoprotection SUNSCREENS Chemical sunscreens were discovered in 1926. By 1928, the first commercial sunscreen, which contained benzyl salicylate and benzyl cinnamate, was marketed in the United States.82 Subsequent sunscreen evolution was primarily directed toward UVB protection to mitigate development of sunburn from overexposure to the sun. Para-aminobenzoic acid (PABA) was first advocated as a sunscreen in 1942; it was patented in 1943 and made commercially available in 1960. By then, national advertisements for sunscreens were promoting the message that people would be able to tan without burning. Sun protection factor (SPF) 15 formulations became available around 1980. More recently, as
TABLE 14-1 Sunscreening Agents Approved in the
United States
Sunscreen Aminobenzoic acid Avobenzone Cinoxate Dioxybenzone Ecamsule* Homosalate Menthyl anthranilate (meradimate) Octocrylene Octyl methoxycinnamate (octinoxate) Octyl salicylate (octisalate) Oxybenzone Padimate O Phenylbenzimidazole sulfonic acid (ensulizole) Titanium dioxide Trolamine salicylate Zinc oxide
Maximal Screen (%) 15 3 3 3 2 15 5 10 7.5 5 6 8 4 25 12 25
Modified from the U.S. Food and Drug Administration: Sunscreen drug products for over-the-counter human use: Final monograph, Fed Reg 64:27666, 1999. *Approved by the U.S. Food and Drug Administration on July 21, 2006.
UVA photodamage has been increasingly appreciated, UVA sunscreening agents such as avobenzone have been introduced. Micronized preparations of titanium dioxide (TiO2) and zinc oxide (ZnO) have become popular, and they provide broadspectrum protection throughout the UVR range. Previously considered “physical” (reflective) as opposed to “chemical” (absorptive) sunscreens, these micronized preparations blur the traditional distinctions. Micronized TiO2 and ZnO are largely transparent and absorb, reflect, and scatter UVR.159 Consequently, chemical and physical labels for sunscreens are of diminishing value and perhaps should be dropped. In the United States, sunscreens are regulated over-the-counter drugs. The U.S. Food and Drug Administration’s (FDA) Final Overthe-Counter Drug Products Monograph on Sunscreens, which was published in the Federal Register on May 21, 1999, established the allowable sunscreening agents, testing procedures, and labeling claims for efficacy, water resistance, and safety.295 On June 17, 2011, the FDA published a final rule that updated the labeling claims and testing procedures of the 1999 Final Monograph.296 The current FDA-approved sunscreening ingredients are listed in Table 14-1. Two names are sometimes given for the same agent, because the U.S. Pharmacopeia changed the names of several sunscreening agents (effective September 1, 2002) to better conform to international standards.297 PABA is an effective UVB absorber that has fallen out of favor. Poorly water soluble, PABA must be formulated in an alcohol vehicle. On the skin, it binds epidermal proteins, thus enhancing its resistance to water removal (substantivity) but provoking contact and photocontact dermatitis in approximately 4% of exposed subjects. Further limiting its acceptability, PABA can permanently stain fabrics a dull yellow color. As a consequence, PABA has been largely replaced by PABA esters such as amyl dimethyl PABA (padimate A) and octyl dimethyl PABA (padimate O). These absorb well in the UVB range, are easier to formulate in nonalcoholic vehicles, and are less staining and less allergenic. Cinnamates are the next most potent UVB absorbers. They often replace PABA in PABA-free sunscreens, but octyl methoxycinnamate (octinoxate; Parsol MCX) is an order-of-magnitude less potent than padimate O.175 Octocrylene, which is a cinnamate derivative, is a weak UVB absorber that also absorbs UVA modestly up to 360 nm. Cinnamates are poorly bound to the stratum corneum and may cause contact dermatitis. Cinoxate is the most frequent contact sensitizer, with cross-sensitization to related cinnamates in coca leaves, balsam of Peru, and cinnamon oil.65 Salicylates, including homosalate and octyl salicylate (octisalate), are relatively weak absorbers of UVB, and they are consequently most often used in combination with other sunscreening agents. They have the advantages of being nonsensitizing and water insoluble, and they help to solubilize benzophenones in commercial products.84 303
CHAPTER 14 Exposure to Radiation From the Sun
proliferation. UVB also causes mutations in ras, thereby disrupting mitogenic signaling pathways. In particular, mutations in BRAF, which is a critical component of the ras protein kinase pathway, are found in a large percentage of nevi168 and melanomas,231 especially melanomas that arise on intermittently sunexposed skin.186 However, BRAF mutations occur only rarely in melanomas that arise in chronically sun-exposed or completely sun-protected skin,186 which suggests multiple genetic pathways for melanoma induction. Moreover, mutations of BRAF and p53 may interact to form melanoma.231 Oxidative damage is another mechanism, in addition to mutation, by which UVR contributes to photocarcinogenesis. Although UVA is less directly mutagenic than is UVB, it is more potent with regard to causing cellular oxidative damage by producing reactive molecular oxygen and nitrogen species that in turn damage DNA, proteins, and lipids. This damage contributes to carcinogenesis via inflammation, immunosuppression, and, ultimately, mutation.120 In addition, a group of zinc-dependent enzymes, known as matrix metalloproteinases, increase in response to UVR by altering the cutaneous extracellular environment to favor tumor invasion and spread.38,139
PART 3 BURNS, FIRE, AND RADIATION
Anthranilates are similarly weak UVB absorbers that also filter UVA. They display peak absorption at 340 nm.175 The single commercially available agent from this class is methyl anthranilate (meradimate). Phenylbenzimidazole sulfonic acid (ensulizole) is a unique UVB absorber. Unlike other chemical absorbers, which solubilize in the oil phase of emulsion formulations, phenylbenzimidazole sulfonic acid is water soluble. This physiochemical property has resulted in its increasing use in oil-free cosmetic sunscreens.175 Benzophenones are broader-spectrum sunscreening agents, with good absorption in the UVB and UVA ranges up to 360 nm.175 The three benzophenones available in the U.S. market are oxybenzone, dioxybenzone, and sulisobenzone. In the United States, dibenzoylmethanes are represented by a single agent: avobenzone (Parsol 1789, butyl methoxydibenzoylmethane). It is a potent UVA absorber, with little or no absorption in the UVB range.175 Its absorption peak at 358 nm falls nearly to zero at 400 nm.252 Concerns have been raised that photodegradation may limit its effectiveness. Under simulated solar light, avobenzone can be degraded 36% in as little as 15 minutes.261 However, these data are disputed, and there is debate regarding whether any significant decrease occurs with typical use, especially given the mitigating effect of combined sunscreening agents in commercially available preparations.261 For example, a patented complex known as Helioplex—a combination of avobenzone, oxybenzone, and diethyl 2,6-naphthalate—is remarkably photostable.51 In addition, select stabilizing compounds such as vitamin C, vitamin E, and iron chelators may retard photodegradation.199 Ecamsule (Mexoryl SX) is the newest sunscreening agent to be approved by the FDA, although it has been available in Europe and elsewhere for several years. It is an excellent UVA filter, with maximal absorbance at 345 nm and with modest absorption in the UVB range as well. Ecamsule is distinguished by being highly photostable and thermostable. It effectively protects skin from repeated exposures to UVA, thereby preventing the histologic changes associated with photoaging.267 Physical sunscreens traditionally refer to opaque agents that primarily reflect, scatter, and, to a lesser extent, absorb UVR. These include calamine, ichthammol, iron oxide, kaolin, red veterinary petroleum, starch, talc, TiO2, and ZnO. In the wilderness, extemporaneous physical blockers can be made from ashes, mud, and leaves. A sunscreen with a physical filter typically protects throughout the UVR and visible spectra and may even protect against IR-induced erythema.227 However, classic physical blockers are messy, uncomfortable, and cosmetically undesirable. Preparations of TiO2 and ZnO with a submicron (i.e., nano) particle size are now widely available. In contrast, with normal TiO2 and ZnO size ranges (150-300 nm for TiO2 and 200-400 nm for ZnO), in which the larger size permits these particles to reflect and scatter light, the submicron dimensions (typically 20-150 nm for TiO2 and 40-100 for ZnO) make these particles more soluble in their vehicle base and minimally reflective of visible light. Cosmetically, this is an advantage, because it makes them more transparent (or nearly so) in thin coats. The lower refractive index of ZnO in the visible range makes it less white and more transparent than TiO2.207 However, submicron-sized preparations significantly absorb UVR, thereby providing broad-spectrum protection from UVB and UVA and blurring the distinction between chemical and physical sunscreens, as mentioned previously.64,175,260 TiO2 and ZnO are sometimes marketed as “chemical-free” sunscreens, which is clearly a misnomer. In addition, products that contain “physical” sunscreening agents are often marketed as “sunblocks,” which is a misleading term that was eliminated in the 1999 FDA Final Monograph.295 Of note is that metal oxide nanoparticles, with their potential to be absorbed through the skin, have received a great deal of media attention in recent years but have not been comprehensively evaluated with regard to their potential longterm effects on human health. Likewise, the ecologic impact of product use and disposal and the fate and toxicity of nanoparticles in the environment will most likely be influenced by a number of factors (e.g., aggregation, stability, transport, sedimentation, biouptake) that remain to be rigorously studied.225 New sunscreens are on the horizon, with imaginative observation leading to future sources of sunscreening agents. For example, Saikawa and colleagues258 determined that the viscous 304
“red sweat” of the hippopotamus is an excellent broad-spectrum sunscreen, with absorption in the 200 to 600 nm range.258 Sunscreen Vehicles Sunscreen vehicles affect efficacy and acceptability. The ideal vehicle spreads easily, maximizes skin adherence, minimizes interaction with the active sunscreening agent, and is noncomedogenic, nonstinging, nonstaining, and inexpensive. In practice, the best vehicle is highly dependent on personal preference. Creams and lotions (emulsions) are most popular. Both are oilin-water or water-in-oil preparations, although lotions spread more easily. Most sunscreening agents are lipid soluble, which results in an objectionable greasy feel. Increasingly popular “dry lotions” minimize the lipid component and often include at least one water-soluble sunscreening agent to reduce oiliness.175 In contrast, sunscreen oils contain only a lipid phase. Oils spread easily but thinly, thus limiting the achievable concentration of active sunscreening agent and thereby limiting protectiveness. In addition, oils are oily and cosmetically less acceptable. Other anhydrous vehicles, such as ointments and waxes, may be desirable for climbers and winter campers by reducing the risks of chapping and frostbite. Gels are generally nongreasy but tend to wash or sweat off easily. In addition, gels seem to produce more stinging and irritation. Sticks typically incorporate sunscreening agents into wax bases, but applying stick preparations to larger areas is not easy. Aerosols can cover large areas quickly but tend to be wasteful, with spray lost to the air, and they usually form an uneven film175; they also need to be rubbed in to provide adequate and uniform protection.18 Sunscreens are increasingly being incorporated into cosmetics, including foundations, lipsticks, and moisturizers. Sun Protection Factor The ability of a sunscreen to protect the skin from UVR-induced erythema is measured by the SPF. The SPF is defined as the ratio of UVR required to produce minimal erythema (1 MED) in sunscreen-protected as opposed to sunscreen-unprotected skin.147,295 It can be represented by the following formula: SPF =
MED of sunscreen-protected skin MED of unprotected skin
Testing conditions are standardized by the FDA.295 The agent to be tested is applied at a standard concentration of 2 mg/cm2. Testing is performed indoors with a solar simulator on the back between the beltline and the scapulae. The SPF is typically determined on a panel of 20 (or a maximum of 25) subjects with skin types I, II, or III (see Box 14-2). The mean is then determined to be the approved SPF. Although indoor testing with a solar simulator is more reproducible than outdoor natural sun exposure, it may yield a falsely high SPF value. In outdoor testing of more than 30 sunscreens labeled SPF 15, none were found to actually have an SPF of more than 12.230 Several factors are responsible for lower SPF values with outdoor testing, including sweating; clothing, towel, and sand abrasion; and application variability. In addition, solar simulators generally have reduced outputs of UVA as compared with sunlight.261 SPF determinations use erythema as their measurable endpoint. Erythema is predominantly a result of UVB and not UVA exposure. Consequently, SPF is primarily a measure of UVB protection. The relationship of SPF to UVB absorption is given in Table 14-2. How high an SPF is necessary? Given that SPF 15 blocks 93% of UVB, some argue that SPF 15 is sufficient187 and that higher labeling claims are misleading and costly for consumers. However, in several studies, higher SPF sunscreens conferred clinical and histologic benefits. In children on Florida beaches, a single application of SPF 25 sunscreen protected just as well as multiple applications of SPF 15 for up to 6 hours of exposure.221 Histologically, an SPF 30 sunscreen provides better protection against sunburn cell formation than does an SPF 15 sunscreen.145 Sunscreen Application Perhaps the most persuasive argument in favor of higher-SPF sunscreens derives from variations in application technique. The
B Radiation Absorption
Sun Protection Factor 2 4 8 15 30 50
Ultraviolet B Radiation Absorption (%) 50.0 75.0 87.5 93.3 96.7 98.0
protection provided by sunscreen is related to the amount of product that is applied.263 In the real world, sunscreens are applied at much lower concentrations than the 2 mg/cm2 at which they are tested. When used ad lib, sunscreens are typically applied in concentrations of 0.5 to 1 mg/cm2.21,262 The resultant SPF is considerably reduced, typically to about 50% of the labeled SPF for chemical sunscreens.40 Some suggest that the reduction is even greater and that the actual SPF is only 20% to 50% of the labeled value.283 Physical sunscreens tend to be applied even more thinly, typically at two-thirds the concentration of chemical sunscreens, most likely because of their cosmetic visibility.62 For TiO2 products, application concentrations of 0.65 mg/cm2 result in SPF values of only 20% to 30% of the intended labeled value.283 Not surprisingly, persons who burn more easily tend to apply thicker concentrations of sunscreen.62 There is no difference in the applied concentrations of higher versus lower SPF formulations. Uneven application further reduces sunscreen protection. With the use of a fluorescent dye, a pattern of spotty use emerges. Individuals typically cover the forehead adequately, but the temples, ears, and posterior neck are often undertreated or missed entirely.99,177,244 Newly available sunscreens that contain disappearing colorants are popular because they provide visible assurance of complete coverage. Adequate coverage of just the chronically exposed areas (i.e., the face, ears, and dorsal surfaces of the hands) requires 2 to 3 g (0.07 to 0.11 oz) of product per day;175 this requires the use of an 8-oz bottle of sunscreen every 80 to 120 days. Application delay imposes a further decrease in protectiveness. In a study of families on Chicago beaches in the summer,249 sunscreen was applied only after arriving at the beach in 98% of families. The median delay from arrival to sunscreen application to the last family member was 51 minutes. Underapplication, uneven application, and delayed application of sunscreens result in unnecessary photoexposure and photodamage. In addition, for hikers, the concomitant use of sunscreen and insect repellent that contains diethyltoluamide lowers the effective SPF by 34%.212 In an effort to balance these issues with consumer concerns about SPF inflation, the FDA set a labeling limit of SPF 30+ in the 1999 Final Monograph295 that was effective May 21, 2001. This was subsequently extended to December 31, 2002, and later deferred indefinitely until the FDA develops a more comprehensive set of requirements to address both UVA testing and labeling. It is expected that the FDA will announce these changes officially in October 2010. Ultraviolet A Radiation Protection Factors With increased understanding of UVA-induced photodamage and the recent addition of better UVA-blocking agents (e.g., avobenzone, ecamsule, micronized TiO2 and ZnO), more attention has been focused on measuring UVA protection. Several measures of UVA protectiveness have been suggested, but none have been widely accepted or used. Among them are the UVA protection factor, which is analogous to SPF.253 The principal drawback of UVA protection factor determination is related to the lengthy exposure times required to induce erythema. A second method, the phototoxic protection factor, shortens exposure times by sensitizing skin to UVA with oral or topical psoralens. However, the relevance of phototoxic protection factor data to real-world conditions has been challenged. Other UVA protection factors involve measuring UVA-induced immediate pigment darkening, suppressing UVA-induced sunburn cell formation in psoralen-treated skin, and UVA-induced photocurrent transmission through various
media.84 In its 1999 Final Monograph, the FDA chose not to impose a specific UVA protection factor but allows a sunscreen to make UVA protection claims as long as it contains an approved UVA sunscreening agent.295 However, Rosenstein and co-workers255 found that sunscreens with a labeling claim of UVA protection allow for transmission of 6% to 52% UVA. Proposed New Sun Protection Factor and Ultraviolet A Radiation Labeling Requirements The FDA revised sunscreen labeling and effectiveness testing standards in a final rule, published in the Federal Register on June 17, 2011.296 Prepared in response to nearly 2900 public submissions, the FDA’s final rule represents the most significant changes to sunscreen labeling and testing in more than a decade. Effective for all products with annual sales less than $25,000 by June 17, 2013, and for all other products by June 18, 2012, the final rule establishes labeling and effectiveness testing for over-the-counter sunscreen products marketed without an approved application under Section 505 of the Federal Food, Drug, and Cosmetic Act. It does not address issues related to sunscreen active ingredients or certain other issues regarding the Generally Recognized as Safe and Effective (GRASE) determination for sunscreen products. The FDA chose to publish this final rule, even as it continues to work toward a comprehensive final monograph, with the immediate goals of public health in mind. More specifically, the FDA hopes the new rule will provide the following services to the public: • Help ensure currently marketed products be appropriately labeled and tested for both UVA and UVB protection • Promote proper use of these sunscreens and greater consumer protection from the damaging effects of UV radiation • Identify claims that render a product “misbranded” or claims that are not allowed on any over-the-counter sunscreen drug product marketed without an approved application; for example, terms like “sunblock,” “sweatproof,” and “waterproof” have been deemed misleading and are no longer permitted The final regulations establish new testing parameters that reduce the number of subjects required in SPF testing from 20 to 10 subjects, and require only a single in vitro test to demonstrate broad spectrum protection. Performance is determined on a pass/fail basis using a critical wavelength of 370 nm. The critical wavelength is defined by FDA as the wavelength at which the integral of the spectral absorbance curve for a particular sunscreen product reaches 90 percent of the integral over the UV spectrum from 290 to 400 nm:
Where λc = critical wavelength, A(λ) = mean absorbance at each wavelength, and dλ = wavelength interval between measurements.297 Products that pass testing (i.e., possess a mean critical wavelength ≥ 370 nm) will be labeled Broad Spectrum and SPF 15 (or higher) on the front, demonstrating protection against both UVB and UVA radiation. The new labeling will also inform consumers on the back of the product that sunscreens labeled as both Broad Spectrum and SPF 15 (or higher) not only protect against sunburn, but, if used as directed with other sun protection measures, can reduce the risk of skin cancer and early skin aging. For these broad spectrum products, higher SPF values also indicate higher levels of overall protection. Conversely, sunscreen products that are not broad spectrum, or that are broad spectrum with SPF values from 2 to 14, will be labeled with a warning that reads: “Skin Cancer/Skin Aging Alert: Spending time in the sun increases your risk of skin cancer and early skin aging. This product has been shown only to help prevent sunburn, not skin cancer or early skin aging.” The FDA also now requires that instructions for reapplying sunscreen at least every two hours, after swimming or sweating, and immediately after towel drying be included on labels. Likewise, a new “direction statement” will be included that states: 305
CHAPTER 14 Exposure to Radiation From the Sun
TABLE 14-2 Skin Protection Factor and Ultraviolet
PART 3 BURNS, FIRE, AND RADIATION
Sun Protection Measures: Spending time in the sun increases your risk of skin cancer and early skin aging. To decrease this risk, regularly use a sunscreen with a Broad Spectrum SPF of 15 or higher and other sun protection measures including: Limit time in the sun, especially from 10 a.m.-2 p.m. Wear long-sleeved shirts, pants, hats, and sunglasses. Required warnings on all covered over-the-counter products will also include the following (Figure 14-10, online): • “Do not use on damaged or broken skin.” • “When using this product keep out of eyes. Rinse with water to remove.” • “Stop use and ask a doctor if rash occurs.” Concomitant to announcing its final rule for sunscreen labeling and testing, the FDA also released three additional regulatory documents that may affect future sunscreen regulations. The proposed rule would limit the maximum SPF value on sunscreen labels to “50+” because, according to the FDA, there is not sufficient data to show that products with SPF values higher than 50 provide greater protection for users than products with SPF values of 50; the proposal creates the opportunity for the submission of data to support the inclusion of higher SPF values in the final rule. The advance notice of proposed rulemaking will allow the public a period of time to submit requested data addressing the effectiveness and the safety of sunscreen sprays, and to comment on possible directions and warnings for sprays that the FDA may pursue in the future among other issues regarding dosage forms for sunscreens. Finally, the Draft Enforcement Guidance for Industry outlines information to help sunscreen product manufacturers understand how to label and test their products in light of the new final rule and other regulatory initiatives. Substantivity The ability of a sunscreen to resist being washed off by water is referred to as substantivity. The FDA’s 2011 final rule changed testing and labeling requirements significantly in order to make it clearer and easier for consumers to understand water resistance as part of their purchase decision. Of interest, the new testing requirements were based on marketing data that indicated individuals at the beach or pool spend an average of 21 minutes in the water, and go into the water an average of 3.6 times per outing.296 Conditions for testing substantivity are set by the FDA. Freshwater immersion is required in an indoor fresh water pool, whirlpool, or hot tub maintained at 23° to 32° C (73° to 90° F). Fresh water is defined as clean drinking water that meets Environmental Protection Agency standards established in 40 CFR, part 141. Sunscreens that are newly labeled “water resistant (40 minutes)” or “water resistant (80 minutes)” will have passed testing requirements that include water immersion (with moderate activity) for 20 minutes with 15-minute drying times (no towel drying), repeated once or thrice, respectively.296 The conditions under which substantivity testing is performed raise some concern for “real world” relevance and applicability. For example, the effect of relative humidity, sunscreen dosage (i.e., amount applied), immersion time, and activity level should be considered. Similarly, the MED for skin that has been bathed in salt water is less than the MED for skin that has been bathed in fresh water, and both are lower than the MED of dry skin.90 Furthermore, cold churning water, sand abrasion, and toweling may add to sunscreen loss, which begs the question of whether water-resistant sunscreens are truly surf-resistant. The concerns about saltwater substantivity, which have been amplified by surfer folklore, have led to an almost cultish market of “surf shop” sunscreens, although few published data indicate whether these products are more substantive in a saltwater environment. Select sun screening agents, primarily PABA and PABA esters, are intrinsically substantive as a result of bonding to stratum corneum proteins. Other sunscreens must be incorporated into vehicles that confer substantivity. By applying sunscreen 15 to 30 minutes before water exposure, substantivity can be increased. Reapplication after swimming or sweating helps to ensure protection. Today dozens of affordable, UVA- and UVB-protective, water-resistant sunscreens are commercially available (Table 14-3). 306
Stability Photostability, which is a sunscreen’s ability to remain intact and effective after sun exposure, has been questioned for a number of sunscreens, most notably avobenzone. Questions regarding photostability have also been raised about octyl dimethyl PABA and octyl methoxycinnamate. Marot and colleagues190 demonstrated that photodegradation of octyl methoxycinnamate allows histologic and enzymatic injury to the skin and that failure of a photolabile sunscreen may result in genotoxicity.191 In a European study of 27 photoprotective lipsticks, 14 showed photoinstability; in other words, they became partially photoinactive after moderate UVR exposure.185 Twelve were photolabile in the UVA range, one was in the UVB range, and one in both the UVA and UVB ranges. Photostability can be significantly improved with the use of combinations of sunscreening agents. For example, octocrylene stabilizes avobenzone in a number of sunscreen formulations, whereas 4-methylbenzylidene camphor can be used to stabilize octyl methoxycinnamate.30 Vehicle formulations also affect stability; butyloctyl salicylate and butyloctyl benzoate contribute to photostability.30 There are few published data regarding packaging, storage, and shelf life of sunscreens. Packaging may affect sunscreen acceptability and stability. For example, octyl methoxycinnamate turns polyvinyl chloride a bright yellow color. In a recent study by Santoro and co-workers,259 benzophenone-3 and octyl methoxycinnamate maintained stability for 60 days in both glass and plastic containers at room temperature (25° C [77° F]) and at 35° C (95° F), with only minor changes in concentrations seen at 10° C (50° F) and 45° C (113° F). The generally accepted wisdom is to keep sunscreens out of glove compartments and similar locations where they are exposed to extremes of temperature for long periods. Shelf life is presumed to be at least 1 year or more for most commercially available sunscreens, although data are lacking. Sunscreen Prevention of Chronic Photodamage Sunscreens prevent sunburns in addition to mitigating UVRinduced histologic damage, UVR-induced immunosuppression, photoaging, and photocarcinogenesis. Sunscreens reduce UVRinduced DNA damage,300 but not entirely.44 Reductions are seen in pyrimidine photoproducts in humans44 as well as in UVRinduced p53 mutations and skin cancer in mice.5 Sunscreen nearly eliminates the overexpression of p53 in mice after acute236 and chronic90 UVR exposure. In humans, an SPF 15 sunscreen reduces p53+ cells by 33% after chronic UVR exposure.24 The published effects of sunscreen on immunosuppression are contradictory, largely resulting from the complex relationships of UVR dosing and sensitivity in different experimental models. SPF is not a reliable measure of a sunscreen’s ability to block UVRinduced immunosuppression; two sunscreens with identical SPF values may vary considerably with regard to their immunoprotectant effects.242 SPF and immune protection factor are not synonymous or equivalent.322 Overall, sunscreens mitigate but do not abrogate UVR-induced immunosuppression. In mice, sunscreens prevent the UVR-induced depletion of Langerhans’ cells, with higher-SPF sunscreens conferring greater protection.19 However, earlier studies noted little or no immunoprotectant effect from sunscreens.19 A broad-spectrum SPF 15 sunscreen prevents the UVR-induced suppression of contact hypersensitivity to dinitrochlorobenzene, a potent topical allergen, in humans.268 In C3H mice transplanted with NMSC, sunscreen blocks UVR-induced immunosuppression, thereby allowing for tumor rejection and again demonstrating increased protection with higher SPF values.248 However, in susceptible mice that have been injected with melanoma, sunscreens fail to adequately suppress UVB enhancement of melanoma growth.313 This finding has been overinterpreted and misinterpreted by some to support a peculiar antisunscreen stance. However, the most appropriate interpretation is that sunscreens by themselves are not sufficient to prevent all of the immunosuppressive sequelae of UVR exposure and that sunscreens should be used as part of a larger sun-protective strategy that includes avoidance and clothing protection. Sunscreens reduce sunburn cell formation and solar elastosis33 in humans. The histologic changes of photoaging in mice are
Product
Sun Protection Factor
High Sun Protection Factor Waterproof Broad-Spectrum Creams and Lotions Bain de Soleil Oil-Free Protecteur Sunscreen Lotion Banana Boat Sport 50 Blue Lizard Australian Sunscreen Lotion Bullfrog SuperBlock Lotion Coppertone Sport Ultra Sweatproof Dermatone Sunscreen Lotion DuraScreen Lotion Hawaiian Tropic Ozone Sunblock Kiss My Face Sunblock Lotion Neutrogena Ultra Sheer Dry-Touch Sunblock Ocean Potion Anti-Aging Sunblock Ombrelle Sunscreen Lotion Extreme Panama Jack Sunscreen Lotion Sea & Ski Sport SolBar PF Cream TI Screen Moisturizing Sunscreen Lotion Water Babies Sunblock Lotion High Sun Protection Factor Gels Bullfrog Quik Gel Coppertone Sport Sunblock Gel Pre-Sun Ultra Gel Ti-Screen Sports Gel High Sun Protection Factor Sprays Banana Boat Sport Quik Block Sunblock Spray Bullfrog Fast Blast Spray Sunblock Coppertone Sport Sunblock Spray Neutrogena Healthy Defense Oil-Free Spray Ti-Screen Sunscreen Spray High Sun Protection Factor Sticks Banana Boat Sport Sunscreen Stick Bullfrog Quik Stick Hawaiian Tropic Ozone Oil-free Sunblock Stick Neutrogena Healthy Defense Sunblock Stick Ocean Potion Sport Stick Shade Sunblock Stick Specialty Sunscreens AloeGator Super Waterproof Gel Bullfrog Surfer Formula Gel Dermatone Skin Protector Pomade SolRx ProSport Lip Screens Banana Boat Aloe Vera Lip Balm Coppertone Sport Lip Guard Dermatone Medicated Lip Balm Hawaiian Tropic Aloe Vera Sunblock Lip Balm Neutrogena Lip Moisturizer Ti-Screen Lip Protectant “Physical” Sunscreens Neutrogena Sensitive Skin Sunblock Lotion Pre-Sun Sensitive Skin Sunblock Vanicream Sunscreen Moisturizers Containing Higher-SPF Sunscreens Anthelios SX Daily Moisturizing Cream Aveeno Positively Radiant Daily Moisturizer Eucerin Extra Protective Moisture Lotion Lubriderm Daily Moisture Lotion Neutrogena Healthy Defense Daily Moisturizer Oil of Olay Complete Defense Daily UV Moisturizer Purpose Dual Treatment Moisture Lotion
Active Ingredients
35 30 30+ 45 30 36 30 70 30 55 50 40 45 50 50 30 45
A, B, OC, S B, C, OC, S B, C, OC, ZO B, C, MA, OC, S, TI B, C, S C, PBSA, ZO B, C, PBSA, S, TI B, C, PB, S, TI C, TI A, B, OC, S A, B, C, S A, B, OC, S B, C, OC, S B, C, S, ZO B, C, OC, S A, B, C, OC, S B, C, S
36 30 30 20
B, C, OC, S A, B, OC, S A, B, C, S B, C, S
48 36 30 30 23
A, B, C, OC, S B, C, OC, S B, C, S A, C, S B, C, MA, OC
30 36 50+ 30 60 30
B, C, OC, S B, C, OC, S A, B, OC, S A, C, S A, B, S B, C, S
40+ 36 23 44
B, B, B, B,
30 15 23 45+ 15 15
B, C, PB, S B, C B, PB C, OC, S B, C B, C
30 28 15
TI TI TI, ZO
15 15 30 15 30 30 15
A, E, OC A, C, S C, OC, PBSA, TI, ZO B, C, S C, OC, PBSA, ZO C, OC, S, ZO C, MA, TI
C, C, C, C,
OC, S OC PB OC, S
A, Avobenzone; B, benzophenones; C, cinnamates; E, ecamsule; MA, methyl anthranilate (meradimate); OC, octocrylene; PB, para-aminobenzoic acid or paraaminobenzoic acid ester; PBSA, phenylbenzimidazole sulfonic acid (ensulizole); S, salicylates; TI, titanium dioxide; ZO, zinc oxide.
prevented by pretreatment with SPF 15 sunscreen.155 In mice that have been exposed to UVB for 10 to 20 weeks, subsequent sunscreen use prevents further photodamage and promotes repair of previous damage, even with continued exposure.156 Higher-SPF sunscreens provide increasing protection against UVB-induced wrinkling in mice.28 Similarly, histologic and clinical
signs of UVA-induced photoaging are prevented by broadspectrum sunscreens.124 Sunscreen use reduces formation of precancerous actinic keratoses216,289 and promotes resolution of preexisting lesions.289 In a 2-year trial of sunscreens in humans with actinic keratoses, those who benefited most had the greatest number of keratoses at 307
CHAPTER 14 Exposure to Radiation From the Sun
TABLE 14-3 Select Sunscreen Products
PART 3 BURNS, FIRE, AND RADIATION
enrollment,216 thereby underscoring the value of continuing sunscreen use in adults. Daily use of SPF 15 sunscreen in adults reduces the incidence of SCCa but not of BCCa.114 Stern and colleagues281 estimated that using an SPF 15 sunscreen from birth until the age of 18 years would reduce the lifetime risk of NMSC by 78%. Liquid base makeup, even without sunscreen, provides an SPF of approximately 4 because of the pigments used in the foundation.175 For women who use lipstick, the incidence of SCCa is lower than in nonusers and men.234 Sunscreens, Melanoma, and Vitamin D Controversy regarding the effects of sunscreen use on the incidence of melanoma has intensified as melanoma incidence and sunscreen sales have both risen over several decades. Previous epidemiologic studies have, in general, failed to demonstrate conclusive evidence of decreased melanoma incidence with sunscreen use. Paradoxically, several studies have suggested an increased risk of melanoma with sunscreen use.12,63 In 1996, Donawho and Wolf 63 reviewed retrospective studies that evaluated melanoma risk in sunscreen users; only one showed decreased risk,135 whereas seven showed increased risk. Subsequent studies have continued to show contradictory results; a case-control study in southern Spain, which was published in the same year as the meta-study by Donawho and Wolf, showed decreased melanoma risk with sunscreen use in a Mediterranean population.251 In 1993, Garland and co-workers94 proposed that sunscreens, by primarily blocking UVB and sunburn, permit longer exposures to UVA in sunlight and that this increased UVA exposure results in increased incidence of melanoma. Confounding all of these studies, however, are the following points: • Persons who are at the highest risk for melanoma (i.e., those with fair complexions who burn easily) may be precisely the same persons who use sunscreens. • Earlier sunscreen products had lower SPFs and narrower spectrums. Modern sunscreens are typically more substantive, with higher SPFs, and substantially broader and better UVA protection. • Because sun exposure during childhood appears to be the most provocative for melanoma, surveying adults about their sunscreen habits may be irrelevant and misleading. Importantly, in 2010, Green and co-workers113 published a large, community-based study that provides strong evidence that daily application of sunscreen may directly reduce melanoma risk. Between 1992 and 1996, 1,621 randomly selected residents of Queensland, Australia, ages 25 to 75 years, were randomized into two groups. In the “daily” sunscreen group, participants were given free and unlimited supply of broad-spectrum sunscreen (SPF 16) and asked to apply it each morning to their head, neck, arms, and hands, with reapplication advised after heavy sweating, bathing, or long sun exposure. Participants in the “discretionary” group continued using sunscreen of any SPF at their usual discretionary frequency, which could include no use at all. Participants were also independently randomized to receive either 30 mg beta carotene or placebo supplements. The groups were then observed for incidence of primary melanoma and followed for an additional 10 years. By the end of the study, risk for developing any first primary melanoma was reduced by 50% (P = 0.051) and risk for invasive melanoma was reduced by 73% (P = 0.045) in “daily” users compared with “discretionary” users. There were no significant between-group differences in either in situ melanomas or melanomas at prescribed application sites. No direct effects of beta carotene were observed. Limitations of the study include the borderline significance of the risk reductions (though a discussion of the rigorous statistical methods are reviewed in an accompanying editorial by Gimotty and Ganz107) and the study’s applicability to different geographical locations and populations (i.e., different skin types). When considered in total, however, the results of this uniquely ambitious study provide support for sunscreen use as a means of helping to reduce the risk of melanoma. The effect of sunscreens and clothing protection on the numbers of nevi in children and adolescents, which is a prominent risk factor for melanoma,93 is controversial as well. In Australian children between the ages of 0 and 35 months, 308
sunscreen use is associated with modestly decreased nevus counts.125 However, in a study of adolescent twins in the United Kingdom,302 sunscreen use did not decrease nevus counts. In fact, there was a modest increase in benign nevi in adolescents who regularly used high-SPF sunscreens, possibly because of increased exposure times among sunscreen users. In this U.K. study, clothing protection had no effect on nevus counts. However, in a separate study of first- and fourth-graders in British Columbia, those who regularly used sunscreens developed fewer nevi, especially on intermittently sun-exposed sites.173 It remains unclear why intermittent sun exposure, especially during childhood, is associated with an increased risk of melanoma, whereas chronic occupational exposure is partially protective.91 An increasingly popular explanation is that vitamin D, which is formed by the action of sunlight on the skin, may be protective. Data are amassing to support this hypothesis. Mortality rates of several common cancers in the United States (e.g., breast, colon, prostate) increase with increasing latitude.68 In 1990, Garland and colleagues95 suggested that decreased cutaneous synthesis of vitamin D at higher, less-sunny latitudes might explain increased mortality from breast cancer in the northern states. Recently, Smedby and co-workers274 reported that sunlight reduces the risk of non-Hodgkin’s lymphoma. Among men in the Navy, Garland and colleagues96 determined that regular sun exposure reduces melanoma risk. In a population-based study of 528 patients with melanoma, Berwick and co-workers25 found that increased survival is associated with sun exposure. These data suggest that melanoma may be among the tumors for which vitamin D has a salutary effect. Supporting this hypothesis are laboratory data that demonstrate the presence of vitamin D receptors on melanoma cells, with growth inhibition occurring in response to this vitamin.52 In a case-control study of 502 melanoma patients and 565 control patients, Millen and colleagues202 found that diets rich in vitamin D and carotenoids were associated with a reduced risk of melanoma. These findings beg the following question: Do sunscreens, by absorbing UVB, reduce vitamin D levels sufficiently to pose an increased risk of melanoma and perhaps other cancers as well? Holick131 states that there is an “unrecognized epidemic” of vitamin D deficiency in the United States. Nonetheless, concerns regarding sunscreen-induced vitamin D depletion may not be warranted. Although regular sunscreen use can decrease cutaneous synthesis of vitamin D3194 and the circulating levels of measurable 25-hydroxyvitamin D,195 even the most conscientious sunscreen users appear to maintain normal levels of vitamin D. Using an SPF 17 sunscreen throughout an Australian summer 113 subjects maintained adequate vitamin D levels,188 and 24 subjects who were using SPF 15 sunscreen for 2 years maintained normal parathyroid hormone levels and normal bone metabolic markers.77 Moreover, eight patients with XP maintained normal vitamin D levels for the 6 years that they were observed, despite rigorous photoprotection with sunscreens, clothing, and sun avoidance.276 Part of the controversy surrounding vitamin D stems from unclear or varying recommendations regarding the recommended dietary allowance (RDA) and the difficulty involved with getting adequate amounts from diet and supplements. For example, in 2008, the American Academy of Pediatrics published guidelines that recommended a daily intake of vitamin D of 400 IU per day for all infants and children beginning during the first few days of life; these updated guidelines were based in part on new clinical trials, and effectively doubled the dose recommended in the previous 2003 guidelines.303 Human milk typically contains a vitamin D concentration of 25 IU/L or less, therefore supplementation is recommended for all breast-fed infants. If an infant is weaned to vitamin-D–fortified infant formula and consuming at least 1000 mL per day, or if a child who is 1 year of age or older is weaned to vitamin-D–fortified milk, then further supplementation is not necessary, according to the American Academy of Pediatrics report and the U.S. Centers for Disease Control and Prevention. Some authors advocate for more aggressive supplementation to meet physiologic need, particularly for individuals who are deprived of sun exposure. This is important as vitamin D’s role in the maintenance of innate immunity and the prevention of
thiazides, sulfonamides, benzocaine, and hair dyes that contain paraphenylenediamine may occur.245 Paradoxically, sunscreens have become the leading cause of photoallergic contact dermatitis.290 Oxybenzone is the most commonly implicated. In 283 cases of photodermatitis, 35 people were photoallergic to oxybenzone, and 17 were allergic to PABA.286 In a separate study of 108 patients with photodermatitis, four were photoallergic to oxybenzone, and four were allergic to other sunscreening agents.290 Stinging or burning without accompanying erythema, scaling, or dermatitis is common, especially in periocular areas and particularly in patients with rosacea, although the addition of skin “protectants” (i.e., dimethicone or cyclomethicone) to the sunscreen vehicle can mitigate this.218 Certain vehicles (e.g., alcoholic gels) may be more stinging. Even when periocular application is avoided, perspiration, water immersion, and rubbing may cause sunscreen to migrate, thus producing symptoms. Comedogenicity is primarily related to ingredients in the vehicle base. Certain common excipients (e.g., almond oil, cocoa butter, isopropyl myristate, isopropyl palmitate, olive oil) are possible comedogens. TiO2 and ZnO can generate reactive molecular species, called free radicals, with sun exposure.64 TiO2 is more photoactive than is ZnO.207 Electromagnetic radiation with wavelengths of less than 412.5 nm has sufficient energy to excite TiO2 electrons from the valence band to the conduction band.159 Photoactivated TiO2 can damage DNA in vitro.129 In vivo, however, it is unlikely that TiO2 particles penetrate the stratum corneum to reach underlying epidermal cells that contain DNA. Transmission electron microscopy fails to demonstrate TiO2 penetration of the stratum corneum.66 Data also demonstrate that ZnO is not absorbed and that Zn levels are unchanged after application.98 Coating TiO2 or ZnO with silicone halts photoproduction of reactive species.64 Still, some concerns have been raised regarding the use of these agents on broken skin. Some sunscreening agents have weak estrogenic or anti androgenic activity.266 In particular, benzophenone-3, octylmethoxycinnamate, and 3-(4-methylbenzylidene) camphor may have estrogenic effects on human breast cancer cells in culture.265 To assess their endocrinologic safety, Janjua and co-workers141 studied the whole-body application of these three sunscreening agents on humans daily for 1 week with the use of a liberal concentration of 2 mg/cm2. Plasma and urine levels of all three agents were detectable in men and postmenopausal women; luteinizing hormone and follicle-stimulating hormone were unchanged, and there were only minor changes in testosterone and estradiol (in men only). The authors concluded that these endocrinologic alterations are clinically insignificant and that these sunscreen products are safe for use, at least for adults.
Sunscreens and Herpes UVB is a potent stimulus for the reactivation of herpes labialis in outdoor enthusiasts.141 Although sunscreen is ineffective for preventing recurrences in skiers on the slopes,204 it is quite effective for preventing recurrences in the clinical laboratory,254 which perhaps reflects a difference in application techniques.
CLOTHING PROTECTION
Sunscreen Side Effects Sunscreen side effects are generally mild and limited. In a prospective study of 603 subjects who applied SPF 15 sunscreen or vehicle control,81 19% in both groups had adverse reactions. Most reactions were irritant in nature, and fewer than 10% were allergic. More than one-half of the individuals who developed irritation were atopic. These data support the notion that most contact irritant dermatitis to sunscreens is attributable to excipients. Similarly, allergic reactions to sunscreens are more often the result of preservatives and fragrances than of active sunscreening agents.65 As a consequence—and contrary to popular belief— higher-SPF sunscreens are not more irritating than lower-SPF sunscreens.269 Nonetheless, most sunscreening agents can cause allergic or photoallergic contact dermatitis.147 For example, PABA is now rarely used, because it sensitizes approximately 4% of exposed subjects. After an individual is sensitized, cross-sensitization with
Clothing is a crucial part of sun protection, and provides substantial coverage to broad surface areas. However, clothing varies considerably in its ability to block UVR. Robson and Diffey250 determined the SPF of 60 different clothing fabrics, ranging from 2 (polyester blouse) to 1000 (cotton twill jeans). The most important factors for determining SPF are the tightness of the weave101,179,250 and then the actual fabric. An extreme example of this is Lycra, which blocks nearly 100% of UVR when lax and only 2% when maximally stretched.179 Other determinants include wetness and color. Dry and dark fabrics have a higher SPF than otherwise identical but wet and white fabrics.101 A typical dry white cotton T-shirt has an SPF of 5 to 9. Accumulating data show that clothing prevents chronic photodamage. In European children, clothing coverage is associated with fewer nevi.9 Blue denim reduces UVR-induced p53+ cells twice as effectively as does an SPF 15 sunscreen.24 Denim greatly reduces the formation of skin cancers in patients with XP.22 Standardized testing of clothing fabrics has produced a new measure, the ultraviolet protection factor, which is analogous to the SPF for sunscreens. A collimated UVR source is passed through flat, tensionless fabric, with resultant transmission measured by a spectroradiometer or broadband sensor.101,250,327 However, the resultant ultraviolet protection factor is generally 309
CHAPTER 14 Exposure to Radiation From the Sun
diseases such as diabetes and certain cancers comes to light.264 Given the remarkably brief sun exposures that are needed to synthesize vitamin D,132 Holick suggests an approach of sensible sun exposure, which involves 5 to 10 minutes of exposure two or three times weekly in conjunction with the dietary intake of vitamin D and vitamin supplements.131 This recommendation has raised considerable controversy and concern in the dermatologic community, where the rise in melanoma incidence and sunscreen use has been considered a reflection of increased recreational sun exposure.217 Weighing in on the debate, the Institute of Medicine, at the request of agencies of the U.S. and Canadian governments, assembled an expert panel of 14 scientists to review the increasing body of research on vitamin D and update its 1997 Dietary Reference Intakes (DRIs). After systematic review of the data was performed, the expert committee, on November 30, 2010, concluded that bone health was the only outcome for which causality and sufficient dose-response evidence were established. Importantly, vitamin D’s role in cancer prevention was not found to be conclusively demonstrated. In addition, the group formally recognized the limitations of 25-hydroxyvitamin D as a biomarker of effect, pointing out that more aggressive vitamin D dosing regimens are based on higher target serum 25-hydroxyvitamin D levels that, in these experts’ opinions, were not justified by the evidence. In total, the new RDA for vitamin D, which assumes minimal sun exposure, suggests the following: • 1 to 70 years, 600 IU per day • 71 years or older, 800 IU per day The committee continued to recommend 400 IU per day as the adequate intake (AI) reference value for infants 0 to 12 months of age. The group also established tolerable upper intake levels (UL) for vitamin D, taking into account emerging evidence of U-shaped associations (i.e., increased risk at both low and high levels and lowest risk at moderate levels of serum 25-hydroxyvitamin D) for all-cause mortality, cardiovascular disease, vascular calcification, pancreatic cancer, falls, frailty, and fractures. The recommended UL for vitamin D is as follows:140 • 9 years and older, 4000 IU per day • 4 to 8 years, 3000 IU per day • 1 to 3 years, 2500 IU per day • 6 to 12 months, 1500 IU per day • 0 to 6 months, 1000 IU per day Scientific literature demonstrates that vitamin D plays a clear role in older adults who are at higher risk for osteopenia and fractures,109 and for infants at risk for rickets (especially breast-fed infants, who may get inadequate vitamin D in human milk).97,162 What still lacks are long-term studies that prove causation and dose-response for what role—if any—vitamin D plays in skin cancer prevention. Further research in the field will help put an end to this dermatologic controversy.
PART 3 BURNS, FIRE, AND RADIATION
much lower than the values seen with actual use, because natural sunlight is scattered and reflected to a far greater extent than a collimated beam.241 In the United States, sun-protective clothing is regulated as a medical device (Figure 14-11, online). Several manufacturing strategies are used to achieve high SPFs. One approved product, Solumbra, is made of tightly woven nylon with an SPF of 30 or more. In hairless mice, this fabric is significantly better than cotton for reducing formation of UVR-induced SCCa.201 In contrast, SolarKnit uses chemically treated cotton and cotton– synthetic blends to achieve an SPF of 30 or more. Rayosan, which is a UVR-absorbing agent, bonds to various fabrics and increases their SPF by up to 300%; it stays on the clothing through several washings.179 A unique chemical UVR protectant, Tinosorb FD, may be incorporated into detergents to increase the SPF of clothing with each wash. Ladies’ hosiery provides a surprisingly low SPF: black hose has an SPF of 1.5 to 3, and beige hose has an SPF of less than 2.270 Perhaps this explains in part why skin cancers are more common on the lower legs of women than those of men. Hats are also protective, with protection varying as a function of brim diameter and wearing style. Small-brimmed (<2.5 cm [≈1 inch]) hats adequately protect the forehead and the upper nose; medium-brimmed (2.5 to 7.5 cm [≈1 to 3 inches]) and wide-brimmed (>7.5 cm [≈3 inches]) hats protect increasing proportions of the nose, cheeks, chin, and neck,61 with largebrimmed hats providing an equivalent SPF of 7 for the nose, 3 for the cheeks, and 2 for the chin. Baseball-style caps are especially useful as a part of an overall sun-protective strategy for children. When these hats are used to protect the forehead and periocular areas, sunscreen application can be limited to areas below the cheekbones, thus mitigating the risk of stinging from application near the eyes. Glasses, contact lenses, and sunglasses protect the corneas from most UVB and from variable amounts of UVA.256 Surprisingly, price is unrelated to protection.3 A complete discussion of this is provided in Chapter 28.
SUN AVOIDANCE An indoor lifestyle is protective but undesirable for most persons. More practical is the avoidance of excessive midday sun (i.e., from 10 AM to 3 PM), which significantly reduces UVB exposure.177 Shade provides variable and often less protection than is generally assumed. In one study, shade beneath leafy trees provided an SPF of less than 4.229 Shade cloths allow significantly more UVB exposure than does clothing of the same fabrics, largely because of atmospheric scattering and surface reflection.314 Automobile windshields block UVB and some UVA, whereas side windows typically block only UVB.292 This may explain why photodamage is more prominent on the left side of the face of Americans (and on the right side of the face of Australians) who drive a great deal.272 Factors that affect UV-protective properties of glass include color, type, coating, and interleave between layers of glass. Transparent plastic films that meet legal requirements in all 50 states can be applied to block more than 99% of UVR (e.g., LLumar UV Shield).
SUNLESS TANNING Bronzers Most artificial tanners and bronzers contain dihydroxyacetone (DHA). DHA reacts with amino groups of keratin proteins via the Maillard reaction to form brown-pigmented products known as melanoidins.174 With DHA, bronzing can occur in as little as 1 hour. Often, however, it requires multiple applications to achieve the desired depth of color. Maintaining this bronzed look requires reapplication every few days, because the stained stratum corneum is shed from the skin surface. The depth of color is related to the thickness of the stratum corneum and the amount and frequency of application.175 Cosmetic complaints include difficulty with obtaining an “even” tan and yellowing of the palms. DHA plus lawsone (a henna dye) was previously used as a sunscreening agent. However, DHA alone is an inadequate 310
sunscreen. It absorbs no UVB; rather, DHA absorbs higherwavelength UVA I and lower-wavelength visible light,85 which makes it useful for select photosensitivity disorders, such as porphyrias and polymorphous light eruption. Some commercial bronzing products now contain sunscreen in addition to DHA. Although the artificial tan produced by these combination products lasts for days, the photoprotection lasts for only hours. Consequently, the FDA Final Monograph requires that bronzers without sunscreens display a warning that they do not protect against sunburn. Certain other products to promote indoor tanning have been used, but few are safe and effective. Tan accelerators that contain melanin precursors such as tyrosine have no discernible benefit.142 Sunscreen preparations that containing psoralens (most commonly 5-methoxypsoralen [oil of bergamot]) are available in Europe. Although these stimulate melanin synthesis, they are tumorigenic in mice.48 Psoriasis patients who have been treated with psoralen plus UVA (PUVA) have a higher incidence of SCCa279 and, with prolonged use, melanoma.280 Users of psoralencontaining sunscreen have an increased risk of subsequent melanoma.12 Oral carotenoids, especially canthaxanthin, have been promoted as tanning pills. However, these are potentially toxic and consequently not approved in the United States. Tanning Salons Although precise data are lacking, approximately 25 million North Americans—many of them adolescents—use tanning salons each year.285 In a survey of high school students in St Paul, Minnesota, 34% admitted to using tanning salons at least four times during the previous year.222 Tanning has even been evaluated as a possible dependency in certain populations.220 Until 1980, most sunlamps emitted mostly UVB.12 Today’s tanning salons make use of high-output UVA tanning beds and market their services as a way to tan without burning, with a subtle but incorrect message that such tans are safe. In fact, chronic suberythemal UVA contributes to photoaging, immunosuppression, and carcinogenesis. In addition, there is significant variation in the radiation output of tanning beds. In a study of 50 tanning beds in England,317 UVA output varied by a factor of 3, and UVB output varied by a factor of 60. Typically, tanning bed outputs are contaminated with 2% to 10% UVB,304 which is more than the average UVB content of natural sunlight. In 38 Scottish tanning units, 10 minutes of exposure yielded the same carcinogenic risk as did 30 minutes of peak summer sun at the same latitude.214 Tanning bed exposure for 15 to 20 minutes induces DNA damage in fibroblasts.315 Several case-control studies document a positive association between tanning bed use and the later development of melanoma.10,305,312 In a Swedish study of 400 patients and 640 controls, persons who used sunbeds or sunlamps before the age of 30 had a 7.7-fold increased risk of melanoma.312 In 420 patients from Germany, France, and Belgium, melanoma risks increased 8.97-fold when sunlamps or sunbeds were used for tanning.11 Ironically, UVA tans are less effective than are natural tans for conferring protection against subsequent sunburn.146 In addition, maintaining a yearlong tan provides no protection against subsequent melanoma development.135 Too often, tanning salons ignore photosensitizing risks in their patrons.41 Furthermore, the damage from tanning salons is insidious. Public awareness of the danger needs to be heightened, and health and government regulators are now taking the lead.316 Recently, the World Health Organization stated that no one less than 18 years old should use tanning beds. Increasingly, states and individual counties within the United States are restricting access to tanning parlors by minors. Currently, a majority of states regulate the use of tanning facilities by minors. Several states have banned access to indoor tanning facilities to anyone younger than 14 years of age unless medically necessary.49,288 Melanin and Thymine Dimers Cyclobutane T-T dimers, which are produced by the action of UVR on skin, stimulate melanin synthesis and subsequent pigmentation.105 Eller and co-workers70 exposed melanocyte cultures to synthetic T-T dimers and noted twofold to threefold increases in tyrosinase messenger ribonucleic acid and sevenfold
UNIQUE PHOTOPROTECTANTS Systemic Sunscreens Safe and effective oral sunscreens remain elusive. Clearly, these would have an advantage with regard to convenience, coverage, and substantivity. Several oral agents have been evaluated, but few are significantly effective or have favorable risk-to-benefit ratios in normal individuals. However, three botanicals appear promising: green tea, turmeric, and extracts of the fern Polypodium leucotomos.243 Currently, a few oral agents are used for patients with photosensitivity disorders: beta-carotene is helpful for individuals with erythropoietic protoporphyria, chloroquine is used for patients with lupus erythematosus, and psoralens helps those with polymorphous light eruption. Antioxidants UVR exposure results in reactive oxygen species that contribute to DNA damage232 and peroxidative destruction of membrane lipids.137 These effects contribute to DNA structural abnormalities, inflammation, and immune alterations. Protecting the skin from reactive species are various natural antioxidants (vitamins A, C, and E; reduced glutathione; urocanic acid; melanin) and enzymatic systems (catalase, superoxide dismutase).137 However, chronic exposure to UVR depletes the skin of these antioxidants.183 Applying antioxidants before UVR exposure delays skin damage in hairless mice.27 Select forms of vitamin E, especially tocopherol sorbate, diminish photoinduced free radicals and skin wrinkling in mice.144 Topical application of vitamins C and E provide protection against the histopathologic changes of photodamage in swine skin.57 In this animal model, sunscreen plus vitamins C and E provide more protection than does sunscreen alone.57 Although vitamin C does not act as a sunscreen (it does not absorb UVR), it protects against erythema and sunburn cell formation by quenching free radicals that are at least partially causative.56 The beneficial effect of topical vitamin C in swine skin persists for 72 hours after application, which suggests a potential strategy for longer-term photoprotection. Resveratrol, which is a potent antioxidant found in grapes, nuts, and red wine, mitigates the UVB-associated damage in mouse skin. It reduces UVB-induced edema, inhibits lipid peroxidation, and decreases production of enzymes associated with tumor promotion.2 Silmarin, which is a flavonoid derived from milk thistle, also has antioxidant, antiinflammatory, and salutary immunomodulatory effects when applied topically.148 Topical applications of aloe and tamarind xyloglucan have similarly been shown to protect against UVR-induced immunosuppression by acting as antioxidants rather than sunscreens.284 Oral antioxidants may also be of value for preventing photodamage. In humans, a combination of 2 g of vitamin C in combination with 1000 IU of vitamin E given orally for 8 days increased MED, albeit modestly.67 A more recent and larger study of human volunteers involving the use of a combination of oral vitamins C and E for 3 months documented a significant decrease in the clinical signs of sunburn and thymine dimer formation after UVB irradiation.233 In a mouse model, dietary addition of lutein, which is a carotenoid antioxidant, decreased edema and suppression of contact hypersensitivity after UVB exposure.172 Green tea given orally to mice reduced cutaneous oxidative damage and abnormal matrix metalloproteinase formation in response to UVB.301 There are some concerns about the routine use of antioxidants. For example, topical vitamin E may provoke contact sensitization and may occasionally serve as a tumor promoter.206 In addition, both topical and oral antioxidants might interfere with the normal functioning of p53 protein to produce apoptosis of photodamaged keratinocytes via oxidative enzymes. Repair Enzyme T4 Endonuclease V There has been considerable interest in postexposure therapy for sunburn with the topical application of the DNA repair enzyme
BOX 14-3 Common Oral Photosensitizing Medications Antihistamines Fluoroquinolones Nonsteroidal antiinflammatory drugs Oral contraceptives Phenothiazines Sulfonamides Sulfonylureas Tetracyclines Thiazides Tricyclic antidepressants
T4 endonuclease V (T4N5). When it is applied in liposomes, T4N5 localizes in the epidermis and the appendages,320 thereby enhancing repair of UVR-induced DNA damage in mice and humans.318 T4N5 prevents UVR-induced immunosuppression166 and reduces UVR-induced skin cancer in mice.319 In a study of 30 patients with XP, T4N5 in a liposomal base significantly reduced the incidence of new actinic keratoses and basal cell carcinomas after 1 year.321 Given these qualities, T4N5 may serve in the future as a “morning-after” cream.
Photosensitivity Disorders ENDOGENOUS PHOTOSENSITIVITY DISORDERS Sun protection is especially important for persons with endogenous photosensitizing disorders, persons who take photosensitizing medications (Box 14-3), and persons who are exposed to topical photosensitizers (Box 14-4). The most common endogenous photodermatosis is polymorphous light eruption, which affects 10% to 14% of whites and predominantly females who are less than 30 years old. Clinically, this manifests with pruritus, erythema, macules, papules, or vesicles on sun-exposed skin arising 1 to 2 days after exposure and resolving spontaneously over the next 7 to 10 days. It is most common with initial sun exposures during the spring or early summer; “hardening” of the skin may occur with subsequent exposures. The action spectrum is unclear, although it is most commonly 290 to 365 nm.84 Patient education is very important for persons with this group of disorders. Sun avoidance and protective clothing are critical. Liberally applied sunscreens are helpful; a broad-spectrum sunscreen that contained padimate O and avobenzone was quite effective in one study.86 For medication-related photosensitization disorders, identifying the specific causative agent is crucial, and discontinuation or substitution, whenever possible, should be considered. For polymorphous light eruption, super- or highpotency topical steroids in several daily to weekly pulses— frequently in combination with systemic antihistamines (e.g., diphenhydramine, hydroxyzine, doxepin)—can help to manage pruritus and control the eruption. Hardening of the skin in the spring with UVB, narrow-band UVB, or PUVA can be very effective. Systemic antimalarials (e.g., 200 to 400 mg/day of hydroxychloroquine sulfate, started in late winter) are generally less effective than phototherapy; beta-carotene has been used with varying success. For patients with severe issues, azathioprine, cyclosporine, thalidomide, and mycophenolate mofetil may be considered. Lupus erythematosus may be exacerbated by sunlight. Although UVB is typically causative, UVA can contribute to this condition in some patients. Consequently, broad-spectrum sunscreens in combination with sun avoidance and clothing protection are most appropriate. A broad-spectrum sunscreen that contained padimate O and avobenzone diminished clinical severity in a 4-week study.45 Systemic antimalarials may also be used in more serious cases. Porphyrias are caused by inherited abnormalities in heme synthesis. Clinical manifestations vary with the genetic subtype, but photosensitivity is common with this group of disorders. Typically, the action spectrum is in the Soret band at 400 to 311
CHAPTER 14 Exposure to Radiation From the Sun
increases in melanin production. Topical application to guinea pigs increases pigmentation. This raises the question of whether the induction of protective pigmentation in humans might be possible with T-T dimers.
PART 3 BURNS, FIRE, AND RADIATION
BOX 14-4 Topical Phototoxins and Photoallergens Topical Phototoxic Compounds Dyes Eosin Methylene blue Medications Phenothiazines Sulfonamides Psoralens Methoxypsoralen Trimethylpsoralen Tars Creosote Pitch Topical Phototoxic Plants Angelica Carrot Celery Cow parsley Dill Fennel Fig Gas plant Giant hogweed Lemon Lime Meadow grass Parsnip Stinking mayweed Yarrow Topical Photoallergenic Compounds Antiseptics Chlorhexidine Hexachlorophene Fragrances Methylcoumarin Musk ambrette Phenothiazines Salicylanilides Sulfonamides Sunscreens Benzophenones Cinnamates Dibenzoylmethanes Para-aminobenzoic acid Para-aminobenzoic acid esters
410 nm. Consequently, sunscreens other than “physical” blockers are generally inadequate, although topical DHA and oral betacarotene may be useful adjuncts to sun avoidance and protective clothing. Chronic actinic dermatitis manifests as persistent macules and plaques that are often infiltrated and lichenified on chronically sun-exposed sites on older men. These patients may demonstrate dermatitic flares on involved areas with even modest photoexposure to UVR and shorter-wavelength visible light. Histologically the disorder can demonstrate progression from dermatitis to T-cell lymphoma. Broad-spectrum sunscreens, sun avoidance, and clothing protection (including the wearing of brimmed hats) are essential. For advanced cases, therapy with azathioprine, cyclosporine, PUVA, and retinoids has been used. Persons with persistent light reaction display a peculiar and persistent overreaction to sun exposure as a result of a prior topical photoallergy. Musk ambrette, which is found in many 312
perfumes, has been reported to provoke persistent light reaction.245 UVB is most often causative, although UVA may be involved as well. Broad-spectrum sunscreens, sun avoidance, and clothing protection provide appropriate prophylaxis. For disorders in which melanocytes are defective or absent (e.g., albinism, vitiligo) and for disorders in which DNA repair mechanisms are deficient (e.g., XP), the protective triad of sunscreens, sun avoidance, and clothing protection is required.
PHOTOTOXICITY Most oral photodrug eruptions are phototoxic, and they clinically manifest as exaggerated sunburn on exposed skin. Typically, there are sharp cutoffs at the “V” of the neck and the short-sleeve line. Less commonly there may be photo-onycholysis, which causes the distal fingernails to separate from their underlying beds. Photodrug eruptions are usually triggered by UVA. The most common offending drugs are listed in Box 14-3. Topical photosensitizers may cause phototoxicity, photoallergy, or both. Phototoxicity results in an exaggerated sunburn that is typically followed by postinflammatory pigmentation. Phototoxicity is nonimmunologic. The action spectrum for most topical phototoxic sensitizers is in UVR. A surprisingly large number of plants contain photosensitizers that can produce phototoxic reactions in exposed human skin (see Box 14-4), which results in a condition known as phytophotodermatitis. The most common chemical precipitants are furocoumarins, especially psoralens, which are found in limes, lemons, and certain other plants (Figure 14-12). Phytophotodermatitis is common among farmworkers, bartenders, cannery packers, and vacationers to sunny climates. Oil of bergamot, which contains 5-methoxypsoralen, is a frequent cause of phototoxicity related to perfumes (berloque dermatitis). Streaks of erythema and subsequent pigmentation on exposed skin of the face, neck, and wrists typify this eruption. Meadow-grass dermatitis among hikers is another example of phytophotodermatitis. Various common weeds, including meadow parsnip, contain furocoumarins, which cause whiplike erythematous streaks and pigmenting on skin after exposure to sunlight. Psoralens have been incorporated into sunscreens in Europe to promote tanning, although their use is associated with increasing risks of burns and carcinogenicity.48 PUVA is used therapeutically for psoriasis and select other dermatoses.
PHOTOALLERGY Although phototoxic reactions may occur in anyone, photoallergic reactions occur only in previously sensitized individuals. Photoallergic reactions are uncommon. They are typically provoked by interaction of UVA with a topical proallergen, and result in contact dermatitis within 48 hours. Unlike phototoxic reactions, which are limited to exposed skin, photoallergic reactions can spread to sun-protected adjacent sites. Sunscreens are
FIGURE 14-12 Phytophotodermatitis on a teenager after a “lime fight” that took place during an outdoor summer picnic.
Changing Attitudes Toward Photoprotection During the 20th century, a tan became desirable. It was equated with health, wealth, and stylishness. Characterizing the times was Coco Chanel’s pronouncement in 1929 that “a golden tan is the index of chic.” Sadly, this attitude led to dangerous behaviors and resulted in an epidemic of skin cancer. Psychological and attitudinal barriers remain some of the most challenging to overcome. Several studies have documented current attitudes toward photoprotection. In a study of Connecticut beachgoers, 70% said that they were there to obtain or maintain a tan.330 College students who were questioned in North Carolina stated that they rarely if ever used sunscreens.298 In a U.S. study of 2459 whites, 59% admitted to sunbathing, and 25% stated that they had sunbathed more than 10 times during the preceding year.158 Among spring skiers, only two-thirds used sunscreens, and of those, one-third were sunburned at the time of the survey.199 A survey in Leicester, England found that onehalf of all children were sunburned at least once a year.31 A 2003 Fact Sheet from the Centers for Disease Control and Prevention reported that 43% of white children who were less than 12 years old in the United States had one or more sunburns within the prior year.118 Even patients with sun-related problems often do not adopt adequate sun-protection habits. One study documented that patients with dysplastic nevus syndrome, who are at higher risk for melanoma, do not avoid sunburning.34 Among Israeli patients 1 year after treatment for BCCa, only 49% wore hats or long sleeves in the summer, and 62% used less than two bottles of sunscreen per year.127 Sunscreen use correlates with knowledge of the harmful effects of sun exposure and an understanding of SPF values.26 In a survey of 1001 adults in the United States, only 42% were aware of the term melanoma, and only 34% knew that it was some type of skin cancer.203 Many mistakenly use sunscreens in the belief that sunscreens will promote tanning. Clearly more education is needed. For 146 college students in Southern California, a 12-minute videotape about photoaging in conjunction with ultraviolet facial photography resulted in improved sunprotective behaviors 1 month after the education.184 In Australia, where a significant educational effort is under way, three-fourths of adults visiting their family physicians reported that they used sunscreens.192 Australian state-sponsored and privately sponsored programs stress sun avoidance and clothing protection over sunscreens, and increasingly Australian fashion magazines feature more hats and more models who are less tan.50 Prevention and early diagnosis programs have yielded results: sun-seeking behaviors and sunburns have decreased. More importantly, the incidence of melanoma has decreased, and melanoma survival has increased in younger Australian cohorts.196 Photoprotection education needs to begin during childhood. Considerable sun exposure occurs by the age of 18 years,
and childhood exposure may be more significant than lifetime exposure for determining the subsequent risks of BCCa and melanoma. Children who use or who are compelled to use sunscreens at an early age are more likely to use sunscreens as adolescents.17 However, sun-protection policies in U.S. schools are lacking, with one 2006 study demonstrating that only 10% of the 484 secondary schools in 27 cities surveyed had a formal policy in place.42 This situation thus requires the education of parents. Sadly, parents too often ignore or are ignorant of photoprotective measures. On beaches in Galveston, Texas at midday in July, only 42 of 82 parents interviewed had applied sunscreen to their children.182 Only a history of prior painful sunburns was correlated with sunscreen use, and this finding was documented in other studies as well.329 Physicians should try to alter parental behavior through education, beginning with the first well-baby visit. In the Galveston study, photoprotection was discussed during only 18% of well-baby checkups. Sun avoidance and clothing protection should be advocated for infants who are less than 6 months old, and sunscreen should be added to the photoprotective regimen for older toddlers and children. Consistent use of sun protection during childhood would decrease the number of sunburns and provide lifelong reduction in photoaging and NMSC.281 Advertisers and the fashion industry continue to glorify tanning with the use of bronzed models. Even sunscreen advertisements seem to have a dual and medically incompatible message: tan beautifully while protecting your skin. No wonder the public is confused by oxymoronic enticements regarding a “healthy tan.”240 Recently in the United States there has been a glimmer of progress toward photoprotection education in the public media. In a review of models in six popular American fashion magazines between 1983 and 1993, there was a trend toward lighter tans, more sunscreens, and more articles about sun awareness, although men’s magazines did not demonstrate this trend.100
Conclusion Sun exposure is associated with both acute and chronic deleterious sequelae. Sun protection significantly mitigates these sequelae. Appropriate sun-protective strategies include a combination of sun avoidance, clothing protection, and sunscreens. Sunscreens have evolved to become increasingly elegant and effective. Despite occasional concerns, sunscreens have enjoyed an excellent safety record for more than 5 decades.103,176 Still, some issues remain controversial and unanswered. For example, further research is needed to answer concerns about vitamin D deficiency with strict sun protection. It is conceivable that minimal and “sensible” sun exposure in adults may be part of that answer. For now, the best advice remains to use sun protection. Sun protection should begin during infancy and continue throughout life; educating parents and children is key to the success of this plan. With the introduction of high-SPF, broad-spectrum, waterproof sunscreens and high-SPF clothing fabrics, the wilderness enthusiast can enjoy the outdoors more safely.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
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paradoxically the current leading cause of photoallergy.60,136 During the 1970s, the fragrance 6-methylcoumarin, which was added to a tanning product, was responsible for a number of cases of photoallergy.245 During the 1960s, there was a virtual epidemic of photoallergic reactions that resulted from antibacterial salicylanilides used in soaps.245 Prevention requires excellent UVA protection, including use of broad-spectrum sunscreens.
CHAPTER 15
Volcanic Eruptions, Hazards, and Mitigation JOANNE N. FELDMAN AND ROBERT I. TILLING
Volcanic eruptions are spectacular, violent, and often quite dangerous expressions of Earth’s dynamic internal processes (Figure 15-1). More than 80% of the earth’s surface above and below sea level is of volcanic origin, and gaseous emissions from volcanoes helped form the earth’s oceans and atmosphere.22 On average, about 60 to 70 eruptions occur worldwide each year; half of these are continuations of previously erupting volcanoes, and the others are new eruptions.63,69 There are approximately 600 active volcanoes in the world and probably another 800 that have erupted at least once during the past 10,000 years.69 Some volcanoes erupt only once in their lifetime, whereas others erupt repeatedly or even continuously. The largest explosive eruptions occur infrequently; in general, the longer the time interval between eruptions, the larger the next eruption tends to be. Some of the worst volcanic catastrophes in history have occurred at volcanoes believed to be extinct, including the famous eruption of Vesuvius in AD 79, which destroyed the cities of Pompeii and Herculaneum (see later).69 In fact, in the past two centuries, 12 of the 17 largest eruptions were the first eruptions known in historical times.57,63 Table 15-1 lists some notable historical eruptions, the most recent of which occurred at Chaitén Volcano in southern Chile, coming back to life after being inactive for 9400 years.37 The Chaitén eruption, which began in May 2008, has continued nonexplosively into June 2010. This eruption has special volcanologic significance, because it is the world’s first major rhyolitic eruption since the 1912 eruption of Novarupta, Alaska—the largest in the 20th century (Figure 15-2; see Table 15-1). Volcanic eruptions have been responsible for the deaths of approximately 300,000 people in the past 400 years. In recent
years, the average is two to four fatal volcanic events per year.64 Causes of death and number of fatalities are not well documented.64 Most deadly of the volcano hazards, pyroclastic flows have claimed the most lives, whereas tephra is the most common killer (Box 15-1). Long after the eruption, famine and disease epidemics are responsible for up to one-third of the total fatalities attributed to explosive eruptions (Tables 15-2 and 15-3).64 Compared with other natural disasters, volcanic eruptions occur infrequently, affect few people, and are responsible for only a small percentage of fatalities. Only some 2% of all natural disasters are from volcanic activity.33,65 The deadliest volcanic eruption in history, Tambora, Indonesia, in 1815, killed approximately 60,000 people, whereas 1 million people were killed in the worst hurricane (Ganges Delta in Bangladesh, 1970) and 830,000 were killed in the worst earthquake (Shaanxi earthquake in China, 1556).36,62,69 Nevertheless, volcanoes have the potential to unleash one of the most destructive forces on Earth. Approximately 74,000 years ago, an Indonesian volcano named Toba
A
B
FIGURE 15-1 Eruption of Mt St Helens on May 18, 1980. (Courtesy Robert M. Krimmel, U.S. Geological Survey.)
314
FIGURE 15-2 A, Satellite view of an ash plume produced during the explosive phase of the ongoing eruption of Chaitén Volcano, southern Chile; plume is drifting downwind across Argentina and dissipating over the Atlantic Ocean. B, Aerial oblique view in January 2010 of the actively growing 2008-2010 lava dome within Chaitén’s 3-km (1.9-mile)wide summit caldera. (A MODIS/NASA image, May 3, 2008; B courtesy John Pallister, U.S. Geological Survey.)
For online-only figures, please go to www.expertconsult.com
Volcano
Country
Year
Significance
Santorini
Greece
1650 BC
Vesuvius
Italy
AD
Laki
Iceland
1783
Tambora
Indonesia
1815
Krakatau
Indonesia
1883
Montagne Pelée Novarupta
Martinique United States
1902 1912
Mt St Helens
United States
1980
El Chichón
Mexico
1982
Nevado del Ruiz
Colombia
1985
Mt Pinatubo
Philippines
1991
Chaitén
Chile
2008
One of the largest explosive eruptions on Earth; may have contributed to the decline of Minoan civilizations First major historical eruption to occur within range of major cities; first eruption to be well documented by an eyewitness (Pliny the Younger) Largest historical lava flow eruption on Earth; catastrophic impact on Iceland’s population from famine caused by loss of livestock from poisoning by hydrogen fluoride emissions Largest historical volcanic eruption on Earth; highest estimated eruption column (43 km [27 miles]); largest known death toll of over 60,000 (12,000 directly by pyroclastic flows* and tephra*; 48,000 indirectly from starvation and disease); global sulfuric acid aerosols caused worldwide climate change resulting in the “Year Without a Summer” in 1816; abnormally low temperatures in the northern hemisphere caused famine from widespread crop failure First large eruption of the modern age; two-thirds of the island destroyed; tsunami* killed 36,000 people living in adjacent coastal areas Classic example of a moderate-sized eruption causing severe loss of life: 29,000 people died Largest eruption in the world in the 20th century; occurred in uninhabited part of Alaska; no fatalities First major explosive eruption to be monitored intensively with modern technology; worst volcanic disaster in U.S. history; $1 billion worth of damage but only 57 people died because timely forecasting prompted evacuation Erupted violently three times; first eruption came as a complete surprise; pyroclastic flows killed 2000; worst volcanic disaster in Mexican history Example of small eruption causing severe loss of life; lahar* caused 23,000 deaths and $212 million of damage; worst volcanic disaster in Colombian history; disaster demonstrates that in densely populated areas, even very small eruptions can cause widespread devastation and kill thousands Second-largest eruption of the 20th century; major societal impact in Philippines; important but temporary global atmospheric effects; despite its huge size, eruption directly caused only 300 deaths because of timely evacuations prompted by precise forecasts by scientists Largest eruption in the 21st century to date; volcano had been dormant for 9400 years before abrupt onset of eruption in May 2008; activity is continuing nonexplosively through mid-June 2010; lahars and ashfalls caused relatively few deaths but severe socioeconomic impacts in southern Chile and downwind neighboring Argentina
79
Data from Sigurdsson H: The history of volcanology. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000, Academic Press; Tilling RI: Volcanic hazards and their mitigation: Progress and problems, Rev Geophys 27:237, 1989; Clemens JA: Volcano! Evacuation and military medical implications, ADF Health 3:25, 2002; and Lara LE: The 2008 eruption of Chaitén Volcano, Chile, Andean Geology 36:125, 2009. *See definitions in Box 15-1.
exploded and ejected 2800 km3 (672 cubic miles) of ash, dust, and volcanic gases high into the stratosphere, where it was carried around the world by high-altitude winds. The particulate matter interfered with solar radiation and is thought to have led to a 10° C (22° F) temporary global cooling of the earth’s surface.62,77 Such a degree of cooling today would be catastrophic on a global scale. We can expect more fatalities from volcanic eruptions as human settlements inexorably encroach on areas with high-risk volcanoes.4 Current estimates suggest that about 500 million people, or 10% of the world’s population, live within 100 km (62 miles) of a volcano that has been active in the historical record.4,53 Auckland, New Zealand, occupies an area of young volcanoes. Seattle–Tacoma, Washington, is on land that could be devastated by mudflows from an eruption of Mt Rainier. Naples, Italy, is built on the flanks of Vesuvius, where in the first minutes of a major eruption more than 100,000 people could be
BOX 15-1 Glossary of Terms Lahar Lava Magma Pumice Pyroclastic flow Tephra Tsunami Volcanologist
Volcanic mudflow Magma that has erupted at the earth’s surface Molten rock inside the earth Lightweight solidified fragments of magma ejected explosively from an eruption Ground-hugging ash and rock clouds that sweep down slopes at hurricane speeds Explosively erupted airborne volcanic material such as ash, pumice, and rocks Seismic sea wave generated by an earthquake or eruption Scientist who studies volcanoes
killed (Figure 15-3).4,9,57 Latin America and the Caribbean are areas of particularly high risk because of population density. During the 20th century, 76% of all fatalities from volcanic eruptions occurred in this region, and in the past 10 years, one-half of the most powerful eruptions occurred in this area. In general, most fatalities occur in densely populated, less developed countries (Table 15-4).53 Although volcanic eruptions constitute a significant natural hazard, other processes and products of volcanism can be highly beneficial to society, explaining in part why so many people live on or near volcanoes.62 Volcanic ash rejuvenates soil and can prevent the loss of phosphorus, resulting in highly productive agricultural land (Figure 15-4, online). Volcanic ore deposits supply diamonds, copper, gold, silver, lead, and zinc. Products of volcanic activity are used as building materials, as abrasive and cleaning agents, and for many chemical and industrial uses.22 Geothermal heat and steam can drive turbines to generate electricity, heat homes and industries directly, and be enjoyed by people at hot spring resorts (Figure 15-5, online). The beauty of volcanoes and volcanic activity also generates income for communities through tourism.
Vesuvius,
AD
79
The best-known volcanic eruption was Vesuvius on August 24, AD 79. This eruption killed thousands of people, devastated the surrounding countryside, and destroyed at least eight towns, most notably Pompeii and Herculaneum. Before this eruption, Vesuvius was seen as a benign mountain with lush vineyards planted on the slopes and human settlements on the mountain’s flanks. Unlike the nearby often-erupting volcanoes Etna and Stromboli, Vesuvius was not considered volcanic. Even a series of preeruption earthquakes, as is typical before eruptions, did little to raise concern that Vesuvius was an active volcano. The eruption was witnessed and documented by Pliny the 315
CHAPTER 15 Volcanic Eruptions, Hazards, and Mitigation
TABLE 15-1 Notable Historical Eruptions
PART 3 BURNS, FIRE, AND RADIATION
TABLE 15-2 Causes of Fatalities From Notable Volcanic Disasters Since 1000 AD No. of Deaths According to Primary Cause Volcano
Country
Year
Pyroclastic Flow
Merapi Kelut Vesuvius Etna Merapi Awu Oshima Cotopaxi Makian Papadayan Laki Asama Unzen Mayon Tambora Galunggung Nevado del Ruiz Awu Cotopaxi Krakatau Awu La Soufrière Montagne Pelée Santa María Taal Kelut Merapi Lamington Hibok-Hibok Agung Mt St Helens El Chichón Nevado del Ruiz
Indonesia Indonesia Italy Italy Indonesia Indonesia Japan Ecuador Indonesia Indonesia Iceland Japan Japan Philippines Indonesia Indonesia Colombia Indonesia Ecuador Indonesia Indonesia St Vincent Martinique Guatemala Philippines Indonesia Indonesia Papua New Guinea Philippines Indonesia United States Mexico Colombia Totals: GRAND TOTAL
1006 1586 1631 1669 1672 1711 1741 1741 1760 1772 1783 1783 1792 1814 1815 1822 1845 1856 1877 1883 1892 1902 1902 1902 1911 1919 1951 1951 1951 1963 1980 1982 1985
1000 — — — 300 — — — — 2960 — 1150 — 1200 12,000 — — — — — — 1560 29,000 6000 1330 — 1300 2940 500 1900 57 >2000 — >65,197
Lahar
Tsunami
Lava Flow
— 10,000 — — — 3200 — 1000 3000 — — — — — — 4000 1000 3000 1000 — 1530 — — — — 5110 — — — — — — >25,000 >57,840
— — — — — — 1480 — — — — — 15,190 — — — — — — 36,420 — — — — — — — — — — — — — 53,090 >261,467
— — 18,000 10,000 — — — — — — — — — — — — — — — — — — — — — — — — — — — — — 28,000
Posteruption Starvation — — — — — — — — — — 9340 — — — 48,000 — — — — — — — — — — — — — — — — — — >57,340
Modified from Tilling RI: Volcanic hazards and their mitigation: Progress and problems, Rev Geophys 27:237, 1989; and Tanguy J-C, Ribière C, Scarth A, et al: Victims from volcanic eruptions: A revised database, Bull Volcanol 60:137, 1998.
Younger. In two letters written to the Roman historian Tacitus, Pliny wrote that the first explosion began in the early afternoon and ended in the evening of the following day. At first, Vesuvius produced an enormous eruption cloud that ejected ash, pumice, and volcanic gases vertically up to 30 km (19 miles) high. Then, from a darkened sky, ash and pumice rained down on the towns of Pompeii and Straide, causing roofs to collapse under the weight of the ash fall and burying the towns (Figure 15-6, online). The town of Herculaneum, lying at the foot of Mt Vesuvius on a cliff overlooking the sea, was initially spared from burial. The prevailing wind blew away from the town and toward TABLE 15-3 Fatalities From Volcanic Eruptions,
1783-2000
Fatalities Volcanic Hazard Posteruption famine and disease epidemics Pyroclastic flows Lahars Volcanogenic tsunamis Debris avalanches Volcanic ash Volcanic gases Lava flows TOTAL
No. 75,000 67,500 42,500 42,500 10,000 10,000 1750 750 250,000
TABLE 15-4 Fatalities From Volcanic Eruptions by
Region, 1600-1982
% 30 27 17 17 4 4 <1 0.3 —
Modified from Baxter PJ: Impact of eruptions on human health. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000, Academic Press.
316
Pompeii. But in the early hours of August 25, Vesuvius exploded again, this time ejecting hot gases, ash, and pumice down the mountain’s slopes as a pyroclastic flow. Herculaneum was destroyed, buried beneath more than 20 m (66 feet) of pumice and ash. Whatever remained of Pompeii was also destroyed at that time.56 At about that time, Pliny the Younger wrote of the death of his uncle, Pliny the Elder, who probably died of asphyxiation from being caught too close to a pyroclastic flow.4 The remains of more than 2000 people found amid the ruins offer clues as to the causes of death. People unwilling or unable to flee their homes were instantaneously suffocated as hot volcanic ash and gases entered buildings. Others had multisystem trauma as the force of the explosion and pyroclastic flows scooped up rocks and building materials and smashed them into anything in their path. Skeletons recently uncovered in beach
Fatalities Region Indonesia Caribbean Japan Iceland Everywhere else TOTAL
No.
%
161,000 31,000 19,000 9400 19,000 239,400
67 13 8 4 8 100
Modified from Blong RJ: Volcanic hazards: A sourcebook on the effects of eruptions, Orlando, Fla, 1984, Academic Press.
THEORY OF PLATE TECTONICS
B
C FIGURE 15-3 A, Mt Eden, one of 50 geologically young but dormant volcanoes in the Auckland Volcanic Field, within the city of Auckland, New Zealand. B, Mt Rainier sits just 137 km (85 miles) southeast of Seattle–Tacoma, Washington. C, Bay of Naples, Italy, with Mt Vesuvius in the background. (A courtesy Lloyd Holmer, Institute of Geological and Nuclear Sciences, New Zealand; B courtesy Lyn Topinka, U.S. Geological Survey; C courtesy Robert I. Tilling, U.S. Geological Survey.)
The global distribution of volcanoes, as well as the origin and distribution of mountain ranges and earthquakes, are explained by plate tectonics.54,69 This theory suggests that the earth’s outermost layer is broken into a number of rigid plates that move relative to one another as they float atop the hotter, semisolid, more mobile material of the mantle. The nature and distribution of volcanic activity depend on the formation, movement, and destruction of these plates at their margins (Figure 15-10). When two tectonic plates move away from each other, or diverge, new crust is created as molten rock pushes up from the mantle and oozes out onto the earth’s surface or the seafloor. One well-known, mostly oceanic, divergent boundary, the MidAtlantic Ridge, is a submerged mountain range in the Atlantic Ocean that extends from the Arctic Ocean to beyond the southern tip of Africa. Along the Mid-Atlantic Ridge are numerous volcanoes, including those that rise above sea level in Iceland (Figure 15-11). Another prominent divergent boundary, entirely continental, is the 11,000-km-long (6835-mile-long) Great African Rift. About 75% of Earth’s volcanism occurs unseen along divergent boundaries, deep on the ocean floor. Two plates can also move toward one another, or converge. How two converging plates interact depends on the type of crust—continental or oceanic. Continental parts of plates, composed largely of granitic rocks, are relatively lightweight compared with the much denser and heavier oceanic parts of plates, which are composed of basalt. When two continental plates collide, both buckle upward to form a mountain range. The Himalaya Mountains are the result of the Indian plate colliding against the Eurasian plate (Figure 15-12). Few volcanoes are located in zones of continental collisions.
caves in Herculaneum suggested that the cause of death was the intense heat, roughly 500° C (932° F) (Figure 15-7).12,44,67
Volcanoes and Their Global Distribution Different images are associated with the word volcano—for example, a violently erupting Mt St Helens, a peaceful-looking snow-capped Volcán Villarrica in Chile, or rivers of lava flowing down the flanks of Kilauea Volcano in Hawaii (Figure 15-8). Volcano also means the opening, or vent, in the earth’s crust through which molten rock, ash, and gases are ejected. Molten rock, while underground, is called magma. It becomes lava once it reaches the surface. Whether a volcano erupts explosively (like Vesuvius or Mt St Helens) or nonexplosively (like the lava flows of Kilauea) depends on the magma—its composition, temperature, gas content, viscosity, and crystal content.62 Magma that is fluid and hot tends to erupt frequently (every few years) and generally nonexplosively. This type of volcano most commonly produces fountains or rivers of red-hot lava.72 In contrast, magma that is less fluid and cooler, and that contains trapped gases, tends to rise sluggishly and can plug up the volcanic vent. If enough pressure builds up as trapped gases
FIGURE 15-7 The “Garden of the Fugitives,” in Pompeii, Italy, reveals 13 adults and children huddled together in a futile attempt to shield themselves from pyroclastic flows from the eruption of Vesuvius in AD 79. The human casts are obtained by filling cavities left in hardened ash with liquid chalk. (Courtesy Lancevortex.)
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CHAPTER 15 Volcanic Eruptions, Hazards, and Mitigation
A
expand during ascent, the pent-up pressure can blow the plug, abruptly unleashing the expanding gases and producing a violent eruption.35 The most volcanically and seismically active zone in the world, called the Ring of Fire, coincides roughly with the borders of the Pacific Ocean (Figure 15-9).35 The volcanically active countries in this zone include Russia, Japan, the Philippines, Indonesia, Papua New Guinea, New Zealand, and the countries on the Pacific coasts of North, Central, and South America. Volcanoes are also scattered in the Atlantic and Pacific Oceans—in Hawaii, Iceland, and the Galapagos.
PART 3 BURNS, FIRE, AND RADIATION
A
B
C
FIGURE 15-8 A, Violently erupting Mt St Helens on May 18, 1980. B, Villarrica Volcano, Chile, looks peaceful and even has a ski lift on its flanks, but the mountain is actually the most active volcano in Chile. C, A long river of lava flowing downhill from Kilauea Volcano in 1983. It ultimately enters the ocean 12 km (7.5 miles) away. (A courtesy Keith Ronnholm; B courtesy Robert I. Tilling, U.S. Geological Survey; C courtesy J. D. Griggs, U.S. Geological Survey.)
Many of the world’s volcanoes are located at the convergent boundary between a continental plate and an oceanic plate. When these plates converge, the heavier oceanic plate dives, or subducts, below the lighter continental plate. This produces tremendous pressure and heat, melting the rock deep in the mantle. This molten rock, or magma, traps gases, such as carbon dioxide (CO2) and sulfur dioxide (SO2), making it buoyant in the surrounding denser, solid rock, and it begins to rise through the surrounding solid rock. Magma movement causes earthquakes that can be recorded with sensitive volcano-monitoring equipment. If the rising magma finds an area of weakness at the earth’s surface, a volcano is created either just inland from the coast—for example, the volcanoes in eastern Russia, the Cascades in North America, and the Andes in South America— or just off the coast, such as the volcanic island arcs of the Aleutian Islands in Alaska,
FIGURE 15-9 The Ring of Fire, a zone of frequent earthquakes and volcanic eruptions encircling the Pacific Ocean. Where the plates come together, they form deep oceanic trenches (green). (From Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office.)
318
and Indonesia (Figure 15-13). Because of their proximity to a continent’s coastline or to an island, subduction volcanoes are often near populated regions and thus can have a significant human impact. Eruptions tend to be violent and explosive, such as the 1980 eruption of Mt St Helens or the 1991 eruption of Mt Pinatubo in the Philippines.62 Some volcanoes are found far from plate boundaries. The Hawaiian volcanoes are more than 3200 km (1988 miles) from the nearest plate boundary, and Yellowstone, with over 10,000 geysers, hot springs, and boiling mud pools, is located in the interior of the North American plate. At both of these locations, an inferred hot spot below the plate melts overriding rock to produce magma that can rise toward the surface and ultimately erupt onto the seafloor or land. It has been assumed that the hot spot is stationary, whereas the tectonic plate above it moves. However, recent studies have questioned the fixedness of hot spots, prompting substantial debate among Earth scientists. Examination of oceanic hot spots shows that in a series of islands created by plate movement, the islands farthest from the hot spot are the oldest. For example, a 6000-km (3728-mile) chain of volcanoes stretches from the older Emperor Seamounts (underwater sea mountains) off Alaska to the younger Hawaiian Islands. These were all created by passage of the Pacific Plate over the Hawaiian hot spot. This hot spot, currently located under the Big Island of Hawaii, has remained stationary for about 45 million years, whereas the Pacific Plate has been slowly moving to the northwest. According to the stationary-hot-spot model, as the plate continues to move over the hot spot, a new Hawaiian island will eventually emerge above sea level. In fact, just 35 km (22 miles) southeast of the Big Island there is an underwater volcano, Loihi, that has risen 3 km (1.9 miles) above the seafloor and is within 1 km (0.6 miles) of the ocean surface (Figure 15-14). At hot-spot volcanoes, eruptions tend to be nonexplosive and are rarely life threatening.35 Huge volumes of fluid lava pour out, often creating large volcanic mountains, such as Mauna Loa, the largest single volcano in the world, standing 8851 m (5.5 miles) above the sea floor.
Types of Volcanoes As erupted material accumulates around a volcanic vent, a volcano is formed and progressively grows. Classified by
Isl
Oc
an d
Convergent plate boundary
ea
Tr
c
Shield volcano
en
ar
tle pla
M an
te
ng
ti uc
Lithosphere Asthenosphere
Moho Hotspot
bd
nc h
Oceanic crust
Sub
Continental crust Ma ntl Moho ting e plat e
duc
Mantle Mantle plume ?
Su
Tre g
ch
Stratovolcano
nic rid spre ge ad in
Continental rift zone (young divergent plate boundary)
Ex tra te ob rrestr jec t ial
Divergent plate boundary
Not to scale
Schematic cross section of plate tectonics
FIGURE 15-10 Cross section of the main types of plate boundaries. (From “This Dynamic Planet,” a wall map produced jointly by the U.S. Geological Survey, the Smithsonian Institution, and the U.S. Naval Research Laboratory.)
Divergent boundary
Oc
ea
ni c rid spr ge ead i
Tre n
ch
ng
structure, the most common types of volcanoes are composite volcanoes, calderas, shield volcanoes, subglacial volcanoes, and flood basalts. These can be roughly grouped as either explosive or nonexplosive volcanoes. However, volcanoes can show both explosive and nonexplosive behavior during their lifespan. For example, Kilauea typically erupts nonexplosively, spewing out fountains and rivers of lava, yet a 1924 eruption was spectacularly explosive, and new studies show that Kilauea’s explosive eruptions are as frequent as those of Mt St Helens.
GENERALLY EXPLOSIVE VOLCANOES Lithosphere Oceanic crust
Asthenosphere
A
B
C
FIGURE 15-11 A, Cross section of an oceanic divergent boundary. B, Map of the Mid-Atlantic Ridge, along which the Eurasian and African plates are pulling away from the North American and South American plates. Note the ridge rising above sea level in Iceland. C, Exposed segment of the Mid-Atlantic Ridge at Thingvellir, Iceland. Left of the fissure, the North American Plate is pulling westward away from the Eurasian Plate (right of the fissure). (A from “This Dynamic Planet,” a wall map produced jointly by the U.S. Geological Survey, the Smithsonian Institution, and the U.S. Naval Research Laboratory; B and C from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office.)
Composite Volcanoes Composite volcanoes, or stratovolcanoes, have steep sides and are typically associated with subduction zones at converging plate boundaries. Mt Fuji in Japan, Mt Pinatubo in the Philippines, and Mt Rainier in the United States are classic examples. However, composite volcanoes can also be formed at divergent plate boundaries (e.g., Hekla in Iceland and Mt Kilimanjaro in Tanzania) or at hot spots (e.g., Mt Erebus in Antarctica and Tenerife of the Spanish Canary Islands).56,57 The steep-sided shape results from the deposition of viscous lava flows alternating with pyroclastic flows and ashfall deposits. The explosive nature of composite volcanoes comes from the high viscosity and volatility of the magma (Figure 15-15). Calderas Formed by the collapse of a volcanic structure, calderas are circular or elliptical depressions, generally over 1 km (0.62 mile) in diameter. Crater Lake in the U.S. Cascade Range is a large, partially filled caldera 10 km (6.2 miles) in diameter and 600 m (1970 feet) deep, formed when Mt Mazama exploded 7700 years ago. Krakatau, in Indonesia, was created by an 1883 eruption that involved rapid emptying of the magma chamber and subsequent collapse of the volcano.56 Kilauea Crater is another well-known caldera (Figure 15-16). Very large calderas fed by huge active magma chambers have been called supervolcanoes and are capable of producing enormously explosive eruptions. Yellowstone Caldera, 85 km (53 miles) long by 45 km (28 miles) wide, the largest and most worrisome in the United States, has a magma chamber that is 40 km (25 miles) long, 20 km (12 miles) wide, and 10 km (6 miles) deep.57 Yellowstone has produced explosive eruptions 1000 times larger than the 1980 Mt St Helens eruption. Two other geologically young, large calderas located in the United States are Long Valley Caldera in California and Valles Caldera in New Mexico. Outside the United States, very large calderas include Campi Flegrei in Italy, Kamari Caldera on the island of Kos in the eastern Aegean, and Rabaul Caldera in Papua New Guinea. Fortunately, very large caldera-forming eruptions were rare events, occurring approximately once in hundreds of thousands of years (Figure 15-17, online).57 319
CHAPTER 15 Volcanic Eruptions, Hazards, and Mitigation
Transform plate boundary
Convergent plate boundary
Hig hp late au
ou
e
ng
ra
M
Continental crust
Continental crust
Lithosphere
Lithosphere
A
Asthenosphere
Ancient oceanic crust
B
FIGURE 15-12 A, Cross section of two continental parts of plates converging, resulting in the formation of a mountain range. B, The snow-capped Himalayas and the Tibetan Plateau are produced by the collision of the Indian-Australian Plate (left) against the Eurasian Plate (right). (A from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office; B courtesy NASA, photo STS41G-120-22. http://eol.jsc.nasa.gov/sseop/EFS/printinfo.pl?PHOTO=STS41G-120-22.)
GENERALLY NONEXPLOSIVE VOLCANOES
of Hawaii, are classic examples of shield volcanoes (Figure 15-18).
Shield volcanoes have gentle slopes and are formed almost exclusively of layers of lava that have often flowed great distances from the eruptive vents. The magma, unlike that of explosive volcanoes, is predominantly of low viscosity and low volatility. Shield volcanoes are mostly formed at hot spots, although some are located at convergent or divergent plate boundaries—for example, Erta Ale in Ethiopia and Mt Etna in Italy. The largest volcanoes on Earth, Mauna Loa and Mauna Kea
Subglacial Volcanoes Historically active volcanoes located under glaciers, called subglacial volcanoes, are known only in Iceland and Antarctica. They can erupt explosively, but thick ice cover generally inhibits material from being ejected high into the atmosphere. Instead, lava flows out, often melting ice and creating subglacial lakes and rivers. If this subglacial water suddenly escapes onto the glacier’s surface (a glacial burst, or jökulhlaup), a huge river can form
Tr en
Volca n
ch
ic arc
Shield Volcanoes
Oceanic crust
Kronotsky Volcano
Continental crust
Lithosphere
Lithosphere
Ocean
Asthenosphere
Oceanic crust Lithosphere
Pacific
rc da an Isl
nc
h
A
Tr e
PART 3 BURNS, FIRE, AND RADIATION
nt
ain
Continental crust
B
Lithosphere
Asthenosphere
C
D FIGURE 15-13 A, Cross section showing subduction of an oceanic plate resulting in the formation of continental volcanoes and mountains. B, Kronotsky Volcano, at 3525 m (11,570 feet) above sea level, lies at the margin of the Pacific Ocean on the Kamchatka Peninsula of Russia. It was formed from the subduction of the Pacific Plate (right) under the Eurasian Plate (left). C, Cross section illustrating subduction of an oceanic plate with formation of volcanic island arcs. D, View of steep-sided, symmetric Carlisle volcano on Carlisle Island in the central Aleutian Islands. The 1620-m (5315-foot)-high stratovolcano has erupted several times since the late 1700s. (A and C from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office; B modified from NASA, photo STS61A-45-0098. http://eol.jsc.nasa.gov/sseop/EFS/photoinfo.pl?PHOTO=STS61A-45-98; D courtesy M. Harbin, University of Alaska Fairbanks, U.S. Geological Survey.)
320
TE PLA
i ua Ka est) d (ol hu Oa
ui
Ma
So
lid
aii Haw est) g n (you
de
nse
roc
k
Zone of magma formation Fixed "Hot Spot"
A
B FIGURE 15-14 A, Cross section of the Hawaiian hot spot. B, Map of the 6000-km (3728-mile)-long Emperor Seamount–Hawaiian Ridge formed by the passage of the Pacific Plate over the Hawaiian hot spot over a span of 70 million years. (A from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office; B from “This Dynamic Planet,” a wall map produced jointly by the U.S. Geological Survey, the Smithsonian Institution, and the U.S. Naval Research Laboratory.)
and destroy anything in its path. Grímsvötn volcano, in Iceland, lies largely beneath the vast Vatnajökull icecap. The caldera lake is covered by an ice shelf 200 m (656 feet) thick, and only the southern rim of the 6- by 8-km (3.7- by 5-mile) caldera is exposed (Figure 15-19).57 Eyjafjallajökull, a subglacial volcano 120 km
Flood-Basalt Plateaus Flood-basalt plateaus are massive areas of hardened lava produced from the largest volcanic events known on Earth.29 Found on all continents and ocean floors, flood-basalt plateaus are created when basaltic magma erupts rapidly from fissures to form sheets of lava flows, typically tens of meters thick and covering tens of thousands of square kilometers.29 Good examples are the Columbia River Plateau (Figure 15-20, online) and the Deccan Plateau of India. The rate of erupting lava can be 20 times the average eruption rate of a hot-spot volcano, and the eruption is on average 1000 times bigger than that of a supervolcano.57 Not surprisingly, the copious release of volcanic gases during the eruptions of flood basalts can severely affect the climate, and there is a strong correlation between mass extinction on Earth and the eruption of flood basalts (see Figure 15-20).57 Undersea Volcanoes Most undersea volcanoes are found at oceanic divergent plate boundaries. Others are found at undersea hot spots or near island arcs at convergent plate boundaries. Where two plates diverge, magma is injected along the space created. If the magma reaches the seafloor, pillow lava (from slow effusions) or sheets of lava (from more rapid effusions) form. Sometimes, if the magma supply to a single point is sufficiently large and persistent, a cone-shaped volcano, called a seamount, rises from the seafloor. Seamounts found at undersea hot spots become island shield volcanoes, like the Hawaiian volcanoes, if they rise above sea level. Seamounts at subduction zones become island-arc volcanoes, like the volcanoes of Indonesia, above sea level. It is not uncommon for hot-spot seamounts to emerge above sea level and then later sink as the seamount moves away from the hot spot and the seafloor subsides under the weight of the lava. Atolls, found in equatorial regions, are the coral reefs around drowning island volcanoes, after they become inactive and sink below sea level (Figure 15-21, online).57
Volcano Hazards Some volcanic eruptions cause injury, death, and destruction within minutes to hours. Others produce hazards that pose risks to human life, livestock, and the environment for months to years after the eruption. Explosive and nonexplosive
Central vent Pyroclastic layers Lava flows
A
B
FIGURE 15-15 A, Cross section of a composite volcano (also called a stratovolcano). B, Mt Fuji, Japan, is a perfect example of a composite volcano. (Courtesy Thomas C. Pierson, U.S. Geological Survey.)
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IFIC PAC
(75 miles) from Reykjavik, Iceland, began to erupt on March 20, 2010, after being dormant since 1823. During the eruption, hot lava melted the overlying glacial ice and generated jökulhlaups (see Figure 15-19, C ) that caused destructive flooding and prompted evacuation of more than 800 inhabitants. Then, on April 14, the eruption entered a much more explosive phase and propelled an enormous ash plume more than 8 km (5 miles) into the atmosphere.61 The easterly drift of this plume over northern Europe provides an illustrative example of the potential hazards of volcanic ash for aviation safety (see Volcanic Ash, later). As of June 2010, the Eyjafjallajökull eruption is continuing, although at a reduced level of activity.
PART 3 BURNS, FIRE, AND RADIATION
B
I
C II
III Lake
IV
D
A FIGURE 15-16 A, Cross section of the formation of a caldera. B, Crater Lake, Oregon, was formed by the caldera-forming eruption of Mt Mazama 7700 years ago. C, When that mountain erupted cataclysmically, the summit collapsed, forming a caldera that eventually filled with water to form Crater Lake. D, Kilauea Caldera, Hawaii, in 1954 after an eruption within the caldera (dark area is the new lava). (B courtesy Peter Dartnell, U.S. Geological Survey; C courtesy Crater Lake Natural History Association; D courtesy U.S. Geological Survey.)
volcanoes generate unique hazards, but explosive eruptions are usually associated with much larger numbers of deaths.
HAZARDS FROM EXPLOSIVE VOLCANOES Volcanoes with explosive characteristics are extremely dangerous. They can cause thermal injury from hot gases and ash; mechanical injury from mud flows, debris avalanches, and falling tephra; chemical injury from toxic gases, and, rarely, electrical injury from lightning or ionizing radiation injury from radon gas (Figure 15-22).4 Most volcano-related deaths, injuries, and psychosocial effects occur because the volcano erupts violently and rapidly, leaving little or no time for people to escape or take shelter.50 However, significant fatalities have been associated with mud flows and release of toxic gases during noneruption periods. Unfortunately, the global distribution of explosive volcanoes, mostly along convergent plate boundaries, places them in densely populated areas.7 Fortunately, explosive eruptions occur infrequently, and technologic advances have increased the ability of 322
volcanologists to predict an eruption. Before the 1980 and 2004 eruptions of Mt St Helens and the 1991 eruption of Mt Pinatubo, high-risk zones around the volcanoes were evacuated because of timely warnings. Pyroclastic Flows and Surges Commonly, when an explosive volcano erupts, a volcanic cloud of gas, ash, and lava fragments rises vertically into the atmos phere. If this rising eruption cloud becomes denser than the surrounding air, it collapses and falls back toward the ground. Such gravitational collapse of the cloud leads to the formation of a hot, high-speed avalanche of ash, volcanic gases, lava fragments, and heated air, called a pyroclastic flow.56 Pyroclastic surges are similar to flows but are more dilute and less dense (Figure 15-23) and can travel farther.4 There is little chance for survival in the direct path of a pyroclastic flow or surge traveling at 300 km/hr (186 mph) or even greater, with temperatures of 600° to 900° C (1112° to 1652° F).57 Everything living is carbonized by the extreme
Summit caldera
Magma reservoir
A
has been rebuilt, but the population now is only 5000, much below the 1902 level (Figure 15-24). Mitigation. Mitigation of future disasters from pyroclastic flows depends on evacuation before an impending eruption. Failure for any reason to evacuate in time will result in many deaths. Unfortunately, many countries with human settlements close to active volcanoes do not have the resources to closely monitor volcanic activity, as the United States did for Mt St Helens. In Latin America and the Caribbean alone, nearly 60% of all deaths from volcanic eruptions are caused by pyroclastic flows.53 Survival is possible without evacuation far from the volcano, if there is adequate shelter to protect against high temperatures, asphyxiating gases, falling trees, and projectiles. Once persons are sheltered, windows, doors, and dampers should be closed. Skin should be completely covered, the head swathed in cloth and, to prevent severe lung damage, the breath should be held during the seconds to minutes when the hot cloud passes by. Emergency medical personnel should be prepared to treat burns and blunt trauma injuries.
Ice cap
B
Subglacial lake
A
FIGURE 15-18 A, Cross section of a shield volcano. B, Snow-capped Mauna Loa as seen from the Hawaiian Volcano Observatory on the Big Island of Hawaii. (B courtesy Robert I. Tilling, U.S. Geological Survey.)
temperatures and swept away by the hurricane force of gas, ash, and rock sweeping downhill. Most human victims die as a result of asphyxiation (from breathing overwhelming amounts of ash or from oxygen deprivation), exposure to the intense heat, or burial under volcanic debris. Moreover, fatal traumatic injuries can result from associated devastating winds that can flatten trees and throw rocks. Survivors might have severe and extensive burns to their skin and respiratory tracts, or blunt trauma injuries.53 Although the main impact only lasts a few minutes, pyroclastic deposits can remain extremely hot for weeks and pose a lingering danger.4 Subsequent fires could cause further injury and death. Some of the most famous volcanic disasters have involved pyroclastic flows and surges. The AD 79 eruption of Vesuvius sent pyroclastic flows down the volcano flanks, killing thousands in nearby towns. The 1980 eruption of Mt St Helens created a pyroclastic surge cloud that enveloped over one hundred people as it moved at locally supersonic speeds. The 57 people closest to the crater died. Many were buried by volcanic debris, and others died from exposure to intense heat or from asphyxia. One man was killed by a falling tree and another by a rock that flew through his car windshield. Two men died in the hospital from lung injury (acute respiratory distress syndrome) caused by inhaling fine ash.4 Two others, near the edge of the pyroclastic surge, survived with minimal injury. More people would have died, but the area surrounding Mt St Helens had been evacuated after swarms of earthquakes and changes in the shape of the mountain signaled an impending eruption. Two weeks after the eruption, ash deposits on the volcano were still 300° to 400° C (572° to 752° F).70 Gophers were the only animals to survive, because they were below ground. The most devastating eruption of the 20th century occurred on May 8, 1902, when Montagne Pelée, on the Caribbean island of Martinique, sent pyroclastic flows moving greater than 100 km/ hr (62 mph) down the mountainside. Within minutes, the city of Saint-Pierre, 6 km (3.7 miles) away, was annihilated and 29,000 people were killed. Only two survived in the town. At sea, ships were capsized and demasted, and people burned by hot air fall.57 Since then, Montagne Pelée has been relatively quiet. Saint-Pierre
B
C FIGURE 15-19 A, Cross section of a subglacial volcano. B, Subglacial volcano Grímsvötn in Iceland lies largely beneath the vast Vatnajökull icecap. The caldera lake is covered by a 200-m (656-foot)-thick ice shelf. A volcanic plume rises, during the November 2004 eruption, from the exposed southern rim of the 6- by 8-km (3.7- by 5-mile) caldera. C, Aerial view of jökulhlaups from the 2010-to-present eruption at Eyjafjallajökull, Iceland (see text). (B courtesy Freysteinn Sigmundsson, Nordic Volcanological Center.)
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Central vent
PART 3 BURNS, FIRE, AND RADIATION
Eruption cloud (volcanic ash cloud)
Prevailing wind Eruption column
Tephra (ash) fall Acid rain
Debris avalanche (landslide)
Ballistic projectiles (bombs, blocks)
Lava dome collapse Pyroclastic flow Mud or debris flow (lahar) Lava flow
Lava dome
Vent
Pyroclastic flow Pyroclastic surge Fumaroles
Ground water
FIGURE 15-23 Pyroclastic flow sweeping rapidly downslope from Unzen Volcano, Japan, in 1991. (Courtesy Shigeru Suto, Geological Survey of Japan.) Crack
Magma
(After Myers et al., 1998)
FIGURE 15-22 Common volcanic hazards. (Modified from Bobbie Meyers, U.S. Geological Survey.)
Lahars (Volcanic Mudflows) Lahars, the Indonesian term for volcanic mudflows, can accompany most active, explosive volcanoes (particularly those with snow or ice cover), and historically they have been almost as devastating as pyroclastic flows.53 They occur when hot or cold volcanic debris mixes with water. Because the mixture has a high proportion of sediment, lahars behave like liquid cement and may cover 20 times the area of equivalent rock avalanches.35 The
mass of rock, mud, ash, and water sweeps down valleys, and when it reaches lowland plains, it slows down and spreads out to cover hundreds of square kilometers. Lahars destroy buildings, bridges, and other structures and leave thick deposits behind (Figure 15-25, online). Most fatalities occur when victims are caught in the flow and are killed by trauma resulting from this destruction, by flying debris, and by burial.4 More deaths occur later from famine and disease as people are displaced from their homes and local water sources become contaminated. Lahars are especially dangerous because they come unheralded. They can form during or after an eruption, or they may be completely unrelated to eruptive activity.4 Water is the key ingredient. Lahars need at least 10% water by weight to become mobile.57 During an eruption, hot pyroclastic material can melt glacial ice or snow, producing water that mixes with ash on the volcano’s flank. The water may come from a crater lake drained during an eruption or from the volcano’s own subsurface geothermal system. A subglacial eruption can form a subglacial lake that subsequently breaks out to the surface and mixes with glacial debris. Heavy rainfall occurring during an eruption can initiate
A
B
C
FIGURE 15-24 A, City of Saint-Pierre, Martinique, with Montagne Pelée in the background, before the 1902 eruption. B, City of Saint-Pierre showing the destruction from pyroclastic flows from Montagne Pelée, May 8, 1902. C, Seven months later, another, smaller pyroclastic flow sweeps down the flank of Montagne Pelée on December 16, 1902. (A from an anonymous source; B and C courtesy Academy of Sciences, France.)
324
FIGURE 15-26 Armero, Colombia, after devastating lahars from Nevado del Ruiz swept down the steep-sided valley (top center) on November 13, 1985. (Courtesy Richard Janda, U.S. Geological Survey.)
lahar formation. Shortly after an eruption, when new volcanic material is on the volcano’s flank and there is no ground cover, rainfall can mix with the ash to create a lahar. Even long after an eruption, under circumstances such as a sustained intense rainfall, water may mix with ash and a lahar (now called a secondary lahar) can start to flow. Posteruption secondary lahars have caused more fatalities than during the catastrophic eruption of Mt Pinatubo, in the Philippines, on June 15, 1991. Lahars can flow far from the site of the eruption. It is not necessarily the largest ones that produce the highest fatality rate; other factors include the victims’ proximity to the hazard and the efficacy of a warning system. The greatest volcano tragedy of recent times began late at night on November 13, 1985, with a small eruption of the Colombian volcano Nevado del Ruiz. Small pyroclastic flows melted the snow cap and glacial ice on the mountain at 1656 m (5433 feet). The water mixed with volcanic ash, forming lahars that swept down the steep valleys and destroyed the town of Armero 50 km (31 miles) away, killing 23,000 inhabitants (Figure 15-26). Around midnight, the first lahar struck the town, which was completely unaware of the danger, and covered it with 3 to 4 m (10 to 13 feet) of mud, burying three quarters of the population.4 Causes of death included suffocation from mud aspiration, trauma, hypovolemic shock, and, later, gangrene. Of the 834 survivors, 578 (69.3%) had lacerations, 343 (41.1%) had penetrating injuries, 312 (37.4%) had fractures, and 272 (32.6%) had eye injuries; many had multiple injuries.76 Armero had been rebuilt on the site of previous settlements destroyed by similar lahars in 1595 and 1845. Local officials were warned by an on-site scientific team but failed to act. Another devastating lahar occurred in 1953 when Ruapehu volcano in New Zealand claimed 151 lives after an ash and ice dam retaining its crater lake collapsed. The resultant lahar swept away the Tangiwai railway bridge just minutes before the arrival of the Wellington-Auckland express, and five train cars plunged into the river.57,72 Mitigation. For communities at risk for being struck by a lahar, evacuation is as important as when the threat is a pyroclastic flow. Early warning systems include using trip wires stretched across lahar channels, seismic instrumentation (e.g., acoustic flow monitors), video cameras, automated rain gauges, and human observers. Also, lahars might be partly diverted or contained by creating channels, and they might be held back by dams and retention basins.57 To reduce the water source, reservoirs or crater lakes can be lowered in level. Survival is possible without complete evacuation if the population at risk can be quickly moved to higher ground. Caution should be taken when crossing bridges. Emergency medical personnel in high-risk areas need to be prepared to treat blunt and penetrating trauma (crush injuries, lacerations, fractures, eye injuries), hypovolemic shock, and wounds with gangrene complications. Access to victims buried in the thick cement-like mud can be difficult and prolonged.
Tsunami, the Japanese term for harbor wave, is a seismic sea wave triggered by an earthquake or by volcanic activity. Specific triggers include major earthquakes along subduction zones, submarine landslides, underwater explosions, eruptions of island volcanoes, and avalanches on the flanks of a volcano.35 Waves can move at speeds of more than 800 km/hr (497 mph), and travel hundreds or even thousands of kilometers away from the source. In deep water, a tsunami is generally less than 1 m (3 feet) high and of no threat, but as the wave approaches the shore, its speed falls and its height increases until it becomes a steep breaking wave or an enormous surging wall of water. Though relatively infrequent, tsunamis pose a severe risk that cannot be ignored, as was illustrated by the 2004 Indian Ocean Banda Aceh undersea earthquake, magnitude 9.0, which generated a tsunami that devastated the shores of Indonesia, Sri Lanka, India, Thailand, and other countries, with waves of up to 15 m (49 feet) high, killing approximately 228,000 people, although it is hard to know the exact figure (Figure 15-27). Tsunamis caused by volcanic activity have directly killed more than 42,500 people, which is as many as have been killed by lahars. Tsunamis, like lahars, can come unheralded to settlements close to the source but can also affect distant coastal regions. Fortunately, many of these distant communities can now receive forewarning from the Pacific Tsunami Warning System and the newly established Indian Ocean Tsunami Warning System. Death and destruction occur when a tsunami slams ashore and destroys low-lying coastal communities (Figure 15-28, online). Fatalities associated with volcanogenic tsunamis include those triggered by Mt Unzen, Japan, in 1792 and Krakatau, Indonesia, in 1883. Mt Unzen, on the Japanese island of Kyushu, is an island-arc volcano created above a subduction zone. In 1792, part of the volcano collapsed, probably as a result of seismic activity. The subsequent debris avalanche swept 6 km (3.7 miles) down the volcano to devastate the city of Shimabara, killing over 9500 people. Most of the debris then emptied into the sea and triggered a tsunami that struck much of the seacoast of Ariake, killing another 5000 people in villages and on farms, even those
FIGURE 15-27 Hundreds of dead bodies and debris are piled along the coast, a dramatic demonstration of the devastation caused by tsunamis affecting the Indian Ocean basin, this one triggered by the Banda Aceh earthquake, December 26, 2004. (Photographer unknown.)
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CHAPTER 15 Volcanic Eruptions, Hazards, and Mitigation
Tsunamis
PART 3 BURNS, FIRE, AND RADIATION
A
B
FIGURE 15-29 A, Tsunami buoy contains pressure sensors for determining a wave’s size by gauging the weight of the water column passing over it. B, “TsunamiReady” sign. (Courtesy National Oceanic and Atmospheric Administration.)
as high as 30 m (98 feet) above sea level, along nearly 100 km (62 miles) of coastline.56 The famous eruption of Krakatau in 1883, involving volcano collapse and sending pyroclastic flows into the sea, set off a series of tsunamis that washed away 165 coastal villages on Java and Sumatra, killing 36,000 people.35,57 Mitigation. Volcanic islands at risk for being hit by a tsunami include the islands of Hawaii, the Marquesas, the Canaries, Tristan da Cunha, and Réunion.57 Other low-lying coastal regions are at risk. Key to mitigation is a worldwide tsunami warning system similar to the Pacific Tsunami Warning System, which was created in 1965 to warn of impending tsunamis in the Pacific Basin. In Hawaii, the warning system consists of sirens throughout the islands. Lobbies of coastal high-rise buildings are designed to allow water to pass through them without causing structural damage.57 In addition, tsunami-warning-system buoys are scattered throughout the Pacific Ocean, and many coastal communities are educated to flee to high ground in case of earthquake or volcanic eruption (Figure 15-29). As a result of the 2004 Indian Ocean Banda Aceh undersea earthquake and tsunami, three more tsunami warning systems have been established. The Indian Ocean Tsunami Warning System became active in June 2006, whereas the other two, the Caribbean Sea and Adjacent Regions Tsunami Warning System and the Northeastern Atlantic, the Mediterranean and Connected Seas Tsunami Warning System, have been established but are not operational. The United Nations Intergovernmental Oceanographic Commission, through the International Tsunami Information Center, coordinates the four systems. Evacuation to higher ground is essential to reduce the morbidity and mortality associated with tsunamis, and effective evacuation depends on public education of the officials and inhabitants of coastal communities. Emergency medical personnel need to be prepared to treat near drownings, the effects of trauma, and disease epidemics. Debris Avalanches Volcanoes, especially steep-sided composite volcanoes, can be the site of catastrophic debris avalanches at any time.56 In 1792 at Mt Unzen, mentioned previously, it was a debris avalanche that swept down the side of the volcano, killing thousands before emptying into the sea and setting off a devastating tsunami.56,57 Also in Japan, in 1888, an avalanche from the north flank of Bandai volcano sent 1.5 km3 (0.36 cubic mile) of debris down the mountainside, killing 400 people below.56,57 A debris avalanche also contributed to the eruption of Mt St Helens in 1980. 326
Triggered by an earthquake, a debris avalanche on the north flank of the mountain removed rock overlying a shallow magma chamber. Pent-up volatile gases in the magma, no longer contained by the overlying pressure of the rock, quickly expanded, causing explosive fragmentation of the magma and the first eruption. Mitigation. Mitigating danger from debris avalanches includes mapping the zones of potential slope collapse and avoiding travel to and high-density development within those areas. Fatalities and injuries are associated with blunt trauma and burial beneath rock debris. A victim caught in a rock fall should immediately seek some sort of shelter, and roll into a ball to protect the head. Health care professionals need to be prepared for victims of blunt trauma. Tephra Tephra is the general term for fragmented rock of any size (volcanic blocks, glass shards, pumice, ash) ejected into the air by volcanic explosions. Tephra can range in size from large ballistic ejecta (over 1 m [3 feet]) to ash (less than 2 mm). The largest tephra fall back to the ground at high speeds in the immediate vicinity of the volcano. Smaller fragments stay airborne longer, and the smallest are carried away by prevailing winds before ultimately being deposited, even at distances of many hundreds of kilometers from the volcano. Ballistic Ejecta. An erupting volcano can eject huge ballistic fragments at high velocities (Figure 15-30). They can travel kilometers away from the volcanic vent and can cause significant damage (skull injuries, lacerations, blunt trauma of the chest and abdomen) to humans on impact.4,57 The zone of damage from volcanic ballistics is generally limited to about 5 km (3 miles)— the maximum recorded range—so this is rarely a major human health hazard.4 However, in Italy in 1944, three men were killed at Terzigno by falling volcanic rocks from Mt Vesuvius 5 km (3 miles) away. In 1924, an explosive eruption at Kilauea knocked a photographer down with flying stones and severed his leg. He died later that day, probably from toxic gas exposure.9 Fire is a more common hazard, because hot flying ejecta can set fire to wooden structures, forests, or grassland. Volcanic Ash. Smaller-sized tephra, especially ash, pose a much greater danger than do blocks and bombs. Drifting volcanic ash can be deposited hundreds to thousands of kilometers downwind from a volcano. Heavy accumulations of ash fall can collapse
CHAPTER 15 Volcanic Eruptions, Hazards, and Mitigation
A
B
FIGURE 15-30 A, Spectacular explosive spray of ballistic ejecta when hot lava from Kilauea Volcano entered the ocean in 2008 in Hawaii; observers (left corner) give scale. B, A large ballistic block thrown up onto the shore from a previous lava entry into the ocean in the 1980s. (A courtesy Michael Poland, U.S. Geological Survey; B courtesy Christina Heliker, U.S. Geological Survey.)
roofs, interfere with driving, clog machinery, and damage vegetation (Figure 15-31). A layer of ash only 10 cm (4 inches) thick is enough to collapse a flat roof, especially if it is wet with rainfall.53,57 Approximately 10,000 fatalities have been directly associated with ash fall, and the majority of these are from collapsed roofs. In 1991, Mt Pinatubo in the Philippines erupted during an untimely typhoon. Subsequent ash mixed with rain collapsed roofs and killed at least 300 people.57 Decreased visibility from airborne ash and slippery ashcoated roads pose a danger to drivers of motor vehicles. During and after an eruption, the incidence of motor vehicle accidents and associated injuries rises. Moderate amounts of ash fall can also directly damage motors and other machinery, as fine ash clogs engine filters and lubrication systems.57 Damaged machinery is rarely a risk to human health, except in the case of jet engines. Volcanic ash clouds contain a combination of fine rock and glass particles. If a jet aircraft flies into a volcanic ash cloud, even thousands of kilometers away, the ash can damage engines, avionics, and airframes. Ash particles can block fuel nozzles, air filters, and external navigational equipment. Abrasion damage can badly scratch cockpit windows, landing lights, and turbine blades. Volcanic glass sucked into the engine will melt in the heat, accumulate and solidify into a glassy layer that chokes fuel nozzles, coats turbine engines, and interferes with sensors, leading to reduced engine performance and ultimately total engine failure. High levels of static electricity in volcanic material can also interfere with radio communication. Comprehensive summaries of the damage and impacts of volcanic ash on aircraft operating and support systems are described in works by Casadevall13 and Miller and Casadevall.46 In the last 30 years, over 80 commercial aircraft have accidentally flown into eruption clouds, and 7 of these encounters caused in-flight loss of jet engine power.48 In 1982, two jetliners
flew into the eruption cloud from Galunggung volcano on Java. The first, a British Airways jumbo jet carrying 240 people, lost all four engines and plummeted 7500 m (24,600 feet) in 16 minutes before cold air chilled and shattered the volcanic glass and the engines could be restarted. The jet made an emergency landing at Jakarta airport with three functioning engines and flying blind because the windshield was opaque from ash abrasion. A few weeks later, a Singapore Airline jumbo jet flew into a volcanic ash cloud from the same volcano, lost three engines and dropped 2400 m (7874 feet) before one engine restarted, and the aircraft made an emergency landing (Figure 15-32).9 Fortunately, to date no lives have been lost from aircraft–volcanic ash encounters. However, in mid-April 2010, the high eruption cloud from the Eyjafjallajökull eruption (Figure 15-33, A) and its easterly drift over northern Europe (Figure. 15-33, B) raised serious concerns of possible damaging encounters between commercial aircraft and volcanic ash. As a precautionary measure, aviation officials closed many airports and grounded flights in the United Kingdom, France, Germany, Norway, Sweden, Finland, and Spain; many Europe-bound flights from the United States were also cancelled. The airport closures and flight cancellations resulted in the biggest disruption in commercial aviation since that caused by the September 11, 2001, terrorist attacks on the United States. Heavy ash can strip vegetation from leaves and coat surviving leaves. Destroyed vegetation and crops result in starvation of animals and can ultimately lead to famine in areas dependent on agriculture for subsistence. Famine from ash-related destruction of crops was the number one cause of fatalities associated with volcanic eruptions before the 20th century. With global communication and world relief organizations, famine is less common. Most volcanic ash poses little direct danger to humans. Eye irritation may cause conjunctivitis and corneal abrasion, especially in persons wearing contact lenses, but treatment is 327
PART 3 BURNS, FIRE, AND RADIATION
disease.47,59 For example, after Mt St Helens erupted in 1980, there was a fourfold increase in the number of asthma patients and a twofold increase in the number of bronchitis patients visiting emergency departments in two large hospitals.6 However, no study has shown significant long-term consequences of regularly breathing ash, even in the densely populated regions around Mt Sakurajima in Kyushu, Japan, where eruptions occur hundreds of times each year.75 Some studies have shown some types of ash, especially ash with a high content of the mineral cristobalite, can cause lung inflammation, but there is no evidence of any fibrogenic lung changes.31,38,60
A
B
Mitigation. To prevent injury from large tephra, danger zones around the volcano should be mapped, and they should be closed when eruption is a possibility. If closure is not possible, concrete shelters can be built in danger zones for the public to access. Hard hats should be worn at all times, and anyone caught near an erupting volcano should watch for missiles and dodge them.4 Emergency medical personnel need to be prepared for blunt trauma to the head and torso and for burn victims. To minimize injury from ash, drive slowly, minimize engine use, and wear eye protection and a dust mask. All vehicles and machinery should be put inside a garage or barn. Animals and livestock should be brought into closed shelters. Consider evacuating children and high-risk individuals (asthmatics and persons with chronic bronchitis) until ash levels are lower. Although communities used to be advised to keep flat roofs clear of ash buildup, this is not now recommended, as people have been injured or killed from falling off roofs while cleaning off ash (Figure 15-34). Health care professionals should be ready for an increase in emergency visits from motor vehicle collisions, eye injuries, and respiratory problems. To mitigate the dangers associated with aircraft travel near volcanic ash clouds, air traffic is routed away from eruption
C FIGURE 15-31 A, An enormous ash cloud from the 1980 eruption of Mt St Helens passing over the small town of Ephrata, Washington, 233 km (145 miles) to the west. B, Ash-covered village of Parentas, Java, after one of the eruptions of Galunggung Volcano in 1982. C, In the city of Yakima, central Washington, ash made roads slippery and decreased visibility after the 1980 eruption of Mt St Helens. (A courtesy Douglas Miller; B courtesy Maurice Kraft; C courtesy U.S. Geological Survey.)
simple.34,53 Inhalation of ash, typically thought to be a significant health hazard, is for the most part benign, except for people with preexisting lung disease, and heavily exposed workers, such as gardeners, road workers, and police.* Most ash particles are too large to be respired, high-dust concentrations are of brief duration, and ash is biologically inert.53,72 However, fine ash particles of less than 10 µm in diameter can irritate the lungs. They are especially dangerous for people with asthma and chronic bronchitis, and they result in increased visits to emergency departments for exacerbation of chronic lung *References 6, 8, 10, 14, 24, 43, 58, 75.
328
A
B FIGURE 15-32 A, Eruption cloud from Rabaul Volcano, New Britain Island, Papua New Guinea, September 1994. Note the difference in appearance between the eruption cloud and the ordinary mete orologic clouds. B, Aircraft damage after flying into an eruption cloud from Redoubt Volcano in Alaska, December 1989. (A cour tesy NASA, photo STS064-116-47, http://eol.jsc.nasa.gov/sseop/EFS/ photoinfo.pl?PHOTO=STS064-116-47; B courtesy Joyce Warren.)
B FIGURE 15-33 A, A high-rising eruption cloud from the explosive phase of the ongoing eruption of the subglacial volcano Eyjafjallajökull in Iceland. B, The airspace of northern Europe affected by the drifting eruption ash cloud from Eyjafjallajökull Volcano ( ). (Courtesy U.K. Met Office.)
clouds based on the analyses of a global system of Volcanic Ash Advisory Centers. These centers—-working with volcanic observatories—coordinate and disseminate information on atmospheric volcanic ash clouds that may endanger aircraft. In addition, if aircraft accidentally fly into an ash cloud, pilots are now trained in what to do at the first sign of engine failure. Pilots will turn around the plane to fly out of the eruption cloud and will try to cool the engines by idling. With engine cooling, the glassy coating will break off, thus preventing total engine failure. Volcanic Gases Gases dissolved in magma can separate explosively or passively from the molten rock and be discharged into the atmosphere. During an explosive eruption, 10 million to a billion tons of volcanic gases can be released into the atmosphere over a period of a few hours to a few days. During noneruptive periods, gas can also escape continuously from fissures, geysers, and other sites of volcanic activity. The most abundant gas released from magma is water vapor (H2O). Second is CO2, closely followed by SO2. Carbon monoxide, hydrochloric acid, hydrogen, and hydrogen sulfide (H2S) are other common gases released in appreciable quantities.56 CO2 and H2S are by far the most dangerous. Because they are both denser than air, they collect in lowlying areas and cause harm if inhaled by unsuspecting individuals.53 CO2 is an asphyxiant, and at concentrations higher than 20%, even a few breaths can very quickly lead to unconsciousness and death from acute hypoxia, severe acidosis, and respiratory paralysis. H2S, the colorless gas that smells like rotten eggs, is so toxic that a high-level exposure can kill a human after a single breath.57 H2S, much like cyanide, arrests cellular respiration and thus aerobic metabolism. There are numerous accounts of fatalities associated with CO2 emissions from volcanic activity. Perhaps the most lethal tragedy occurred in 1986 at Lake Nyos, Cameroon, when dangerous amounts of dissolved CO2, once trapped in the lower
FIGURE 15-34 Ash removal in Moses Lake, eastern Washington, after the 1980 eruption of Mt St Helens. Keeping roofs clear of ash is not advised because of the risk of falling off. (Photographer unknown.)
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CHAPTER 15 Volcanic Eruptions, Hazards, and Mitigation
A
levels of this volcanic crater lake, suddenly rose to the surface and were abruptly released like champagne suddenly uncorked.28 The gas rose 80 m (262 feet) before the CO2 settled to the ground and rolled down valleys and into villages up to 20 km (12 miles) away, instantly suffocating 1746 people and 3000 livestock. About 1500 others survived and suffered transiently from burns, headache, nausea, vomiting, cough, dyspnea, hemoptysis, and chest pain (Figure 15-35, online).1 Only 2 years earlier, at nearby Lake Monoun, a similar but smaller cloud of CO2 welled up from the lake, flowed downhill, and killed 39 people.28 In Indonesia, in 1979, a release of CO2-rich volcanic gas from Sinila Crater (Dieng Plateau) killed 142 local inhabitants as they evacuated the area via a low-lying valley.39 Less dramatically, CO2 leaking from underground volcanic systems in Italy has been linked to the deaths of animals and two children. In the Mammoth Lakes region in eastern central California, accumulation of volcanic CO2 trapped under snow may have contributed to the death of a cross-country skier as well as three ski patrol members.11,27 There are a few reports of H2S-associated fatalities. Six downhill skiers on Kusatsu-Shirane volcano in Japan died in 1971, and four hikers who wandered into the lowest part of the summit crater on Adatara volcano in Japan died in 1997. Neither volcano was erupting at the time.30,57 Chronic low-level H2S exposure may also have deleterious health effects. In Rotorua, New Zealand, where 30% of the city’s population lives downwind of an actively degassing geothermal field, preliminary findings indicated there is a spatial relationship between exposure and an increase in respiratory symptoms, especially in individuals with chronic obstructive pulmonary disease.21 SO2 is an irritant to mucous membranes, can induce respiratory distress, and can have an adverse effect on pulse rate and blood pressure, but it has never been proved to directly cause death.2,40-42,57 However, in Japan, SO2 emissions from Mt Oyama on the island of Miyake forced evacuation of Miyake’s 3900 residents to the mainland from September 2000 to February 2005.16 Since the return of residents to the island of Miyake, despite ongoing SO2 emissions, research has showed a relationship
PART 3 BURNS, FIRE, AND RADIATION
between SO2 concentrations and acute respiratory symptoms such as cough, sore throat, and shortness of breath.32 Similarly, there are no fatalities associated with hydrogen fluoride (HF), but indirectly HF was responsible for the death of 10,000 Icelanders in 1783. HF from the prolonged Laki fissure eruption poisoned much of the pastureland and crops, causing the death of half the livestock and crop failure, which ultimately led to famine and death.55-57 Mitigation. Mitigating the danger associated with toxic volcanic gases depends on the type of gas and how it is released. Since the Lake Nyos disaster, scientists have placed 12 pipes into the lake at different depths to allow CO2 to escape continuously rather than accumulating to dangerously high levels. Danger zones can be mapped, and warnings signs can be posted. Equipment can be stationed to monitor gas emissions. Recreationists should be educated to avoid certain activities at times of gas release or buildup under snow. Low-lying areas where poisonous gases can collect should be avoided. Emergency medical personnel should remove victims from the source of toxic gases, place them on high-flow oxygen, and treat other injuries accordingly.
2:58 PM, July 2, 1983
A 3:11 PM, July 2, 1983
HAZARDS FROM NONEXPLOSIVE VOLCANOES In general, nonexplosive volcanoes pose little direct danger to humans. Few fatalities are associated with them because lava usually flows slowly enough for people to avoid it.4,5 Generally, those who died either lingered to watch the lava or returned to their homes too early. On the other hand, rivers of lava can cause significant property damage as they set fire to, knock down, or bury buildings and roads. On rare occasions, flows of lowviscosity lava have been witnessed to travel down steep slopes at speeds as high as 100 km/hr (62 mph). Lava Flows Fatalities associated with lava flows account for only about 0.3% of total deaths from volcanic activity. The most deadly lava flow took place at Mt Nyiragongo, Congo.4 Nyiragongo is among the few volcanoes with an active lava lake inside its summit crater, and during an eruption in 1977, this lake suddenly drained through fissures in the crater wall. A very fluid lava flow, estimated to be traveling at 100 km/hr (62 mph), swiftly engulfed small towns, killing hundreds of people.4,51,56,57 In 1947, a scientist filming a lava flow at Mt Hekla in Iceland was killed by a glowing lava block rolling downslope.9 Other hazards include methanefueled explosions when lava overruns vegetation, and explosions or scalding steam when lava flows over ice or snow or into water (Figure 15-36).57 Mitigation. Because lava flows rarely pose a significant health hazard during volcanic activity, they are not a high priority for health planning.53 However, to limit property damage, lava-flow diversion is a possibility. In 1973, after 6000 years of inactivity, Eldfell volcano on the island of Heimaey in Iceland reawakened and lava poured out, threatening the most important port of the Icelandic fishing industry. To stop or divert the lava flow, cold seawater was sprayed onto the advancing lava front, and after 2 weeks of nonstop work, the port was saved.56,57 Other attempts at diversion, including building rock and dirt barriers, and aerial bombings,69 have not been successful. Health care professionals should be prepared to treat burns from contact with lava or scalding steam. Jökulhlaups A jökulhlaup is a large outburst flood associated with the eruption of a subglacial volcano. The heat from the volcano melts overlying ice, forming a subglacial lake. As the lake rises, the overlying glacier is lifted and begins to melt, forming a subglacial river. If this river bursts to the surface, disastrous flooding can occur. When this happened in 1996 from a subglacial eruption at Grímsvötn in Iceland, water escaped from a 3.5-km (2.2-mile) crevice at a maximum rate of 45,000 m3/sec (12 million gal/sec) to form, temporarily, the second-largest river on Earth.57 Miles of road and bridges were destroyed. A smaller jökulhlaup emerged 330
B FIGURE 15-36 A rapidly advancing lava flow from Puu Oo vent, Kilauea Volcano, Hawaii, engulfs vehicles. (Courtesy Robert W. Decker, U.S. Geological Survey.)
in November 2004, from volcanic activity at Grímsvötn, with a peak discharge of up to 4000 m3/sec (1 million gal/sec), but this time no roads or bridges were destroyed.66 In 2010, jökulhlaups of the Eyjafjallajökull eruption (see Figure 15-19, C ) caused substantial destruction of roads and infrastructure locally, but fortunately no deaths or injuries.
POSTERUPTION HAZARDS Major eruptions can be hazardous long after the eruption is over. Large quantities of gas released into the atmosphere can cause air pollution, produce acid rain, and deplete ozone, possibly affecting global climate for a few years.4 Water supplies can be contaminated and crops destroyed, leading to disease epidemics and famine.3 Moreover, overcrowding and poor sanitation conditions—commonly associated with temporary evacuation camps—pose health hazards and sometimes lead to disease epidemics. After the eruption of Mt Pinatubo in June 1991, a measles outbreak, diarrhea, and respiratory infections resulted in the death of hundreds of children from an isolated tribe forced to live in evacuation centers.23 Ongoing smaller eruptions can also cause problems (Figure 15-37, online). In Italy, Mt Etna is the largest continuous source of volcanic SO2 globally, and Stromboli is probably the second largest in Europe.20 During the 8 months that the Laki fissure in Iceland was erupting in 1783, at least 122 million metric tons (MT) of SO2, 7 MT of hydrogen chloride, and 15 MT of HF were released into the atmosphere.73 HF poisoned Icelandic sheep and destroyed crops, contributing to the death of about one-fifth of Iceland’s entire population.55 In addition, the Laki eruptions were probably responsible for the death of more than 10,000 people in England during the summer of 1783 and winter of 1784.55,73 Noting that the mortality rate was 16.7% above normal for this time period, experts in the United Kingdom suggest that a cloud of volcanic gases and particles swept south from Laki into England and was responsible for the very hot 1783 summer and subsequent severe winter.55,73 Combing climatic data, burial records, and written accounts, they read of a summertime “volcanic haze” or “dry fog” that shrouded the moon and sun, reduced visibility, withered vegetation, and caused health problems.20,55 Like smog, the dry fog caused headache and eye irritation, exacerbated lung disease,
Risk Reduction From Volcanic Hazards Humans are vulnerable to severe, unpreventable volcanic eruptions. Risk reduction starts with comprehending the seriousness of volcanic hazards and being prepared for the associated dangers. Nearly 99% of fatalities associated with volcanic eruptions are from pyroclastic flows and lahars, yet one-tenth of the world’s population lives in cities and homes near volcanoes, sometimes on the volcano slopes or on the remains of a previous pyroclastic flow, lahar, or debris avalanche.53,57 Fortunately, most volcanic eruptions are preceded by premonitory events, such as earthquakes and other measurable phenomena, far enough in advance to enable scientists and emergency workers to plan for disaster. However, a few of the most severe eruptions have occurred with little or no warning, and most of the world’s dangerous volcanoes are in densely populated countries that lack the resources or political interest to monitor them.5,69 Nevertheless, emergency planning for an eruption, including creation of hazard-zone maps and hazard evaluation, should be routine for all populated areas near volcanoes, regardless of their location or apparent state of activity.5 Risk reduction includes volcano monitoring, eruption prediction, and effective coordination between volcanologists, scientists, health care professionals, and the community at risk. In addition, with tourism increasing to volcanic destinations, the tourist industry, practitioners of travel medicine, and adventure travelers need to educate themselves and others about the potential health hazards when in volcanic environments.25
VOLCANO MONITORING Scientists monitor volcanoes for seismic activity (earthquakes), changes in volcano shape (ground deformation), surface temperature, magma level, gas emissions, and other chemical and physical attributes (Figure 15-38, online).50 Earthquakes and ground
deformations are the most reliable diagnostic observations for helping scientists predict when a volcano might erupt or when it is no longer likely to erupt.45,68 The importance of monitoring cannot be overstated. During the last half of the 20th century, most eruptions from monitored volcanoes were anticipated weeks or months in advance. These include the eruptions of Mt St Helens in 1980 and 2004 and Mt Pinatubo in 1991 (see next). Often, the problem is not predicting when the volcano will erupt but convincing government officials to act on the warning. Before 1985, authorities in Armero, Colombia, were warned that lahars could devastate their town, but the warning was disregarded, and the eruption at Nevado del Ruiz and the subsequent lahars destroyed the town and killed over 25,000 people.57
ERUPTION PREDICTION AND MT PINATUBO: EFFECTIVE VOLCANIC-EMERGENCY RESPONSE In April 1991, the Philippine volcano Mt Pinatubo began to erupt weakly for the first time in recorded history. Ultimately, the activity escalated into the world’s largest eruption in the preceding eight decades, yet only 300 people were killed, even though at least 600,000 people lived in cities, villages, and military bases around the volcano. The larger tragedy was prevented by effective cooperation between local authorities and scientists of the Philippine Institute of Volcanology and Seismology (PHIVOLCS) and the U.S. Geological Survey (USGS). Two months before the climactic eruption on June 15, PHIVOLCS consulted the USGS’s Volcano Disaster Assistance Program (VDAP), a mobile volcano-response team (i.e., an eruption SWAT [special weapons and tactics] team) of experienced volcanologists and other scientists who rapidly respond to a developing volcanic crisis with state-of-the-art portable monitoring equipment (Figure 15-39, online). The request for assistance came after there was an increase in the number of earthquakes, up to 500 per day, explosions, and new cracks opening in the volcano. The VDAP team set up a base camp at Clark Air Force Base and began to monitor and interpret seismic activity, ground deformation, and gas emissions. They also gathered data about Pinatubo’s previous eruptions to predict the types of hazards that could be expected and to create a map of the area, delineating zones at risk during an eruption. Finally, the PHIVOLCS-USGS team worked with local authorities to develop an evacuation plan and educate the people. A 30-minute video, “Understanding Volcanic Hazards,” produced after the tragedy of Armero, Colombia, in 1985, was shown to local officials and populations to raise awareness of hazardous volcanic processes. On June 7, a month and a half after the USGS team arrived, a warning was sent out of a possible major eruption within 24 hours. Villages and cities were evacuated. Five days later, the first in a series of powerful explosive eruptions began. An eruption cloud rose 19 km (12 miles) into the air, and small pyroclastic flows started down to the north and northwest. Additional eruptions took place over the next 2 days. On June 15, a cataclysmic eruption took place during a typhoon. The eruption cloud rose 12 km (7.5 miles) into the atmosphere and spread out like an umbrella more than 200 km (124 miles) in all directions. Wet ash covered a 4000-km2 (1544-square-mile) area, burying crops and collapsing roofs, and many destructive lahars were generated.15 Ash fell as far away as the Indian Ocean. The warning saved at least 5000 lives and a great deal of property damage.
COORDINATION BETWEEN VOLCANOLOGISTS AND HEALTH CARE PROFESSIONALS Coordination between geologists, other scientists, and health care professionals is essential to prepare communities for volcanic emergencies. Planning for future eruptions requires determining the history of a volcano’s past eruptions and their impacts, developing a hazard-zone map, anticipating when a volcano might erupt, and describing the types of hazards to be expected and their potential effects on health (Figure 15-40). Furthermore, health care professionals need to identify high-risk populations, prepare for disaster victims, and help volcanologists educate the community about potential health effects for each volcanic hazard.50 Evacuation of communities, especially in low-lying 331
CHAPTER 15 Volcanic Eruptions, Hazards, and Mitigation
and irritated mucous membranes. Wintertime deaths were associated with unusually cold temperatures. Benjamin Franklin, U.S. ambassador to France in Paris at the time, was the first to link the effect of Laki’s eruption on climate, and presented a scientific paper on the topic. Eruption clouds that penetrate the upper atmosphere can spread volcanic particles and gases across an entire hemisphere.57 During the 3 months it can take fine ash particles to settle out, solar heating is reduced and the lower atmosphere is cooled. The 1991 eruption of Mt Pinatubo in the Philippines created a large volcanic cloud that drifted around the world and caused a temporary average global temperature drop of 0.5° C (0.9° F).35 The largest eruption in recorded history, in 1815 at Tambora, Indonesia, reduced the average global temperature by 3° C (5.4° F) for several years.35 This eruption directly or indirectly caused the death of an estimated 60,000 people in Indonesia and was responsible for a typhus epidemic in Great Britain, cholera in India, and mass migration from northern Europe and Russia. It ruined farms in New England and spurred westward migration.57 The greatest eruption since humans evolved was that of Toba in Indonesia, about 74,000 years ago. The global temperature dropped 5° C (9° F) for many years, causing a global environmental catastrophe. It may have resulted in an estimated decrease in the population of Homo sapiens from over 100,000 to less than 2000.57 Some volcanic soils may also pose a health risk. Nonfilarial elephantiasis, otherwise known as podoconiosis or mossy foot, appears to be caused by chronic exposure of unprotected feet to irritant alkalic red clay soils rich in volcanic particles. Microscopic particles absorbed through abrasions in the feet penetrate the lymphatic system, causing inflammation, lymphatic fibrosis, and ultimate blockage. As the lymphatics are obstructed, the lower extremities swell, resulting in elephantiasis. Podoconiosis is predominately found in high-altitude areas (>1,250 m [4101 feet]) of tropical Africa, Central America, and North India.17-19,49,71,74 Fluoride leached from volcanic rocks into drinking water can also cause disease. In eastern Turkey near Tendurek Volcano, mottled enamel from high levels of fluoride, called endemic dental fluorosis, has been observed in humans and livestock since the 1950s.52
PART 3 BURNS, FIRE, AND RADIATION
TABLE 15-5 Casualties Caused by Pyroclastic Flows in 20th-Century Explosive Eruptions Eruption
Year
Deaths (N)
Ratio of Dead to Injured
Montagne Pelée, Martinique La Soufrière, St Vincent Taal, Philippines Lamington, Papua New Guinea Mount St Helens, United States Unzen, Japan Merapi, Indonesia Soufrière Hills, Montserrat
1902 1902 1911 1958 1980 1991 1994 1997
28,000 1565 1335 2942 58 43 63 19
230 : 1 11 : 1 10 : 1 44 : 1 16 : 1 5 : 1 3 : 1 4 : 1
Survivors After Treatment 163 treated, 123 survived 194 treated, 120 survived Not known 70 treated, 67 survived 130 airlifted, 9 treated, 7 survived 17 treated, 4 survived (minor burns) 86 treated, 11 dead on arrival 7 treated, all survived
From Baxter PJ: Impact of eruptions on human health. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000, Academic Press.
areas and river valley regions, is of utmost importance. Goggles and masks should be distributed, especially to individuals who must work in dusty conditions.
EMERGENCY MEDICAL RESPONSE Emergency medical care plays a small role in severe volcanic eruptions. The number of injured who could benefit from treatment is much smaller than the number of victims killed within minutes of a catastrophic eruption (Table 15-5).5 Therefore prevention is of utmost importance, and evacuation is the key to decreasing morbidity and mortality.5 Health care professionals should be prepared to treat a variety of medical problems in persons who survive (Box 15-2), and they must be aware that access to victims will be limited by high ash conditions, burial beneath volcanic debris, and ongoing hazards. Transient increases in emergency department visits and hospital admissions will require additional resources.8
GEOTOURISM With the increased interest in visiting volcanic environments, the numbers of injuries and illnesses are increasing. Areas like Hawaii Volcanoes National Park have experienced a high rate of injuries and illness because of inexperienced hikers entering high-risk environments and disregarding warning signs.26 People working or traveling near an active volcano or volcanic environment should heed these safety recommendations: • Read about the volcanic environment, including past eruptions and accidents. • Know the current volcano warning level, and obey local authorities.
BOX 15-2 Summary of Health Effects From Volcanic
Eruptions
Physical • Blunt trauma from pyroclastic material, lahars, debris avalanches, tsunamis, and tephra • Burns, wounds, and gangrene complications • Asphyxiation from lack of oxygen or inhaled ash • Acute irritation of the respiratory tract caused by ash • Exacerbation of prior respiratory disease caused by inhaled particles • Respiratory tract and lung burns caused by inhalation of hot steam • Conjunctivitis and corneal abrasions • Toxic effects of gases such as CO2, H2S, SO2, HF, CO, and radon • Gastroenteritis • Skin irritation from acid water • Drowning in lahars or tsunamis Psychological • Depression • Anxiety • Nightmares • Psychomotor disorders • Irritability • Insomnia • Confusion • Neurosis • Stress Modified from Zeballos JL, Meli R, Vilchis A, et al: The effects of volcanoes on health: Preparedness in Mexico, World Health Stat Q 49:204, 1996. CO2, Carbon dioxide; CO, carbon monoxide; HF, hydrogen fluoride; H2S, hydrogen sulfide; SO2, sulfur dioxide.
• Travel with a guide experienced in local conditions. • Leave travel details with a responsible person. • Wear a hard hat and take a gas mask, if appropriate. • Beware of the sources of danger on a volcano: • Rock falls • Avalanches • Hazardous gases • Look for warning signs of an eruption. • Immediately leave the area if it becomes dangerous. • Do not approach lava flowing through vegetation. FIGURE 15-40 First of a series of powerful explosions beginning on June 12, 1991, Pinatubo Volcano, Philippines (see text); note within the yellow oval a farmer and buffalo plowing. (Courtesy David Harlow, U.S. Geological Survey.)
332
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 16
Injury Prevention: Decision Making, Safety, and Accident Avoidance EUNICE SINGLETARY AND DAVID S. MARKENSON
For many, it is the wild in wilderness that fuels a passion for the wilderness experience. Wilderness areas are considered the last areas that humans do not control and have not developed. This lack of human control in undeveloped terrain, combined with the enthusiasm of wilderness explorers, is an ideal recipe for unintentional injury. Managing the risk through sound decisions and efforts to improve safety and reduce accidents is a critical component of wilderness medicine and the focus of this chapter. Contributing to overall risk for injury is the growing feasibility of exploration by wilderness novices, children, elders, and persons with disabilities or chronic health issues by using offroad vehicles, watercraft, and aircraft or via improved access. For persons who venture into the wilderness, there are growing technologic advances in communications equipment, global positioning systems, sporting equipment design, water purification and disinfection, and food processing and preservation techniques, all of which extend the duration of expeditions and permit exploration of remote wilderness once accessed by only the most skilled and experienced persons. Environmental hazards, such as exposure to cold, heat, snow, or altitude, can be minimized through proper planning and training. Wilderness sports activities, such as hunting, snowmobiling, and backcountry ski touring, are safer today not only because of advances in technologic and safety equipment, but because of efforts to educate the public about associated risks and how to manage or reduce these risks and efforts to train the public in wilderness first-aid and medicine (Figure 16-1, online). Despite the growth in numbers of practitioners of wilderness medicine and improved ability to provide care for many injuries and illnesses in remote settings, evacuation of injured victims from the wilderness remains daunting and can turn a minor problem into a major medical situation with a protracted rescue. There are 78 million hectares (193 million acres) of land in the U.S. National Forests and Grasslands. Thousands of rivers and lakes are parts of the National Forests, and there are 247,000 km (153,000 miles) of trails, primarily for nonmotorized use. It is estimated that 178 million people recreate each year in the national forests.152 Sixty-four percent of 446 million visits to national parks in 2009 were considered recreational, with 1.9 million categorized as backcountry overnight visits.97 The National Sporting Goods Association estimates that between 1994 and 2004, the number of Americans involved in backpacking and wilderness camping climbed from 10.2 million to 13.3 million. During the same time period, the number of hikers increased from 25 million to 29.8 million.98 With increased access comes the potential for higher numbers of injuries, illnesses, and fatalities. According to the Centers for Disease Control and Prevention (CDC), in 2005 a total of 173,753 injury-related deaths occurred in the United States, and during 2006 an estimated 29,821,159 persons with nonfatal injuries were treated in U.S. hospital emergency departments.26 The number of injuries and injury-related deaths as a result of wilderness activities is unknown and can only be extrapolated, particularly from National Park Service (NPS) data. Between 2003 and 2006, there were 12,337 search and rescue (SAR) operations in national parks, involving 15,537 visitors and involving 522 fatalities and 4860 ill or injured visitors.60 From a public health point of view, the physical, financial, and emotional consequences of injury can 334
be wide ranging, devastating, and long lasting. The CDC’s National Center for Injury Prevention and Control (Injury Center) was formed partially as a result of a recommendation of the 1985 Institute of Medicine report Injury in America, which concluded that supporting injury research is necessary to substantially reduce injury rates.30 The Injury Center strives to prevent injury and reduce its consequences, using a public health approach that describes the problem, identifies risk and protective factors, develops and tests prevention interventions and strategies, and promotes widespread adoption of effective interventions and strategies. Although the Injury Center includes intentional as well as unintentional injuries in its focus on injury prevention, their efforts and approach may prove to be a model for future research and methods for injury reduction in the wilderness setting. This chapter reviews basic principles of injury applied to the wilderness environment. Individual (human/host) factors and behavior and how they apply to injury risk and prevention are detailed, including preparation, planning, anticipation of problems, and errors of omission or commission. Problems are approached from the perspective of environmental hazards, rather than from a particular activity, because many hazards are common to different wilderness activities. Throughout this chapter, prevention of injury is the focus. Details of pathophysiology and treatment are found in the referenced chapters throughout this text.
Principles of Wilderness Injury and Prevention THE INJURY FIELD: BASIC PRINCIPLES Injury prevention is a key component of public health and medical care. It is a long-held belief of physicians and public health practitioners that injury prevention is far superior to injury treatment. Underlying injury prevention is the concept that when an injury occurs it is usually the result of a series of events under specific circumstances that had they been identified in advance might have been avoided, addressed, and/or eliminated to prevent or mitigate the injury. In the field of injury prevention, accidents are defined as unpredictable acts of fate or chance events, whereas injuries are defined as damages resulting from a sequence of accidents or intentional actions. Injuries are prevented by stopping or reducing the number of accidents causing them and/or eliminating the intentional actions and situations that lead to them. By applying this principle, practitioners of injury prevention estimate that 90% of all injuries are predictable and preventable. For example, by inspecting, testing, and replacing equipment, individuals may prevent accidents related to equipment failure. The need for this approach is even greater in wilderness medicine than in many other fields of medicine. In medicine we attempt to prevent injury, but if that prevention fails, we then provide emergency care and rehabilitation to limit the lasting effects of injury and return the person to good health. In the case of wilderness injuries, which may occur in areas with limited immediate care and often with significant distance and time to reach definitive care, our ability to limit the extent of injury is less, magnifying the need for prevention.
For online-only figures, please go to www.expertconsult.com
Injury prevention can occur at many points along the continuum, beginning before injury through rehabilitation. In classic injury prevention and epidemiology, opportunities for prevention are divided into primary, secondary, and tertiary phases. Primary prevention avoids development of a disease. Most population-based health promotion activities are primary preventive measures. In addition, many environmental or regulatory controls are primary. Secondary prevention activities are aimed at early disease detection, thereby increasing opportunities for interventions to prevent progression of disease and emergence of symptoms. In the field of injury prevention this would include early recognition of injury to limit the extent and impact of an injury should it occur. An example in wilderness medicine is early recognition of foot blisters and use of protective coverings or footwear alteration to prevent skin breakdown and further extension of blisters or infections. Wearing protective equipment is both primary and secondary if it limits the extent of injury. Interventions may cross multiple stages of prevention. Tertiary prevention reduces the negative impact of an already established disease by restoring function and reducing diseaserelated complications. In the field of injury prevention, this traditionally includes prompt and appropriate medical rehabilitation. An example is early splinting of a fracture in the field to prevent further injury and to limit swelling and associated complications. Quaternary prevention is the set of health activities that mitigate or avoid the consequences of unnecessary or excessive interventions within the health system. This stage is the latest addition to the classic three stages of prevention and is not always included in descriptions of injury prevention.
EPIDEMIOLOGIC FACTORS: HUMAN OR HOST, AGENT, AND ENVIRONMENT One of the most commonly used methods of categorizing the factors that lead to injury is “human (host), agent, and environment.” Numerous human factors can lead to injury and be used as opportunities for prevention. Examples include predisposition to injury, such as osteoporosis predisposing to fractures; behaviors that may be high risk for injury, such as alcohol consumption and intoxication; decision making, such as a choice to proceed on an icy trail; and different body habitus, ages, or conditions, such as pregnancy. The next factor is the agent. Broadly defined, the agent is what causes the injury. Although this may seem straightforward, the lines can be blurred. For example, if someone decides to strike a branch with his or her hand to break it, is the branch the agent or is the human who made the decision the agent? Most would agree the branch is the agent and the human factor was the decision to strike it. Classic descriptions of agents would be propelled objects, items that strike people, falls from heights, or malfunctioning mechanical devices. In the wilderness, the items include failing ropes or belts when climbing, branches and rocks when falling, wet ground causing a slip, a poorly positioned or inappropriately worn backpack leading to back injury, or a hot object that causes burns. The last factor is the environment, which includes the situation in which the injury occurred. This might be temperature conditions, such as extremes of heat or cold, but may also include a situation where there is only one option for moving forward through less-than-ideal terrain without the option to turn back.
CONCEPTUAL MODELS A more comprehensive conceptualization for intervention and prevention can be done by combining stages of injury prevention with the host, agent, and environment approach. This combination was proposed by Dr. William Haddon, Jr., who is widely considered the father of modern injury epidemiology. Haddon’s matrix is an injury prevention brainstorming tool originally designed for motor vehicle safety that combines the epidemiology triangle (host, agent, environment) and levels of prevention. This combination allows planning for injury interventions and prevention strategies by phases in time of the event.
In addition to planning interventions, this matrix can also be used to collect data to determine the factors that cause injuries. The following are the steps to complete Haddon’s matrix: 1. Assess the contributing factors or characteristics of an injury from the perspective of the following: • Host or human factors • Agent of energy or vehicle (such as crashworthiness of a vehicle) • Physical environment (such as roadway design or safety features) • Social environment (such as passage and enforcement of seat belt laws) 2. Then combine them with time phases: • Pre-event: What factors affect the host before the event occurs? • Event: What are factors related to the crash phase? • Postevent: What are factors related to the postevent crash phase? 3. Place the items with the possible intervention in the appropriate location in Haddon’s matrix. Haddon’s 10 Strategies for Reducing Injuries In addition to developing the matrix, Haddon also proposed strategies for reducing injuries. These strategies have been grouped into 10 specific approaches, commonly known as Haddon’s 10 Strategies (with examples): 1. Prevent creation of the hazard. • Perform preparticipation musculoskeletal physical examination to identify underlying pathologic problems of the knee joints. • Provide treatment and rehabilitation before sports participation. • Provide warm-up programs involving neuromuscular and proprioceptive training to stabilize the knee. 2. Reduce the amount of the hazard. • Limit the physical areas for activities. Provide limitations on activities or exposure to the environment. 3. Prevent the release of the existing hazard. • Ensure that waste is kept properly distant from potable water sources. 4. Modify the rate or partial distribution of release of the hazard from its source. • Limit activity to an individual’s ability. • Substitute individuals as necessary during a specific activity. 5. Separate, in time or space, the hazard and that which is to be protected. • Limit climbing to certain weather conditions. • Perform strenuous activity only when ambient conditions are appropriate. 6. Separate the hazard and that which is to be protected by interposition of a material barrier. • Use well-fitted gear. • Employ protective gear. 7. Modify basic relevant qualities of the hazard. • Avoid surfaces that increase the potential for injury. 8. Make what is to be protected more resistant to damage. • Provide fitness training, including stretching, strengthening, and improving balance and movement. 9. Begin to counter the damage already done by the hazard. • Seek and receive prompt medical care as soon as the injury is noted. 10. Stabilize, repair, and rehabilitate the object of the damage. • Provide rehabilitation, and use stabilization devices, such as knee braces.
ENVIRONMENTAL, EDUCATIONAL, AND ENFORCEMENT APPROACHES TO INJURY PREVENTION In addition to describing possible interventions using Haddon’s matrix approach, it may be helpful to characterize the type of intervention. One way to categorize injury prevention efforts is by the three E’s: 335
CHAPTER 16 INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE
THE CONTINUUM OF INJURY PREVENTION
PART 4 INJURIES AND MEDICAL INTERVENTIONS
• Environment makes the environment or product safer. • Education provides information to individuals. • Enforcement relies on change through laws. Comprehensive injury prevention projects employ strategies that include all of these. Environmental Approach The environment includes physical surroundings (e.g., roadway), products (e.g., vehicles), and the social environment (e.g., societal attitudes toward drinking and driving). The environmental approach is a strategy that does not depend on action by those being protected; it is passive, automatic, and constant in its protective effects. As a result, this approach is considered the most effective strategy. In some cases, there is the technology available to make products safer, but industry has not adopted it, often because of economic disincentives. In classic injury epidemiology, environmental interventions refer to the following: • Physical surroundings • Product design, protocols, and practices • Social environment The following are key concepts for environmental modifi cation: • Design safer surroundings • Pool fencing • Handrails • Antislip surfaces • Playground surfaces • Roadways • Bike/walking paths • Design safer products • “Kill switches” • Childproof packaging • Crib slat spacing • Flame-resistant sleepwear • Vehicle design • Protocols and practices • “Traffic calming” • Walk-light timing at crosswalks • Bus stop placement • Lighting for crime reduction • Factory settings for water heaters • Social environment • Alcohol consumption and operating motorized devices while drunk • Domestic violence • Violence on television • Safety devices Educational Approach Preventive measures defined as an educational approach involve education of large populations, targeted groups, or individuals and efforts to alter specific injury-related behaviors. Many injuries result less from lack of knowledge than from failure to apply what is known. Three goals of educational interventions are as follows: 1. Provide information regarding injury risks and how to avoid them. 2. Change attitudes away from risks and toward safer practices. 3. Alter behaviors. It is not enough to know that seat belts save lives, but one must actually use the seat belt for it to be effective. An educational approach may be appropriate in the following instances: • New knowledge about a risk is needed (e.g., defective equipment, better approaches to an activity, newer and safer technology available) • No other approach exists (e.g., an activity that is inherently unsafe and avoidance is the only strategy) • To influence decision makers, lawmakers, and design engineers • To teach specific behaviors and skills (dialing 9-1-1, crawl under smoke, self-care of injuries) 336
Limitations of the educational approach include the following: • It uses an active approach. Passive approaches are pre ferred. • It may be an inappropriate message for the target audience. Targeted, at-risk populations are not always reached through mass-media educational campaigns. • There are variations in learning style among adults and possible language barriers. In education, “one size doesn’t necessarily fit all.” There are variations in learning styles unique to children and adults, cultures, and socioeconomic status. • There may not be cultural acceptance of the message. Messages should be tested with a focus group to be certain that they are not offensive. Enforcement Approach This approach uses a strategy that seeks to require change in behavior, the environment, or product by enacting law and policy. Enforcement initiatives and laws are directed toward individuals, products, and environmental conditions. The following are examples of laws targeted to individuals: • Requiring: • Seat belts • Child restraints • Helmet use • Prohibiting: • Drunk driving • Excessive speed The following are examples of laws targeted to products: • Requiring: • Motor vehicle standards • Helmet standards • Childproof packaging • Prohibiting: • Fully automatic weapons • Flammable fabrics The following are examples of laws targeted to the environment • Requiring: • Swimming pool fence • Smoke detectors • Prohibiting: • Firearms in airports/schools • Rigid structures on highways Characteristics of successful laws include the following: • There are few exceptions to compliance. • Detection is easy (measuring speed with radar, observing helmet use). • Punishment is certain, swift, and sure. • There is publicity about enforcement. Enforcement and laws can have a much greater impact on changing behavior when enforcement is highly visible and media are used to let the public know about enforcement campaigns. Controversies arise when legislation is perceived to restrict personal freedoms.
SOCIAL-ECOLOGIC MODEL In addition to the classic epidemiology approach of host, agent, and environment enhanced by the stages of prevention and articulated by Haddon in his matrix, another conceptual model attempts to describe injury prevention but with more focus on the interplay of different factors. The social-ecologic model has its foundation in human development and has been refined to apply to injury prevention and epidemiology. The social-ecologic framework was created by Urie Bronfenbrenner19 in the context of understanding human development and is very compatible with a broader view of public health.76 Social-ecologic theory defines various levels of the social environment, depicting the nested roles of intrapersonal factors, interpersonal factors, institutional elements, and cultural elements. This social-ecologic framework enhances the standard public health model of agent-host-environment.88,120,135 With respect to understanding injury prevention, intrapersonal factors include both developmental and sociobehavioral features
RISK AND EFFECT MODIFICATION IN INJURY PREVENTION EPIDEMIOLOGY Two basic epidemiologic concepts are risk and effect modification. Risk is the likelihood of disease occurrence and is often operationalized as relative risk to aid in decision making. This is a method to describe how one option versus another option may lead to different disease outcomes. In injury prevention, one always must consider risk. Some activities are inherently risky, and all one can do is provide interventions that protect the individual or minimize the impact of a potential injury. In other cases, there may be several options each with different risk, so that one can determine the relative risk. Major human risk factor examples are age, gender, and experience. Another basic epidemiologic concept that can be applied to injury prevention is that of effect modification. An effect modifier is a variable that lies in the pathway from independent/main explanatory variable and the dependent/outcome variable. When applying this to injury prevention, one can think of an effect modifier as something that lies in the pathway between the event and the injury, and that can alter the injury outcome from similar events. An example might be wearing a helmet, so that when thrown from a horse the injury to one’s head is less than if not wearing a helmet. Human factors can be considered from the perspective of effect modifiers. For example, when caught in bad weather, the more experienced hiker will be less likely than the novice to be injured.
ACTIVE VERSUS PASSIVE INJURY PREVENTION STRATEGIES Before proceeding to implement methods of injury prevention, it is important to recognize that injury prevention strategies are either active or passive.112 Active injury prevention strategies require change in behaviors by individuals before or when exposed to risks.145 For example, individuals must be convinced that wearing seat belts reduces the risk for injury and then must take the action of buckling up. Passive injury prevention
strategies are preferable because they require no action on the part of the individual.54,72 For example, recent advances in automotive safety have been gained by placement of air bags. A more classic passive approach has been referred to as environmental controls. An example of this is a fence placed around a pool to prevent entry of unsupervised children, thus reducing drowning incidents.
MORBIDITY AND MORTALITY STATISTICS FOR WILDERNESS INJURY The difficulties of obtaining data about injury prevention in the wilderness are the diversity of activities covered and lack of a single source for the data. As a result, data are often only for a selected activity and in a single location. Some data involve several activities. An example is a CDC study released in 2008 of nearly 213,000 people who had been treated each year in emergency departments for outdoor recreational injuries from 2004 to 2005.44 Of those injured, about 109,000 (51.5%) were young people between the ages of 10 and 24. For both men and women of all ages, the most common injuries were fractures (27.4%) and sprains (23.9%). Of these, most injuries were to the arms or legs (52%) or to the head or neck (23.3%). Overall, 6.5% of outdoor injuries treated were diagnosed as traumatic brain injury. Researchers found that snowboarding (25.5%), sledding (10.8%), and hiking (6.3%) were associated with the highest percentage of injuries requiring emergency department visits. The study points out that wilderness injury prevention begins with planning, preparation, and problem anticipation, which are discussed later in this chapter. An example of event-specific data is for backpacking and camping. Data reveal that more than 11 million people participated in backpacking or wilderness camping in 1990. The morbidity and mortality figures from eight national parks in California between 1993 and 1995 are 1708 injuries and 78 fatalities.95 Another event-specific activity for which there are data is scuba diving. There are more than 9 million certified scuba divers in the United States, with approximately 650,000 annual certifications.35 The Divers Alert Network37 at Duke University Medical Center (Durham, NC) reported approximately 1000 serious diving-related injuries and approximately 90 diving-related fatalities annually between 1995 and 2002. In addition to event-specific data, one can examine equipmentbased data, which can include data based on certain types of vehicles. For example, from 1990 through 1995, an estimated 32,954 persons were involved in injuries related to personal watercraft.18 Lastly, one may search data to learn about specific types of injuries or deaths. An example of this type of data is a western Washington study of 40 pediatric wilderness-activity related deaths between 1987 and 1996.100 Ninety percent of the victims were male, and 83% were 13 to 19 years of age. The most common cause of death was drowning (55%), followed by closed head injury (26%). Injuries or deaths resulted from lack of preparation, lack of training for wilderness activities, and inadequate basic safety equipment; alcohol use and rescue delays were contributing factors. Of note, the presence of adults did not appear to be significant in reducing the incidence of mortality.
PUTTING INJURY PREVENTION INTO PRACTICE Planning Careful planning is the foundation for a safe activity that minimizes risk and avoids injury. Planning begins by gathering all relevant data for the planned activity. This includes up-to-date information regarding weather, trail, and campground conditions, best times to travel, permit requirements, equipment needed, and special considerations unique to the activity. After gathering all available information, one develops a plan for activities. The plan may be very brief and purely a mental exercise for some activities such as brief hikes, camping trips, rock climbing, or day diving. For longer excursions, the planning phase will include a detailed, written plan. Planning activities may include activity-specific 337
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of individuals (i.e., the host), for example, a young child’s curiosity and exploratory behaviors through touching, tasting, and crawling; an adolescent’s propensity to take risks and the varied responses to parent and peer influences; or an older adult’s suicide risk due to a sense of hopelessness in the face of an incurable chronic disease, or avoidance of walking in certain locations because of fear of falling or assault. Likewise, biologic features of the host, such as a young child’s lack of balance and strength, high center of gravity, and small size, relate to some of the hazards encountered. For an older adult, biologic characteristics such as bone brittleness; reduced visual acuity, reaction time, and balance; and thinner skin all increase susceptibility to injury events such as traffic crashes, pedestrian injuries, falls, and burns. Interpersonal factors are those that result from the interactions between two persons, for example, intimate partners, parent and child, employer and employee, or adolescents. In the injury sphere, this relates to intentional injury as a result of behaviors associated with disciplinary practices or conflict resolution. Institutional elements are those that reflect organizations in which individuals function, for example, schools, places of worship, and workplaces. How these organizations promote or control activities and environments can affect injury risks. Work sites contain many hazards and adopt many types of safety practices, whereas places of worship may either encourage or discourage certain safe or unsafe practices. Prehospital trauma care and inpatient health care systems are institutions that affect injury outcomes.105 Cultural elements include broad social values and norms as well as governmental policies that guide or mandate behaviors of individuals or organizations. Examples are values placed on individual freedom; social norms about drinking or corporal punishment; and laws, policies, and regulations about producing, selling, and storing firearms. Any health problem can be viewed as resulting from and being alleviated by the interactions among these dynamic factors.
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planning that addresses unique risks or needs. For example, to plan for a climb that includes high altitude, allowance is made for ascent and descent to allow time for acclimatization. Planning may include provision of equipment specific to the activity, such as scuba gear or helmets. Two of the most important planning factors are personal limitations and required preparation. It is important to establish criteria under which the activity can be undertaken safely. The level of detail is based on the risks. For events with high risk or multiple risks, these criteria need to be detailed. There are many factors that figure into a “go” or “no-go” decision plan. Some factors, such as weather, local conditions, physical conditioning for the activity, sleep, and wellness, may apply to all activities, but others may be activity specific, such as water conditions for rafting and kayaking. Once the criteria are established, the most important thing is to adhere to them. Injuries often occur when the desire to perform an activity causes someone to participate in a situation that is either unsafe or exceeds personal abilities. At a minimum, one must address the following: • Predetermined “go” or “no-go” criteria, which may include the following: • Weather and environmental conditions at the activity site • Personal criteria such as sleep, preparation time, preexisting illness, departure time and window • Required participants • Equipment • Comprehensive equipment checklist • Timeline • Alternative plans • Communication methods, including emergency communi cations • Emergency procedures, including the following: • Medical emergencies • Unexpected weather or local conditions • Equipment failure Preparation After planning, the next step in a good injury prevention approach is to prepare for the activity so as to minimize risk and put into place factors that are targeted at the human, agent, and environmental issues that can lead to injury. Preparation activities can be grouped into human factors (physical and mental preparation) and material factors, such as equipment preparation. Physical Preparation. Physical preparation includes maintaining excellent fitness and health in anticipation of the activity and the added stresses over daily activities. This may include conditioning, medical evaluation for physical abilities and health to undertake the activity, better medication adjustment for persons with chronic illness, and/or disability-specific planning for those with disabilities. In addition to general physical preparation there are unique considerations for physical preparation related to the genitourinary tract (see Injury Prevention for the Genitourinary Tract, later). Mental Preparation. Mental preparation emphasizes thinking through the plan, ensuring that one is well rested, focusing on the activity, and being confident about the activity. Mental preparation also includes proper education and training. This should include training specific to the activity and emergency medical training. Discuss and agree on a travel route. Select a leader, and review each member’s capabilities and what equipment and supplies are necessary. Equipment Preparation. Material preparation involves acquiring proper equipment (both routine and for emergencies and unplanned events), testing and organizing equipment, and having backup equipment. Carry sufficient equipment to survive for extended periods if unforeseen changes occur and under the worst possible environmental conditions for the season. This includes ensuring that preventive maintenance has been performed for equipment and that equipment is in good working condition. Review each person’s responsibility for equipment. Make sure that equipment and weight are properly distributed, taking into 338
account abilities. Equipment should be appropriate for the activity and the environment (e.g., waterproof, ruggedized). Selecting battery-powered items that require the same size and type of batteries minimizes items to be carried. Maintain an equipment checklist. If using specialized equipment, know its proper use and maintenance. Courses are available through retail outlets, clubs, and wilderness organizations to prepare and train participants for most outdoor activities. The minimum equipment list should include, but is not limited to the following: • Emergency equipment • Emergency blankets • Emergency bag • First-aid kit • Flashlight • Maps, compass, navigation equipment • Communication and emergency communication equipment • Footwear • Skin and eye protection • Backpack • Water, extra food • Extra clothing • Timepiece • Survival/unplanned conditions equipment may include the following: • Fire starter, matches • Shelter (e.g., emergency tube tent) • Survival whistle • Water • Water disinfection system • Avalanche beacon • Personal locator beacon, rescue laser, ground insulation Problem Anticipation Even with good planning and preparation, problems occur. For most activities and trips, major problems can be anticipated. A good exercise before undertaking any activity (and during the activity at various times) is to think through the five most likely problems and the two rare but significant problems, to both plan and prepare for them. Standard problem anticipation approaches include bringing adequate protection from environmental and recreational hazards, having all the appropriate immunizations, safe drinking and food hygiene practices, and ensuring that everyone has a working knowledge of first aid. Physical Disabilities (see Chapter 102) For persons with disabilities, it may be a great challenge to access wilderness. In federally designated wilderness areas, Congress reaffirms in the Americans with Disabilities Act that nothing in the Wilderness Act prohibits use of a wheelchair in the wilderness by a person whose disability requires its use. There are 54 million persons with disabilities in the United States, and this number is expected to grow. The challenge for the future will be ensuring that persons with disabilities have the same opportunity to participate in wilderness activities and programs as do persons without disabilities, without necessarily making wilderness access easier.153 The principles of injury prevention apply to people with disabilities who participate in wilderness activities. Their preparation, planning, and anticipation of problems must take into account the specific disability and unique physical and mental challenges of that disability.
Individual Factors and Injury Prevention SPECIFIC TOOLS FOR PLANNING AND PREPARATION IN THE WILDERNESS Maps and Orienteering People should have the ability to tell where they are and where they are going. A single wrong turn can have disastrous consequences. Maps are useful tools for planning, and the Global Positioning System (GPS) gives an accurate determination of actual location. Traditional two-dimensional maps, such as road maps, identify a sampling of features on the ground, with symbols
Global Positioning System Devices The GPS is a U.S. space-based global navigation satellite system that provides continuous positioning, navigation, and timing services to users from anywhere on Earth. Use of a GPS device requires an unobstructed view of four or more GPS satellites, each of which broadcasts signals that GPS receivers use to provide absolute locations in three dimensions (latitude, longitude, and altitude), velocity of movement and orientation, and precise time. GPS receivers have become commonplace for navigation on ground, air, and water. Modern GPS receivers often overlap graphic displays of terrain or nautical features to further assist navigation. A GPS unit can assist SAR organizations with recovery of lost or stranded travelers. Because line of sight is required for GPS receivers to function, their use may be limited in dense forests or jungles or below steep cliffs or rock overhangs. In addition, they are sensitive to extremes of temperature, moisture or humidity, and mishandling. They depend on battery power, so users should carry spare batteries. They should not be used as total replacement for traditional maps or compasses for navigation and positioning or use of natural references, such as sun position, wind, or topography. Communication Devices Traditionally, emergency communications from wilderness settings have been limited to signaling with devices such as a mirror or other reflector, whistle, fire, smoke, or flare (Figure 16-2). Newer laser devices encased in waterproof housings have been found to be very effective in identifying people during aerial searches, particularly at night. Commercially available “rescue laser flares” are small, lightweight, and rugged handheld laser devices that project a wide line, rather than the pinpoint light normally associated with a laser. They allow the user to sweep across an area with a dispersed red or green light beam that can be seen from up to 30 miles away (3 miles in daylight). The device is powered by lithium batteries that when used continuously will last for up to 72 hours, depending on the model.111 The international distress signal (SOS), which can be used with many signaling devices, consists of three short signals, followed by three long signals, and then three short signals, repeated at
intervals. Signals may communicate the general location of an injured person, but to provide more detailed information about injuries or illness, some form of vocal or written communication is needed. Vocal communication allows rescuers to obtain an accurate, on-site victim report with descriptions of injuries, mechanism of injury and the specific location of the victim. Ongoing communications with a reporting party can help guide rescuers to the victim and allow them to provide advice about first aid before their arrival. Cell phone technology is useful only when travel is within an area with cell phone relay stations, making its use limited in the wilderness. Wireless access for cell phone use is becoming more common inside U.S. national parks but is limited to the more populated areas where the park service often provides audio tours. Signals may be weak or unreliable. Cell phones in national parks are controversial: Conservationists argue that parks run the risk of becoming too civilized. Critics argue that the presence of cell phone towers in wilderness areas and national parks creates a false sense of security. Despite the controversies, cell phones are being used increasingly within national parks to notify authorities of mountaineering and recreational accidents. If a cell phone is used within a park, it is best to program in the direct number for park dispatch, because dialing 9-1-1 will often reach a county sheriff, who must then relay the call. Once dispatch is reached, state your location and call-back number early in the conversation in case of connection failure. A member of a party may need to hike to the nearest trailhead to obtain cell phone service. Completion of a standard incident report form before leaving the scene will allow the caller to provide critical information about the nature of the incident, location, and initial care provided. Cell phones with GPS (E911) technology can be useful for providing the location of an injured person. As a result of a mountaineering accident with three fatalities on Mt Hood in 2007, the Oregon state legislature proposed bills that mandate electronic signaling devices (personal locator beacons, mountain locator beacon, GPS receiver with cell phone/two-way radio) for all climbs above 3048 m (10,000 feet) on Mt Hood. Although local rescue personnel and climbers are reported to encourage the use of such equipment, they do not believe its use should be required.127 One survey of climbers found that 14% of them always carry a cell phone. Twenty-one percent of climbers who reported carrying a cell phone indicated that they had used it to report an accident.8 If a cell phone or GPS unit is carried into the wilderness, consider using a waterproof box or case to prevent damage from crushing, dropping, or water, along with a backup battery. In most cases, portable radios serve as a good choice for communication between party members. When carrying a portable radio, determine which frequencies are allowed for personal use and which frequencies are monitored in your area. Radiofrequency interference from transmitting cell phones (code division multiple access [CDMA]) or two-way radios can cause interference with some avalanche beacons. Playing an iPod at close range has also been found to cause radio frequency interference in all beacons.38 A common intermediate (processing) frequency for cell phones or digital cameras is 455 kHz, which is very close to the 457 kHz radio frequency of avalanche beacons. In addition, false signals may be produced in some beacons from cell phones cycling their transmission to “handshake” with their cell. To ensure there is no radio frequency interference, electronic equipment, including cell phones and digital cameras, should be turned off while doing an avalanche transceiver search with any brand of digital or analog transceiver.149 Satellite phones connect with orbiting satellites and have the potential to be used worldwide. The size and weight of early “sat phones” once limited their use in the wilderness, but current versions are as small as a “smartphone” or mobile PDA (Figure 16-3, online). The cost of newer satellite phones can top $1000, prohibiting their use by many wilderness adventurers. In addition, most satellite phones will only work with a corresponding network and cannot be used if the network is switched. Depending on the type of satellite phone service used, there may be a delay in transmission of voice or data. Geostationary satellite phone systems depend on line of sight for service. 339
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to represent physical objects. Topographic maps, also known as “topo” maps or contour maps, use contour lines or shaded relief to represent the shape of land surface. Contour lines connect contiguous points at the same altitude. Topo maps usually depict significant bodies of water, forest cover, or other features and are prepared using interpretation of aerial photography or remote sensing techniques. The U.S. Geological Survey (USGS) produces several series of national topographic maps, the largest and best known of which is the 7.5 minute, 1:24,000 scale, quadrangle nonmetric scale map, each of which covers an area of 0.125° latitude by 0.125° longitude spaced 7.5 minutes apart (an area of about 49 to 64 square miles). The 7.5 minute series of maps has been abandoned recently in favor of The National Map, a collaborative effort of the USGS and federal, state, and local agencies to improve topographic information in the United States and contributing to the development of a new generation of digital topographic maps.141 An accurate graphic information system (GIS), such as a digital elevation (terrain) model, allows wilderness explorers to extract and analyze additional information via three-dimensional digital representation of surface terrain or topography. An offshoot of GIS is location-based services, which allows GPS-enabled mobile devices (such as cell phones, personal digital assistants [PDAs] and laptop computers) to display their location in relation to fixed or mobile assets (such as a gas station or police car) or to relay their position back to a central server for display or other processing. This is a potentially useful future application in national parks. GIS has led to the explosion of Internet mapping services, such as Google Maps and MapQuest, which allow users access to aerial satellite imagery useful in the planning and preparation stage of wilderness travel. Whether a two-dimensional planimetric, topographic, or graphic display map is used for wilderness travel, it is essential that the user carry the map and know how to use it. In addition, ingress points, checkpoints, and egress points should be established before traveling.
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A
B
C
D
E
FIGURE 16-2 A, Smoke signal. B, Handheld flare. C, Marking location with flare. D, Rocket flare. E, The Rescue Laser Flare Magnum. (A to D courtesy Eunice Singletary; E copyright Greatland Laser, Anchorage, Alaska. http://www.greatlandlaser.com.)
Low-Earth-orbit systems (<2000 km [1243 miles] above the earth’s surface) depend less on line of sight. Two such systems in the United States are Globalstar (http://www.GlobalstarUSA.com) and Iridium (http://www.Iridium.com). Globalstar does not provide coverage of the polar caps because of the inclination of their orbiting satellites; Iridium claims worldwide coverage. Satellite phones are banned in a number of countries, such as North Korea and Myanmar, because their use bypasses local telecommunication systems, hindering efforts at censorship. In disaster situations, large spikes in call volumes may lead to cascading failures of a network, similar to cell phone network failures noted in past disasters. Protective Gear Engineering accomplishments have improved protective equipment for wilderness travel and recreational activities. Clothing. Waterproof and breathable fabrics, sealed seams, lightweight high-loft insulation, quick-dry material, and material with sun-blocking properties have been at the forefront of outdoor clothing offerings. Sometimes referred to as technical clothing, these fabrics have temperature regulation properties embedded in the yarns and retained with washing. Microfiber materials are used as an alternative to down for insulation in sleeping bags and clothing, because they retain heat when damp or wet. Microfiber material wicks moisture and sweat away from the body and keeping wearers drier and warmer in cold weather and cooler in hot weather. A combination of yarn selection, fabric 340
construction, and finishes is used to create sun-blocking protection, which is often rated with the Ultraviolet Protection Factor (UPF) system.7 A rating of 15 earns a product a rating of “good”; a rating of 30, “very good”; and a rating of 40 or 50+, “excellent.” Foot and Hand Wear. Ideal footwear in the wilderness accommodates environmental factors (extremes of heat, cold, terrain), user comfort, and protection needs. Proper fit and hygiene are crucial for comfort and to prevent “hot spots,” blisters, or toenail problems. The purposes of footwear are protection, cushioning, support, and grip. Selecting, fitting, breaking in, and caring for footwear help it last a long time and maximize comfort. It is important to properly size footwear, including accommodating for swelling that may occur during prolonged activities. Each foot should be properly fitted. When sizing footwear, it is important to consider not only the length and width, but the ball-to-heel (arch) length. For hiking, wear shoes that extend above the ankle to reduce likelihood of an ankle sprain. Footwear should fit comfortably with moderate tension on the laces, so that they can be tightened or loosened as needed. To avoid blister formation, seams should not rub against any part of the foot. The tongue of the footwear should be aligned and laced properly. Otherwise, the tongue can slide into an incorrect position and cause blisters. Ankles should be comfortably supported by stiff heel counters or heel cups and should not slip with toe flexion, causing blisters because of repetitive rubbing. With the foot on the ground, there should be no more than 6 to 12 mm (0.2 to 0.5 inches) of heel lift.
Helmets. Helmets are used for many wilderness and remote activities, including mountain biking, skiing and snowboarding, rafting, kayaking, and climbing. Most helmets are designed for specific activities. The use of helmets by recreational bicyclists dates back to the mid-1970s. Early helmets had polycarbonate hard shells with an expanded polystyrene liner and little or no ventilation. Helmets for children were not introduced until 1984. Since the 1990s, bicycle helmet design has evolved, with incorporation of vents—critical for cooling in high-exertion riding— and cradles to fit the head more precisely. Bicycle helmets today come in either a hard shell design or a soft/micro shell. Helmets for racers often have a streamlined, elongated back (Figure 16-4). The back of the head is covered less with bicycle helmets than with other helmets. For this reason, bicycle helmets are not appropriate for skating, skateboarding, and other activities in which falls backward are more common. The Snell Memorial Foundation131 created the first standards for helmet design in 1985. Today, the U.S. Consumer Product
FIGURE 16-4 Bicycle helmets with varying designs. (Courtesy Eunice Singletary.)
Safety Commission (CPSC)140 requires standards for helmets sold in the United States. CPSC standards have been criticized as being less stringent than current Snell B95 standards and as having weakened over time.144 The trend in bicycle helmet design today is to make them thinner and with larger vents, which may compromise the ability of certain helmets to protect against head injury. In addition, there is concern that the liners of many bicycle helmets are too rigid to properly cushion and protect the head.31 One of the most important elements of helmet selection for any activity is proper fit. One study showed that 96% of helmets were improperly fitted.104 Fit can be adjusted on helmets using cushioned pads, or by use of a band inside the helmet that may be adjusted with a tightening wheel or plastic clips. The chinstrap can be adjusted to help with fit, and it should be kept fastened under the chin to help keep the helmet in place during falls. Should a helmet be damaged by a fall, or should the helmet exceed 5 years of age (or less according to the manufacturer), the Snell Memorial Foundation recommends replacement.4 Helmets are not without criticism. Laws mandating use for bicyclists have been paradoxically blamed for a decrease in use. Helmets have been blamed for an increase in accidents, because some feel they restrict peripheral vision and decrease hearing. It is speculated that use of a helmet encourages risky behavior. Goggles. Goggles provide a thermal barrier and help protect eyes from wind, snow, rain, dryness, and ultraviolet (UV) or bright light. Sunglasses provide some protection from the elements and UV light, especially when they “wrap” the face or have plastic or leather side guards. Goggles should fit well on the wearers face. The foam on the frame should fit uniformly and snugly around the entire goggle, because gaps increase airflow and contribute to drying of the eyes. Depending on the activity of the wearer, other desirable features may include helmet compatibility, polychromatic or interchangeable lenses for varying light conditions and to improve contrast, and prescription lens inserts. Fogging lenses are a common problem. Most goggles are vented to help prevent fogging, and many have antifog coatings. Goggles with a spherical double lens provide high-quality optics and fog-free vision. In general, ski goggle design has changed little over the years. Zeal Optics has recently designed a new goggle (Transcend GPS) with an integrated heads-up display system that shows GPS, speed, altitude, vertical odometer, time, and temperature, all of which can be viewed on the spherical polarized lens by scrolling with buttons on the side of the goggle. Although more expensive than traditional goggles, this new design may have applications for backcountry snow-sports enthusiasts. Future plans for the goggle include trail maps, text messaging, emergency calling, buddy tracking, and music controls. Body Armor. Once popular with football players and dirt bike enthusiasts, body armor and padded clothing are promoted for water sports, snow sports, cycling, and other outdoor sports. Snowboard gloves or mittens with integrated wrist guards are purported to decrease the risk for hand, wrist, and forearm 341
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Thermal insulation is the most important factor in footwear designed for protecting feet from cold and is influenced greatly by moisture control. Although foot comfort is affected by the interaction of sock, sole, and shoe, the choice of footwear is influenced by factors such as intended activity, fit, shoe weight, insulation, vapor barrier, waterproofing, protection, flexibility, and durability. Mechanical injuries to the toes can be avoided with shoes or boots with integrated steel caps and soles. Sole design can prevent slippage; the design should be based on the intended use. Materials with good friction at moderate temperatures tend to become hard with cold temperatures and to lose their grip. On wet ice, virtually all shoe materials become slippery. Insulation is an important factor with low ambient temperatures. Adding heat sources such as disposable chemical foot and toe warmers, warm air or water circulation, or battery powered electrical heaters can reduce heat loss. Additional heat sources generally reduce volume inside the shoe or boot, potentially compromising fit and maneuverability, and also add weight. A 100-g (3.5 oz) increase in the weight of footwear has been shown to increase oxygen consumption by 0.7 to 1.0%, the equivalent of adding five times that weight carried on the torso.70,71,83 Insulating qualities of footwear largely depend on air being trapped inside the fabric of the shoe and between the sole of the foot and the shoe, and can be increased by addition of socks, so long as the footwear is large enough to accommodate the socks without becoming too tight.78 Socks play a large role in moisture management by absorbing sweat. Sweat rates vary widely in the foot, with lower rates in cold weather of 3 g/hr at rest. Newer synthetic materials, such as polypropylene, Capilene, and Thermax, wick moisture quickly, making them good choices for an inner layer. Pile or fleece socks do not wick moisture very well. Wool offers many advantages. It is warm in winter, cool in summer, absorbs and wicks sweat, and keeps the feet warm when wet. Furthermore, during long trips, it rinses well in cold stream water, can be worn for days at a time without wear, and does not mat down like cotton socks with terry loop liners. Impermeable or semipermeable footwear materials prevent external moisture from entering footwear and wetting insulation. Moisture from sweat inside a shoe reduces insulation qualities and increases heat loss by 5%. Walking and the subsequent pumping effect of moving air in footwear removes moisture and in ordinary shoes removes about 40% of humidity.78 Footwear requires drying to retain insulation and protect feet from the cold. Moist socks and insoles should be changed, and shoes with removable liners should have the liners removed. Placing footwear in a warm, well-ventilated location will assist with drying. Hand protection from cold requires gloves or mittens with insulation, moisture barrier, and adequate space for air trapping. Mittens allow more air trapping and heat retention than do gloves, but with a tradeoff for dexterity. Mittens with glove liners or finger inserts allow improved dexterity without loss of insulation and may include pockets for placement of disposable chemical heaters. For other wilderness activities where gloves are needed but dexterity is critical (such as fly-fishing or climbing), fingerless gloves may be appropriate.
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injuries in snowboarders, but may increase the risk for elbow, upper arm, and shoulder injuries.55,121 Knee and elbow pads, padded pants or shorts, spine and back protectors, and upper body protectors are promoted to offer protection from injury, but with little evidence of effectiveness outside of football.90 Such gear is often articulated, thermal-formed, or soft foam-padded clothing or wraps designed to be lightweight and flexible, usually fitting underneath underwear or outerwear. Some gear includes molded plastic plating or shoulder cups. Mouth Guards. The efficacy of mouth guards in preventing or reducing dental trauma is debated. There are studies that show significantly lower rates of dental injuries and soft tissue injuries among users of mouth guards in football and basketball than among nonusers.43,79 Other studies have found no significant difference in oral, head, or neck injuries between users and nonusers of mouth guards.16 Although the American Dental Association reports that mouth guards can reduce the severity and incidence of oral injuries, they also recommend further research on currently available models.2 The CDC has pointed out the need for high-quality research into the effectiveness of mouth guards.24 Avalanche-Specific Protective Gear. According to the Colorado Avalanche Information Center,29 there has been an annual average of 25 deaths in the United States due to avalanches over the past 10 winters, with 36 fatalities in the 2009-2010 season. Avalanche fatalities most commonly involve backcountry snowmobilers, skiers, and snowboarders, but ice climbers, snowshoers, and hikers are also occasionally killed (Figure 16-5, online). Fatalities from avalanches are most commonly due to asphyxiation, followed by trauma with asphyxiation, or trauma alone.91 The key to reducing the risk for being caught in or killed by an avalanche is not safety equipment, but rather education and training, along with avalanche awareness and smart decision making. The skills acquired require repeated practice. Traveling in avalanche country with a trusted and trained partner is a key element of avalanche safety. Additional tools that may help one avoid or survive an avalanche include a digital or analog transceiver; a lightweight shovel for digging test pits or for recovering a buried victim; and a collapsible probe to pinpoint the exact location of a buried victim following a transceiver search.128 Snowshoers and snowmobilers tend to underestimate avalanche danger when traveling in backcountry.129 The RECCO Rescue System (http://RECCO.com) was introduced in 1983 and is used by over 600 rescue organizations worldwide, including more than 100 ski areas, rescue organizations, and helicopter companies in the North America. It consists of a RECCO detector used by search organizers and a reflector permanently integrated into the helmet, boots, or clothing of the wearer. The system uses harmonic radar to pinpoint a victim’s exact location. The reflector has advantages of requiring no batteries or training, but it is not designed for self-rescue or as a replacement for traditional avalanche transceivers. It is an additional tool for search and rescue that compliments transceivers when worn in an area where the RECCO detector is readily available. More recent technologic advances are designed to improve the chances of survival by an avalanche victim. The AvaLung is a 9-oz sling type of apparatus worn over the shoulder that prolongs the time a victim can breathe while trapped under snow. Two other devices use one or two inflatable air bags holding up to 45 L of gas to allow a victim caught in an avalanche to float to the surface, avoiding burial and enhancing visibility for searchers. The ABS system deploys two air bags from a backpack when a handle is pulled. Nitrogen canisters that inflate the bags are replaceable, allowing the system to be reused. Snowpulse SA markets an air bag in a backpack that when released, envelops the head, providing similar flotation along with head protection. Snowpulse cartridges for air bag inflation are refillable (see Chapter 2). Training and Education William Haddon’s strategy for reducing the magnitude and burden of injuries involves the pre-event phase, the event phase, 342
and the postevent phase.137 The pre-event phase focuses on prevention. Education and training in this phase includes courses that provide wilderness explorers the ability to recognize and avoid dangers in the environment and courses that teach acquisition of basic skills and techniques necessary to safely perform activities in the wilderness. Such courses include topics such as avalanche awareness and safety, rock and ice climbing, rope use, caving, mountaineering, map reading, orienteering, and kayaking. Courses are available through clubs, colleges, and specialty organizations that represent these activities. The Outdoor Wilderness Leadership School, the National Outdoor Leadership School (NOLS), and Outward Bound are examples of organizations that offer instruction in many different wilderness activities, as well as courses for instructor development. Education and training for wilderness medical care or SAR techniques are a component of the third (postevent) phase of Haddon’s injury matrix. Salvaging people and property is the focus of this phase. Initial (field) emergency care SAR operations, extrication, and transportation to advanced medical care for victims of wilderness injuries all fall into this phase. Different levels of providers may provide emergency care in the wilderness. As the popularity of wilderness excursions and wilderness medicine have grown, so have the number and variety of courses in wilderness emergency care. Although there is no national standardized curriculum or certification for wilderness first aid, courses are available through organizations such as the American Red Cross, Wilderness Medical Associates, and the Wilderness Medical Institute. These courses are generally 16 hours in duration.147 Some organizations offer a 36-hour advanced wilderness first-aid course and are ideal for wilderness enthusiasts without medical backgrounds. Guides, SAR team members, and outdoor educators without medical backgrounds complete courses with more comprehensive curricula and practical training, such as a 70-hour wilderness first responder course or a wilderness emergency medical technician (EMT) course. Unlike standard first responder and EMT courses, these programs include content that prepares an individual to deliver emergency medical care in harsh environments, when evacuation times may be lengthy, and when equipment may need to be improvised. Wilderness EMT courses are designed for EMS personnel working in search and rescue, on expeditions, in disaster situations, or in remote settings. For medical professionals with Advanced Life Support certification, a 36-hour Wilderness Advanced Life Support course is offered by Wilderness Medical Associates and other organizations. Supervision and Buddy Systems. The number of children and adolescents exploring backcountry wilderness areas has steadily increased, accounting for 25% of backpackers and wilderness campers in the United States.98 Children and adolescents typically enter wilderness areas either in a family group or through a sponsored group youth expedition or outing (Figure 16-6). Groups are accompanied and supervised by adults trained as instructors in various recreational disciplines or in wilderness emergency care. There are few studies looking at wilderness injuries or fatalities in children or adolescents. A retrospective study of visitor fatalities at all NPS units for 2003 and 2004 found that of 356 fatalities, 13% (46) occurred in children and adolescents 19 years or age or younger.62 A second study found that children and adolescents account for 21.2% of all NPS visitors nationwide requiring SAR assistance.59 The most common activities reported at the time of request for SAR were hiking, mountaineering, and boating. A study in Washington State identified 40 recreational wilderness fatalities among children and adolescents between 12 months and 19 years, with hiking and swimming the most common activities preceding death. Four out of five pediatric fatalities in this study involved children drowning after falling out of boats or into water while playing at a campsite.100 Supervision of children or lack thereof in wilderness fatalities or injuries is rarely mentioned in these retrospective studies, although a lack of personal flotation devices was noted for nonscuba drowning fatalities in the latter study. For supervised expeditions, one study found that only 13% of all 1646 reported health problems were related to trauma,33 whereas a study by Sadnicka122 found that 10% of medical problems among 2915
travelers between 15 and 18 years of age in 250 expeditions to multiple countries were the result of trauma. Organizations such as NOLS strive for safety in outdoor activities. Through their risk management program, NOLS decreased the number of injuries to a rate of 1.18 per 1000 program days for the years 2002 to 2005. NOLS attributes this reduction to prevention strategies that include reduced (11-kg [25-lb]) backpack weights, carefully planned course routes, avoiding overly demanding terrain early in a trip, emphasizing warm-up and stretching before hiking and strenuous activities, and deliberately teaching students how to hike on rugged and uneven terrain.92 Just as risk management programs and supervision of participants in organized group wilderness recreation activities may potentially decrease the incidence of injury, use of a buddy system is desirable for individual activities. People who engage in climbing, backcountry skiing, snowmobiling, and other solo activities in the wilderness are encouraged to do these activities with a buddy (Figures 16-7 and 16-8). The buddy should be someone with whom they are familiar. If unfamiliar with a buddy, one should use a half-day outing at a lower level of activity to become acquainted with their skills, styles, and physical condition. Wilderness partners need to be aware of each other’s previous experience for the planned activity; level of training in pertinent topics such as avalanche fundamentals, companion rescue, or wilderness emergency medical care; and what medical supplies are being carried. Additional points that should be addressed include the following: • What gear, specialty equipment, personal clothing, food, water, communications, and safety equipment are being carried? • Maps and route of travel. What are the potential hazards and current condition of the planned route? What is the weather forecast? What are the contingency plans in case a route or access conditions have deteriorated? What will be the turn-around or pull-out time, and how will you decide whether to continue on or turn back? • In the event of a serious event or injury, what is the emergency plan, and what resources are available? Emergency contact information and pertinent medical information should be shared with each other and with a nontraveling contact. Once wilderness travel plans have been decided, it is best not to change them at the last minute. Likewise, it is a good idea not to change buddies or to add additional travel partners in haste. Problem Anticipation: Acute Illness and Injury Even with the best preparation and planning, acute illnesses and injuries occur. When primary prevention fails, one needs to be prepared to address illnesses and injuries and minimize their impact. This is accomplished through medical clearance and vaccinations, first-aid training and ensuring that one has proper first-aid supplies, medical supplies, and medications. Because supplies may be limited as a result of availability or what one can carry in the wilderness, one must be ready to improvise.
FIGURE 16-7 Lone kayaker surfing the falls. Having a buddy or spotter to accompany individuals in solo wilderness activities is advisable. (Courtesy Haley Buffman.)
First-Aid Training. Every adult participating in wilderness activities at a minimum should have training in cardiopulmonary resuscitation (CPR) and have completed a basic first-aid course that covers common illnesses and injuries. Additional training beyond first aid may be needed, depending on the activity, distance to more definitive medical care, and underlying medical conditions of participants. For example, if one is participating in a remote area with delayed time to further medical care, at least one person needs to have completed a formal wilderness first-aid training program with emphasis on remote conditions and prolonged care.
FIGURE 16-8 Wilderness treks are more fun and less risky with a buddy. (Courtesy Haley Buffman.)
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FIGURE 16-6 Children in wilderness activities are typically supervised by excursion guides, parents, or both. (Courtesy Eric Becker.)
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Medical Clearance. Before participating in any athletic activity, it is prudent to obtain medical clearance. This is especially important for the following: • Activities in remote areas • High-risk activities and extreme sports • Person with chronic illness and/or physical limitations The purpose of medical clearance is to determine appropriate activities, personal limits, and go/no-go decisions. For persons with chronic medical conditions, the goal may be to optimize these conditions. An example is a diabetic with projected increased physical activity and projected altered meal schedule needing to alter the insulin regimen, or a patient on a medication that increases photosensitivity having to adapt to a sunny environment. Vaccinations and Prophylaxis. Tetanus vaccination should be current. If the intended activity requires travel to remote areas or areas subject to endemic diseases, then individuals should consult with a health care provider regarding the need for vaccination and/or drugs for prophylaxis. An example is the need for prophylaxis if hiking or camping in a malaria-risk area. First-Aid/Emergency Medical Supplies. For most activities a first-aid kit should be available. For brief activities with low injury risk that do not require an overnight stay or travel to remote areas, a basic first-aid kit is appropriate. The contents of commercially available first-aid kits vary greatly. In general, a kit should contain the items listed in Table 16-1.146 These recommendations are expanded for more remote locations. For certain extreme sports or very distant locations, extrication equipment may be necessary. Medications. Prescription medications may need to be considered for wilderness activities. At a minimum, bring medications prescribed for those participants sufficient for the entire trip and include an additional supply to cover unforeseen trip extension. For a single-day trip, a rule of thumb is 2 days of medications; for prolonged trips or remote environments, 1 week’s extra should be taken. Additional medications to consider are the following: • Antibiotics • Epinephrine autoinjector • Intravenous fluids
TABLE 16-1 Wilderness First-Aid Kit Item Dressings and Wound Care Adhesive bandage (Band-Aid) Adhesive tape (2-inch roll) Conforming gauze bandage (Kling 3-inch roll) Elastic bandage (Ace 3-inch wrap) Moleskin (l5.5-square inch sheets) Spenco 2nd Skin (3-inch × 4-inch pads) Sterile gauze compresses (4 inches × 4 inches) Equipment Scissors Thermometer Tweezers Oral OTC Preparations Antacid (chewable tablet) Antihistamine (diphenhydramine 50 mg) Bismuth subsalicylate (Pepto-Bismol chewable) Ibuprofen (200-mg tablets) Topical OTC Preparations Alcohol swabs (for cleaning equipment) Antiseptic ointment (Neosporin 0.9-g packets) Hydrocortisone 1% cream (30-g tube) Povidone-iodine solution (individual swabs) Tincture of benzoin (30-mL bottle) OTC, Over-the-counter.
344
Quantity 12 2 2 1 2 4 6 1 1 1 6 6 6 6 10 6 1 8 1
• Oxygen • Resuscitation medications Improvisation in Treatment. In many instances, drugs and supplies are inadequate. One may need to rely on improvisation to address these situations. Planned improvisation refers to situations where a specific piece of emergency equipment cannot be brought, but there is a predetermined plan to improvise the device. The classic example is extrication equipment for a patient whose size and weight are prohibitive. Therefore one must preplan how to convert existing equipment, such as backpack frames, should the need arise. Unplanned improvisation is exemplified by a major injury leading to uncontrolled bleeding. A tourniquet may be required but might not be standard equipment. In such a case, form a tourniquet from nontraditional material, such as a belt. Injury Prevention for the Genitourinary Tract. To prevent genitourinary infections during outings, individuals should maintain attention to genital hygiene and hydration. Infections and irritation of the genitourinary tract are more common in women than in men because the female urethra is shorter, leaving the bladder more vulnerable to colonization by bacteria. The risk for infection can be exacerbated during wilderness activity because of infrequent urination and urethral trauma from vigorous activity or bruising from a bike seat, saddle, or climbing harness. One should provide adequate padding, allow for adequate bathroom breaks, and minimize urethral trauma. To avoid vaginitis, women should keep themselves cool and dry by wearing loose-fitting clothing that maximizes air circulation and minimizes the optimal conditions for bacterial and fungal growth. Avoid nylon undergarments, because they retain humidity. Cotton undergarments or underwear made from a material such as polyester that wicks moisture and is fast drying, are ideal. Women may need to consider sanitary protection for menstruation. If menstruating while in the wilderness, women should change tampons or sanitary napkins just as frequently as at home to avoid infection. Women who handle tampons should make sure that hands are scrupulously clean before insertion. For environmental reasons, tampons with cardboard rather than plastic applicators should be used if wilderness disposal is a possibility. Injury Prevention for the Feet. Proper footwear, including careful selection of shoes and socks, helps prevent problems such as blisters. The soles should be protected with layers of cushioning thick enough to prevent bruising, but pliable enough to allow natural heel-to-toe flexion. Thick soles insulate against cold and heat. The tread provides grip. Support comes from a fit that stops the foot from slipping inside the shoe, but that is not so tight that it prevents the foot from expanding when it swells. Check socks for loose threads, knots, or harsh stitching that might cause blisters or sore spots. Flat seams at the toes are important. Bulky seams rub and cause blisters. Consider wearing one pair of fairly heavy socks (rag wool) and one pair of light liner socks next to the skin. With one sock, the boot and the outer sock tend to move as a unit. They rub against the heel and the tops of the toes at the metatarsal heads. A lightweight liner sock tends to cling to the foot. As the boot moves, the socks rub against each other, not against foot skin. Consider using powder to keep the feet dry. Some boots feature sock liners or booties made from vapor-permeable membranes, such as Gore-Tex and Sympatex, hung between the lining and outer aspect of the boot. These may be appealing initially because of the ability to prevent leaks, but over time they may leak. Their lack of breathability means that water vapor cannot penetrate the barrier, resulting in hot, sweaty feet. In addition to appropriate footwear and socks, one must practice proper foot hygiene. Keep toenails short and cut square. Keep feet dry to avoid skin softening. Immediately stop walking and attend to the first sign of a sore or “hot spot” to prevent further injury. Carry supplies, such as moleskin, tape, or Molefoam, to allow protection of any reddened areas. The covering should extend beyond any redness.
A
The Physical Environment and Injury Prevention The event phase of injury begins when physical forces exert themselves unfavorably on people or property. Prevention of injury at this stage involves intervention to prevent the harmful effects when excessive mechanical, thermal, chemical, electrical, or ionizing radiation energy is contacted. Harmful effects of excessive energy may occur acutely, as with thermal burns, or as a result of prolonged exposure with extended wilderness stays.
ULTRAVIOLET EXPOSURE UV light is the main cause for most skin cancers and cataracts. Anyone who has ever experienced a severe sunburn or solar keratitis is aware of the significant, even disabling pain associated with acute burns to skin and corneas from UV light. Even on a cloudy day, UV light can cause a serious burn. In the wilderness setting, injury from UV light is largely preventable. Photoprotection begins with behavioral changes. Limiting exposure to UV light is an essential prophylactic element and begins with avoiding exposure at peak times of the day (10 AM to 4 PM) and with covering the skin and eyes with UV-blocking clothing and sunglasses. The photoprotective properties of clothing depend on its thickness, weight, and color, with darker fabrics having greater photoblocking ability. Lightweight fabrics treated to enhance UV protection are especially useful in the wilderness setting. Hats provide photoprotection for the scalp, face, and neck; the amount of skin covered varies with the style of hat (Figure 16-9). Sunglasses protect the eyes from the discomfort of bright lights, but not all sunglasses provide UV protection. In the United States, there is an American National Standards Institute (ANSI) standard for sunglasses that includes impact resistance and UV protection.5 ANSI Z80.3 1996 standards require that a lens should have a UV-B (280 to 315 nm) transmittance of no more than 1% and a UV-A (315 to 380 nm) transmittance of no more than 0.3 times the visual light transmittance. When purchasing sunglasses with UV protection, choose a pair labeled “meets ANSI Z80.3 1996 [normal] or [strictest] UV blocking requirements” or “lenses block [X] % of UV-A and [X] % of UV-B” (as close as possible to 100%). Because of the intensity of light at altitude and the reflection of light off snow and ice, sunglasses used in winter
B FIGURE 16-10 Examples of traditional (A) and contemporary (B) sunglasses with side guards to help reduce ultraviolet light at altitude. (Courtesy Julbo.)
wilderness settings often include leather blinders on the sides or broad temple arms to further block light transmission (Figure 16-10). Sunglasses worn for travel at altitude on snowpack or in polar regions should transmit 5% to 10% of visible light and block up to 100% of UV radiation. Some sunglasses also block highenergy visible, or “blue” light, which is postulated to contribute to macular degeneration.52 The best optic quality is achieved with glass lenses, but in the wilderness, glass lenses are easily broken or shattered. Plastic lenses are lighter and more resistant to breaking, but they scratch easily. The lightest and most shatterproof plastic lenses for sunglasses are made of polycarbonate. Polarizing lenses reduce glare and are popular with fishing enthusiasts because they allow one to see below the sunlit surface of water. Sunglasses designed for water sports are constructed for greater impact resistance and flotation and include a nose cushion and retaining strap to hold in place. Lens color, polarizing characteristics, and price do not relate to UV protection, so sunglasses should be sought that meet the requisite UVA and UVB protection. Sunscreens are topical or oral products designed to protect the skin from the harmful effects of UV light by absorbing, scattering, or reflecting UV radiation. Topical “shielding” sunscreens are the most effective at preventing sunburn. Prevention of photoaging depends more on blocking low-energy UV light. Some topical sunscreens have been shown in animal models to also repair preexisting damage from UV radiation exposure.75 Sunscreens are rated by their sun protection factor (SPF), with a higher number correlating generally with greater protection. Faircomplected individuals should use a sunscreen of SPF 30 or higher. Look for a product with broad UV-A and UV-B protection. It is important to apply an adequate amount of the product (approximately 1 oz for the uncovered skin of an average 150-lb adult), to apply the product 15 to 30 minutes before exposure, and to reapply the product 15 to 30 minutes after exposure begins.36 When maximum protection from UV exposure is needed, a topical sunblock should be used. These products contain titanium dioxide or zinc oxide and are more opaque than are sunscreens. When sunscreens are needed on or in the water, use a product that is water resistant. Water resistance does not mean waterproof. The products will resist loss of protection from UV exposure after swimming or with sweating but may still require reapplication.
TEMPERATURE EXTREMES
FIGURE 16-9 Hat with extensions to shade the neck offer increased protection from sunburn. (Courtesy Eunice Singletary.)
Cold Injury The spectrum of cold injuries ranges from localized cold injury (frostbite) to systemic hypothermia. A complete discussion of the pathophysiology and treatment for cold injury is found in 345
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If primary prevention fails to prevent blister formation, try to prevent rupture and infection. Relieve external pressure by applying a doughnut-shaped piece of Molefoam. A blister should not be unroofed unless absolutely necessary. If this is required, wash the area with soap and water, and insert a decontaminated needle (“sterilized” by a flame or with rubbing alcohol) into the edge of the blister. Gently press out the fluid. Apply a sterile dressing. If the blister has already broken, cleanse and cover the area. Topical antiseptic ointment may be beneficial.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Chapters 4 to 9. Prevention of cold injury begins in the pre-event phase with preparation and planning. Weather forecasts should be studied and excursions or expeditions timed to avoid hazardous weather. Climbing, hiking, and backcountry skiing partners or groups should have a travel plan that includes turn-around times and an emergency/crisis plan for potential cold injury. Proper cold-weather clothing (above), including waterproof and windproof outerwear, and dressing in layers are essential for wilderness travel in extreme cold. For short periods of travel, some clothing, including fleece jackets, vests, gloves, and foot beds, are available with wire or carbon microfiber heating elements (ActiVHeat, Therm-ic, Hotronic) that provide up to 5 hours of supplemental heat. Batteries are rechargeable or replaceable, making these garments impractical for excursions lasting more than a day or two, unless spare batteries or a source for recharging are carried. Disposable chemical heaters are available for use in gloves, mittens, shoes, or boots, as well as in pockets. Duration of heat varies; temperature for most brands is high enough to cause burns if placed on bare skin.123 Proper nutrition and hydration are essential for endogenous heat generation. Following an accident when a person has limited mobility, or during long excursions with extreme weather, clothing and nutrition may not be enough to keep a person warm. In these cases, shelters must be used (Figure 16-11, online) or improvised, and a source of exogenous heat is necessary. Sleeping bags offer additional insulation, and a second person in the bag will offer additional warming or protection from heat loss. The heat escape lessening position (HELP) is taught to prevent hypothermia in cold water and involves putting one’s knees together and hugging them close to the chest with both arms. A group of people can gather in this position. A similar position can be used in outdoor settings when no shelter is possible. Figure 16-12 is a risk management process for preventing cold injury applicable to the wilderness setting.23 Heat Illness Heat illness is a spectrum of illnesses ranging from minor cramps and edema to heat exhaustion and life-threatening heatstroke. Heat illness results when heat gain overwhelms the body’s heatloss mechanisms and body temperature rises. In terms of wilderness travel and reducing the risk for heat illness, sources of heat gain include strenuous physical activity and environmental acquisition through conduction, convection, and radiation. Dissipation of excess heat occurs primarily by radiation through the skin and is influenced by clothing. In high ambient temperatures, evaporation becomes the most effective means of heat loss. This is enhanced with sweating. Evaporation is less effective with high ambient humidity. Heat dissipation is hampered by dehydration, cardiovascular dysfunction, skin conditions, certain medications, lack of acclimatization, reduced sweating capability, extremes of age, and hypothalamic dysfunction. When planning for wilderness trips, each participant needs to evaluate his or her risk based on age, presence of preexisting illnesses, and medications (Figure 16-13, online). If traveling during a period of high ambient temperatures and humidity, acclimatization takes 7 to 10 days, so activity level initially needs to be limited. Plan to carry enough water and electrolytecontaining fluids and to wear loose-fitting, lightweight, and lightcolored clothing that enhances evaporation by wicking, while providing shade and protection from the sun (Figure 16-14). Avoid strenuous exertion during the hottest part of the day, and take frequent breaks for hydration and cooling. NOLS guidelines for hydration call for 0.5 L of ingested liquid before strenuous exercise and 0.25 L every 20 minutes during exertion.125 Wilderness excursion leaders who supervise group activities need to emphasize preventive measures, recognize the signs and symptoms of heat illness, know when evacuation is necessary, and be able to provide emergency care. Signs of impending heat illness include headache, dizziness, fatigue, and concentrated urine. Immersion (Trench) Foot and Pernio (Chilblains) Immersion foot and chilblains are nonfreezing cold injuries. Immersion foot is seen when feet have been exposed to moisture at ambient temperatures near or above freezing for prolonged periods.138 Dependent positioning of the feet and overly tight 346
1. Identify/assess hazard How cold is it?
Air temperature Wind Rain Solar load Immersion Sea-state Altitude
2. Identify/assess contributing factors Analyze game/training requirements Determine uniform and equipment available for each person Identify high-risk athletes
Work rates Load carried Duration Availability of clothing/shelter Food and water Experience Fitness Fatigue Health Body fat Nutritional status Time of day
3. Develop controls Implement cold mitigation
Obtain appropriate weather information Train in cold conditions Provide proper clothing and equipment Provide warming facility Provide food and water Implement exposure/rewarming schedules Mandatory clothing changes
4. Implement controls Adopt and implement controls into plans
Changing weather plan Develop standing operating procedures (SOPs) for: Self checks Buddy checks Leadership checks
5. Supervise Evaluate and correct controls
Enforce controls Modify behavior
FIGURE 16-12 A risk management process for preventing cold injury that is applicable to the wilderness setting. (From Castellani JW, Young AJ, Ducharme MB, et al: American College of Sports Medicine position stand: Prevention of cold injuries during exercise, Med Sci Sports Exerc 38:2012, 2006.)
boots are believed to contribute. Keeping the feet dry for at least 8 hours a day often prevents this injury. Pernio (chilblains) is a vasculitis that follows exposure to damp, nonfreezing temperatures, most commonly below 10° C (50° F).107 It is characterized by red to violaceous lesions on exposed skin and is most common in young to middle-age women with Raynaud’s phenomenon or systemic lupus erythematosus. Keeping exposed skin to a minimum and exchanging wet or damp gloves, socks, and face and neck gaiters for dry wear will help prevent this injury.
WIND AND RAIN Wind has a primary effect of increasing convective heat loss, causing an exposed person to cool toward ambient temperature more rapidly than without wind. With moderate to strenuous exer 2 max ]), cise (intensity >60% maximum oxygen consumption [ VO heat production exceeds heats loss at a temperature of 5° C (41° F) in wet clothes with wind velocity of 5 m/sec, and body temperature is maintained. With light or no exercise, heat loss exceeds heat production, and core temperature declines. Exercise in rain leads to rapid declines in core temperature.22,106,109 Wind reduces the insulating value of clothing. Wind-blocking outerwear can counter much of this effect (Figure 16-15, online).
A
WATER
B FIGURE 16-14 A and B, Plan to carry enough water and electrolytecontaining fluids to hydrate adequately in warm weather. (A courtesy Haley Buffman; B courtesy Eunice Singletary.)
Windchill is the apparent temperature felt on exposed skin and depends on wind speed and air temperature. The “windchill factor” is always lower than the ambient temperature; when apparent temperature (what it feels like) exceeds ambient temperature, a heat index is used. Windchill tables have been available through the National Weather Service since the 1970s, with the most recent revised index published in 2001. The index applies to temperatures of 10° C (50° F) or below and wind speeds above 3.0 mph, calculates wind speed at 5 feet (typical height of a human face), and assumes no impact from the sun. Figure 16-16 shows a windchill chart from the National Weather Service.99 Windchill is useful for planning wilderness travel in order to anticipate appropriate clothing and insulation. Wind
Between 2003 and 2006, there were 12,337 reported SAR operations in NPS units, involving 15,537 park visitors. The combined lake, ocean, and river environments accounted for 35% of the total SAR environments—nearly double the number within mountain environments. Motorized boating, swimming, and nonmotorized boating (e.g., canoeing, kayaking, rafting) were three of the top six activities reported by visitors at the time SAR operations were initiated.60 An evaluation of visitor fatalities at all NPS units between 2003 and 2004 found that of 356 fatalities, 16% involved boating incidents or swimming. More than one-half of the swimming fatalities involved rip currents, river currents, and large waves, whereas one-half of boating fatalities involved boats capsizing (Figure 16-18). The most significant risks associated with water immersion or recreational activities on the water are drowning, hypothermia, and trauma from striking an object. Hypothermia is a significant risk from immersion, considering that convective heat loss in water is 25 times greater than that in air, and heat loss by conduction increases as thermal gradients increase in cold water.51 The greater the surface area of a body that is immersed, the greater the heat exchange area and the faster the decline in core temperature.81 Endurance athletes and swimmers are not immune to core temperature drop but can often partially compensate by adapting through cold-water training and by use of wetsuits. When people fall from a boat, kayak, or raft, they usually do not have the advantage of prior cold-water training or a wetsuit. A recent review of U.S. Coast Guard annual boating statistics reports for 1997 to 2006 found that although canoeists and kayakers accounted for 13% of total reported recreational boating deaths, they accounted for 29% of deaths due to hypothermia and 17% of deaths due to drowning (Figure 16-19). In the canoeist/kayaker group, failure to wear a personal flotation device was the primary factor in accidental drowning, and capsizing precipitated two-thirds of injuries or fatalities.103 A
FIGURE 16-16 Windchill chart. (From National Weather Service: NWS windchill chart, 2001. http://www.weather. gov/os/windchill/index.shtml.)
Wind (mph)
Calm 5 10 15 20 25 30 35 40 45 50 55 60
40 36 34 32 30 29 28 28 27 26 26 25 25
35 31 27 25 24 23 22 21 20 19 19 18 17
30 25 21 19 17 16 15 14 13 12 12 11 10
25 19 15 13 11 9 8 7 6 5 4 4 3
20 13 9 6 4 3 1 0 -1 -2 -3 -3 -4
15 7 3 0 -2 -4 -5 -7 -8 -9 -10 -11 -11
Frostbite Times
Temperature (° F) 10 5 0 -5 -10 1 -5 -11 -16 -22 -4 -10 -16 -22 -28 -7 -13 -19 -26 -32 -9 -15 -22 -29 -35 -11 -17 -24 -31 -37 -12 -19 -26 -33 -39 -14 -21 -27 -34 -41 -15 -22 -29 -36 -43 -16 -23 -30 -37 -44 -17 -24 -31 -38 -45 -18 -25 -32 -39 -46 -19 -26 -33 -40 -48 30 minutes
-15 -28 -35 -39 -42 -44 -46 -48 -50 -51 -52 -54 -55
10 minutes
-20 -34 -41 -45 -48 -51 -53 -55 -57 -58 -60 -61 -62
-25 -40 -47 -51 -55 -58 -60 -62 -64 -65 -67 -68 -69
-30 -46 -53 -58 -61 -64 -67 -69 -71 -72 -74 -75 -76
-35 -52 -59 -64 -68 -71 -73 -76 -78 -79 -81 -82 -84
-40 -57 -66 -71 -74 -78 -80 -82 -84 -86 -88 -89 -91
-45 -63 -72 -77 -81 -84 -87 -89 -91 -93 -95 -97 -98
5 minutes
Wind chill (° F) = 35.74 + 0.6215T – 35.75(V0.16) + 0.4275T(V0.16) Where, T=Air temperature (° F) V=Wind speed (mph)
Effective 11/01/01
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speeds do not reflect man-made wind. For instance, a snowmobiler traveling 35 mph on a calm day will be exposed to wind speed of 35 mph across his or her body. In addition, wet skin exposed to wind chills faster than does dry skin. If wet skin is exposed to wind, the ambient temperature used in the windchill chart should be 10° C (18° F) lower than measured actual ambient temperature.17 When windchill temperature falls below −27° C (−17° F), frostbite can occur in 30 minutes of less. Travelers in mountain terrain should presume that wind speed would likely increase as altitude increases and natural barriers to wind (trees) become more sparse. Wind-blown snow is a potential travel hazard. Reduced visibility from blowing snow can cause a person to become disoriented, lost, and even to fall off rocky precipices or into a crevasse (Figure 16-17). Wind makes securing of shelters significantly more difficult and can turn natural and man-made objects into trauma-inflicting missiles.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
fall into water can be associated with traumatic injuries to the head or spine with subsequent drowning (Figure 16-20). If a fall is into swift water, contact with rocks or downed trees (streamers) increases the chance of additional trauma or becoming trapped underwater and drowning (Figures 16-21 and 16-22). Prevention of drowning from falls off boats or rafts begins with use of a personal flotation device. A water-activated light is useful for locating a person in a nighttime rescue. In swift-water boating activities, most wilderness excursion companies and leaders require a helmet to be worn (Figure 16-23, online). If
A
B A
C FIGURE 16-17 A, Wind from blowing snow can reduce visibility and cause climbers or hikers to become lost or fall off rocky precipices. B and C, Wind can make posing for pictures on cliff edges especially precarious. (A courtesy Haley Buffman; B and C courtesy Eunice Singletary.)
B
C FIGURE 16-18 Large waves and river currents are commonly involved in water-related fatalities. (Courtesy Haley Buffman.)
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FIGURE 16-19 A, B, and C, Canoeists and kayakers account for 13% of the total reported recreational boating deaths in the United States. (Courtesy Haley Buffman.)
FIGURE 16-20 A fall into water can be associated with traumatic injuries to the head or spine with subsequent drowning (Courtesy Eric Becker.)
people fall into swift water, they are instructed to position themselves so that they travel downstream feetfirst, which allows them to avoid hitting their head on rocks and to see and avoid objects in the water (Figure 16-24, online). Alcohol ingestion is associated with a higher relative risk for death while boating, even with lower levels of blood alcohol. The risk is the same for passengers as for operators.25,39,130 One of the greatest preventive measures for both operators and passengers engaged in watercraft activities is to abstain from drinking.
SNOW To a wilderness enthusiast, nothing can be more delightful than fresh snow, and yet nothing can be potentially more dangerous. Snow becomes a hazard when it slides (avalanches), when it accumulates in heavy snowstorms to such great depths that a person can asphyxiate following a fall, and when a wilderness adventurer becomes wet, cold, or unable to see due to blowing snow. Non–avalanche-related snow immersion death was described by Cadman20 in 1999. Asphyxiation associated with snow immersion occurs when skiers or snowboarders fall upside down into a snow bank or into a tree well around a conifer. It has been
proposed that snowboarders are at higher risk than are skiers from asphyxiation because of the lack of releasable bindings on snowboards. Preventing injury or death from non–avalanche snow immersion begins with basic precautions. Always ski or ride with a partner; in very deep snow following a snowstorm, always ski or ride a slope within eyesight or voice contact of your partner; ski or ride one at a time on slopes using a spotter; and avoid tree wells on glady slopes.142 In case of accidental submersion, attempt to release bindings; if a ski pole is available, it may be the only means of releasing a binding short of twisting out. Several products designed for surviving avalanche burials are potentially useful to backcountry and sidecountry recreationalists to improve chances of surviving snow immersion. The AvaLung (see above) and the Snow Snorkel may increase survival time under snow by diverting expired air away from the face.150 Inflatable air bag type of devices marketed for improving survival in avalanches (e.g., Snow Pulse) may help prevent snow immersion asphyxiation by allowing a skier or snowboarder to remain in a “head-on-top” position following a fall in deep snow.
HYDRATION If fluid intake is less than fluid loss, dehydration may result. Many individuals do not drink an adequate amount of fluids in the wilderness. In a cold environment, this is because when skin temperatures fall significantly, thirst is less noticeable compared with during hot weather.73 In cold temperatures, moderate fluid loss may not be as important for exercise performance as during hot weather.27 If cold-weather clothing maintains skin and core temperature to what would be expected during exercise in a temperate or hot environment, then dehydration will likely
A
B
C
FIGURE 16-22 A, B, and C, Removal of logs and branches from rivers can lessen the risk for injury or death after falling from a raft or kayak. (Courtesy Haley Buffman.)
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FIGURE 16-21 Downed trees or branches (streamers) increase the chance of additional trauma or becoming trapped underwater and drowning. (Courtesy Haley Buffman.)
PART 4 INJURIES AND MEDICAL INTERVENTIONS
negatively impact performance.49 Individuals with hypohydration or hyperhydration who are exposed to intermittent exercise with normobaric hypoxia demonstrate greater physiologic-strain hypoxemia and acute mountain sickness (AMS) symptoms than do individuals with euhydration.110 Hydration status can be monitored in the wilderness by observing the color (and thus concentration), volume, and frequency of urine output. Oral fluids containing sodium have been shown to aid in fluid retention over several days of cold exposure, as well as in wildland firefighters in heat-stress conditions.32,115 During wilderness excursions, a source of water needs to be readily available and easily reached to permit frequent, ad libitum fluid intake. Severe exercise-associated hyponatremia (EAH) from overzealous hydration is a well-described problem in endurance sports participants, particularly women, individuals with low body weight, and those taking nonsteroidal antiinflammatory drugs (NSAIDs).50,65,66,101 In general, EAH is not frequently encountered in the wilderness setting, although there are reports of EAH in hikers, trekkers, climbers, cold weather endurance athletes, and long-distance cyclists.* Symptoms reflect noncardiogenic pulmonary edema and cerebral edema and include nausea, vomiting, and headache followed by neurologic symptoms such as confusion, disorientation, seizures, or coma. A recommended preventive measure to be considered, especially by those at risk (women, low body weight, planned prolonged exercise duration, extremes of heat), is to refrain from using NSAIDs while participating in sustained physical activity in the wilderness setting. In addition, moderate fluid intake is recommended based on the perceived need (ad libitum) rather than a specific amount. Any fluid intake during prolonged exercise that exceeds combined urine and sweat output (800 to 1000 mL/hr) should be considered high risk for development of EAH.114 Wilderness excursion leaders need to educate and advise their group members on appropriate fluid intake and be able to recognize early symptoms of EAH. There are many marketed hydration systems. These systems use bags (“bladders” or reservoirs) to hold water or other liquid inside an insulated carrier or are integrated into a backpack. Water is sucked through a bite valve from a dispensing tube extending from the reservoir up over the shoulder or through the inside of an insulated shoulder strap. “Wearable” hydration includes garments, such as cycling jerseys, that contain concealed reservoirs. Some hydration system manufacturers use antimicrobial compounds in the reservoir and bag to inhibit bacterial growth. Hydration systems are more difficult to clean than are water bottles but have the advantage of allowing a person to easily carry large amounts of liquids needed for maintaining hydration during prolonged physical activity.
ALTITUDE Wilderness adventurers most commonly encounter changes in altitude during travel through mountainous terrain. As travelers ascend to higher altitude, barometric pressure decreases. Although the fraction of oxygen in the atmosphere remains constant, the partial pressure of oxygen decreases with ascent. Hypoxia is the physiologic insult that is responsible for altitude illness. The altitude where symptoms of altitude illness occur varies between persons. One study of tourists in Colorado found that 71% experienced symptoms of altitude illness following arrival at altitudes of 2103 to 2957 m (6900 to 9700 feet), which represents the elevation of many ski areas.67 There is no absolute elevation where altitude illness can be predicted; rather, it is influenced by the rate of ascent, the altitude reached and where sleep occurs, duration of exposure to altitude, and level of physical activity. Individuals with a prior history of altitude illness are prone to future altitude illness,143 and adolescent girls have a higher incidence than do boys.34 Prevention begins with education. Only just over one-half of respondents on a survey at a major U.S. ski area were aware of the existence of AMS, and one-third were unaware that it could *References 9, 14, 77, 119, 134, 151.
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be prevented. One-half the respondents preferred to receive information about AMS from the Internet. This suggests that the Internet may be an effective means of educating the public about AMS symptoms and means of prevention.57 Because slow, gradual ascent allows time for acclimatization to altitude, this is the primary means of prevention, particularly when ascending to high or extremely high altitude. If symptoms develop during ascent, additional time is needed for acclimatization before resuming ascent. If symptoms do not abate, then descent to an altitude 305 to 914 m (1000 to 3000 feet) lower, particularly for sleep, may be needed. The use of acetazolamide 125 to 250 mg twice daily beginning 1 day before travel and continuing for several days at altitude has been shown to prevent symptoms of AMS.1,28,42 While at high altitude, a dose of 250 mg every 8 hours has been shown to dramatically reduce symptoms.46 Dexamethasone has also been found to prevent symptoms of AMS.41,113 Risk factors and susceptibility for high-altitude pulmonary edema (HAPE) are similar to AMS and include a prior history of HAPE, rapid ascent, and higher altitudes. Additional risk factors include male gender, intense exercise, cold ambient temperatures, and preexisting respiratory tract infection.40,68,132 Preexisting primary pulmonary hypertension and intracardiac shunt, such as ventricular or atrial septal defect, or patent foramen ovale, may predispose to HAPE.3,74,148 As for AMS, primary prevention of HAPE is by gradual ascent. Ascent rate should be limited to no more than 300 to 350 m (984 to 1148 feet) per day above 2500 m (8202 feet) (sleeping altitude) with an additional day of acclimatization added for every 600 to 1200 m (1969 to 3937 feet) above 2500 m (8202 feet).11 Pharmacologic prophylaxis aimed at preventing altitude-induced pulmonary hypertension is most commonly achieved with the calcium channel blocker nifedipine, 30 mg extended release daily or twice daily.12 Sildenafil and tadalafil, both phosphodiesterase-5 inhibitors and pulmonary vasodilators, have been evaluated for prophylaxis and treatment of HAPE but have the potential side effect of causing significant headache. When taken beginning a day before ascent, dexamethasone reduced the incidence of HAPE by 78% and was superior to tadalafil in its efficacy. However, side effects may limit its use as a prophylactic agent.13,86 For individuals who are prone to development of HAPE, the β-agonist salmeterol 125 mcg inhaled twice a day has been found to reduce the incidence of HAPE by 50%. Side effects, notably tachycardia, are similar to those of other β-agonists. Studies do not conclusively support the use of acetazolamide for prevention of HAPE.85 Because of its safety profile and lack of serious side effects other than reflex tachycardia, nifedipine remains the prophylactic drug of choice for individuals with a prior history of HAPE.133 High-altitude cerebral edema (HACE) is the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status change and ataxia in a person without AMS.136 Symptoms typically occur at night, and after several days at altitude; many persons with HACE also have HAPE or AMS. Without rapid treatment, HACE progresses to coma, and death occurs by herniation. There are no studies showing a benefit to prophylactic treatment. However, slow ascent and prophylaxis against AMS are likely beneficial.
BITES AND STINGS The incidence of wilderness-acquired bites and stings and their fatalities is difficult to ascertain, especially because many injuries go unreported, but there is likely a resemblance to statistics maintained by the American Association of Poison Control Centers (AAPCC). Between 2001 and 2005, an annual average of over 92,000 bites or stings were reported to the AAPCC. Over three-quarters (76%) were due to insects and spiders, 7.2% were from snakes, 6.9% from mammals, and 3% from aquatic animals (Figure 16-25, online). Twenty-seven fatalities were reported for the period, with 16 from snakebites.80 A study of long-distance hikers in Vermont found 6.6% of reported injuries in 155 hikers were due to insect bites. Heggie58 found that 7% of wilderness injuries in children under 18 years and 1% of injuries in adults in Mt Rainier and Olympic National Park in Washington were due to insect stings. Just over 2% of injuries reported by NOLS over a 4-year period were due to stings.82
FIGURE 16-26 Stings from hymenoptera commonly cause pain and local allergic reactions. (Courtesy Eunice Singletary.)
A
B FIGURE 16-27 A and B, Bells are frequently worn by hikers to produce noise and avoid startling a bear. Grizzly (A) and black bear (B). (Courtesy Eunice Singletary.)
hospitalization. The vast overall majority (69%) were due to rattlesnakes.102 Preventing snakebites begins with being aware of the presence of snakes and their typical habitats. Snakes tend to hide under debris, rocks, and other objects in the outdoors, so caution is urged when lifting up fallen wood or logs. It is important to not step on or near snakes. Use a flashlight to check for snakes in dark holes, and be aware that snakes can swim. If a snake is spotted, back away from it slowly and do not attempt to capture it. One study found that up to 67% of snakebites were the result of intentional interaction, and up to 40% of snakebite victims had consumed alcohol before the bite occurred.96 Snakes have a strike zone of one-third to one-half of body length. Since snakebites are typically to the lower leg, outfitters recommend specialized snake boots. Hiking boots and several layers of pants legs also help divert bites from many snakes. Keep tents zipped closed, and check inside sleeping bags and clothing before using. Mammalian attacks in the wilderness are unusual and typically provoked. Attacks by bears are a common preoccupation of hikers and campers, although the actual incidence of attacks is believed to be very low. Herrero63 found 77 people with reported injury from 66 incidents involving grizzly bears in North American national parks between 1900 and 1970, most involving bear sows with cubs. Attacks were frequently provoked either intentionally or unintentionally (i.e., surprising/startling a bear in its habitat); only 5 fatalities were reported. Attacks by black bear sows are much less common than those by brown bears (Figure 16-27). Hikers often wear bells to create noise while hiking to prevent inadvertently startling a bear and provoking an attack. Avoiding high-risk areas, such as where carrion or bear scat is located, is a way to avoid an encounter with a bear. It is recommended to keep food out of tents and in bear-proof containers and to burn garbage at least 300 feet downwind of a campsite. In the case of an encounter with a brown bear, it is best to avoid eye contact, to avoid running or turning away, and to assume a submissive posture (“play dead”) until the bear has left the area.53 Predatory encounters by a black bear should be dealt with by standing still, by attempting to intimidate and appear larger by raising one’s arms above the head, or by fighting back with any available 351
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Permethrin is a repellent that helps prevent bites from many crawling and blood-sucking insects. Some permethrin clothing formulations reportedly last up to 6 weeks, even with weekly laundering.124 In the United States, ticks transmit more diseases than do any other insects. When traveling in tick-infested country, wear long pants, bloused at the ankles and tucked into shoes or boots, and a long-sleeved, buttoned or pullover shirt tucked into pants and, if possible, covered with a jacket. Use of 0.5% permethrin spray on shoes and outer clothing is a barrier to ticks. Careful daily inspection of clothing and skin and removal of crawling insects while in tick-infested areas is recommended. Other precautions include avoiding sleeping on a cabin floor, not sleeping in a bed that touches the wall, and changing and laundering all bed linens before use if a cabin has been unoccupied.10 In general, mosquitos in North America cause little problem beyond minor itching and skin irritation. However, certain mosquitos transmit forms of encephalitis. Since 1999, West Nile virus has spread throughout the United States, infecting thousands and killing hundreds of people. Use of long pants and sleeves is a measure for preventing mosquito bites. Mosquito netting is effective for sleeping areas and is used on hats to protect the face and neck. N,N-diethyl-3-methylbenzamide (DEET) is an insect repellent used to reduce mosquito bites, including the species responsible for transmission of West Nile virus in the United States. The higher the percentage of DEET in a repellent, the longer and better the insect-repelling effect. Concentrations of at least 23.8% are highly effective in reducing mosquito bites for up to 5 hours.48 Newer formulations allow a lower percentage of DEET to be as effective as a higher-percentage formulation by mixing DEET in a controlled-release lotion vehicle that can last up to 20 hours. DEET can be absorbed through skin and should not be used on children under 2 years of age. Flies, gnats, and no-see-ums are not repelled as effectively as are other insects by DEET. When traveling in areas with these bothersome insects (coastal regions, southwestern United States), use a repellant containing di-Npropyl isocinchomeronate, or R-326. Some insect repellants are combined with sunscreens, but this may decrease the effectiveness of the repellant and/or the sunscreen. Certain spider bites cause significant morbidity. Prevention includes awareness of habitat; inspection of clothing, shoes, and sleeping bags; and shaking out items before use. Stings from hymenoptera cause local and allergic reactions (Figure 16-26). Limiting exposure to these insects is not easily accomplished. Wilderness travelers with known allergy to hymenoptera may prevent serious reactions to stings by prior desensitization therapy and should carry injectable epinephrine, oral antihistamines, and a corticosteroid. Avoiding brightly colored clothing, perfume or fruity scents, and walking barefoot in areas where stinging insects may be present are maneuvers to help prevent hymenoptera stings. Between 2001 and 2004, an estimated 9873 snakebites were treated each year in emergency departments in the United States, with nearly one-third due to venomous species, 18.7% while the patient was outdoors hiking or camping, and over 25% requiring
PART 4 INJURIES AND MEDICAL INTERVENTIONS
weapon or object.45 Pepper spray (5% to 10% capsicum oleoresin) may be an effective deterrent in the event of a charge by a bear.64 For some predatory species, such as mountain lions and wolves, it may be best to display aggressive behavior or fight back in the event of an attack.15,94 Other mammals that may inflict injuries or fatalities in the wild include bison, cougars, bats, deer and elk, coyotes, wolves, moose, porcupines, foxes, raccoons, skunks, and rodents (Figure 16-28). Human attacks by foxes are usually by rabid animals. One general method of preventing attacks by wild animals includes never approaching or attempting to capture or restrain an animal.
TOXIC EXPOSURES Exposure to inhaled toxins may stem from natural or man-made sources. The most common man-made exposures are most likely smoke from campfires. Fatalities are reported not infrequently from carbon monoxide (CO) inhalation due to accumulation inside of poorly ventilated tents after using camp stoves. Injury or death is preventable by being aware of the symptoms of CO poisoning, by ventilating tents, cleaning ice or snow off tent fabric, using maximum blue flames and avoiding low flames, and avoiding prolonged simmering.84 Wilderness travelers at altitude need to be especially alert to the symptoms of possible CO poisoning, because symptoms may be similar to those of altitude illness, although no relation has been found between increased CO exposure and AMS symptoms.117,118 Climbers on descent were found to have higher carboxyhemoglobin levels and an increased risk for CO exposure with increased hours of stove operation. Volcanoes are another source of possible toxic inhalation injury in wilderness adventurers. Volcanic laze is a dense plume of concentrated hydrochloric acid and seawater mist that forms when hot lava enters the ocean waters. It has been identified as the cause of two fatalities in Hawaii and is a risk for wilderness adventurers seeking close views of active volcanos.61 Volcanoes
A
release a number of potentially toxic gases, including sulfur dioxide, hydrogen fluoride, and carbon dioxide. Injury prevention includes avoiding standing under or downwind of a laze plume, avoiding depressions where carbon dioxide may settle, avoiding proximity to volcanic fumaroles, and avoiding exposure to volcanic ash.21 Poison ivy, oak, and sumac are common sources of allergic plant contact dermatitis caused by exposure to urushiol found throughout the plant (Figure 16-29, online). Exposure may be the result of direct contact, from inhalation of smoke particles from burning plants, and from contact with contaminated clothing, shoes, or gear. A skin protectant containing 5% bentoquatam (quaternium-18 bentonite) in a lotion form has been found to be effective at preventing allergic contact dermatitis from poison oak.89 When combined with skin cleansing using isopropyl and cetyl alcohol wipes and education to recognize offending plants, it may be especially effective at preventing contact dermatitis from Toxicodendron species.126 Prevention of adverse reactions from plants begins with being aware of potentially toxic plants that may be encountered in the area of planned travel, and being able to identify and avoid them. Wearing long-sleeved shirts and pants will help decrease exposure, but contamination is still possible from clothing. If contact with a potentially toxic plant is suspected, the area of contact should be washed thoroughly with water and mild soap and sun exposure to the area avoided. The opportunity to ingest poisons in the wilderness is practically limitless. Mushrooms, berries, roots, fruits, leaves, and other vegetation are tempting to many hikers or campers. Prevention involves being able to definitely identify toxic plants and to not ingest them in a harmful form.
WATER, GERMS, AND HYGIENE Water in wilderness areas is used for drinking, cooking, cleaning, and recreation. When wilderness travelers are concerned about possible water contamination in an area where they plan to drink that water, they should use a viable option for water disinfection. Perhaps the most important means of preventing infectious diarrhea in the wilderness is fastidious hand hygiene and education on hygienic techniques for food handling and preparation. Proper disposal of human waste in high-traffic alpine climbing routes, and all wilderness areas, is encouraged. Exposure to a travel or climbing companion with diarrhea increases the risk for developing infectious diarrhea.93 A revised three-bowl system of washing eating utensils was recently recommended for cleaning and reducing bacterial contamination on expeditions where running water is not available. The first bowl contains detergent to remove food residue and grease. A second bowl contains 20 mL of 4% bleach and is used to wash utensils until visibly clean, and a third bowl of drinkable water is used as a rinse to remove the smell and taste of disinfectant.56
Unique Risks of Select Wilderness Activities BACKPACKING
B FIGURE 16-28 A and B, Attacks by mammals, such as coyotes and porcupines, are uncommon. (Courtesy Eunice Singletary.)
352
The two basic types of backpacks are those with external frames and those with internal frames (Figure 16-30, online). The frames are designed to transfer the weight of the backpack from the shoulders and back to the hips and legs. An ideal backpack weight distribution is 20% on the shoulders and 80% on the hips. This distribution lowers the body’s center of gravity, making the fit more stable and places weight on the location best suited to carrying the weight. Backpack size is an important consideration for injury prevention. Individuals need to be sure that all equipment necessary for the duration of the trip can be carried without putting excessive strain on the shoulders and back muscles. In addition to backpack design, the prime concern regarding stress on the back and muscles is the proper amount of weight an individual can carry. This is determined by the size, body weight, and fitness level of the person. For multiday trips, where there is repetitive stress, a good rule of thumb is to limit the contents to 25% of body weight. To minimize the chance of back injury
Backpacks With External Frames A backpack with an external frame may be preferred because it allows a larger amount of weight to be carried, using a ladderlike frame commonly made of aluminum or plastic. A hip belt and shoulder strap are attached to the frame, usually with clevis pins and split rings. A backpack that is adjustable to fit the length of the spine is best. One should optimally select a design that prevents injuries. Lumbar padding and increased stability via a conical hip belt allow for comfort. Recurved shoulder pads/straps and a chest compression strap improve weight distribution and increase comfort. Additional advantages of a backpack with an external frame are allowing air space between the back and the pack, thus reducing sweating and skin breakdown; and weight carried higher in the pack, allowing for more upright posture. However, the pack may wobble side to side during walking, potentially compromising balance. Backpacks With Internal Frames The advantages of an internal frame backpack are that if well designed and fitted, it will conform more to the body, allowing for better balance, and can be worn comfortably for longer periods of time. With this advantage comes the absence of airflow, leading to problems with back perspiration and possible skin breakdown. Because the weight is carried lower, one must bend more, which in turn alters proper posture and can predispose to low back strain. Backpack Lifting Proper lifting techniques are the key to minimize injury. The least injurious method for donning a backpack is to have someone hold and stabilize the pack while the carrier slips his or her arms into the shoulder straps. If a second person is not available, the backpacker can lift and rest the backpack on an object that is waist high and then slip into it. If a backpack must be donned from the ground, the wearer should lift the backpack onto a bent knee and slide one arm through the shoulder strap. After adjusting the strap so that the backpack rests on the shoulder, the carrier should lean forward and rotate the body slightly, allowing the free arm to slide through the other shoulder strap. While still leaning forward with bent knees, the backpacker adjusts the second strap and hip belt. Backpacks and Children There are specially designed child carriers. Be certain to use a well-structured carrier that provides appropriate support and weight distribution. A child-carrying device should be equipped with restraints that prevent an active child from climbing out. One should not use an ordinary backpack to carry small children. Risks include strangulation if a child becomes entangled in the carrier’s harness, and head and body injury if a child wiggles out of the harness and falls or is struck by an overhead obstruction, such as a tree branch.
HIKING Environmental hazards to be anticipated during hiking include those common to many wilderness activities, such as altitude illness, temperature extremes, UV exposure, plant and insect exposure, and hygiene and water effects. Negotiating trails and uneven and hazardous terrain, including snow, ice, and mud, can be challenging. Because a trail is marked or exists on a map does not mean it is safe, clear, and well maintained. Plan to check actual conditions on the day of travel. The key to a safe and injury-free trip is ensuring proper balance. Watch for unstable rocks and boulders. Keep body weight over feet, with knees bent, and do not lean backward. When crossing rivers and streams, remember that water is very powerful. Use predefined crossing points, safety ropes, or watercraft and flotation devices.
A common injury during hiking and backpacking is low back pain. The most common reason for back injuries is carrying excessive or poorly distributed loads. Using a properly designed backpack and proper lifting techniques can help avoid these injuries. A useful injury prevention adjunct is a hiking pole or staff to provide stability on rough ground and diminish impact on knees and ankles. A staff can support a good walking rhythm and prevent imbalance when carrying a heavy load. Hiking poles allow for probing and identifying hidden rocks and deep spots and can hold back bushes, barbed wire, stinging plants, and other trail obstructions. Although one pole can be helpful, it can often lead to uneven balance and weight shift. Using two poles takes the load off the legs and hips and redistributes part of the weight to the upper body musculature. On a steep area, hiking poles enable tripoding, which is having three points of contact with the ground.
HAMMOCK SAFETY Hammocks safety issues exist. The priorities are strong and secure attachments with clear knowledge by the user of the weight tolerances for the hammock and the hanging hardware. A slight modification to the traditional hammock is the lightweight minihammock, which is popular for camping and backpacking. These hammocks have no spreader bars and can be folded easily. The CPSC warns that children can become trapped and strangle in certain mini-hammocks; two deaths and one nonfatal incident have involved mini-hammocks or backpacker hammocks. If a hammock is rigged too high off the ground, a child will have difficulty climbing into it and may become trapped or entangled, leading to strangulation. To prevent injuries, install a mini-hammock near the ground.139
HUNTING More than 35,000 firearm fatalities have occurred in the United States each year since 1989, and it is estimated that there are three nonfatal firearm injuries for each death associated with a firearm.6 The key elements to injury prevention while hunting are at a minimum the following: • Proper training for hunting and use of firearms, focusing on safety • Hunters wearing appropriate protective clothing; wearing international orange clothing articles when traveling in areas frequented by hunters; and ear and eye protection • Hunting only in approved areas and at safe distances from residential or populated areas • Compliance with all local and state laws and regulations Hunter safety courses are available in every state and are a prerequisite in most states to obtaining a hunting license. Key recommendations include warning nonhunters of hunting season, limiting hunting to designated hunting areas, and wearing international orange clothing articles when traveling in areas frequented by hunters. Hunters should always be sure of their target before shooting. A safety harness should be worn when using a tree stand. Care should be taken to use appropriate techniques when cleaning game to prevent lacerations. Eye protection with impact-resistant lenses should always be worn to prevent injury from ricocheting fragments and shotgun pellets. Ammunition should always be stored separately from guns. The greatest potential serious injury from hunting is a gunshot wound, but this is actually uncommon. A 9-year retrospective review of illnesses and injuries in hunters found that trauma accounted for only 45% of emergency department visits by hunters, with the majority of injuries being knife injuries associated with the field dressing of game. The most common medical visits were for cardiac signs and symptoms, and all emergency department deaths were due to cardiac causes.108 Cardiac evaluation of big game hunters with risk factors for cardiac disease should be considered.
HORSEBACK RIDING In 2005, an estimated 73,576 people were treated in hospital emergency departments for horseback-riding injuries.47 Horsebackriding injuries most frequently occur to the upper extremity as 353
CHAPTER 16 INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE
and allow better stability, the goal is distribution of the weight via maximal use of the frame. To achieve this goal, 50% of the weight should be in the upper one-third of the pack. To accomplish this distribution, lighter and bulkier items should be packed in the bottom and heavier items should be packed in the top close to the frame.
riders try to break a fall. Serious horseback-riding injuries involve the spine, pelvis, internal organs, and head. The following precautions should be taken to prevent horseback-riding injuries: • All riders should always wear riding helmets that meet proper safety standards. • Wear properly fitted, sturdy leather boots with a minimal heel. • Inspect all riding equipment for damage. • Be sure the saddle and stirrups are appropriate for your size and are properly adjusted. • Secure all riding equipment properly. • Amateurs should ride on open, flat terrain or in monitored riding arenas. • Jumps and stunts require a higher level of riding skill. Do not attempt these without supervision.
CLIMBING Climbing is a wilderness activity that poses risks common to many other wilderness activities, such as hypothermia, dehydration, heat illness, altitude illness, trauma from falls, and avalanches (Figure 16-31, online). Hand injuries, including fractures, tendon ruptures, and digital amputations, are common in climbers.87,116 Use of stiffer ropes, reducing rope slack, and grabbing rope in a controlled manner during a fall have all been suggested as means for preventing digital injuries in climbers.69
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 17
Principles of Pain Management STEPHEN D. COLEMAN AND RAYMOND R. GAETA
Pain is ubiquitous in daily life, and multiple treatment modalities are available under normal circumstances. However, the wilderness setting presents significant challenges when available treatments are limited to those that are included with medical supplies for travel into remote locations. Many travelers have medical conditions that may restrict or limit the use of certain therapies. Some travelers may suffer chronic pain and are already receiving treatment with medications or implanted devices. The treatment of pain in remote and extreme environments is guided by patient characteristics, type of injury, and available therapies. Optimal treatment reduces the chances of further injury, decreases suffering, and improves the likelihood of successful rescue. The International Association for the Study of Pain4 defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” This definition indicates that pain is not simply sensory input from tissue damage; rather, it is a complex experience that depends in varying degrees on an emotional component. The emotional component can vary markedly among individuals and circumstances; however, these factors may significantly affect physiology and dramatically alter the impact of pain on an individual patient. For example, fear and anxiety associated with injury in remote areas can exacerbate the situation. The optimal management of pain often requires a multimodal approach. This approach includes treatment of ongoing tissue damage, which may include interventions locally and systemically, non-narcotic medications, opioid and adjuvant medications, and awareness and management of psychological factors that affect an individual’s perception of pain.
Anatomy and Physiology of Acute Nociceptive Pain The early understanding of the transmission of sensation was that pain perception followed nerves that were simple conduits to the brain. As a greater understanding of pain has developed, it is clear that nociceptive pain, which is defined as the pain of tissue injury or potential tissue injury, is initiated by nociceptor activation in the periphery and modulated at multiple levels in the nervous system, thereby allowing for multiple targets for therapy. This sequence of events is categorized into four processes: 354
1. Transduction: Chemical, thermal, or mechanical energy is converted into an electrochemical signal. 2. Transmission: The signal is conducted to the central nervous system via Aδ and C fibers. 3. Modulation: The signal is altered by both positive and negative feedback loops in the spinal cord and the brain. 4. Perception: The signal is finally appreciated as pain. The skin, the periosteum, and the joint surfaces are abundantly populated with nociceptors that are activated by potential or actual tissue damage. Thinly myelinated Aδ and unmyelinated C fibers terminate in the skin as nociceptors and transmit nociception to the spinal cord. Fast-conducting Aδ fibers respond to mechanical stimuli and transmit sharp sensations. Slow-conducting C fibers respond to chemical, thermal, and mechanical stimuli and transmit burning sensations. Acute injury of the skin results in simultaneous transmission through Aδ and C fibers. Cell bodies of the Aδ and C fibers are located in the dorsal root ganglion, and they project fibers to the posterior horn of the spinal cord. Aδ and C fibers synapse with second-order neurons in the dorsal horn of lamina I to lamina V. These second-order neurons cross to the contralateral side of the spinal cord and ascend in the anterolateral spinal tracts to the thalamic nuclei, brainstem, and midbrain, where they synapse with third-order neurons and project to the cerebral cortex. The simple stimulation of nociceptors without tissue damage may result in transmission of an action potential to the spinal cord and higher levels of the nervous system, and this may eventually result in a perception. However, if stimulation results in tissue damage, a host of changes can occur; these include the local release of many chemicals near the site of the injury as well as chemical changes at the spinal cord and higher levels of the central nervous system. Locally released chemicals may be excitatory or inhibitory. Substance P and neurokinin A are excitatory neuropeptides that are released locally during tissue damage that may facilitate nociceptive transmission. Release of calcitonin gene-related peptide and substance P results in tissue edema and erythema by increasing vascular permeability in peripheral vasculature, thereby contributing to inflammation. There are proinflammatory substances released during tissue damage, including bradykinin, which can initiate pain transmission and sensitize nociceptors. Glutamate, nerve growth factor, serotonin, and histamine also potentiate the response of nociceptors. In addition, low pH may reduce the threshold of nociceptors. There are many additional sensitizing chemicals that act locally at the site of tissue injury as well as at the spinal cord level. The opposing system includes
Pain Measurement The experience of pain is completely subjective. Various scales have been introduced that attempt to quantify the level of pain; these include numeric scales (e.g., 0 to 10, with 10 being the worst pain), categoric scales (i.e., none, mild, moderate, or severe), and even face scales (i.e., smile, neutral, or frown). The visual analog scale appears to be more objective because the patient makes a mark along a 100-mm horizontal line that can then be measured to give a pain score of 73 mm, for example. The usefulness of any scale is best determined when making repeated measures for the same patient with the use of the same scale, especially in an acute setting. A baseline value establishes a set point from which higher pain scores should be interpreted as “worse” and lower pain scores interpreted as “better.” Infrequent measures (e.g., for a patient with a chronic condition) are somewhat less reliable. Interpatient reliability is even more problematic, because different people may experience the same injury differently.
Types of Pain The nomenclature of acute pain versus chronic pain is familiar to many, and relies on time as a determining factor; however, it adds little else to the understanding and treatment of pain. Understanding the mechanisms of pain allows pain to be treated on a continuum, with recognition that unmitigated acute pain can become chronic on the basis of physiologic changes that may occur within the nervous system rather than just with the passage of time. With this approach, the rationale for preemptive strategies and aggressive acute strategies comes into clearer view. Coexistence of acute and chronic pain in the same patient is thus treated in an integrated model. With an understanding of the common mechanisms of pain disorders, a rational approach to initial therapy can be developed with the use of three general categories that are based on pathophysiology. Pain may be considered nociceptive, inflammatory, or neuropathic, or it may be a combination of two or all three types with certain forms of injury (Figure 17-1). The categories and initial therapies are as follows:
Nociceptive
CHAPTER 17 Principles of Pain Management
release of pain-inhibitory substances such as endogenous opioids, β-endorphins, acetylcholine, γ-aminobutyric acid, and somatostatin; these substances impede nociceptive transmission. Modulating nociceptive input can inhibit or facilitate the transmission of signals. In addition to local and spinal cord effects of these chemicals, transmission of action potentials to the spinal cord may be modulated by the transmission of signals by other fiber types. A landmark publication by Melzack and Wall3 described the gate control theory, which operates at the spinal cord level. The authors described input from Aβ fibers, which transmit light touch and pressure and have an inhibitory modulation effect on transmission of nociception to the spinal cord. This description of the gate control theory may explain the mechanism for modulating nociception at the spinal cord level when transcutaneous electrical nerve stimulation (TENS) is applied. At the level of the spinal cord, nociception and the autonomic nervous system are under descending inhibitory control from supraspinal levels. A familiar example of descending inhibitory control is found in our normal disregard for the sounds of our heartbeat and respirations. Normally these signals are suppressed, but they are easily called into consciousness by cortical mechanisms. Similarly, the nociceptive system is also under descending inhibition from supraspinal systems, allowing us to ignore our pain at times during stressful situations. Serotonin and norepinephrine appear to be the primary neurotransmitters that regulate descending inhibitory control; however, others (e.g., α2 agonists, cannabinoids) may be involved. Thus the perception of pain involves not simply the transmission of signals from peripheral sensors to the brain. It is in fact a complex system that is initiated by stimulating peripheral nociceptors in the presence of a milieu of local mediators that facilitate or inhibit signal transmission. As transmission of the signal moves centrally, modulating influences exert their influence before the perception of the sensation occurs.
Inflammatory
Neuropathic
FIGURE 17-1 Categories of pain.
1. Nociceptive. Acute pain that is initiated by tissue injury in the form of a laceration, fractured bone, or crush injury is a type of nociceptive pain. It is a consequence of activating specific nociceptors within the skin, muscle, periosteum, joints, and probably the viscera. These receptors are likely the distal terminals of Aδ and C fibers; they may respond to specific stimuli, including chemical, thermal, and mechanical insults, or they may respond to more than one of these stimuli, in which case they are called polymodal receptors. Polymodal receptors represent the majority of nociceptors. The primary medications directed toward treating nociceptive pain are opioids. Opioids have their primary effects on the opioid receptors µ, δ, and κ. Their analgesic effect is produced in the periphery, at the dorsal horn of the spinal cord, and at supraspinal sites. 2. Inflammatory. Inflammatory pain is mediated by elaborating prostaglandins via the cyclooxygenase pathway. Sensitization of peripheral nociceptors is also mediated via this mechanism, which leads to hyperalgesia around the wound. Nociceptive pain and inflammatory pain generally coexist, because the pain stimulus provokes them both. Immunemediated inflammation with or without tissue injury also falls into this category. Nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids are particularly effective for treating inflammation as well as mild to moderate pain. Peripherally decreased production of prostaglandins, including prostaglandin E2 (PGE-2), is the likely mechanism for decreased pain and inflammation. In addition to their peripheral actions, NSAIDs also appear to act on the dorsal horn of the spinal cord. Prostaglandin 2 at the level of the spinal cord is thought to cause release of glutamate both pre synaptically and postsynaptically. Glutamate may augment pain states and hyperalgesia. Inhibition of glutamate release at the spinal cord by reduction of PGE-2 as a consequence of NSAID administration involves a centrally acting mechanism in addition to the well-known peripheral mechanism. 3. Neuropathic. Neuropathic pain results from injury to the nervous system (e.g., peripheral nerve, spinal cord) that may occur as an acute injury of the nerve. Neuropathic pain may be the result of an isolated injury to the nervous system, or it may be the result of an injury that causes nociceptive or inflammatory pain. At the dorsal horn of the spinal cord, after peripheral nerve injury, release of cytokines and growth factors results in upregulation of nociceptive neurons. Although this is considered a broad category, various mechanisms are responsible for maintaining neuropathic pain, which results in multiple agents that are used to treat it. Antidepressants, anticonvulsants, antiarrhythmics, and local anesthetics are considered first-line agents 355
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for treatment of neuropathic pain, and are given empirically. Gabapentin, which is commonly prescribed, was developed for treatment of epileptic seizures and designed to bind to γ-aminobutyric acid receptors. However, its analgesic effect is thought to be related to actions at the α2-δ subunit of L-type calcium channels that block the influx of calcium.
Pretravel Preparation Optimally a pretravel evaluation should assess the individual’s suitability for the wilderness experience and include an assessment of chronic medical conditions. A thorough history and physical examination should include the individual’s use of medications as well as any allergies and intolerances. Determining the use of chronic pain medications is important, because there are common and potential side effects to these medications. Some medications may cause cognitive impairment and psychomotor changes that may increase an individual’s risk for injury. Use of opioids may be associated with side effects including cognitive changes, constipation, and tolerance as well as withdrawal if the medication dose is significantly reduced or terminated abruptly. Termination of adjuvant medications—including antidepressants (e.g., desipramine, duloxetine), benzodiazepines (e.g., lorazepam, alprazolam), and anticonvulsants (e.g., carbamazepine, gabapentin)—can also cause withdrawal-type syndromes. Individuals who are receiving chronic opioids or adjuvants for chronic pain may not have a predictable response to acutely administered analgesic medications for acute injuries. As management of chronic pain has become more complex and as more sophisticated implanted devices have become available, it has become more likely that individuals with chronic pain will be traveling in the wilderness. These devices include spinal cord stimulators, peripheral nerve stimulators, cortical and deep brain stimulators, and implanted intrathecal infusion devices. If an individual has one of these devices, it will be important for him or her to understand how to operate the device and to have contingency plans in case the device fails. For example, individuals with implanted pumps that deliver intrathecal medication require periodic refills of the reservoir, typically every 1 to 3 months. Persons who use these devices and persons with allergies should wear identification bracelets. Device manufacturers have a worldwide network of support that is accessible by telephone or e-mail, but this may not be practical in the wilderness, so written instructions should be available. Having the device information (i.e., the name of the manufacturer and the model number) and contact information for local health care providers and manufacturers will facilitate resolving difficulties when civilization is reached. When medications are transported internationally and specifically by air carrier, the Travel Security Administration in the United States may require specific handling of medications. Because regulations change periodically, one should check for updates before traveling. Medications should be properly labeled with appropriate prescription and patient identification information.
Treatment Modalities After injury, the patient should be assessed with regard to mechanism and severity of injury. Treatment modalities are available for management of acute pain; these include local, regional, and systemic techniques. Local physical modalities (e.g., cold, heat), local anesthetics, and topical medications may be effective. Regionally, nerve blocks of the extremities or other body parts may provide excellent analgesia or even anesthesia for many hours. Systemically, medications include opioids, NSAIDs, and antineuropathics for treatment of acute pain. Preparation of a pain first-aid kit for excursions into the outdoors allows for the greatest number of options for treatment of various maladies (Box 17-1).
PHYSICAL MODALITIES Rest minimizes additional pain and inflammation. If practical, maximize rest and minimize motion until pain is fundamentally 356
BOX 17-1 Pain Management First-Aid Kit* Basics Esmarch bandage, 3 × 36 inches Hot and cold packs Oral Medications Acetylsalicylic acid, 500 mg Acetaminophen, 500 mg Carisoprodol (Soma), 350 mg, or metaxalone (Skelaxin), 500 mg Diazepam (Valium), 5 mg Hydrocodone, 5 mg Injectable Medications Naloxone, two 0.4-mg ampules Ketamine, 50 mg/mL, 5 to 10 mL Lidocaine, 1%, 30 mL Procaine, 1%, 30 mL Midazolam (Versed), 5 mg/mL, 5-mL vial Morphine, 5 mg/mL, 5-mL vial Meperidine (Demerol), 50 mg/mL, 5-mL vial Topical Therapies Capsaicin ointment, 2-g tube Lidocaine ointment, 5%, 30 to 50 g Lidocaine patches, 5% Diclofenac, 1% gel, 100 g Diclofenac, 1.3% patch (Flector Patch) Additional Supplies Intravenous cannula, 20 gauge, three Intravenous cannula, 18 gauge, three Tourniquet Intravenous tubing sets, two Normal saline, 500 mL Intravenous 5% dextrose in lactated Ringer’s solution, 500 mL Acupuncture needles, 50 *Items in this list are subject to the individual’s training and scope of practice. This pain kit should be available in addition to a regular first-aid kit.
gone and the majority of function is restored. Ice or another cold application (e.g., immersing a sprained ankle in a cold stream) can reduce inflammation and pain from an acute injury. Ice should be applied intermittently (e.g., for 20 minutes per hour; by alternating ice with no ice in 20-minute intervals to avoid the risks of decreased blood flow to the region, which could result in decreased oxygen delivery, decreased clearance of cellular by-products, or even frostbite [further ischemia of the limb or local tissue may occur with prolonged contact with ice]). A towel or a similar material should be placed between the ice and skin, and tissue status should be closely monitored. Edema and swelling result from the acute inflammatory process and may cause significant pain and loss of function. As swelling in the extremities increases, there may be compression of the veins, which results in worsening bleeding and swelling. Further swelling may compress nerves and arteries (i.e., compartment syndrome), which will result in ischemia distal to the injury. Elevation reduces swelling by increasing venous return of blood and by minimizing tissue edema. Distended tissues increase pain. If possible, the injured site should be maintained above the level of the heart. If a bandage is applied to reduce swelling, an elastic bandage rather than a tight nonelastic bandage will help to prevent overly aggressive reduction of sufficient blood flow and, potentially, ischemia. Compression Analgesia Wrapping an extremity proximal to the site of injury to compress the relevant peripheral nerves can produce distal analgesia and anesthesia. This may occur intentionally or may be the consequence of placing a compression dressing over an injured site.
Topical Therapies Topical application of analgesic medications may be effective for treatment of mild to moderate pain. The advantages of using a topical preparation include eliminating the need for oral medication administration, beneficial metabolic interactions with other medications, reduced systemic adverse events, direct access to the site of pain, and ease of termination of treatment if a side effect occurs. Topical medications include NSAID gels and patches, lidocaine ointments and patches, and capsaicin creams, lotions, and patches. Topical application of NSAIDs is generally less effective than oral therapy; in addition, there may be localized skin irritation. Any topical analgesic medication should only be used on intact skin. In the United States, the only available topical NSAID is diclofenac, either as a 1% gel or a 1.3% patch. Outside of the United States, other topical NSAIDs may be available. Topical 1% diclofenac gel is applied four times daily over the site of pain, and is indicated for relief of osteoarthritis pain in joints that are amenable to topical therapy. The diclofenac patch (i.e., Flector Patch) is applied twice daily to the site of pain, and is indicated for acute pain that results from minor strains, sprains, and contusions. Topical lidocaine is available as 5% topical ointment, 4% topical cream, and 5% patch. Ointment and cream are applied up to three times per day. Up to three patches at a time may be applied, and the patches are to remain on the skin for no more than 12 hours during any 24-hour period. Lidocaine patches are indicated for postherpetic neuralgia; however, they may be effective for any localized pain condition. Capsaicin is available as a cream, lotion, or patch. Concentrations of capsaicin cream preparations range from 0.025% to 0.25%. A recently approved 8% capsaicin patch has limited usefulness outside of the clinic or hospital setting. Capsaicin results in burning pain at the site of application. Start with the least concentrated formulation of capsaicin, and apply it with lidocaine 5% ointment three or four times a day. Initially use three parts of lidocaine ointment to one part of capsaicin. As the application becomes more tolerable, increase to a one-to-one concentration; this will eventually be followed by full-strength capsaicin. Although the evidence for efficacy of capsaicin is the best for all of the topical agents, analgesia occurs approximately 7 days after the initiation of therapy, thereby limiting its use for acute pain.2 TENS can be an effective technique for management of painful stimuli. This therapy requires special equipment that users may easily bring into the wilderness. TENS is frequently used to treat chronic back pain with placement of electrode patches over the area of pain and then connecting them to the battery and controller. Clinical studies to demonstrate efficacy have been inconclusive. There are many criticisms of these studies, including the use of heterogeneous patient populations and nonstandard lead placement and stimulation parameters. Nonetheless many individuals report significant benefit while using TENS. The proposed mechanism is explained by the gate control theory. Peripheral stimulation of large afferent Aβ fibers by TENS inhibits nociceptive transmission in the dorsal horn. Some studies have noted release of endogenous opioids and serotonin.6,7 In addition, increases in opioid agonists in cerebrospinal fluid have been noted after TENS use. At least two patches are used. Patch placement requires experimentation to find the locations that provide the best analgesia. Pulse width, frequency, and intensity may be adjusted. TENS can be applied at high frequency (>50 Hz) with an intensity that is below motor contraction (i.e., “sensory intensity”) or at low frequency (<10 Hz) with an intensity that produces motor contraction. The device is adjusted to create a sensation at the site of the patch without causing muscle contraction or discomfort. In warm climates, the patches may require additional adhesive,
or else they might become dislodged, thereby limiting effectiveness. Regional Therapy Local anesthetics are membrane stabilizers. They reversibly decrease the rate of depolarization of neurons by inhibiting sodium ion channels in the neuronal cell membrane on the basis of chemical structure. Local anesthetic is considered either an amino ester or an amino amide. Familiar amino ester local anesthetics are procaine, chloroprocaine, and tetracaine. Amino amides include lidocaine, prilocaine, mepivacaine, bupivacaine, and ropivacaine. The principal differences between amino ester and amino amide are metabolic fate and potential for allergic reactions. Amide ester local anesthetics undergo hydrolysis; this results in production of para-aminobenzoic acid, which is more likely to precipitate an allergic reaction than are amino amides, which undergo hepatic metabolism. Local anesthetics also contain preservatives that may cause allergic reactions. An allergic reaction to a local anesthetic of one class does not increase the risk of an allergic reaction to the other class of local anesthetic, unless the reaction is to the preservative. The metabolism of amino amides is slower, so repeated dosing of these agents may result in increased systemic side effects with repeated exposure as compared with the amino esters. Systemic toxicity with local anesthetics is related to plasma concentrations of the drug. Local anesthetic may enter the systemic circulation by direct injection at the time that the block is placed or as a result of ongoing systemic absorption of drug in the tissue after placement of the block. Absorption of local anesthetic depends on the dose administered, vascularity of the site of injection, use of added epinephrine, and chemical properties of the anesthetic. Systemic toxicity with local anesthetics primarily involves the central nervous and cardiovascular systems. As plasma levels of local anesthetics increase, patients may experience perioral and tongue numbness followed by vertigo, tinnitus, and blurred vision. At higher plasma levels, seizures may occur. Intravenous benzodiazepines are effective to suppress seizures as a result of local anesthetic toxicity. Cardiac toxicity generally occurs at higher plasma concentrations than those that are necessary to produce central nervous system side effects. Cardiovascular toxicity results from relaxation of vascular smooth muscle and direct myocardial depression. Effects on the vascular smooth muscle may cause hypotension. Cardiac depression is thought to be related to sodium channel blockade. Slowed conduction can result in prolonged PR and QRS intervals and reentry ventricular dysrhythmias. Local anesthetics to consider having in a first-aid kit may include an amino amide, short-acting, rapid-onset local anesthetic such as 1% lidocaine; a slower-onset, longer-acting medication such as 0.5% bupivacaine or 0.5% ropivacaine; and, if there is need for a nonamide local anesthetic, an amino ester local anesthetic such as 1% procaine. Trigger Point Injections Pains from muscular spasm are readily identified. Palpation of the affected muscle group will localize sites of maximal tenderness, which are known as trigger points. Injecting 2 to 3 mL of local anesthetic will temporarily block pain and spasm. Care should be taken to avoid large volumes (i.e., >15 mL) of 0.5% bupivacaine, which is absorbed quickly from muscles.
NERVE BLOCKS Pain as a result of injuries to extremities may be amenable to placement of nerve blocks. The simplest of these is the field block, which involves local anesthetic being infiltrated around the wound. Injuries to the forearm and hand may be managed with an axillary nerve block (Figures 17-2 and 17-3). Injuries to the hand in an ulnar, radial, or median nerve distribution can be blocked at the wrist or in the forearm by blocking the respective nerves. Digital blocks may be placed for injuries to individual fingers or toes. More sophistication is required for blockade of a major nerve or plexus. With minimal training, the motivated individual can readily instill blocks, such as the femoral block near the inguinal ligament, for the lower extremities. Similarly 357
CHAPTER 17 Principles of Pain Management
In addition to providing analgesia, compression may result in loss of distal pulses, which should be monitored. Compression analgesia may result in development of paresthesias, thereby confounding the diagnosis of compartment syndrome. Therefore compression analgesia is not a recommended technique. However, it may be considered in rare circumstances, such as when a limb is not salvageable.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Median n.
Musculocutaneous n. Supraclavicular n. (lateral antebrachial (cervical plexus) cutaneous n.) Axillary n. Radial n. Radial n. (superficial br.) (inferior lateral brachial cutaneous n.) Humerus Axillary a.
(Palmar br.) Median n. Musculocutaneous n. Ulnar n. (palmar digital br.)
Median antebrachial Intercostobrachial and cutaneous n. medial brachial cutaneous n.
Radial n.
Ulnar n.
FIGURE 17-2 Ventral nerve distribution of the upper extremity. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)
FIGURE 17-4 Axillary block. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)
the entire foot can be blocked by placing local anesthetic at the level of the ankle joint in one of a combination of easily identifiable locations. The use of surface landmarks is adequate for anatomic localization of the appropriate nerves, because nerve stimulators and ultrasound machines are luxuries that are found only in the clinic or operating theater. Blunt-needle placement and administration of local anesthetic guided by paresthesias will usually suffice.
to the skin and then redirected inferior (medial) and deep to the artery, where the radial nerve is located; another 5 to 10 mL of local anesthetic are deposited. Finally, the needle is withdrawn to the depth of the axillary artery, where the ulnar nerve is located, and the remaining 5 to 10 mL of local anesthetic is deposited. During this procedure, the patient may experience paresthesias, which can be used to verify the location of the needle. However, this is not necessary. If the axillary artery is entered, continue to advance the needle through the artery, and then aspirate to make sure that the needle is deep to the artery (not intravascular) before depositing the local anesthetic. If the artery is entered, direct pressure should be maintained over the site for 5 minutes to limit bleeding. If 0.5% bupivacaine without epinephrine is used, the block duration will be 4 to 6 hours; with the addition of epinephrine, it may be 8 to 12 hours. Potential complications include intravascular injection of local anesthetic and vascular or nerve injury.
Axillary Block Sites distal to the elbow can be blocked by placing local anesthetic near the musculocutaneous, median, radial, and ulnar nerves at the distal axilla guided by the axillary artery pulse (Figure 17-4). This block is performed by having the patient supine with shoulder abducted to 90 degrees and externally rotated, with the elbow flexed. Stand or sit at the patient’s side caudal to the arm, and identify the axillary pulse over the proximal humerus. The site of entry is sterilized, and local anesthesia injected locally before a blunt needle is placed. (Blunt needles have a shorter bevel than do traditional hypodermic needles. These needles may be safer when performing nerve blocks, because they may be less likely to injure vascular and neural structures.) A 22-gauge blunt needle is then advanced superior to the pulse. The musculocutaneous nerve lies deep to the artery, and this is where 5 to 10 mL of local anesthetic is deposited. Superficial to the musculocutaneous nerve and the pulse of the axillary artery is the median nerve, where an additional 5 to 10 mL of local anesthetic are deposited. The needle is withdrawn Radial n. Median n.
Median antebrachial cutaneous n.
Ulnar n.
Axillary n.
(Posterior brachial (Posterior cutaneous n.) antebrachial cutaneous n.) (Inferior lateral brachial cutaneous n.)
Radial n.
Musculocutaneous n. Intercostobrachial (lateral antebrachial cutaneous n. cutaneous n.) Supraclavicular n. (cervical plexus)
FIGURE 17-3 Dorsal nerve distribution of the arm. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)
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Wrist Block To accomplish a wrist block, it may be necessary to block one or two of the three nerves that innervate the hand. To perform this nerve block, the shoulder is abducted with the arm supported and the hand in a supine position. The ulnar nerve is located medial to the ulnar pulse at the level of the ulnar styloid. A blunt-beveled needle is advanced, a paresthesia may be obtained, and then 3 to 5 mL of local anesthetic is injected. If no paresthesia is obtained, the needle can be moved in a fanlike distribution while injecting local anesthetic to ensure nerve block. The median nerve is located between the ulnar styloid process and the distal radial prominence and between the flexor carpi radialis and palmaris longus tendons. With the wrist and fingers flexed, these tendons are easily identified. A blunt-beveled needle is advanced deep to the tendons, and 3 to 5 mL of local anesthetic is injected. The radial nerve is blocked by injecting 5 mL of local anesthetic subcutaneously as a field block over the radial aspect of the wrist proximal to the anatomic “snuff box.” The use of 1% lidocaine or 0.25% bupivacaine is sufficient to achieve good analgesia at each of these nerves. Digital Block The dorsal digital and proper palmar digital nerves are located over the medial and lateral aspects of the digits. To perform this block, the hand is pronated and supported. The skin is entered on the dorsal aspect of the digit. A blunt-beveled needle is inserted at the medial and lateral aspect of the proximal phalanx (Figure 17-5), and 1 to 2 mL of local anesthetic is injected on each side of the digit. The use of 0.25% bupivacaine or 1% lidocaine without epinephrine provides good analgesia. Femoral Block The sensory distribution of the femoral nerve includes the anterior and medial thigh and knee as well as the medial lower leg
Femoral nerve Femoral artery Femoral vein
Needle entry sites
Lateral femoral cutaneous nerve Rectus femoris muscle
Dorsal digital nerves Palmar digital nerves
FIGURE 17-5 Digital nerve block. (Courtesy Bryan L. Frank.)
in the saphenous nerve distribution (Figure 17-6). A femoral nerve block can be used for a femur fracture. With the patient supine, the inguinal ligament, anterior-superior iliac spine, pubic tubercle, and femoral pulse at the level of the inguinal ligament are identified. A 4-inch, 22-gauge, blunt-bevel needle is entered through the skin 1 cm lateral to the femoral pulse and advanced in the anterior-posterior plane. As the needle is advanced, a paresthesia may be elicited, although this is variable. A total volume of 20 to 40 mL of local anesthetic is injected while redirecting the needle from the initial medial position adjacent to the femoral artery to a more lateral position, thereby achieving a field block. The use of 0.25% bupivacaine will provide good analgesia; if motor block and anesthesia are necessary, 0.5% bupivacaine should be used. Because this is a field block, it may be slower in onset than other nerve blocks. The femoral artery is in close proximity to the injection site, so arterial puncture of the artery and intravascular injection are possible (Figure 17-7).
FIGURE 17-6 Distribution of the femoral nerve. (From Obrien MD: Aids to the examination of the peripheral nervous system, ed 4, United Kingdom, 2008, Saunders.)
Head of femur FIGURE 17-7 Femoral nerve block.
Common Peroneal Block A common peroneal block may be helpful for distal tibia and ankle trauma (Figure 17-8). With the patient in a lateral position, the fibular head is identified. A blunt-bevel needle is introduced just below the fibular head. A paresthesia can be elicited at a depth of 0.5 to 1 cm, and 5 mL of local anesthetic is deposited (Figure 17-9). Ankle Block To achieve analgesia of the foot, five nerves are blocked at the level of the ankle (Figure 17-10). Depending on the injury, one or more of the nerves may be blocked with local anesthetic. To block the posterior tibial nerve, a 22-gauge blunt-bevel needle is advanced at the level of the superior aspect of the medial malleolus from posterior to anterior, beginning just medial to the Achilles tendon. If a paresthesia is obtained, 5 mL of local anesthetic is injected. If a paresthesia is not elicited, the needle is advanced to the malleolus, and local anesthetic is injected. The sural nerve is blocked by entering the skin lateral to the Achilles tendon at the level of the superior aspect of the lateral malleolus. The needle is advanced from posterior to anterior until a paresthesia is obtained or the needle contacts the lateral malleolus, at which point 5 mL of local anesthetic is injected. The deep peroneal nerve is blocked by entering the skin lateral to the
FIGURE 17-8 Distribution of the common peroneal nerve. (From Obrien MD: Aids to the examination of the peripheral nervous system, ed 4, United Kingdom, 2008, Saunders.)
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CHAPTER 17 Principles of Pain Management
Iliopsoas Sartorius muscle muscle
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Semitendinosus m. Biceps femoris m.
Tibial n.
Popliteal v.
Popliteal a.
Common peroneal n. Fibular head
Tibia
FIGURE 17-9 Common peroneal block. (From Waldman SD: Atlas of interventional pain management. Philadelphia, 2009, Saunders.)
anterior tibial pulse, and then 5 mL of local anesthetic is injected. Field block of the superficial peroneal and saphenous nerves is performed by injecting 5 mL of local anesthetic medially and laterally from the point of entry for the deep peroneal block down to the malleoli.
SYSTEMIC THERAPY The use of various oral and parenteral analgesics forms the basis for the specific treatment of pain related to trauma in the
1 3 Extensor hallucis longus tendon
2
Superficial peroneal n.
Tibia
Posterior tibial a. Posterior tibial n.
Fibula
Flexor hallucis m. Peroneus brevis m. Sural n. Tendocalcaneus (Achilles tendon)
1 2
2
FIGURE 17-10 Ankle block.
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Opioids Opioids that are effective for treatment of nociceptive acute pain are available in many forms and dosages to achieve various routes of administration. Although there can be differences in absorption of various opioids, the general rule of thumb is that titration to beneficial effect best suits the needs of patients. Oral administration remains the easiest form of delivery, and is accomplished with combination medications that contain hydrocodone and acetaminophen (e.g., Vicodin, Norco, Lortab). Care should be taken to avoid consuming more than 4 g of acetaminophen in 24 hours, because hepatic toxicity may occur above these levels. A step up from hydrocodone is oxycodone, which comes as both a sustained-release preparation (OxyContin) and as a shorter-acting agent (Roxicodone). Because there is no acetaminophen in these latter agents, the maximum dose is limited only by efficacy and side effects. Morphine remains the gold standard, and is available for both oral and parenteral use. Intravenous administration of opioids reduces variability introduced by oral administration and decreases the time to onset of analgesia. Intravenous administration can be by intermittent injection or continuous infusion. However, continuous infusion requires additional equipment, so intermittent bolus injections in remote locations are more practical. Intramuscular administration of opioids is feasible in remote areas, but drugs may have variable absorption from different muscle groups, thus making titration to effect and duration of action more difficult to determine. Management of nausea and vomiting, which are the most common side effects of these drugs, can be accomplished with antiemetics. Phenothiazines may cause undue sedation; therefore the use of a 5-hydroxytryptamine antagonist such as ondansetron (Zofran) is advised. Oversedation and respiratory depression are feared complications of opioid use. Naloxone is supplied in 1-mL vials that contain 0.4 mg/mL; when used judiciously in 40-mcg increments, naloxone can reverse many of the minor side effects, such as nausea, vomiting, pruritus, and sedation. Fulldose naloxone is still the appropriate treatment for respiratory depression. Nonsteroidal Antiinflammatory Drugs NSAIDs have both analgesic and antiinflammatory properties. Common agents such as ibuprofen and naproxen are readily available and offer first-line treatment for various minor aches and pains that may be encountered in the outdoors. They offer an inexpensive and effective means of treatment without concern about the possible adverse effects of opioids, and are generally free from regulation in foreign countries.
Deep peroneal n. Tibialis anterior tendon Saphenous n.
Ankle section
outdoors. Familiarity with multiple classes of medications is imperative. Their use should be guided initially on the basis of the mechanism of pain and whether pain is the result of nociceptive, inflammatory, or neuropathic causes (see Figure 17-1). Tables 17-1 and 17-2 list medications from various classes and doses that are calculated for a 70-kg (154-lb) man. Oral and parental doses are listed.
1
Anti-Neuropathic Drugs The efficacy of anti-neuropathic agents is variable because of the complexity of the mechanisms present within neuropathic pain states. Although antidepressants and antiarrhythmics can be effective, anticonvulsants (particularly gabapentin) offer a safe and reasonably tolerated therapy for the pain of nerve injury. Although it is sedating at higher doses, gabapentin that is started at 300 mg 3 times daily and then increased to 600 mg 3 times daily over the course of several days is usually well tolerated. Sedation is the major side effect, so dose escalation is not advised if the patient receives benefit at lower doses or cannot tolerate higher doses. Ketamine Ketamine is a powerful dissociative anesthetic that, when used in a small parenteral dose, can provide profound analgesia. As a centrally acting N-methyl-D-aspartate receptor antagonist, ketamine is effective for all types of pain in the short term. As little as 10 to 20 mg given intravenously or intramuscularly to an adult produces the desired analgesia. If needed, the dose may be
Drug
Dosage (mg)
Salicylates Acetylsalicylic acid
325-650
4-6
300-600
8-12
Gastrointestinal distress; inhibited platelet function; contraindicated in children with viral illness Similar to aspirin
300-1000
4-6
Hepatic toxicity with overdose
50 50-75 10
4-6 4-6 4-6
Similar to aspirin Similar to aspirin Similar to aspirin; use for 5 days or less because of the potential for gastrointestinal bleeding
4-6 4-6 6-8 8 6-8
Similar Similar Similar Similar Similar
Diflunisal Para-Aminophenol Acetaminophen Indoles Indomethacin Sulindac Ketorolac
Interval (hr)
Propionic Acids Fenoprofen 400-600 Ibuprofen 300-400 Ketoprofen 25-50 Dexketoprofen 25 Naproxen 200-275 Cyclooxygenase-2 Inhibitor Celecoxib 100-200 Narcotic Agonists (Oral) Codeine 15-60, with a maximum of 360 mg per 24 hr Hydrocodone 5-10 Hydromorphone 7.5 Levorphanol 4 Meperidine 300 Methadone 2.5-150 Morphine 30-60 Oxycodone 5-10 Extended release, 10
Risks and Precautions
12-24
to to to to to
aspirin aspirin aspirin aspirin, with less gastrointestinal distress aspirin
Gastrointestinal distress; skin rash
4-6
Narcotic side effects; note the cumulative acetaminophen dosage
4-6 3-4 6-8 2-3 4-12 3-4 4-6 12
Narcotic Narcotic Narcotic Narcotic Narcotic Narcotic Narcotic
side side side side side side side
effects; note the cumulative acetaminophen dosage effects effects effects effects effects effects; note the cumulative acetaminophen dosage
From Burnham T, et al, editors: Drug facts and comparisons, St Louis, 1999, Facts and Comparisons Inc; and Emermann CL, Spenetta J: Pain management in the emergency department, Emerg Med Rep 23:53, 2002.
repeated every 2 to 3 hours. Titration to effect or to the presence of side effects is imperative. Psychomimetic effects (e.g., hallucinations, bad dreams) are seen with higher doses and may limit the use of this drug. A calm and quiet setting with minimal stimulation is the ideal setting for use. Benzodiazepines (e.g., midazolam, 2 mg intravenously) are effective for blunting this response.
Muscle Relaxants Muscle relaxants that are centrally acting are reasonable to use to treat acute muscle spasms related to injury. Sedation is a significant side effect that may limit the use of these drugs. Baclofen is a preferred agent because of its activity at the γ-aminobutyric
TABLE 17-2 Common Parenteral Analgesics: Dosage Recommendations for 70-kg (154-lb) Adults Drug
Dosage (mg)
Narcotic Agonists Codeine 15-75 IM Fentanyl 50-100 mcg Hydromorphone 1-2 IM Levorphanol 4 10-20 IM, 2.5 IV Morphine Meperidine 50-100 IM, 25-50 IV Oxymorphone 1 Narcotic Agonists and Antagonists 0.3-0.6 IM Buprenorphine 2-4 IM Butorphanol Dezocine 5-20 IM, 5-10 IV 10-20 IM, 1-5 IV Nalbuphine Nonsteroidal Antiinflammatory Drug 15-30 IM, 2-5 IV Ketorolac Dissociative Analgesic and Anesthetic 50-75 IM, 15-30 IV Ketamine
Interval (hr) 4-6 0.5-1 3-4 6-8 3-5 2-4
Risks and Precautions
3-4
Narcotic side effects Narcotic side effects; wide range of dosages Narcotic side effects; choose over morphine for a patient with hepatic impairment Narcotic side effects Narcotic side effects Narcotic side effects; active metabolite accumulates in patients with renal impairment and may cause seizures Narcotic side effects
6-8 3-4 2-4 3-6
May May May May
4-6
Similar to aspirin
2-4
Increased intracranial pressure
precipitate precipitate precipitate precipitate
narcotic narcotic narcotic narcotic
withdrawal withdrawal withdrawal withdrawal
From Burnham T, et al, editors: Drug facts and comparisons, St Louis, 1999, Facts and Comparisons Inc; and Emermann CL, Spenetta J: Pain management in the emergency department, Emerg Med Rep 23:53, 2002. IM, Intramuscularly; IV, intravenously.
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CHAPTER 17 Principles of Pain Management
TABLE 17-1 Common Oral Analgesics: Dosage Recommendations for 70-kg (154-lb) Adults
PART 4 INJURIES AND MEDICAL INTERVENTIONS
acid B receptor; this makes it different from other agents that also act centrally but that have less specific sites of action, thereby resulting in less desirable side effect profiles. Carisoprodol (Soma), metaxalone (Skelaxin), and cyclobenzaprine (Flexeril) are examples of less preferred agents.
ALTERNATIVE THERAPIES Acupuncture Acupuncture has developed over the past 3 to 5 millennia in Asia, and has been practiced for the past several hundred years in the Western world. In many cases, acupuncture as an art and science was developed in geographic areas and under social and austere conditions that are familiar to wilderness travelers. The use of acupuncture by physicians to treat trauma and illness in wilderness settings has been described recently in the medical literature.1 When properly administered, acupuncture should have a very low risk of morbidity, and may be extremely effective for alleviating pain and restoring function to an injured wilderness traveler. It has been demonstrated that endorphin, enkephalin, monoamine, and adrenocorticotropic hormone are released after stimulation with acupuncture. Furthermore, the gate control theory of pain modulation and altered sympathetic activity may also apply. Clinically improved microvascular circulation may lead to decreases in tissue edema, which in turn may diminish pain and help with restoring function. Release of adrenocorticotropic hormone leads to increased circulating corticosteroids; decreased inflammation may contribute to decreased pain and improved healing. Contemporary medical acupuncturists are typically trained in a variety of styles and traditions. Many physicians make use of a combined approach of acupuncture point selections based on neuroanatomy and the points that are felt to have energetic effects within the body. In addition, acupuncture microsystems in which the entire body is represented in a small area (e.g., the ear, scalp, or hand) are often employed. These microsystems are often quite beneficial for acute pain relief. Sterile acupuncture needles are compact, lightweight, and easy to include in a daypack or a first-aid kit. Integration of acupuncture into the biomedical care of wilderness trauma, pain, and illness may dramatically enhance patient comfort and facilitate extrication from a remote setting. An energetic style of acupuncture that is especially useful for common trauma makes use of the tendinomuscular meridians of the acupuncture energetic subsystems. Indications for activation of the tendinomuscular meridians treatment include acute strains, sprains, abrasions, and hematomas. The method of activation for this style of treatment is to place a needle in the jing-well or ting point of one to three of the meridians involved in the lesion. This is followed by placing a needle in the “gathering point” of the meridians and then by placing needles around the area of induration, swelling, or bruising, approximately 1 cm (0.4 inch) out from the edge. All needles in this treatment are placed only 2 to 3 mm (0.08 to 0.12 inch) deep and are left in place for 20 to 45 minutes.
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FIGURE 17-11 LI4 (ho gu) acupuncture site for headache.
Treatment of headaches is also amenable to acupuncture; a general point of insertion into the web space between the thumb and forefinger, known as LI4 (ho gu), is recommended (Figure 17-11).
PSYCHOLOGICAL TECHNIQUES Guided imagery or self-hypnosis is an often overlooked modality for pain management. The ability to transport the sensorium out of the painful experience into a different context is the aim of this technique. Although it is seemingly in the realm of a vaudeville show, self-hypnosis has been demonstrated to lessen the pain experience of patients with breast cancer, and is putatively felt to activate descending inhibitory pathways. Although these techniques are often thought of in the context of pain relief, their use to heighten the state of concentration has other uses in human performance, so learning the techniques before traveling is worth the investment of time. The mind is capable of extraordinary feats, as illustrated by the experience of Aron Ralston, whose arm was trapped between a rock and a canyon wall while canyon climbing alone in a remote area of Utah in 2004. Aron’s initial attempts to free himself produced excruciating pain. After reassessing his situation, relaxing, and making a plan, he touched his crushed hand and realized that it had lost sensation. This produced a sense that his arm was isolated from his body. He noted the disfigurement of this arm and observed that is was strange that he was not suffering pain. Unable to free himself and stranded alone with a limited water supply, he concluded that he needed to amputate his own arm and to focus all of his attention on this task. Not able to cut the bone, he levered the trapped arm, breaking the ulna and radius bones and thus freeing the arm. Although he felt a “blaze of pain” with the maneuver, he refocused on survival and was able to make his way to rescue.5 This is a story of an extraordinary person that illustrates the power of the human mind.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 18
Taping and Bandaging DANIEL GARZA
Taping and bandaging are both useful skills in wilderness medicine. Taping can be used to support injured joints and soft tissues; bandaging is most often used to secure a wound dressing (Figure 18-1, online). In addition, bandaging with an elastic wrap is an alternative to taping, and, over larger joints such as the knee, it is often preferable. In general, taping requires practice and experience, but some simple techniques can be easily mastered. Taping is most often used for mild to moderate sprains and strains, with which some functional capacities (e.g., weight bearing, lifting), are maintained. Although taping offers dynamic support, it is in no way comparable with splinting, which is intended to immobilize an extremity. The most common tape that is applied is white athletic or “adhesive” tape, which is often used by athletic trainers in organized sports. Athletic tape may be applied to the skin, although it may lose adhesion if the body part is not shaved and if tape adhesive is not applied. Some keys to successful taping include the following: • Avoid leaving any gaps in the tape (i.e., allowing any skin to be visible), because these gaps will lead to blisters. Avoid excessive tension on tape strips that serve to fill such gaps. • Apply tape in a manner that follows skin contours to avoid wrinkles. • Try to overlap one-half of the width of the tape with each successive strip. Bandaging is accomplished with the use of either elastic wraps or gauze rolls of varying widths. After a dressing is applied to a wound, appropriate bandaging allows the patient to feel confident that the dressing will remain secure during reasonable amounts of activity. Regardless of the method used, it is important to remember that taping and bandaging—especially when circumferential— should not be so tight as to limit circulation.
Taping TYPES OF TAPE Athletic tape is composed of fibers that are woven into strips and that are coated with zinc oxide, which is an adhesive compound. Although athletic tape is most commonly colored white, it is available in many colors. Athletic tape is the most commonly used tape in sports and first aid for support and for the prevention of injuries. It is also available in many widths. Although the major advantage of athletic tape is versatility, its major disadvantage is the tendency of zinc oxide to lose adhesive properties with heat and moisture, thereby resulting in a loss of support when the patient sweats. A variety of techniques, which are described later in this chapter, are used to increase the durability of athletic tape under these conditions. Elastic tape (e.g., Elastikon) is cotton elastic cloth tape that incorporates a rubber-based adhesive. The elasticity of this tape allows for greater flexibility, so it is particularly useful for large joints such as the knees and shoulders.
SKIN PREPARATION Skin preparation involves measures that are intended to increase patient comfort as well as the longevity of tape adhesion. If tape is to be applied directly to skin, the area is usually first shaved to remove hair that may interfere with direct contact. Care must
be taken to avoid small abrasions in the skin when shaving, because these can serve as entry sites for infection. If the area cannot be shaved in a clean and deliberate manner, it is advisable to avoid shaving. Any obvious abrasion or other wound should be covered with a thin layer of gauze or a small adhesive bandage before taping. Some commercially available skin adhesives are available in aerosolized form. These preparations (e.g., Tuf-Skin) use benzoin as the adhesive. Skin adhesive is applied after the skin has been shaved and after all abrasions have been dressed. If the area is not shaved, a foam underwrap or prewrap is used to protect the patient’s body hair. Prewrap is available in 3-inch–wide rolls in many colors. After the application of a topical skin adherent (e.g., Tuf-Skin), prewrap is applied over the part to be taped in a simple and continuous circular wrap. The prewrap is sufficiently self-adherent and does not need to be taped. When tape is applied over bony prominences, it can create tension on the skin surface that leads to blistering. Heel-and-lace pads and foam pads are used to provide additional comfort by relieving potential pressure points. Heel-and-lace pads are prefabricated pieces of white foam that are adhered together with petroleum jelly and then applied to the anterior and posterior aspects of the talus when the ankle is taped. Pads of foam can be cut to size to fit over painful areas that need to be taped (e.g., for medial tibial stress syndrome) or used for support in special cases (e.g., for patellar subluxation).
ANKLE TAPING The most common injury to the lower extremity while hiking is a sprained ankle. It is usually the result of inverting the ankle on an unstable surface. Pain and swelling linger for several days, so taping can offer support if the patient is able to bear weight. Because most injuries occur to the lateral ligaments, taping supports the lateral surface by restricting inversion. In general, taping the ankle consists of anchor strips on the lower leg and foot, stirrups that run in a medial to a lateral direction underneath the calcaneus, and support from either a figure-8 or heel-lock technique (Figure 18-2). The heel lock requires expertise to perform, so most operators are initially more comfortable with the figure-8 technique.
TOE TAPING Taping toes that are sprained or fractured is simple and effective. This treatment involves “buddy taping” to the adjacent toe with one or two pieces of tape to provide support. A small piece of gauze, cotton, or cloth should be placed between the toes to avoid skin breakdown. A sprain of the first metatarsophalangeal joint, which is also known as turf toe, can be a painful and chronic condition. Taping for turf toe is done in an attempt to support and stabilize the joint (Figure 18-3).
LOWER-LEG TAPING Medial tibial stress syndrome, which is commonly referred to as shin splints, can be taped for support and comfort. Tape is brought from a lateral to a medial direction. A small foam pad can be placed to cover the area of tenderness. Underwrap should be used over a foam pad to secure the pad in place (Figure 18-4).
For online-only figures, please go to www.expertconsult.com
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PART 4 INJURIES AND MEDICAL INTERVENTIONS
A
B
C
D
E
F
G
H
I
J
K
FIGURE 18-2 Ankle taping. A, With the ankle bent 90 degrees, apply anchors of 1.5-inch–wide tape at the lower leg and the distal foot. B, Apply three stirrups from a medial to a lateral direction in a slight fanlike projection. C, Fill in any gaps with horizontal strips. D, Begin the figure-8 technique. Apply tape across the front of the ankle in a left-to-right direction. E, Continue taping under the foot to the opposite side, and cross back over the top of the foot. F, Complete by wrapping tape around the leg, and end at the anterior aspect of the ankle. G, Apply heel locks for both feet (omit if not familiar with this technique). Start in a left-to-right direction, and apply tape across the front of the joint. H, Wrap tape around the heel (the bottom margin of the tape should be above the superior edge of the calcaneus) to form the first heel lock. I, Continue under the foot to the opposite side, and then cross back over the top of the foot. J, The tape is then brought back around the superior margin of the calcaneus and down and around the heel. K, Finish by wrapping the tape around the ankle. Repeat the figure-8 or heel-lock technique as desired.
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Place the first anchor around IP joint of first toe with 1-inch tape. Place the second anchor around midfoot with 11/2-inch tape. 2. Apply strip of 1-inch tape from distal to proximal anchor along medial aspect.
3. Continue with a strip of 1-inch tape from lateral edge of distal anchor along plantar aspect of first MTP joint to medial aspect of proximal anchor.
4. Cross with a strip of 1-inch tape extending from the medial aspect of the toe to the plantar aspect of the proximal anchor.
5. Begin dorsal strips by applying 1-inch tape from medial aspect of distal anchor across the dorsal aspect of the MTP joint to the proximal anchor.
6. Cross over the previous strip by applying 1-inch tape from lateral aspect of distal anchor to medial aspect of proximal anchor.
PATELLA TAPING Subluxation of the patella is exacerbated by the stress of walking long distances across uneven terrain. Incorporating a piece of foam into the taping of the knee can help to relieve symptoms. As with all taping around the knee, underwrap should not be used (Figure 18-6).
FINGER TAPING Injuries to the fingers are common in outdoor settings. Simple fractures and sprains can be initially treated by taping. The most common scenarios involve fingers that are hyperextended or that are “jammed.” Injuries in this scenario are often to the palmar ligaments and tendons. Patients may find it difficult to flex the finger against the resistance of an examiner’s finger, or they may demonstrate tenderness over the palmar aspect of the finger. Swelling is almost always present, so the precise injury may be difficult to diagnose. This presentation is also seen after reduction of a dorsal dislocation of the proximal interphalangeal joint. In all of these cases, it is always best to splint or tape the finger in slight flexion to avoid further injury to the flexor apparatus. Fingers are buddy taped to the adjacent finger, which serves as a splint (Figure 18-7). The second and third fingers and the fourth and fifth fingers are always paired. If the third and fourth fingers are paired, this makes injury to the second and fifth fingers more likely with subsequent activity. A small piece of gauze, cotton, or cloth should be placed between the fingers to avoid blistering or pressure on a tender joint. Strips of tape should be applied around the fingers but not over the joints. Although they are not as common, injuries of the extensor tendons can occur. These typically occur with hyperflexion, but they may also occur with hyperextension and axial loading.2 “Mallet finger” results from fracturing the base of the distal phalange, which is the site of attachment for the extensor tendon. The resulting inability of the distal phalange to fully extend results in a partially flexed finger. Injuries in which the extensor mechanism is clearly disrupted should be treated with the finger taped in full extension. A straight splint (e.g., a tongue blade, a
1. (Optional) Underwrap is applied over a foam pad.
7. Close with 1-inch strips around the toe and 11/2-inch tape around the forefoot.
FIGURE 18-3 Toe taping.
KNEE TAPING Because the knee is a large joint, taping requires expertise. Underwrap should not be used, because adequate traction to support the joint can only be achieved by taping directly to the skin. The patient’s knee should be shaved 6 inches above and below the joint line. Standard athletic tape should not be used, because it cannot provide sufficient support. Three-inch–wide elastic tape provides the foundation. Taping for injuries of the medial aspect of the knee is shown in Figure 18-5.
2. With the patient placing his or her heel on a rock or roll of tape, begin applying 11/2-inch tape from the superior margin of the malleoli to the calf.
FIGURE 18-4 Lower-leg taping.
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CHAPTER 18 Taping and Bandaging
1. Apply two anchors:
PART 4 INJURIES AND MEDICAL INTERVENTIONS
1. The patient maintains the knee in slight flexion (10 -15 degrees) by placing the heel on a small stone or cap of a spray can.
2. Apply two anchor strips of 3-inch elastic tape 6 inches above and below the joint line.
3. Apply a strip of 3-inch elastic tape from the anterolateral aspect of the lower leg, across the knee joint and up to the posteromedial aspect of the thigh.
1. Cut a piece of foam into a C shape, measured to encircle one-half of the patient’s patella.
2. The patient maintains the knee in slight flexion (10-15 degrees) by placing the heel on a small stone or cap of a spray can.
3. Apply two anchor strips of 3-inch elastic tape 4 inches above and below the patella.
4. Apply a second strip from the posterior calf to anterior thigh, forming an X.
5. Repeat steps 3 and 4 twice.
6. Apply two additional anchor strips of 3-inch elastic tape 6 inches above and below the joint for closure.
7. (Optional) Wrap a 6-inch elastic bandage from mid-calf to mid-thigh to cover the tape and provide additional support.
FIGURE 18-5 Knee taping.
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4. Apply the foam pad cut to fit the patient’s patella. Elastic tape (3-inch) is applied in a manner that reproduces the curvature of the foam pad.
5. Starting from the medial aspect of the lower leg anchors, bring the elastic tape around the lateral aspect of the patella and back to the medial aspect of the upper leg anchors.
6. (Optional) Wrap a 6-inch elastic bandage from mid-calf to mid-thigh to cover the taping and provide additional support.
FIGURE 18-6 Patella taping.
Bandaging Bandaging may be used to wrap and support an injury or to help dress a wound. Many of the techniques described in the previous sections about taping, such as the use of figure-8 patterns, are also used for bandaging.
TYPES OF BANDAGES FIGURE 18-7 Buddy taping of the fingers.
smooth stick) can be placed on the dorsal or volar surface and the finger taped to it for additional extensor support (Figure 18-8). Any significant injury to the fingers or hands should be evaluated by a physician, who can determine whether radiographs are necessary. Given the importance of maintaining optimal functioning of the hands for personal and professional activities, this point cannot be overemphasized.
THUMB TAPING The thumb is frequently injured when it is placed in extreme extension or abduction, which occurs when it is caught in the strap of a ski pole when a person is falling. Taping can prevent reproducing the mechanism of injury, particularly when the individual is grasping an object (Figure 18-9).
The type of bandage depends on the intended purpose. Elastic bandages (e.g., Ace wraps) come in many widths and are used to wrap injuries such as sprains and strains. These bandages generally are accompanied by separate clips or have built-in clips for the purpose of securing the bandage. Of note is that the double-length 6-inch–wide elastic bandage is quite useful for wrapping large joints, such as the knee and the shoulder. Bandaging wounds generally involves rolled gauze or cottonbased wraps that secure a dressing in place. These wraps are more desirable than are elastic bandages for wound care, because they do not place as much tension on the dressing. A triangular bandage, which is often used to create a sling, can be folded two to three times into a strap called a cravat (Figure 18-14). Cravat dressings are useful for applying pressure to a bleeding wound to promote hemostasis. In the discussion of bandaging different parts of the body that appears later in this chapter, the method for using an elastic bandage is described. When securing a wound dressing, the same methods may be used, except that rolled gauze or cotton
WRIST TAPING Wrist sprain generally occurs during a fall. It can initially be difficult to distinguish from a fracture. Although splinting is usually the most desirable treatment, there are two basic taping approaches that can be used, depending on whether the injury occurred with the wrist in hyperextension or hyperflexion. Anchors are first placed around the palm and the distal wrist. Support strips to prevent undesirable movements are placed on the palmar aspect for hyperextension injuries or on the dorsal aspect for hyperflexion injuries (Figure 18-10).
ELBOW TAPING The two most common soft-tissue injuries to the elbow result from hyperextension or excessive valgus force. Each of these injuries can result in significant ligament and tendon injuries. Taping techniques are intended to prevent reproduction of painful movements while maintaining function. Because these techniques allow for substantial joint movement, underwrap should not be used, and tape should be applied directly to the skin to allow for maximal adhesion. Taping for a hyperextension injury involves use of a fan of elastic or tape, which is similar to that used for the wrist, to prevent excessive extension (Figure 18-11). Individuals who have suffered valgus stress injuries require reinforcement with elastic tape placed on the medial aspect of the elbow (Figure 18-12).
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SHOULDER TAPING Taping the glenohumeral joint is rarely performed, mostly because it results in such a significant restriction of movement that the patient cannot effectively function. Thus taping offers little advantage over a sling. However, taping the acromioclavicular joint can be effective in reducing pain and maintaining adequate function at the glenohumeral joint.
B FIGURE 18-8 A and B, Extension taping of the finger with a small splint.
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Injury to the acromioclavicular joint most commonly occurs when a patient falls on the lateral aspect of the shoulder. Sufficient force is transmitted through the acromioclavicular ligament to stretch or tear it, which results in an “AC sprain” or a “separated shoulder.” For this injury, tape should be applied directly to the skin (Figure 18-13).
PART 4 INJURIES AND MEDICAL INTERVENTIONS
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FIGURE 18-9 Thumb taping. A, With the use of 1.5-inch–wide athletic tape, wrap an anchor strip around the wrist. B, With the use of 0.75-inch– wide tape, start at the volar aspect of the wrist and continue along the dorsal aspect of the thumb toward the first web space. C, Allow the patient to crimp the tape as it comes across the web space, and then continue around the base of the thumb. D, Bring the tape around to the volar aspect of the wrist, and then tape at that point. To complete a thumb spica, apply several more strips of tape in succession. To reinforce this, rather than repeating a series of strips, continue as follows. E, Apply an anchor strip from the volar to the dorsal aspect of the wrist through the first web space; note the crimping. F, Apply a strip from the dorsal to the volar aspect of the anchor strip. G, Apply successive strips until the wrist is reached. H, Add a finishing anchor strip through the first web space. I, Complete the wrapping with an anchor strip at the wrist.
bandages should be substituted. If there is a special technique for wound care, it will be described separately.
SECURING BANDAGES Because bandages are not adhesive, they must be secured with tape or clips or by tying them to the body. Two techniques for tying off a bandage are as follows: 1. As you are finishing wrapping the body part with the bandage, bend the free end of the bandage backward over your fingers to create a loop. Double back around the body part, and then tie the remaining free end to the loop to secure the bandage1 (Figure 18-15). 2. As you are finishing wrapping the body part, tear or cut the remaining portion of the bandage lengthwise down the middle. Double back with one of the resulting strips, and then tie off the bandage.
ANKLE AND FOOT BANDAGING Ankle bandaging with a 2- to 3-inch–wide elastic wrap can be used to support a sprain. The bandage can be applied over a sock or directly to the skin. It is usually the most simple to use 368
a series of figure-8 wraps. One may also use a series of heel locks, which were described in the section about ankle taping. Anchors and stirrups are not used. When bandaging the foot, the same technique should be carried out to the metatarsophalangeal joint. Circumferentially bandaging the foot by itself often results in the bandage slipping, which does not occur when the ankle is also bandaged as part of the process.
KNEE BANDAGING A double-length 6-inch–wide elastic bandage can provide support to the knee. Ask the patient to hold the knee in slight flexion by placing his or her heel on a small stone or a piece of wood (Figure 18-16, A, online). The elastic wrap is then applied circumferentially from the mid quadriceps to the mid calf (Figure 18-16, B, online). If using gauze or a smaller-width elastic wrap to secure a dressing, a series of figure-8 wraps can be applied, with the patella left exposed.
THIGH AND GROIN BANDAGING Quadriceps, hamstring, and hip-adductor (i.e., groin) strains can all be treated with an elastic bandage in a hip-spica configuration.
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CHAPTER 18 Taping and Bandaging
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FIGURE 18-10 Wrist taping. A, With the hand wide open, apply one anchor across the palm of the hand and two to three anchors across the distal forearm. B, Measure out the distance between the two anchors, and then construct a fan of four strips at varying angles on a smooth surface. C, For hyperextension injuries, apply these support strips to the palmar aspect; for hyperflexion injuries, apply them to the dorsal aspect. D, Apply another set of anchors over the support strips.
The bandaging is modified slightly for a groin strain (Figure 18-17). Although the quadriceps and hamstring can be supported by wrapping only the leg with a 6-inch–wide elastic bandage, the hip spica helps to prevent slipping and provides additional support.
SHOULDER BANDAGING A shoulder spica is used to support shoulder sprains, strains, and subluxations (Figure 18-21). A triangular bandage can be used to dress a shoulder wound (Figure 18-22).
SCALP BANDAGING WRIST AND HAND BANDAGING Support to the wrist can be supplied with the use of a 2- to 3-inch–wide elastic wrap and a continuous wrapping technique (Figure 18-18). This same technique can be used with gauze to secure a dressing to a wound that involves the palm of the hand. A hand cravat bandage can be used for wounds that continue to bleed despite manual pressure1 (Figure 18-19).
FINGER BANDAGING Finger wounds are generally easily treated with adhesive bandages. However, if the size of the wound or the degree of bleeding necessitates a larger dressing, then the following method may be used. Fold a 1-inch–wide piece of rolled gauze back and forth over the tip of the finger to cover and cushion the wound (Figure 18-20). Next, wrap the gauze around the finger until the gauze is snug. On the last turn around the finger, pull the gauze over the top of the hand so that it extends beyond the wrist. Split this gauze tail lengthwise, and then tie the ends around the wrist to secure the bandage.
THUMB BANDAGING The application of a bandage or dressing to the thumb usually involves a thumb spica, as described in the previous section about taping. The gauze or elastic bandage should be looped continuously rather than applied in individual strips.
Wounds to the scalp often require a dressing to be placed over hair, which makes adhesion very difficult. The dressing can be secured with a triangular bandage in a method that allows for considerable tension if pressure is necessary to stop any bleeding (Figure 18-23).
EAR OR SIDE OF HEAD BANDAGING A wound to the pinna of the ear or other location on the side of the head may require a compression dressing. If the ear is involved, gauze should be placed both anterior and posterior to the ear to allow the ear to maintain its natural curvature. A cravat is used to secure the dressing (Figure 18-24). This method may be used for wounds anywhere along the side of the head or under the chin.
EYE BANDAGING When bandaging an eye, a shield is placed over the eye socket to protect the globe, and this is followed by the application of a bandage over the shield. The shield may be made of commercially available sterile pads, or it may be cut foam or felt, stacked gauze, or a shirt or cravat that has been fashioned into a doughnut shape (Figure 18-25). The bandage is fashioned from a cravat and a spare piece of 15-inch–wide cloth or a shirt. The spare cloth is placed over the top of the head from a posterior to an anterior direction so that the anterior portion lies over the unaffected eye. A cravat is then applied horizontally to hold the shield over the injured eye. To expose the uninjured eye, pull up both ends of the spare cloth, and tie it at the top of the head (Figure 18-26). 369
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1. The arm is supinated and extended just short of where pain is experienced. Apply anchors with 3-inch elastic tape 4 inches above and below the elbow.
1. The arm is supinated and flexed to approximately 30 degrees. Apply anchors with 3-inch elastic tape 4 inches above and below the elbow.
2. Apply 3-inch elastic tape from distal to proximal anchors that form an X over the antecubital fossa. A total of four strips should be applied.
2. Apply 3-inch elastic tape that forms an X over the medial joint line.
3. Apply closure strips above and below the elbow over the original anchors.
The first strip begins at the posterior aspect of the proximal anchor and crosses to the anterior aspect of the distal anchor. The second strip begins at the anterior aspect of the proximal anchor and crosses to the posterior aspect of the distal anchor. Apply a total of four strips.
4. (Optional) Apply a 4- or 6-inch elastic bandage from distal to proximal to secure the taping.
FIGURE 18-11 Elbow taping.
3. Apply closure strips above and below the elbow over the original anchors.
4. (Optional) Apply a 4- or 6-inch elastic bandage from distal to proximal to secure the taping.
FIGURE 18-12 Elbow taping for a valgus stretch injury.
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1. Apply three anchor strips with 3-inch elastic tape. Place the first anchor around the midhumerus. Place the second anchor beginning inferior to the nipple anteriorly and around to the inferior tip of the scapula posteriorly. Apply the third anchor from the anterior portion of the second anchor, over the trapezius and extending to the posterior portion of the second anchor. Note that a 3-inch gauze pad is incorporated into this anchor to protect the nipple. 2. Apply a longitudinal strip of 3-inch elastic tape from the anterior aspect of the first anchor, over the acromioclavicular joint and ending on the posterior aspect of the third anchor.
3. Apply the next strip overlapping two-thirds of the third anchor laterally. It should extend from posterior to anterior portions of the second anchor and cross over the acromioclavicular joint.
4. Apply the next strip from the posterior aspect of the first anchor, over the acromioclavicular joint and ending at the anterior aspect of the third anchor.
5. Repeat steps 2 through 4 two more times. (Optional) Wrap a 6-inch elastic bandage in a shoulder spica for additional support. (See Bandaging section.)
FIGURE 18-13 Shoulder taping.
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1. Wrap a double-length 6-inch elastic bandage around the mid-thigh in a medial to lateral direction and continue proximally.
2. At the groin crease, continue up and around the waist once to help anchor the bandage. FIGURE 18-14 Making a cravat from a triangular bandage. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)
3. Return to the thigh to complete the figure-8. For quadriceps and hamstring strains, concentrate on wrapping the leg, using an additional figure-8 bandage to anchor the wrap. For groin strains, concentrate on supporting the hip adductors by alternating wrapping the leg with figure-8 wraps.
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FIGURE 18-15 A and B, Securing a bandage. (Redrawn from Donelan S: That’s a wrap: Wound bandaging made easy, Ski Patrol Magazine Winter:63, 2005.)
4. Finish wrapping leg.
FIGURE 18-17 Thigh and groin bandaging.
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FIGURE 18-18 Wrist bandaging. A, Begin by encircling the wrist with the bandage two to three times. B, Continue bandaging across the dorsum of the hand, through the first web space, and around the base of the proximal phalanges. C, Continue down and across the dorsum of the hand. D, Circle the wrist, and bring the bandage across the dorsum of the hand to form a figure-8. E, Repeat these steps, and make alternating figure-8 patterns on the dorsum of the hand. Secure the bandage at the wrist.
1. After dressing the wound, the patient closes his fist around rolled gauze.
2. Starting from the anterior aspect of the wrist, wrap one end around the dorsum of the hand, over the fingers and back to the wrist. FIGURE 18-20 To begin a finger bandage, place layers of gauze over the fingertip. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.) 3. With tension, wrap the other end around the dorsum of the hand, over the fingers and back to the wrist, creating an X.
4. Cross both ends around the wrist.
5. Tie the ends to secure the dressing.
FIGURE 18-19 Hand cravat bandage. (Redrawn from Donelan S: That’s a wrap: Wound bandaging made easy, Ski Patrol Magazine Winter:66, 2005.)
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1. Begin by encircling the mid-humerus with a double-length 6-inch elastic bandage and continue proximally while wrapping. Once near the axilla, wrap over the acromioclavicular joint and around the posterior thorax.
2. Continue under the opposite axilla, across the chest and bring down over the acromioclavicular joint and onto the upper arm.
3. Repeat the figure-8 pattern as the length of the bandage allows and finish on the upper arm.
FIGURE 18-21 Shoulder bandaging.
1. Lay the base of the bandage over the shoulder with the apex pointed toward the arm. Tie the two free ends just anterior to the axilla.
1. Drape a triangular bandage just over the eyes and fold the edge 1 inch under to form a hem. Allow the apex to drop over the back of the neck.
2. Roll the apex up the arm to the desired point of coverage and tie off.
2. Cross the free ends over the back of the head and tie in a half-knot.
FIGURE 18-22 Shoulder bandaging with a triangular bandage. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)
3. Bring the free ends to the front of the head and tie a complete knot. At the posterior aspect of the head, tuck the apex into the half-knot.
FIGURE 18-23 Scalp bandaging. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)
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1. Place the cravat over the wound at the cravat’s midpoint. Wrap one end over the head and the other under the chin.
2. Cross the cravat just above ear level and wrap ends in opposite directions.
FIGURE 18-25 Bandaging for the injured eye. A cravat or cloth is rolled and wrapped to make a doughnut-shaped shield, which is then fixed in place over the eye. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)
3. Tie off the ends.
FIGURE 18-24 Ear or side of head bandaging. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
FIGURE 18-26 To hold an eye patch in place with a cravat, hang a cloth strip over the uninjured eye. Hold the patch in place with the cravat, and then tie the cloth strip to lift the cravat off of the uninjured eye. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)
CHAPTER 19
Splints and Slings MISHA R. KASSEL AND ALAN GIANOTTI
Splints and slings have been staples of medical care for thousands of years. For instance, orthopedic splinting was well documented in ancient Egypt more than 5000 years ago1,33 (Figure 19-1, online). First and foremost, splints and slings stabilize injuries by limiting movement (Box 19-1). Limiting movement minimizes pain and decreases potential further tissue damage. Splinting eases transportation from the field, minimizes blood loss, and aids in healing.12 In general, all fractures and dislocations should be splinted before transport unless the patient’s life is at immediate risk or the rescue scene is unsafe.13 Basic splint types include rigid, soft, anatomic, and traction. Splint choice is based on fracture type and available materials. In improvisational situations, splints can be made from just about any material. Examples include newspapers, pillows, umbrellas, and other supportive materials5 (Figure 19-2).
Spinal Immobilization Spinal cord injuries are rare, affecting 40 to 50 individuals per million annually in the United States. These injuries may result in long-term disability.22 The 5 million people each year who are placed in spinal immobilization after traffic collisions contribute
to the majority of spinal cord injuries. In one wilderness study, 3.6% of mountain trauma patients who were alive when rescued had spinal injuries.12 In an attempt to prevent further neurologic damage, prehospital spinal immobilization of urban trauma patients is the standard of care. This may not be practical in wilderness settings, but it should always be considered. Spinal stabilization is first accomplished by manual techniques, and then mechanical devices (e.g., backboards, collars, straps) are required. Indications, risks, benefits, and equipment descriptions are discussed later in this chapter.
INDICATIONS FOR SPINAL IMMOBILIZATION The most common scenario for prehospital spinal immobilization is an injury sustained during a motor vehicle collision. All-terrain vehicles, automobiles, snowmobiles, motorcycles, and other offroad vehicles are the most common causes of high-force spinal trauma in the wilderness setting. Falls and other high-force mechanisms are also concerning. Worrisome symptoms include spine pain or palpable tenderness, altered mental status, neurologic complaints, head injury, extremes of age, or an unreliable examination that involves a distracting injury, alcohol or drug use, or a communication barrier6 (Box 19-2).
For online-only figures, please go to www.expertconsult.com
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BOX 19-1 Principles of Splinting
BOX 19-2 Indications for Spinal Immobilization
Visualize the injured body part. Continually recheck the patient’s neurovascular status. Traction is indicated if the pulse is not palpable. Gentle traction involves less than 10 lbs of force. Cover open wounds with sterile dressings. Immobilize the joints above and below the injury. Padding prevents further tissue damage. Do not reset open or protruding fractures. Splint the extremity in the position in which it was found. Splint the patient before transport (if he or she is stable). Ice and elevate the injury after immobilization.
Spine pain or tenderness Traumatic mechanism of injury Altered mental status Distracting injury Unreliable examination (e.g., as a result of alcohol or drug use) Neurologic complaints Head injury Extremes of age
Modified from Bowman W, et al: Outdoor emergency care: Comprehensive prehospital care for nonurban settings, ed 4, 2003, Sudbery, Jones and Bartlett Publishers; and Campbell J: Extremity trauma. International trauma life support for prehospital care providers, ed 6, Upper Saddle River, NJ, 2008, Brady.
Spinal immobilization is intended to prevent worsening of an existing spinal cord injury or the creation of a spinal cord injury in the case of a ligamentous disruption. The medical literature has multiple reports of worsening neurologic deficits after patients with spinal cord injuries are moved.6,34,35 Extreme settings mandate a different interpretation of “urban” recommendations to fit the survival wilderness scenario. Wilderness data are limited, so prehospital spinal immobilization is prudent when practical. Spinal immobilization is not performed without reservation. Backboards and collars may increase discomfort. Airway management may be restricted and evacuation times increased with spinal immobilization. However spinal immobilization remains the standard of care when practical in the wilderness setting.12 Further research is indicated to better classify appropriate indications and to further assess the risk-benefit ratio for spinal immobilization in the wilderness.
Modified from Brabson T, Greenfield M: Prehospital immobilization. In Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2007, Saunders.
CERVICAL SPINE IMMOBILIZATION High cervical spine (C-spine) injuries have great potential for morbidity and disability. The goals of C-spine immobilization are to minimize movement and maintain a “neutral” alignment. Standard C-spine immobilization is performed with a hard collar in conjunction with a backboard and lateral support devices. The modern standard cervical collar has five contact points and makes use of the head, C-spine, and thorax. The thorax contact points include the trapezius muscles (posterior), clavicle, and sternum (anterior). Hard collars alone do not adequately limit cervical motion. Backboards and lateral support devices are required in conjunction with a hard collar (Figures 19-3 and 19-4). The
FIGURE 19-3 Standard hard cervical collars. (Courtesy Laerdal Medical Corporation.)
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FIGURE 19-2 Improvised cervical spine and ankle stabilization (pillow, towels, cardboard and tape) in Port au Prince, Haiti, 2010. (Courtesy Anil Menon, MD.)
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FIGURE 19-4 A to C, Different lateral support devices. D, Complete spinal immobilization. (Courtesy Laerdal Medical Corporation.)
CERVICAL SPINE APPLICATION The application of a C-spine immobilization device depends on the position in which the patient is found and the device that is available. Universal application diagrams are generally helpful with regard to in-line stabilization, neutral neck alignment, chin positioning, and collar placement. Diagrams for application of C-spine collars on both upright and supine patients are easily referenced and generally intuitive (Figure 19-5). Diagrams for application of improvised C-spine collars or C-spine collars on patients who are found in sitting positions are also helpful (Figures 19-6 to 19-9; Figure 19-8, online).
SPECIAL CONSIDERATIONS Special populations require accurately sized equipment. This includes people with extra long or short necks for which a standard cervical hard collar is not effective. Children who are less than 8 years old are at risk for further injury when immobilized on a standard backboard because of a proportionately large head, which may cause increased flexion during a collision.36 Modifications to counter this anatomic feature include raising the shoulders to the level of the head by placing a pad underneath the shoulders (Figure 19-10). This should be considered for all children who are on backboards.28,29
IMPROVISATIONAL TECHNIQUES The key ingredients to an improvisational C-spine device include maximizing stability and fit while limiting airway compromise and allowing access for mouth opening, thus limiting aspiration risk.14 A “horse collar” technique involves a towel, blanket, or other available and malleable material rolled to the desired thickness and placed underneath the patient’s neck. The ends are then crossed over the patient’s chest and secured. As with the cervical hard collar, the patient’s C-spine is maintained in a neutral position during application and for as long as possible afterward by manual in-line stabilization2,6 (see Figure 19-6). A structural aluminum malleable (SAM) splint can also be molded into a C-spine collar. Studies have shown it to be as effective as a Philadelphia collar, with the advantage of being small, lightweight, versatile, and portable. These characteristics are advantageous in the wilderness setting26 (see Figure 19-7).
COMPLICATIONS OF CERVICAL SPINE STABILIZATION Studies have shown that C-spine collars cause increased intracranial pressure, which may be clinically significant for patients with head injuries. Therefore hard cervical collars should be removed immediately after exclusion of a C-spine injury, especially among patients with head injuries. C-spine collars may also be contraindicated in patients with penetrating neck injuries, because they may interfere with management of neck wounds or even conceal these wounds. Penetrating wounds to the spinal cord are rare. Cervical immobilization creates the real possibility of causing greater morbidity than protection.18,19
THORACOLUMBAR IMMOBILIZATION A full-length backboard best accomplishes immobilization of the thoracolumbar spine. In addition, a cervical collar, lateral neck stabilizers, and backboard straps are essential for full spinal immobilization. If the patient is already upright, standing, or lying supine, application of a full-body backboard is straightforward, as described later in this chapter. However, with the suspected cervical injury of a seated patient, an intermediate device is
required. There are many forms of this short board, such as a Kendrick Extrication Device (see Figure 19-9). Short boards are applied only after manual in-line stabilization and cervical collar placement. When the short board is in place, the patient can be safely transferred to a full backboard device.6 Strict contraindications for spinal immobilization are few but include emergency evacuation from an unsafe environment. Examples of such environments, with the risk of impending danger, include toxic spills, fire hazards, congested traffic areas, and other situations in which the application of an immobilization device would delay immediate evacuation to safety. In these dangerous situations, expedited removal with manual cervical stabilization is advised.21 When the patient is in a safe location, full spinal immobilization should be applied. Choices for full-body splints include hard backboards, scoop stretchers, and full-body vacuum splints (Figures 19-11 to 19-13). Full-body hard backboards are used for their ease of application, availability, and effectiveness. Unfortunately, their size and weight make them undesirable for backcountry use, so they are often improvised in the field. Secured straps minimize spinal movement during transport. These are especially important with vomiting patients, when the airway is potentially compromised and a quick change of position is required to allow for removal and drainage of emesis.6 Hard backboards are uncomfortable. Spinal pain that is induced by a backboard may be misinterpreted, and this can complicate and delay therapy.16 Vacuum splint devices offer certain advantages over rigid hard backboards. They can be applied more quickly, and are significantly more comfortable. They also offer a similar degree of spinal immobilization.20 During mountain rescue, vacuum splints are the preferred device for total spinal immobilization (see Figure 19-12).
FULL SPINE IMMOBILIZATION From a supine (lying) position and after the placement of a cervical collar, the patient is logrolled and placed onto a board or vacuum splint. Three people are required to transfer a patient onto a board. The first person is positioned at the head and applies in-line stabilization, the second is at chest level, and the third is at pelvis level. On the command of the person at the head, the patient is rolled onto his or her least-injured side. The board is then slid underneath the patient while the back is evaluated for injuries. Body straps and lateral neck stabilizers are then placed.6 Logrolling is not required with scoop stretchers, thereby minimizing spinal movement (see Figure 19-13). Full spinal immobilization can also be applied to a standing patient (see Figure 19-5). Complications of full spinal immobilization are listed in Box 19-3.
Upper-Extremity Splinting The most common upper-extremity injury scenario is bracing from a ground-level fall. Rigid and soft splints are used to stabilize upper-extremity injuries. It is always important to leave fingertips exposed to allow continuous assessment of neurovascular status.6 Common examples of upper-extremity splints include malleable, cardboard, air, vacuum, pillow, and sling and swathe splints. Specific splinting recommendations for upperextremity injuries are given in Table 19-1. When feasible, upperextremity injuries are splinted in a position of function (Table 19-2).
Lower-Extremity Splinting Although the principles of lower-extremity splinting are similar to those of upper-extremity splinting, the ramifications are not the same in terms of evacuation. Lower-extremity fractures are more likely to involve weight-bearing bones and thus to require rigid splinting. Specific recommendations, including positions of function, are found in Tables 19-2 and 19-3. One needs look no further than Joe Simpson’s 1985 epic selfrescue from the Peruvian Andes, which was described in Touching the Void, to appreciate the pain of an unsplinted weight-bearing fracture: 377
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patient’s neck requires manual stabilization in a neutral, in-line position until he or she is fully immobilized. Standard emergency medical services equipment includes lateral support devices (foam or plastic). In the wilderness setting, these devices can be improvised by rolling clothes, sheets, or blankets and placing them on both sides of head while securing everything in place with tape17 (see Figure 19-2).
PART 4 INJURIES AND MEDICAL INTERVENTIONS
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FIGURE 19-5 Full spinal immobilization from a standing position. A, Step 1: Manual stabilization. B, Step 2: Apply a rigid collar. C, Step 3: Insert a long backboard. D, Step 4: Center the backboard. E and F, Step 5: Rescuers grasp the board with the use of a handle that is higher than the patient’s armpit. G, Step 6: Slowly lower the patient. H, Step 7: Fully immobilize the torso and then the head and neck. (From Elling R, Politis J: Backboarding the standing patient, JEMS 12:9, 1987. Used with permission.)
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FIGURE 19-6 Improvisational “horse collar.” (Courtesy Ferno-Washington, Inc.)
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FIGURE 19-7 Improvised cervical spine collar from a SAM splint. A, Fold 36-inch splint 5 inches from the end. B, While bracing the thumbs on either side of the fold, pull the edges to create a V-shaped chin rest. C, Place the chin rest below the patient’s chin, and place the rest of the splint loosely around the patient’s neck. D, Bring the end forward and down in an oblique direction until it touches the chest. E, While supporting the chin, bring the chest portion of the splint around the chin to create a chin post. Squeeze to deepen the chin post. F, Insert the index fingers on either side of the splint and pull. G, Squeeze to create lateral posts to ensure a snug fit. H, Squeeze the back of the splint to create more stability. I, Fold up any excess splint and secure it with wrap or tape. (Courtesy SAM Medical Products.)
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FIGURE 19-9 A, Kendrick Extrication Device (KED). B, Manual in-line stabilization of the cervical spine with the KED slid behind the patient. C, Applied KED with cervical collar in place. D, Patient transferred to long board. (Courtesy Ferno-Washington, Inc.)
BOX 19-3 Complications of Spinal Immobilization Tight straps and a rigid board may cause discomfort or distress. Tight straps may cause vascular compromise. An immobilized position may interfere with normal respiratory function. Complications from emesis include aspiration. Loose straps may be inadequate for spinal immobilization From Brabson T, Greenfield M: Prehospital immobilization. In Clinical procedures in emergency medicine, ed 5, Philadelphia, 2007, Saunders; Campbell J: Extremity trauma. International trauma life support for prehospital care providers, ed 6, Upper Saddle River, NJ, 2008, Brady; Hamilton RS, Pons PT: The efficacy and comfort of full-body vacuum splints for cervical-spine immobilization, J Emerg Med 14:553, 1996; and Kwan I, Bunn F, Roberts I: Spinal immobilisation for trauma patients, Cochrane Database Syst Rev (2):CD002803, 2001.
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The moment I jumped I knew I would fall…. I had lain face-down in the gravel, clenching my teeth, waiting for the pain to subside. It remained with me, burning my knee unbearably as it had never done before… I stood and fell, writhed where I fell, cried and swore, and felt sure in my heart that these were my last spastic efforts before I lay still for good.32
Rigid Splints Rigid splints can be improvised from materials such as cardboard, wood, and wire. Proprietary vacuum splints and air splints are commonly used in the field. Rigid splints are attached to the extremity with a variety of fasteners, including tape, straps, gauze, and Velcro. For all splints, ample padding is essential, especially over bony surfaces and swollen tissue to minimize pressure damage and pain.5
CHAPTER 19 Splints and Slings
A
B
C FIGURE 19-10 Backboard considerations and increased cervical flexion for children who are younger than 8 years old. A, A young child immobilized on a standard backboard. Note how the large head forces the neck into flexion. Backboards can be modified by B, an occiput cutout or C, a double mattress pad to raise the chest. The actual clinical consequences of this observation are unknown. (Modified from Herzenberg JE, Hensinger RN, Dedrick DK, et al: Emergency transport and positioning of young children who have an injury of the cervical spine, J Bone Joint Surg Am 71:15, 1989.)
Cardboard splints have the advantage of being lightweight, inexpensive, easy to apply, and radiolucent.6 They can be premade or improvised (Figures 19-2, 19-14 to 19-16; Figure 19-16, online). When improvising, it is important to cut the cardboard so that the corrugations run lengthwise to maintain the material’s intrinsic strength. Splints can be individually fitted
FIGURE 19-12 Example of a full-body vacuum splint used for wilderness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff Department, Utah.)
using the unaffected extremity as a model and then placed on the affected extremity. They are usually secured with adhesive tape. Disadvantages include loss of integrity when wet and greater laxity as compared with other splinting options. The distorted and grossly swollen extremity is difficult to splint using this technique.12 Although they are initially malleable, vacuum splints are a type of rigid splint (Figure 19-17, online). These splints are made of many tiny plastic pellets in a closed, airtight bag. The bag is placed around the injured extremity, and then air is manually extracted via a hand pump to form a rigid “mold” of the injured extremity. The extremity is left in its position of injury to minimize pain (Figure 19-18). No external force is applied, thereby maximizing circulation.6 Unfortunately vacuum splints are expensive, moderately bulky, affected by changes in altitude, and penetrable. In addition, any perforation renders the splint nonfunctional.12 A lightweight, inexpensive, and popular rigid splint is the SAM splint (Figures 19-7, 19-8, and 19-19 to 19-33; Figure 19-8, online). Constructed of an aluminum center that is sandwiched between thin strips of foam, this splint is also malleable and versatile.6 It is very strong and pliable, and it can be used for
TABLE 19-1 Upper Extremity Splints Splint
Indication
Figure-8 splint Sling and swathe splint Sugar-tong splint Proximal Distal Posterior arm splint Volar splint
Medial clavicle fractures Shoulder and humeral injuries
Gutter splint Thumb spica splint Volar finger splint
FIGURE 19-11 Standard rigid splint. (Courtesy Laerdal Medical Corporation.)
Humeral fractures Wrist and distal forearm fractures Stable elbow and forearm injuries Wrist fractures and fractures of the second through fifth metacarpals Phalangeal and metacarpal fractures Scaphoid fractures, thumb dislocations and fractures, and ulnar collateral ligament injuries Fractures of the distal phalanges and the interphalangeal joints
Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint use: Recommendations for treatment protocols, Am J Emerg Med 19:137, 2001; Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel G: An introduction to clinical emergency medicine, Cambridge, UK, 2005, Cambridge University Press; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, Saunders.
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TABLE 19-2 Splinting Guidelines: Positions
of Function
Splint
Position
Volar wrist splint
Neutral forearm (thumb up) with the wrist in 20 degrees of flexion Neutral forearm with the wrist in 20 degrees of extension; metacarpophalangeal joint in 50 degrees of flexion; proximal interphalangeal joint in slight flexion (e.g., 10 degrees); distal interphalangeal joint in extension Forearm neutral with the wrist in 20 degrees of extension and the thumb slightly flexed to allow for thumb–index finger opposition and alignment of the thumb and the forearm Finger in slight flexion Elbow at 90 degrees of flexion with a neutral position of the forearm and the wrist
Ulnar and radial gutter splints
A
Thumb spica splint Finger splint Sugar-tong and posterior arm splints Posterior leg splint
Ankle at 90 degrees
Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint use: Recommendations for treatment protocols, Am J Emerg Med 19(2):137, 2001; Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, WB Saunders.
B
C Long backboard
Short backboard
Board splint
Ladder splint
D FIGURE 19-13 A, Scoop stretcher. B, Stretcher placed beside the patient. C, Stretcher slid under the patient. D, Stretcher locked in place with straps secured. (Courtesy Ferno-Washington, Inc.)
Padded board
Cardboard splint
Aluminum splint
Half ring
Air splint
FIGURE 19-14 Premade Washington, Inc.)
382
cardboard
splint.
(Courtesy
Ferno-
FIGURE 19-15 A variety of splints. (From Geiderman JM, Katz D: General principles of orthopedic injuries. In Marx J, Hockberger R, Walls R, editors: Rosen’s emergency medicine: Concepts and clinical practice, ed 7, Philadelphia, 2009, Saunders. Used with permission.)
Splint
Indication
Knee immobilizer splint Posterior ankle splint
Knee injuries Distal tibia and fibula injuries; ankle, tarsal, and metatarsal fractures Ankle fractures Toe fractures Femur fractures
Stirrup splint Buddy taping Traction splint
CHAPTER 19 Splints and Slings
TABLE 19-3 Lower-Extremity Splints
Modified from Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel G: An introduction to clinical emergency medicine, Cambridge, UK, 2005, Cambridge University Press; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, Saunders.
nearly all extremity requirements. Other malleable splints include ladder splints (i.e., pliable metal splints) and rolled-wire splints, both of which are readily available at most outdoor sporting goods stores5 (Figure 19-34). Given their weight, size, reliability, versatility, and cost, malleable splints have become a popular choice for the universal wilderness medical kit.12
Soft Splints A soft splint earns its name from the soft, padded material that is used to secure the injury. Soft splints include sling and swathe splints, pillow splints, and blanket-roll splints7 (see Figure 19-2). Soft splints allow for more laxity than rigid splints, but they can be combined with rigid splints for extra stability. Pillow splints are soft splints that are adapted for wrist and hand injuries. Their main advantages are ease of application and comfort.6 As with other soft splints, they allow for more movement at the fracture site, but are bulkier than other splints. Sling and swathe splinting can be used alone or in combination with other forms of splints. Shoulder, clavicle, upper arm, elbow, forearm, wrist, and even hand injuries are commonly stabilized with a sling and swathe. For a shoulder injury with which it is not possible to adduct the arm, a pillow (or similar material) can be used to bridge the empty space, with the sling supporting the arm and the swathe stabilizing it.6 This technique takes advantage of the chest wall to provide the splint foundation. Distal humeral injuries necessitate a sling and swathe splint in combination with rigid splints. Sling and swathe splinting is used alone for many clavicle, shoulder, and proximal humeral injuries. Advantages are its weight, portability, and improvisational versatility. Air splints are hybrid splints that are made from inflatable yet durable plastic. These splints are most often used for the elbow, knee, and ankle (Figure 19-35). They are placed around the injured extremity and inflated to the desired pressure and rigidity.5 They have the advantages of being lightweight and portable. Variable external pressures can be used to control hemorrhage. External pressure has the potential to limit distal perfusion. Air splints should be temporarily deflated (e.g., for 5 minutes every 90 minutes) to decrease the risk for ischemic damage.7 Air splint pressure varies with altitude and temperature. For these reasons, it is important to reevaluate neurovascular status during transport.12
FIGURE 19-18 Upper and lower body vacuum splints used for wilderness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff Department.)
A
B
“Click”
SAM Splints Malleable splints such as SAM splints37 no longer fall into the category of improvised splinting. These splints are commonly found in the standard wilderness medical kit. They are lightweight, reusable, versatile, and padded, and they are not affected by changes in pressure or temperature. They are also radiolucent to allow radiographs to be taken with the splint in place. The malleable SAM splint is pliable in its native form yet easily strengthened with creasing. The basic SAM splint adaptations are depicted in Figure 19-22. In addition, the SAM splint can be
C FIGURE 19-19 Application of the SAM pelvic sling. A, Remove all objects from the pockets. Place the sling under the patient’s hips. B, Place the black strap through the buckle, and pull it completely through. C, Hold the orange strap with one hand, and then pull the black strap in the opposite direction under tension until a click is heard. Maintain tension, and place the black strap against the sling surface to secure. (Courtesy SAM Medical Products.)
383
PART 4 INJURIES AND MEDICAL INTERVENTIONS
A
B
D
C
E
FIGURE 19-20 The Slishman femur traction splint. A, Apply the ankle strap. B, Apply the groin strap. C, Extend the middle pole from the outer side of the leg, and lock it in place for coarse adjustment. D, Pull the cord to apply traction. E, Lock the splint in place. F, Splint the injured extremity. (Courtesy Sam Slishman, MD.)
F
A
A
B
B
C FIGURE 19-22 Basic SAM splint adaptations. A, C-curve. B, Reverse C-curve. C, T-curve (maximum strength). (Courtesy SAM Medical Products.)
FIGURE 19-23 Shoulder splint. A, Fold a 36-inch splint into three equal sections. Fold the outer sections along the longitudinal axis, and leave the middle section flat. Hook the outer ends together to make a triangle splint. B, Place the triangle splint under the patient’s axilla to support the abducted arm. The splint can then be held in place by the patient or secured with wrap. (Courtesy SAM Medical Products.)
SAM
SPLINT
®
CHAPTER 19 Splints and Slings
A
B
D
C
E
FIGURE 19-24 Humeral shaft splint. A, Fold one-third of a 36-inch splint on itself. B, Curve the double-layer portion into a fishhook shape, and secure it with tape or wrap. C, Form a C-curve along the shank of the fishhook to create strength, and then mold it to the arm. D, Apply the splint to the arm. Fold any excess splint back on itself. E, Secure the splint with wrap, and apply a sling and swath splint for additional support. (Courtesy SAM Medical Products.)
B
A
D
E
C
F
G FIGURE 19-25 Dislocated elbow splint. A. Use the unaffected arm as a model, and extend a 36-inch splint from under the patient’s armpit to the knuckles. B, Fold under the portion of the splint that extends past the knuckles. C, Form a C-curve along the entire length of splint. D, Use your own arm as a template, and shape the splint. E, You may reverse the C-curve bends on the edges for more strength. F and G, Apply and secure the splint to the patient with wrap or tape. (Courtesy SAM Medical Products.)
385
PART 4 INJURIES AND MEDICAL INTERVENTIONS
A
D
B
E
C
F
G
FIGURE 19-26 Sugar-tong splint. A, Fold a 36-inch splint in one-half. B, To determine the proper length, fold the splint around the patient’s elbow to the knuckles. C, Form a C-curve in each one-half of the splint, but no more than two thirds down each one-half. D, Shape the splint to fit, using your own arm as a template. E, Pad any bony prominences around the wrist and elbow. F and G, Fit and secure the splint with wrap or tape. (Courtesy SAM Medical Products.)
molded to form an adequate C-spine collar (see Figures 19-7 and 19-8, online).
lie in less effectiveness compared with commercial splinting devices.12
Improvised Extremity Splints
Pelvic Splinting
Improvised splints can be made from branches, boards, padded pack straps, or rolled-up newspapers or magazines. Anatomic splints involve an uninjured neighboring body part, primarily a digit. Slings can also be made from unused clothes.5 In these cases, one need not pack additional materials. Disadvantages
Pelvic fractures are potentially life-threatening injuries.24 Splinting is essential for pain and hemorrhage control. Pelvic fractures are often difficult to diagnose in the field, but must be suspected with a high-force mechanism in the face of pelvic pain or altered sensorium. A pelvic compression device should be applied.12
A
B
C
D
E
F
G FIGURE 19-27 Volar wrist splint. A. Roll the end of a 9-inch splint for children or an 18-inch splint for adults over to provide comfort for the patient’s fingers. B, Apply a C-curve. C, Mold the splint into a position of function, using your own wrist as a template. D, Create a generous curve for the base of the thumb. E, Fold up the ulnar side for additional strength. F and G, Apply and secure the splint with wrap or tape. (Courtesy SAM Medical Products.)
386
B
C
D FIGURE 19-28 Ulnar gutter splint. A, Fold a 9-inch splint longitudinally. B, Mold the splint into a desired shape, using the ulnar aspect of your own wrist and hand as a template. C, Apply the splint to the patient. D, Make fine adjustments to the splint, and secure it with wrap or tape. (Courtesy SAM Medical Products.)
A
B
D
C
E
FIGURE 19-29 Thumb spica splint. A, Use a 9-inch splint. B, Use your hand and thumb to mold the splint to create a generous curve for the thumb. C, Add a reverse C-curve to strengthen the splint. D and E, Apply and secure splint with tape or wrap. (Courtesy SAM Medical Products.)
387
CHAPTER 19 Splints and Slings
A
Appropriate stabilization with such a splinting device slows hemorrhaging and stabilizes fracture fragments.6 “Open-book” fractures (i.e., diastasis of the pubic rami with posterior pelvic disruption) create a large surface area for potential hemorrhage. Circumferential compression of the pelvis is recommended for emergency stabilization.4 This can be accomplished by pelvic circumferential compression devices, a pneumatic antishock garment (PASG), or improvised techniques such as pelvic sheeting7 (see Figure 19-16, online). Optimal pelvic stabilization is achieved by applying a sling around both greater trochanters and the symphysis pubis.4 Pelvic circumferential devices are similar in function (see Figure 19-19). A pelvic compression device can be improvised in the wilderness. Sheets, jackets, and other long fabrics are readily available on most expeditions. The sheet or fabric is wrapped around the pelvis over the greater trochanters and the symphysis pubis and then pulled tight and secured to increase pressure at the wound and to decrease the potential space for hemorrhage. The PASG and the military antishock trouser, which were commonly used in the past, have generally fallen out of favor (Figure 19-36). Proponents of PASG and military antishock trouser use point to the position paper of the National Association of EMS Physicians for support. The paper states that the PASG is beneficial in the setting of a ruptured abdominal aortic aneurysm and that it is potentially beneficial in many other scenarios (e.g., hypotension from pelvic fractures, gynecologic bleeding, ruptured ectopic pregnancies, severe traumatic hypotension, and uncontrolled lower extremity hemorrhage).11 Postulated successful mechanisms for correcting hypotension include increasing peripheral vascular resistance, tamponade of local hemorrhage, and increasing blood return from the lower extremities.23 PASG disadvantages include prolonged scene time, pressure changes with altitude (e.g., potential compartment syndrome with air travel), and interference with normal pulmonary function.27 In addition, animal studies have demonstrated lactic acidosis after prolonged use. Rapid deflation may cause hypotension as a result of volume redistribution. Studies have not shown improvement in hospital duration, and others have actually shown increased mortality rates.9 PASGs are bulky and expensive. Absolute contraindications for PASG use include diaphragmatic rupture, penetrating thoracic injury, a splinted lower-extremity fracture, a gravid uterus, or abdominal evisceration.23 Thus the routine use of the PASG in the field is not recommended. In the case of isolated femur fracture, a PASG can be used, but other viable options are more readily available in the wilderness.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
A
B
C
FIGURE 19-30 Finger splint. A, Form a C-curve B, Place the affected finger into the curved splint, and then squeeze the tip to make a fingertip guard. C, Secure the splint with wrap or tape. (Courtesy SAM Medical Products.)
Hip and Femur Splinting Femur fractures result from high-force trauma. These fractures can be diagnosed clinically in the appropriate wilderness setting. Deformity, swelling, and tenderness along the thigh and in the face of significant trauma are highly suggestive of a femur fracture.15 Femur fractures produce significant hemorrhage; a closed femur fracture may bleed more than 1 L into the thigh.10 Femoral shaft fractures also have a high mortality rate that ranges from 20% to 54%.25 Traction splints minimize blood loss, pain, and other adverse sequelae while achieving realignment of bone fragments.6 Contraindications to traction splint placement are fractures that involve the knee, pelvis, or ankle, or that include damage
A
B
to the sciatic nerve.25 Unfortunately, such comorbidities are common with severe wilderness injuries, which makes it impossible or dangerous to anchor the traction splint.3 Controversy exists regarding whether a traction splint should be placed with an open femur fracture, but this is not a strict contraindication. An indication for traction splint placement is any suspected femur fracture in the nonambulatory patient.6 There are many femur traction splint devices, and all are based on the same principle: a rigid frame that anchors at the proximal pelvis and that extends traction beyond the distal heel. The proximal aspect is padded against the ischial tuberosity. Traction to the fractured femur is then applied with a heel strap that is anchored off of the distal frame. The thigh, knee, and leg are also secured with soft straps.12 Traction devices that have a halfring design (e.g., Thomas or Hare splints) can cause hip flexion (i.e., up to 30 degrees). This can cause incomplete fracture realignment unless the leg is elevated to match the angle.6 Traction splints that do not have a posterior half ring (e.g., Sager) do not compress the sciatic nerve and can be used with groin injuries. They can also be used for patients with pelvic fractures or for bilateral femur fractures by making use of two splints (i.e., one applied to each leg).31 Traction splint application is not always intuitive (Figures 19-20, 19-21, 19-37, and 19-38; Figure 19-21, online). Two rescuers are needed for proper placement.5 Manual traction should be applied to reduce the fracture until the splint can be placed.1 As with any splint placement, it is important to establish pain control, to check neurovascular status both before and after splint placement, and to fully explain the process to the conscious patient. After the proximal femur splint is in place, the thigh strap is fastened. The ankle harness is then placed just above the malleoli and attached to the distal splint. Traction (6.8 kg [15 lbs]) is applied, and the remaining straps are applied. After the traction splint is in place, the patient should be logrolled onto a backboard to minimize fracture fragment movement.5 Traction splint complications result from improper strap and splint placement and include sciatic or peroneal nerve injury, pressure wounds, hemorrhage and pain.7,12,25,31
Ankle Splinting C
D FIGURE 19-31 Thomas half-ring femur splint. A, The foot support is made by cutting an 8-inch section from the ski pole. Drill or puncture two holes that are 15 cm (6 inches) apart, with the entry hole being larger. Use duct tape, cord, and safety pins to secure. Create a half-ring support by placing two ski poles, handle facing handle, on the outer thirds of a 36-inch SAM splint. B, Roll the splint tightly around each handle, and secure with duct tape. Bend the splint so that the poles are now parallel and facing down. Firmly fit the pole ends through the foot support. C, Duct tape the thigh and calf supports, and reinforce them with cloth and elastic straps. An improvised ankle strap is required for traction. (Courtesy SAM Medical Products.)
388
Ankle sprains are common orthopedic injuries incurred during expeditions and the most common sprain.2 There are literally hundreds of examples of readily available over-the-counter ankle supports, braces, and splints. These include but are not limited to leather bracing, canvas bracing, air stirrups, air bladders, air casts and air boots, plastic splints with Velcro strapping, and malleable varieties, including wire ladder splints. On the basis of the high incidence of ankle sprains, it appears prudent to have a readily available lightweight ankle splint in one’s medical kit. The goal is to offer ankle support that will fit within the size constraints of the patient’s hiking boot. The time-tested alternative is athletic tape. The taped sprained ankle has talofibular ligament support (for a limited duration), and tape does not add significant weight to the medical kit. All wilderness health care providers should be adept at taping ankles.
Shoulder Dislocation Anterior shoulder dislocation is a common injury. The arm is most comfortable in an abducted position. This can be accomplished with a rolled blanket, a pillow, a jacket, or a SAM splint that has been fashioned into a triangle (Figure 19-23).
CHAPTER 19 Splints and Slings
SAM
SPLINT
NT
SA ® M LI
B
SP
SAM®
SPLIN T
SAM®
SPLIN T
A
C SAM
SAM
SAM
SA
M®
D
E F
G
FIGURE 19-32 Knee immobilizer splint. A, Fold a 36-inch splint in the center to create two equal lengths. Fan the halves so that the splint is twice as wide at one end as compared with the other. B, Apply tape to the top and middle of the splint to keep the fan shape. C, Create a second fan-shaped splint. D, Form a C-curve in each splint. E, The C-curves should appear as shown. F, Place the splints on each side of the knee. G, Secure the splint with tape. (Courtesy SAM Medical Products.)
Humeral Shaft Injury
Thumb Injuries
Humeral shaft fracture is often treated with a sling or with a sling and swathe splint alone. For pain control, a splint is often desirable (see Figure 19-24).
A thumb spica splint is used for suspected scaphoid (navicular) fractures, thumb dislocations and fractures, and ulnar collateral ligament injuries (see Figure 19-29).
Elbow Dislocation
Finger Injuries
A dislocated elbow can be reduced in the field with the appropriate analgesia and experience. The dislocated elbow can also be splinted in place and the patient transported for definitive care (see Figure 19-25).
Finger splints are used for finger fractures, fingertip injuries, and lacerations (see Figure 19-30).
Elbow Fracture A sugar-tong splint is useful for most elbow injuries. These most commonly include supracondylar, olecranon, and radial head fractures (see Figure 19-26).
A femur traction splint can be improvised in a variety of ways with a SAM splint. One practical wilderness example involves the use of ski poles and a SAM splint. An improvised version of a half-ring splint is made from two ski poles, a small piece of metal, and a 91.4-cm (36-inch) SAM splint (see Figure 19-31).
Wrist Fracture
Knee Injuries
The volar wrist splint is used for most wrist fractures, dislocations, sprains, lacerations, and other wrist injuries. A T-beam volar wrist splint (i.e., apply a T-curve to the folded SAM splint) can be used for greater support, when traveling over rough terrain, or when more support is desired (see Figure 19-27).
A knee immobilizer splint is used for knee injuries, patella tendon injuries, dislocations, and other severe ligamentous sprains when immobilization is required (see Figure 19-32).
Metatarsal Fractures
Long-leg splints are used for tibial and fibular fractures. Depending on the amount of stabilization needed, a single or double long-leg splint can be applied. The double long-leg splint offers more stabilization (see Figure 19-33).
Ulnar gutter splints are used for fourth and fifth metatarsal injuries and for corresponding digit injuries (see Figure 19-28).
Femur Fracture
Leg Fractures
389
PART 4 INJURIES AND MEDICAL INTERVENTIONS
B
A
SAM®
SPLINT
C
D
E
F
FIGURE 19-33 Single long-leg splint. A, Place padding around any bony prominences on both sides of the ankle. B, Make a C-curve out of 30 of the splint’s 36 inches, and leave the last 6 inches flat. C, Apply a reverse C-curve to the edges for extra strength. D, Place the splint against the outside of the leg, and fold the last 6 inches under the foot. E, Adjust the splint to fit the leg. F, Secure the splint with wrap or tape. (A double long-leg splint is made by repeating steps B to F so that the splints are on both sides of the leg.) (Courtesy SAM Medical Products.)
FIGURE 19-34 Pliable metal ladder splints. (Courtesy FernoWashington, Inc.)
FIGURE 19-36 Military antishock trouser/pneumatic garment. (Courtesy Common Cents EMS Supply.)
FIGURE 19-35 Lower-extremity air splint used for a wilderness rescue. (Courtesy Ed Gray.)
390
antishock
A
C
B
F
E
D
FIGURE 19-38 Applying the Sager traction splint. A, Position the splint between the patient’s legs, and rest the splint cushion against the ischial tuberosity. B, Fold down the number of comfort cushions needed to engage the ankle above the medial and lateral malleoli. C, Use the ankle straps to secure the splint snugly. D, Pull the control tabs to tightly engage the ankle harness against the crossbar. Grab the padded shaft of the splint with one hand and the traction handle with other, and then gently extend the inner shaft to obtain the desired traction. E, Adjust the thigh strap at the upper thigh securely. F, Firmly secure the elastic leg cravats. G, Apply the foot strap around the feet to prevent rotation. Check the patient for sensation and pulses. (Courtesy Minto Research and Development, Inc.)
CHAPTER 19 Splints and Slings
FIGURE 19-37 Ferno traction splint. A, Adjust the length of the splint to fit the patient. Use the patient’s uninjured leg to determine the desired length. B, One operator supports the injured leg and places the ankle wrap under the ankle. C, Center the foot, wrap the strap around the ankle, and secure it with the fastening strip. D, Support the leg, slide the splint under the injured leg until the pad rests against the lower pelvic bone, and then fasten the hip strap. E, Attach the S-hook to the D-ring, and apply traction. F, Reposition the splint, and then fasten the straps. (From Ferno-Washington Inc. Used with permission.)
B A
C
E
D
F
G 391
A
B
D
C
E
FIGURE 19-39 Ankle stirrup splint. A, Pad any bony prominences. B, Fold a 36-inch splint in half. C, Apply C-curves two thirds of the way down each half. Add reverse C-curves for strength. D, Fold the stirrup splint around the foot and ankle. E, Secure the splint with tape or wrap. (Courtesy SAM Medical Products.)
A
B
C
D
E
FIGURE 19-40 Figure-8 splint. A, Pad any bony prominences. B, Lay a 36-inch splint flat. Put the patient’s foot in middle, with the splint just in front of the heel. C, Conform one side of the splint around the ankle. D, Repeat with the other side of the splint around the opposite side of the ankle. Crimp to fit. E, Secure the splint with tape or wrap. (Courtesy SAM Medical Products.)
Ankle and Foot Injuries Ankle stirrup and figure-8 splints provide for the immobilization of ankle injuries. The ankle stirrup splint can also be used for fractures (Figures 19-39 and 19-40). The combination of an ankle stirrup splint and a figure-8 splint offers maximal support; this is done by first applying the figure-8 splint and then adding the ankle
stirrup splint last. The combination of the two splints provides greater stabilization and immobilization. This procedure could potentially be used for weight-bearing metatarsal fractures.30
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 20
Emergency Airway Management SWAMINATHA V. MAHADEVAN Emergency airway management encompasses assessment, establishment, and protection of the airway in combination with effective oxygenation and ventilation. Timely and effective airway management can literally mean the difference between life and death, and it takes precedence over all other clinical considerations. Airway management in the wilderness must often be provided in austere or unusual environments under less-than-ideal circumstances. Many of the resources that are readily accessible in a hospital or emergency department setting are not available in the wilderness, so improvisation may prove invaluable. 392
Airway Anatomy Internally, the airway is composed of many structures and welldefined spaces. It originates in the nasal and oral cavities (Figure 20-1). The nasal cavity extends from the nostrils to the posterior nares or choanae. Because resistance to airflow through the nose is almost twice that of the mouth, patients who require high flow rates (e.g., during exercise) often breathe through their mouths. The nasopharynx extends from the end of the nasal cavity to the level of the soft palate. Tonsillar lymphoid structures are the primary impediments to airflow through the nasopharynx. The
For online-only figures, please go to www.expertconsult.com
Nasopharynx
Hyoid bone Thyroid membrane Thyroid notch Laryngeal prominence Thyroid cartilage Cricothyroid membrane Cricoid cartilage Tracheal rings
Oral cavity
Oropharynx Epiglottis
Thyroid gland
Vallecula Laryngeal inlet Laryngopharynx
Larynx Glottis
FIGURE 20-1 Lateral airway anatomy. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)
oral cavity is bounded by the teeth anteriorly, hard and soft palates above, and the tongue below. The oropharynx, which communicates with the oral cavity and the nasopharynx, extends from the soft palate to the tip of the epiglottis. The tongue is the principal source of obstruction in the oropharynx. The oropharynx continues as the laryngopharynx (hypopharynx), which extends from the epiglottis to the upper border of the cricoid cartilage at the level of the C6 vertebral body. The larynx, which lies between the laryngopharynx and trachea, serves as an organ of phonation and a valve to protect the lower airway from aspiration. The larynx is made up of muscles, ligaments, and cartilages, including the thyroid, cricoid, arytenoids, corniculates, and epiglottis. The flexible epiglottis, which originates from the hyoid bone and base of the tongue, covers the glottis during swallowing and provides protection from aspiration. During laryngoscopy, the
FIGURE 20-2 External airway anatomy. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)
epiglottis is an important landmark for airway identification and laryngoscopic positioning. The vallecula is the space at the base of the tongue that is formed posteriorly by the epiglottis and anteriorly by the anterior pharyngeal wall. The laryngeal inlet is the opening to the larynx that is bounded by the epiglottis, aryepiglottic folds, and arytenoid cartilages. The glottis is the vocal apparatus, which is made up of the true and false vocal cords and the glottic opening, which is a triangular fissure between the vocal cords and the narrowest segment of the adult larynx. Externally identifiable landmarks are also important to airway assessment and management (Figure 20-2). The mentum is the anterior aspect of the mandible that forms the tip of the chin. The hyoid bone forms the base of the floor of the mouth. The thyroid cartilage forms the laryngeal prominence (i.e., the “Adam’s apple”) and the thyroid notch. The cricoid cartilage, which lies inferior to the thyroid cartilage, forms a complete ring that provides structural support to the lower airway. The cricothyroid membrane lies between the thyroid and cricoid cartilages and serves as an important site for surgical airway management. Knowledge of the anatomic differences between adults and infants is integral to effective pediatric airway management. These important differences are summarized in Table 20-1 and Figure 20-3.
TABLE 20-1 Anatomic Airway Differences Between Children and Adults Anatomy
Clinical Significance
Large intraoral tongue that occupies a relatively large portion of the oral cavity High tracheal opening: C1 in infancy as compared with C3 or C4 at the age of 7 years and C4 or C5 in adulthood Large occiput that may cause flexion of the airway; large tongue that easily collapses against the posterior pharynx
High anterior airway position of the glottic opening as compared with that of an adult Straight blade preferred over curved blade to push distensible anatomy out of the way to visualize the larynx Sniffing position is preferred; the large occiput actually elevates the head into the sniffing position in most infants and children; a towel may be required under the shoulders to elevate the torso relative to the head in small infants Uncuffed tubes provide an adequate seal, because they fit snugly at the level of the cricoid ring; correct tube size is essential, because variable expansion cuffed tubes are not used <2 yr old, high anterior 2-8 yr old, transition >8 yr old, small adult Blind nasotracheal intubation not indicated for children; nasotracheal intubation failure
Cricoid ring is the narrowest portion of the trachea as compared with the vocal cords in adults Consistent anatomic variations with age, with fewer abnormal variations related to body habitus, arthritis, or chronic disease Large tonsils and adenoids may bleed; more acute angle between the epiglottis and the laryngeal opening results in nasotracheal intubation attempt failures Small cricothyroid membrane
Needle cricothyroidotomy difficult and surgical cricothyroidotomy impossible in infants and small children
Modified from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.
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Nasal cavity
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Tongue
Vocal cords
Epiglottis
Cricoid membrane Cricoid ring
Junction of chin and neck Infant
Vocal cords
Tongue
Cricoid membrane
Epiglottis
Cricoid ring Junction of chin and neck
Adult FIGURE 20-3 Anatomic airway differences between infants and adults. The anatomic differences particular to infants include the following: (1) a higher and more anterior position for the glottic opening (note the relationship of the vocal cords to the chin–neck junction); (2) a relatively larger tongue in the infant that lies between the mouth and the glottic opening; (3) a relatively larger and more floppy epiglottis in the infant; (4) the cricoid ring is the narrowest portion of the pediatric airway; in adults, the narrowest portion is the vocal cords; (5) the position and size of the cricothyroid membrane in the infant; (6) the sharper and more difficult angle for blind nasotracheal intubation; and (7) the larger relative size of the occiput in the infant. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)
Assessment of the Airway and Recognition of Airway Compromise Assessment of the airway begins with an evaluation of airway patency and respiratory function. The goal is to determine whether the airway is patent and protected and whether breathing is present and adequate. This is accomplished by inspection, auscultation, and palpation, which is commonly known as the “look, listen, and feel” approach. Visual signs of airway compromise include agitation, obtundation, and cyanosis. Blue, gray, or ashen skin—especially around the eyes, lips, and nail beds—is a worrisome finding. Significant airway compromise may manifest without cyanosis; examples include an allergic reaction with upper airway edema and vasodilation (causing flushed red skin) and unconsciousness as a result of carbon monoxide poisoning. Bradypnea, tachypnea, and irregular respirations may be signs of impending respiratory compromise. Breathing that is shallow, 394
deep, or labored may indicate respiratory insufficiency. Respiratory muscle fatigue may result in recruitment of the accessory muscles of respiration; this is clinically manifested as suprasternal, supraclavicular, or intercostal retractions. Traumatic injury to the chest (e.g., flail chest) or an aspirated foreign body may result in paradoxic or discordant chest wall movement. In children, visual signs of airway compromise and respiratory distress include tachypnea, cyanosis, drooling, nasal flaring, and intercostal retractions. A child with severe upper airway obstruction may sit upright with the head tilted back (i.e., “sniffing” position) to straighten the airway and reduce occlusion. A child with severe lower airway obstruction may sit up and lean forward on outstretched arms (i.e., “tripod” position) to augment accessory muscle function. Under most circumstances, hearing the victim speak with a normal voice suggests that the airway is adequate at that moment. Unusual sounds or noisy respirations may be present with partial airway obstruction. Snoring indicates partial airway obstruction at the pharyngeal level; gurgling may be heard with blood or secretions in the airway; stridor may be associated with partial airway obstruction at the level of the larynx (inspiratory stridor) or at the level of the trachea (expiratory stridor); hoarseness suggests a laryngeal process. The central face and mandible should be assessed for structural integrity, because injuries to these structures may lead to airway distortion and compromise. The anterior neck should be carefully inspected for penetrating wounds, asymmetry, or swelling that may herald impending airway compromise. The palpation of subcutaneous air suggests direct airway injury. In the unconscious victim, feel for air movement at the mouth and nose. Open the mouth to inspect the upper airway, taking care not to extend or rotate the neck. Identify and remove any vomitus, blood, or other foreign bodies. Look for swelling, bleeding, or other abnormalities of the oropharynx. The gentle use of a tongue blade may facilitate this task. The victim’s ability to spontaneously swallow and handle secretions is an important indicator of intact airway protective mechanisms. In the unconscious victim, absence of a gag reflex has traditionally been linked with loss of protective airway reflexes. Auscultation of the lung fields should demonstrate clear and equal breath sounds. Diminished breath sounds may result from a pneumothorax, hemothorax, or pleural effusion. Wheezing and dyspnea are often associated with lower airway obstruction.
Opening the Airway Opening the airway and ensuring airway patency are essential for adequate oxygenation and ventilation; these are the first priorities of airway management. The conscious victim uses protective reflexes and the musculature of the upper airway to maintain a patent airway and to protect against aspiration of foreign substances, gastric contents, or secretions. In the severely ill, compromised, or unconscious victim, these protective airway mechanisms may be impaired or absent. Upper airway obstruction in the unconscious victim most commonly results from posterior displacement of the tongue and the epiglottis at the level of the pharynx and the larynx. Head positioning, manual airway techniques, and mechanical airway adjuncts may be employed to alleviate upper airway obstruction.
HEAD POSITIONING If the mechanism of injury or physical examination raises concern for cervical spine injury, the head and neck should be stabilized in the neutral position. Care should be taken to not flex, extend, or rotate the victim’s head. After cervical spine immobilization, the airway should be reevaluated for obstruction. The optimal head position for airway alignment and patency varies with age. A supine infant’s large occiput contributes to flexion of the head and neck and resultant airway obstruction; this may be alleviated by elevating the shoulders with a small towel (Figure 20-4). In children, slightly extending the head into the sniffing position helps to relieve airway obstruction. In adults,
Infant
Small child
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A
Older child/adult
B FIGURE 20-4 A, The clinical determination of optimal airway alignment with the use of a line passing through the external auditory canal and anterior to the shoulder. B, The application of the line to determine the optimal position. In this small child, the occiput obviates the need for head support, yet the occiput is not so large as to require support of the shoulders. Note that the line traversing the external auditory canal passes anterior to the shoulders. With only slight extension of the head on the atlanto-occipital joint, the sniffing position is achieved. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)
placing a folded towel or article of clothing under the occiput, which flexes the neck at the torso, followed by gentle hyper extension of the head at the atlanto-occipital joint, provides for the optimal alignment of the airway axes.
MANUAL AIRWAY TECHNIQUES Manual airway techniques are effective but often require con tinuous involvement of a single provider to maintain airway patency.
FIGURE 20-5 Head tilt with chin lift. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)
An alternative to piercing the patient’s lower lip is to pass a string through the safety pins and then secure the end of the string to the victim’s shirt button or jacket zipper (Figure 20-8), thereby exerting traction on the tongue.
MECHANICAL AIRWAY ADJUNCTS Several airway adjuncts are available to maintain airway patency while freeing up the health care provider to perform other duties. Oropharyngeal Airway The oropharyngeal airway (OPA) is an S-shaped device that is designed to hold the tongue away from the posterior pharyngeal wall (Figure 20-9). When the OPA is properly placed, it prevents the tongue from obstructing the glottis, and also provides an air
Head Tilt With Chin Lift The head tilt with chin lift (Figure 20-5) is a simple and effective technique for opening the airway. The palm of one hand is placed on the victim’s forehead and applies firm backward pressure to tilt the head back. Simultaneously, the fingers of the other hand are placed under the bony part of the chin and lifted to bring the chin forward. These fingers support the jaw and maintain the head-tilt position. This maneuver extends the neck and should not be used if cervical spine injury is a concern. Jaw Thrust With Head Tilt If a cervical spine injury is not suspected, the jaw thrust with head tilt maneuver may be used to gain additional forward displacement of the mandible. Position yourself at the top of the victim’s head, and then grasp the angles of the mandible with both hands and lift to displace the jaw forward while tilting the head back. Jaw Thrust Without Head Tilt If a cervical spine injury is suspected or cannot be excluded, the jaw thrust without head tilt (Figure 20-6) can be performed while maintaining neutral cervical spine alignment. With this maneuver, the jaw thrust is performed without extending or rotating the neck. Tongue Traction If the patient is unconscious or in extremis, the airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins (Figure 20-7).
FIGURE 20-6 Jaw thrust without head tilt. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)
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FIGURE 20-7 Tongue traction. The airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins.
channel and suction conduit through the mouth. These devices are most effective for unconscious and semiconscious victims who lack a gag reflex or cough. Use of an OPA in a victim with a gag reflex or cough is contraindicated, because the OPA may stimulate retching, vomiting, or laryngospasm. OPAs are made of disposable plastic, and come in varying sizes to accommodate children and adults. The size is based on the distance in millimeters from the flange to the distal tip. The proper OPA size is estimated by placing the OPA’s flange at the corner of the mouth so that the bite-block segment is parallel with the victim’s hard palate; the distal tip of the airway should reach the angle of the jaw. Two types of OPAs are commonly employed. The Guedel makes use of a tubular design, whereas the Berman is distinguished by having airway channels on each side. Technique for insertion: 1. Open the mouth and clear the pharynx of any secretions, blood, or vomitus. Remove dentures or partial dental plates, if present. 2. In an adult or older child, insert the OPA upside down or at a 90-degree angle to avoid pushing the tongue posteriorly during insertion. Slide it gently along the roof of the mouth. As the OPA is inserted past the uvula or the crest
FIGURE 20-8 Tongue traction. An alternative to piercing the lower lip is to pass a string through the safety pins and then exert traction on the tongue by securing the end of the string to the victim’s shirt button or jacket zipper.
396
FIGURE 20-9 Oropharyngeal airway. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)
of the tongue, rotate it so that the tip points down the victim’s throat. 3. In a child, grasp the tongue and gently pull it forward or use a tongue blade to displace it inferiorly and anteriorly. Insert the OPA with the tip pointing toward the tongue and throat (i.e., the intended position after placement). 4. The OPA flange should rest against the victim’s lips, and the distal portion should rest on the posterior pharyngeal wall. If the OPA is too short, it may displace the tongue into the hypopharynx and occlude the airway. If the OPA is too long, it may displace the epiglottis and thereby cause an airway obstruction. Nasopharyngeal Airway The nasopharyngeal airway (NPA) is an uncuffed trumpet-like tube that provides a conduit for airflow between the nares and the pharynx (Figure 20-10). The NPA is inserted through the nose rather than the mouth, and it has a flange at the outer end to prevent displacement or slippage beyond the nostril. These devices are better tolerated than are OPAs, and they are commonly used with intoxicated or semiconscious victims. They are also effective when trauma, trismus (i.e., clenched teeth), or other obstacles (e.g., wiring of the teeth) preclude OPA placement. NPAs are contraindicated in victims with basilar skull or facial fractures, because inadvertent intracranial placement may occur.
FIGURE 20-10 Nasopharyngeal airway. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)
Technique for insertion: 1. Lubricate the nasopharyngeal airway with a water-soluble lubricant to minimize resistance in the nasal cavity. Do not use petroleum jelly or a non–water-based lubricant. 2. If the NPA has a beveled (angled) edge, place the airway in the nostril with the bevel directed toward the nasal septum. 3. Gently insert the NPA straight back along the floor of the nasal passage (i.e., perpendicular to the coronal plane of the face). 4. If resistance is met, rotate the tube slightly, reattempt insertion through the other nostril, or try a smaller-diameter tube. Do not force insertion of the tube, because injury to the nasal mucosa can result in bleeding. 5. After insertion, the NPA flange should rest on the victim’s nostril, and the distal portion of the airway should rest in the posterior pharynx, behind the tongue. Any flexible tube of appropriate diameter and length can be used as an improvisational substitute for the NPA. Examples include a Foley catheter, radiator hose, solar shower hose, siphon tubing, or an inflation hose from a kayak flotation bag or sport pouch. An endotracheal tube (ETT) can be shortened and then softened in warm water to substitute for a commercial nasal trumpet. The flange can be improvised with the use of a safety pin through the nostril end of the tube (Figure 20-11). Although OPAs and NPAs help to establish artificial airways, they do not provide definitive airway protection from aspiration.
RECOVERY POSITION In the spontaneously breathing unconscious victim who is not at risk for cervical spine injury, the recovery position (Figure 20-12) allows for airway patency while reducing the risk of aspiration. In the recovery position, the tongue is less likely to fall back and occlude the airway, and vomitus is more likely to be expelled than inhaled. Even a diminutive rescuer can place a large person in the recovery position if the proper technique is employed.
Foreign-Body Airway Obstruction Foreign bodies—most commonly a piece of meat—may cause partial or complete airway obstruction. A victim with partial airway obstruction can usually phonate or produce a forceful
FIGURE 20-11 Improvised nasal trumpet.
CHAPTER 20 Emergency Airway Management
NPAs made of soft and pliable rubber or plastic come in varying sizes to accommodate children and adults. Sizes (as indicated by internal diameter) range from 12 to 36 Fr. Proper NPA length is determined by measuring the distance from the tip of the patient’s nose to the tragus of the patient’s ear.
FIGURE 20-12 Recovery position.
cough in an attempt to expel the foreign body. When encountering a victim with a partially obstructed airway, if air exchange is adequate, do not interfere with the person’s attempts to clear the airway. Encourage forceful coughing, and closely monitor the victim’s condition. If the obstruction persists or if air exchange worsens or becomes inadequate, the victim should be managed as if a complete airway obstruction exists. Worrisome findings that should prompt immediate aggressive airway management include a weak or ineffective cough, increased respiratory difficulty, decreased air movement, and cyanosis. A person with a complete airway obstruction cannot speak (aphonia), exchange air, or cough. The person will often grasp the neck (i.e., the universal distress signal for choking) and open the mouth widely. The unconscious victim with complete airway obstruction will not demonstrate any typical chest movements or other signs of adequate air exchange. Individuals with complete airway obstruction from a foreign body require immediate medical attention. Failure to rapidly relieve the obstruction can lead to cardiac arrest. A complete summary of the treatment for complete airway obstruction caused by foreign bodies in adults and children is provided in Table 20-2.
Suction All sick or injured victims are at risk for airway obstruction and pulmonary aspiration, typically of gastric contents or blood. Lifesaving interventions, such as bag-mask ventilation (BMV), may increase this risk. Suction is essential for removal of vomitus, secretions, blood, and foreign bodies that may occlude the airway or increase the risk for pulmonary aspiration. Portable suction devices, which are available from a number of manufacturers, are ideal for the wilderness setting. These portable units should provide enough vacuum flow for adequate pharyngeal suction. Portable devices may be powered by oxygen, air, or electricity, or they may be manually powered (Figure 20-13, online). Hand-operated units are popular because they are lightweight, compact, reliable, and inexpensive. All units should have large-bore, nonkinking suction tubing, an unbreakable collection container, and a sterile disposable suction catheter. Flexible (i.e., “French”) suction catheters are used to suction the nose, mouth, and oropharynx, whereas rigid suction catheters are used to suction the mouth and the oropharynx. These suction catheters should not be inserted beyond the base of the tongue. Adults should not be suctioned for more than 10 to 15 sec to prevent oxygen deprivation; children should be suctioned for less time. Care should be taken when using rigid suction catheters in children, because stimulation of the oropharynx may 397
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TABLE 20-2 Relief of Choking Adults and Children >1 Year Old
Children <1 Year Old
Signs
Rescuer Actions
Signs
Rescuer Actions
Mild airway obstruction
Good air exchange Responsive and can cough forcefully May wheeze between coughs
Good air exchange Responsive and can cough forcefully May wheeze between coughs
1. Do not interfere with the victim’s own attempts to expel the foreign body, but stay with the victim and monitor his or her condition. 2. If mild airway obstruction persists, activate EMS.
Severe airway obstruction
Poor or no air exchange Weak and ineffective cough or no cough at all High-pitched noise when inhaling or no noise at all Increased respiratory difficulty Possible cyanosis (turning blue) Unable to speak Clutching neck with thumb and fingers (universal choking sign) Unable to move air
1. As long as good air exchange continues, encourage the victim to continue spontaneous coughing and breathing efforts. 2. Do not interfere with the victim’s own attempts to expel the foreign body, but stay with the victim and monitor his or her condition. 3. If mild airway obstruction persists, activate EMS. 1. Ask the victim if he or she is choking. If the victim nods yes and cannot talk, severe airway obstruction is present, and you must activate EMS. 2. Perform abdominal thrusts (Heimlich maneuver). It may be necessary to repeat the thrusts several times to clear the airway. 3. Repeat until the object is expelled from the airway or the victim becomes unresponsive. 4. If the patient is pregnant or obese, perform chest thrusts instead.
Poor or no air exchange Weak and ineffective cough or no cough at all High-pitched noise when inhaling or no noise at all Increased respiratory difficulty Possible cyanosis (turning blue) Unable to cry Unable to move air
Choking in the unresponsive victim
Choking victims may be initially responsive and then become unresponsive. In this circumstance, you know that the choking has caused the victim’s symptoms.
Adults 1. Activate EMS. 2. Open the airway. 3. Remove the object if you see it. Children from 1 year old to puberty 1. Open the airway. 2. Remove the object if you see it. 3. Begin CPR. 4. After 2 min (or five cycles) of CPR, activate EMS.
Choking infants may be initially responsive and then become unresponsive. In this circumstance, you know that the choking has caused the victim’s symptoms.
1. If the victim cannot make any sounds or breathe, severe airway obstruction is present, and you must activate EMS. 2. Deliver five forceful back slaps between the victim’s shoulder blades with the use of the heel of your hand. 3. If the airway remains obstructed, perform five quick downward chest thrusts just below the nipple line at a rate of one per second. 4. Repeat the back slaps and chest thrusts until the object is removed or the victim becomes unresponsive. 1. Place the infant onto a flat surface. 2. Open the airway. 3. Remove the object if you see it. 4. Do not perform blind finger sweeps, because the foreign body may be pushed back into the airway, thus causing further obstruction or injury. 5. Begin CPR. 6. Each time you open the airway, look for the object, and remove it if you see it. 7. After 2 min (or five cycles) of CPR, activate EMS.
Modified from the American Heart Association: BLS for healthcare providers, Dallas, 2006, American Heart Association. CPR, Cardiopulmonary resuscitation; EMS, emergency medical services.
cause bradycardia. A bulb syringe may be used to suction the nose and mouth of infants up to 4 months old because they are obligate nose breathers. If time permits and supplies are available, a “mucus trap” suction device can be improvised from a jar with two holes poked in its lid and two tubes or straws duct taped into the holes (Figure 20-14). One straw goes to the rescuer, who provides suction, and the other is directed toward whatever has accumulated in the airway. The jar serves to trap the removed secretions, thereby preventing the rescuer from suctioning 398
bodily fluids or foreign substances (e.g., mud) directly into his or her mouth. In the absence of suction or in the presence of large pieces of foreign material, visible debris can be swept from the mouth of an unconscious victim with the use of a finger that is gloved or wrapped in cloth. When using this “finger-sweep” technique with infants and children, be sure to use your little finger. Never attempt to blindly sweep the mouth if you do not see debris. In addition, do not probe the mouth of a conscious victim, because this may precipitate gagging, vomiting, and aspiration. Victims
Tubing
Jar
FIGURE 20-14 Improvised mucus trap suction device.
without risk for cervical spine injury may be placed in the recovery position (i.e., with the head turned to the side) to facilitate clearing the mouth.
Supplemental Oxygen Supplemental oxygen therapy should be provided to all sick or injured people with cardiac disease, respiratory distress, shock, or trauma, even if their measured arterial oxygen tension is normal. Start with a high oxygen concentration and then titrate downward to maintain adequate oxygenation. Although oxygen should never be withheld from a hypoxic patient with respiratory distress, care should be exercised when administering oxygen to patients with chronic hypercarbia (e.g., patients with chronic obstructive pulmonary disease). Unmonitored treatment of such patients with high oxygen concentrations can result in respiratory depression from diminished hypoxic ventilatory drive. A variety of oxygen delivery techniques may be employed, depending on the desired oxygen concentration and clinical circumstances (see Chapter 76).
Ventilation Even with an open airway and supplemental oxygen, a person who is not adequately ventilating cannot conduct sufficient gas exchange. Adequate ventilation implies the inhalation of enough air to deliver oxygen to the alveoli and exhalation of enough air to facilitate the removal of carbon dioxide. The sequence of interventions for the inadequately ventilating victim is opening the airway and then providing positive-pressure ventilation (i.e., via mouth-to-mouth, mouth-to-nose, mouth-to-mask, or BMV). It is advisable to use barrier protection (e.g., a face shield) when performing mouth-to-mouth or mouth-to-nose ventilation. Face shields are clear plastic or silicone sheets that feature a centrally located one-way valve. They are placed over a victim’s face to allow rescue breathing while preventing direct contact with the victim. Face shields are compact, flexible, portable, and manufactured by a number of companies.
RESCUE BREATHING Rescue breathing techniques that make use of exhaled air from the rescuer will deliver approximately 16% to 17% inspired oxygen concentration to the victim, ideally producing an alveolar oxygen tension of 80 mm Hg. Mouth-to-Mouth Ventilation Mouth-to-mouth ventilation is an efficient approach to assisting ventilation. Failure to use a barrier device during mouth-to-mouth ventilation places the rescuer at risk for exposure to infectious bodily fluids. Technique: 1. Open the airway using the head tilt with chin lift approach if cervical spine trauma is not suspected.
Mouth-to-Nose Ventilation Some people have conditions (e.g., injuries to the mouth or mandible, missing teeth or dentures) that make mouth-to-mouth ventilation ineffective. Under such circumstances, mouth-to-nose ventilation should be considered. The mouth-to-nose technique is similar to mouth-to-mouth ventilation, with a few specific differences. Technique: 1. Open the airway using the head tilt with chin lift approach if cervical spine trauma is not suspected. 2. The victim’s nose is left open. 3. Maintain the head tilt with the heel of one hand placed on the victim’s forehead. 4. Support the victim’s chin with the other hand while sealing the victim’s lips (i.e., closing the mouth) with the thumb and forefinger. 5. Take a deep breath. 6. Place your mouth around the victim’s, nose and make a tight seal with your lips against the victim’s face. 7. Exhale slowly into the victim’s nose until you see the victim’s chest rise and feel resistance to the flow of your breath. 8. Break contact with the victim’s nose, and open the victim’s mouth to allow passive exhalation. Mouth-to-Mask Ventilation Mouth-to-mask ventilation is the safest and most effective technique for rescue breathing (Figure 20-15). The pocket face mask or a similar barrier device allows the rescuer to provide ventilation without making direct contact with the victim’s mouth and nose. The mask has a one-way valve in the stem to prevent exhaled gases and bodily fluids from reaching the health care provider. In addition, a disposable high-efficiency particulate air filter may be inserted into the pocket mask to trap infectious air droplets and secretions. The pocket face mask is made of a soft plastic material and can be folded and carried in a pocket. Some masks are available with an oxygen inlet to allow for supplemental oxygen administration. These devices are available in a number of sizes. Technique: 1. Open the airway using the head tilt with chin lift approach if cervical spine trauma is not suspected. 2. Connect the one-way valve to the mask. 3. If available, connect oxygen tubing to the inlet port, and set the flow rate at 15 L/min. 4. Position yourself at the head of the victim. 5. Clear the victim’s airway of vomitus, secretions, and foreign bodies, if necessary. 6. Insert an oral or nasopharyngeal airway. 7. Place the mask on the victim’s face. 8. Apply pressure to both sides of the mask with the thumb side of the palms to create an airtight seal. Apply upward pressure to the mandible (i.e., jaw thrust) using the index, middle, and ring fingers of both hands while maintaining a head tilt. 9. Take a deep breath and exhale into the port of the one-way valve, and observe for chest rise. 10. Allow the victim to passively exhale between breaths. 399
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Duct tape
2. If needed, clear the airway of vomitus, secretions, and foreign bodies. 3. Pinch the victim’s nostrils closed with the finger and thumb of one hand; the heel of that same hand may be placed on the forehead to maintain the head tilt. 4. Support the victim’s chin with the other hand, and hold the victim’s mouth slightly open. 5. Take a deep breath. 6. Place your mouth around the victim’s mouth, which should be open, and make a tight seal with your lips against the victim’s face. 7. Exhale slowly into the victim’s mouth until you see the victim’s chest rise and feel resistance to the flow of your breath. 8. Break contact with the victim’s mouth to allow passive exhalation.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
transferred by BMV is a clinical estimate that is based on patient weight.
Definitive Airway Management The presence of a definitive airway implies patency and protection. Provision of a definitive airway requires a tube in the trachea with the cuff inflated, secured in place, and attached to an oxygen-rich ventilation device. Whether in the wilderness or at the hospital, inability or failure to secure a timely and definitive airway can lead to disastrous or fatal consequences for the victim. Approaches to definitive airway management include immediate oral endotracheal intubation, awake oral intubation, rapid sequence oral intubation, nasotracheal intubation, and surgical airways (e.g., cricothyrotomy). Although the ultimate decision to endotracheally intubate a patient can be complicated and may depend on a variety of clinical factors, several clinical situations mandate definitive airway management: (1) failure of ventilation or oxygenation; (2) the patient’s inability to maintain or protect the airway; (3) the potential for deterioration on the basis of the patient’s clinical presentation; and (4) patient safety and protection. FIGURE 20-15 Rescuer using mouth-to-mask ventilation. The rescuer is providing rescue breathing with a face mask and supplemental oxygen during cardiopulmonary resuscitation. The rescuer is using the cephalic technique (i.e., the rescuer is positioned at the top of the victim’s head). Both of the rescuer’s hands are used to hold the mask securely in position while keeping the victim’s airway open. The rescuer’s thumbs and forefingers hold the mask in place while the third, fourth, and fifth fingers of each hand lift the jaw (i.e., jaw thrust) and maintain an open airway with the head tilted. Alternatively, the thumbs and a portion of the rescuer’s palms can anchor the mask, and the index and remaining fingers can lift the jaw and hold it against the mask. (Redrawn from American Heart Association, International Liaison Committee on Resuscitation: Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 3: Adjuncts for oxygenation, ventilation and airway control, Circulation 102:I95, 2000.)
BAG-MASK VENTILATION The self-inflating ventilation bag with face mask (i.e., the BMV device) provides a means for emergency ventilation with high concentrations of oxygen. The device is equipped with several valves that allow coordinated airflow into and out of the victim. This includes a one-way valve that prevents exhaled air from reentering the victim’s lungs (Figure 20-16). When it is attached to a high-flow oxygen source (15 L/min), the BMV device can supply an oxygen concentration of nearly 100%. The adapter of the face mask is interchangeable with an ETT, so the same bag can be used after intubation. Competence with a BMV device is a vital emergency skill and prerequisite to the use of paralytic agents for endotracheal intubation. When using the single-hand mask hold technique, substantial proficiency is required to use only one hand to maintain an adequate mask seal, to position the victim’s head, and to ensure airway patency while using the other hand to ventilate with the proper tidal volume, neither underventilating or hyperventilating the patient. Although the mastery of solo BMV technique is imperative, recruitment of another individual allows one person to perform a jaw thrust and to ensure a good mask seal with both hands while the second individual squeezes the bag. Successful BMV depends on an adequate mask seal and a patent airway. Placement of an oral airway should always be considered before BMV. Slow and gentle ventilation minimizes the risk for gastric inflation and subsequent regurgitation. The efficacy of BMV can be determined by watching the chest rise and fall, feeling resistance in the bag, and monitoring the victim’s oxygen saturation. Smaller BMV devices are employed for infants and children to prevent overinflation and subsequent barotrauma. In the absence of a BMV device that precisely regulates the volume of air transferred by the device, the amount of air 400
A
B FIGURE 20-16 Detailed view of a bag-mask ventilation device. A, The rescuer provides ventilation with a bag and mask attached to an oxygen supply. The rescuer is using the E-C technique to hold the mask to the face by creating a “C” with the thumb and forefinger while lifting the jaw along the bony portion of the mandible with the last three fingers of the same hand; these fingers make the “E.” The second hand squeezes the bag while the rescuer watches the victim’s chest to ensure that the chest rises with each ventilation. The rescuer is keeping the victim’s airway open with both a head tilt and a jaw thrust. B, Details of a bag-mask ventilation system with supplemental oxygen. The system consists of a self-refilling bag with an oxygen inlet; either a no pop-off valve or a pop-off valve (as shown) that can be disabled during resuscitation to ensure the delivery of adequate tidal volumes despite high pressures; and standard fittings (in this case, the bag is joined with a standard fitting to a mask). This system is capable of delivering high concentrations of oxygen, because it contains an oxygen reservoir. If additional gas is required during ventilation, it is drawn from the oxygen reservoir rather than from room air so that a high concentration of oxygen can be delivered during ventilation. (Redrawn from American Heart Association, International Liaison Committee on Resuscitation: Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 3: Adjuncts for oxygenation, ventilation and airway control, Circulation 102:I95, 2000.)
Intubation
Time
Action
Zero minus 10 min Zero minus 5 min Zero minus 3 min —Time zero— Zero plus 20-30 sec Zero plus 45 sec Zero plus 45 sec Zero plus 1 min
Preparation Preoxygenation Pretreatment Paralysis with induction Protection and positioning Placement Proof Postintubation management
IMMEDIATE ORAL INTUBATION (CRASH INTUBATION) Individuals who present with respiratory arrest, agonal respirations, or deep unresponsiveness require immediate oral intu bation without the use of paralytic or sedative medications. Advantages of crash intubation are technical ease and rapidity. Disadvantages include the potential for increasing intracranial pressure from the stress of intubation and inducing vomiting and subsequent aspiration.
AWAKE ORAL INTUBATION Awake oral intubation is an approach that makes use of titrated intravenous sedation and liberal topical airway anesthesia before inspection of or intubation of an awake victim’s airway. This approach conveniently allows for preservation of the victim’s protective airway reflexes and spontaneous respirations while the laryngoscopist takes a gentle “awake” look at the glottis, vocal cords, and internal airway anatomy. The decision to intubate the victim immediately or to perform a controlled rapid sequence oral intubation depends on the potential for progression of airway difficulty or compromise. During the “awake” look, the clinician might elect to intubate a victim with an airway burn or anaphylaxis with progressive airway swelling, because that moment may be the most opportune time for airway management.
is limited, a patient may take eight vital capacity (i.e., largest possible) breaths in rapid succession from a 100% oxygen source to quickly preoxygenate. The time to desaturation after preoxygenation is determined by the duration of preoxygenation as well as by the type of victim. Young children, pregnant women, and obese adults tend to desaturate more rapidly than do normalsized adults. Pretreatment During RSI, the act of laryngoscopy as well as use of succinylcholine, which is a depolarizing neuromuscular blocking agent, can lead to a number of adverse effects, such as bronchospasm in patients with reactive airway disease, increased intracranial pressure, increased intraocular pressure, increased intragastric pressure, increased sympathetic discharge, and bradycardia (especially in children). Certain pretreatment medications may be administered before laryngoscopy to mitigate these adverse effects. These medications and their indications, mechanisms of actions, and doses are summarized in Table 20-5. Paralysis with Induction The next step in RSI is rapid intravenous administration of an induction agent to produce a complete loss of consciousness, which is followed immediately by administration of a neuro muscular blocking agent (NMBA) to induce complete motor paralysis. Induction agents. All patients, with few exceptions, should receive an induction agent before neuromuscular blockade. Paralyzing a patient without providing adequate sedation can lead to detrimental physiologic and undesirable psychological sequelae. In addition induction agents that are administered in combination with NMBAs enhance muscle relaxation, thereby creating optimal intubating conditions.
TABLE 20-4 SOAP ME Mnemonic Suction Oxygen
RAPID SEQUENCE ORAL INTUBATION Rapid sequence intubation (RSI) is a coordinated series of procedures that allows for the rapid intubation of a victim without interposed BMV. Because victims who require emergent intubation may not have fasted, BMV can inadvertently lead to gastric distention, regurgitation, and aspiration. To perform RSI, the victim is first preoxygenated to allow for a period of apnea without interposed assisted ventilation. Sequential administration of an induction agent and a rapidly acting neuromuscular blocking agent induces a state of unconsciousness and paralysis, respectively. This allows the victim to be intubated without the need for BMV. The steps that make up RSI can be thought of as “the eight P’s” (Table 20-3).
Airway equipment
Preparation Before RSI, careful preparation is essential to achieve success. The mnemonic SOAP ME summarizes the necessary preparatory steps and essential equipment (Table 20-4). Preoxygenation During RSI, the process of direct laryngoscopy and ETT placement precludes oxygen delivery to the paralyzed apneic victim. This could potentially lead to rapid arterial oxygen desaturation (i.e., <90%). However, by preoxygenating the victim, an oxygen reservoir is established within the patient’s lungs and body tissues to allow for prolonged apnea without detrimental arterial oxygen desaturation. Preoxygenation effectively leads to “nitrogen washout” or replacement of any room air (i.e., about 80% nitrogen and 20% oxygen) within the lungs with near-100% oxygen. Administering 100% oxygen to a patient for 5 minutes before paralysis typically provides adequate preoxygenation. When time
Pharmacy
Monitoring Equipment
Suction should be tested and readily available at the bedside. A high-flow oxygen mask and a bag-valve ventilation device should be ready for use. At least two functioning laryngoscope handles and the appropriately sized and shaped laryngoscope blades should be obtained. The anticipated blade of choice should be clicked into position to ensure that the light functions properly. An endotracheal tube (ETT) should be chosen on the basis of the patient’s anatomy, and one of a smaller size should be prepared as well. The average adult male will require a 7.5- or 8.0-mm ETT, and the average adult female will need a size 7.0 or 7.5 mm. In children, the ETT size in mm may be estimated by the formula 4 + (age in years/4). The ETT cuff should be inflated to test for an air leak. A stylet should be inserted within the ETT to shape it into a configuration that will facilitate insertion into the airway. Care must be taken to ensure that the tip of the stylet does not protrude from the end of the ETT or through the small distal side port (i.e., Murphy’s eye). The patient should have at least one intravenous line placed, and patency of the line should be verified. The specific rapid sequence intubation medications, proper dosing, and sequence of administration should be determined, and the agents should be drawn up and labeled. Cardiac monitoring, blood pressure monitoring, and pulse oximetry are mandatory for all patients. If available, an end-tidal carbon dioxide monitor should be readied as well. In a wilderness setting, many of these hospitalbased amenities may not be available.
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TABLE 20-3 The Eight P’s of Rapid Sequence
PART 4 INJURIES AND MEDICAL INTERVENTIONS
TABLE 20-5 Pretreatment Medications Adult Dose (Intravenous)
Pediatric Dose (Intravenous)
Decreases intracranial response to intubation; mitigates bronchospasm with RAD Blunts sympathetic response to laryngoscopy
1.5 mg/kg
1.5 mg/kg
3-6 mcg/kg
1-3 mcg/kg
Mitigates bradycardic response to SCh
2.0 mg
0.02 mg/kg (minimum dose, 0.1 mg)
Drug
Indication
Mechanism
Lidocaine
Increased ICP and RAD
Opioid (fentanyl)
Increased ICP, ischemic heart disease, and aortic dissection Children <10 yr old; adults receiving a second dose of SCh
Atropine
Notes
Use with caution in young children
From Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. ICP, Intracranial pressure; RAD, reactive airways disease; SCh, succinylcholine.
TABLE 20-6 Clinical Characteristics of Induction Agents Induction Agent
Induction Dose (Intravenous)
Onset of Action
Duration of Action
Methohexital
1-3 mg/kg
<30 sec
5-10 min
Midazolam
0.2-0.3 mg/kg
30-60 sec
15-30 min
Etomidate
0.3 mg/kg
15-45 sec
3-12 min
Ketamine
1-2 mg/kg
45-60 sec
10-20 min
Benefits
Precautions
Decreased ICP Short duration Reversible Amnestic Anticonvulsant Decreased ICP Rarely decreased BP
Decreased BP Laryngospasm, seizures Apnea No analgesia Variable dosing Myoclonic jerks Vomiting No analgesia Increased secretions Increased ICP Emergence phenomenon
Increased BP Bronchodilator Dissociative amnesia
From Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. BP, Blood pressure; ICP, intracranial pressure.
There is no single induction agent of choice for RSI in the field or emergency department. The choice of an induction agent is based on the clinical circumstances and the agent’s attributes. The clinical characteristics of the most commonly used induction agents are summarized in Table 20-6. Neuromuscular blockade. NMBAs are used to completely paralyze the patient to facilitate rapid endotracheal intubation. These agents do not provide analgesia, sedation, or amnesia. The ideal NMBA should have rapid onset action, short duration of action, and few adverse side effects. Succinylcholine (SCh), a depolarizing NMBA, comes closest to fulfilling these traits, and it is the most commonly used NMBA. At the neuromuscular junction, SCh binds tightly to acetylcholine receptors, causing depolarization of the motor endplate and the ensuing muscle contraction. Clinically this manifests as muscle fasciculations followed by complete paralysis. Intravenous administration of SCh results in muscle fasciculations in 10 to 15 seconds, and this is followed by complete paralysis after 45 to 60 seconds. Because of the short duration of action, patients may begin spontaneous breathing within 3 to 5 minutes. The dose of SCh is 1.5 mg/kg given via rapid intravenous push in adults; 2 mg/kg via rapid intravenous push in children less than 10 years old; and 3 mg/kg via rapid intravenous push in newborns. An insufficient dose of SCh can lead to inadequate paralysis and can adversely affect laryngoscopy and intubation. The main disadvantages of using SCh are its side effects, which include muscle fasciculations, bradycardia, hyperkalemia, prolonged neuromuscular blockade, malignant hyperthermia, and trismus (i.e., masseter muscle spasm). 402
Nondepolarizing NMBAs (e.g., rocuronium) cause paralysis by competing with acetylcholine for receptors at the neuromuscular junction. Although these agents are most commonly used for postintubation patient paralysis, they may also be used as the primary RSI paralytic agent for specific patient populations or for patients who have a contraindication to SCh. Although they possess fewer side effects than SCh, these agents are generally less effective for intubation because of their delayed time to paralysis, prolonged duration of action, or both. Specific attributes of both depolarizing and nondepolarizing NMBAs are listed in Table 20-7.
TABLE 20-7 Neuromuscular Blocking Agents Neuromuscular Blocking Agent Depolarizing Succinylcholine
Intubating Dose (Intravenous) 1.5 mg/kg (adult) 2 mg/kg (child) 3 mg/kg (infant)
Nondepolarizing Rocuronium 1.0 mg/kg Vecuronium 0.15 mg/kg Pancuronium 0.1 mg/kg
Onset
Duration
45-60 sec
6-12 min
50-70 sec 90-120 sec 100-150 sec
30-60 min 60-75 min 120-150 min
From Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press.
PA LA
FIGURE 20-17 Cricoid pressure (Sellick’s maneuver). (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department. Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)
FIGURE 20-19 Head elevated on pad, neutral position. LA, Laryngeal axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)
Positioning
Protection After sequential administration of the induction and paralytic agents, the patient will predictably lose consciousness and become apneic. Application of Sellick’s maneuver (i.e., approximately 10 lb of manual pressure to the cricoid cartilage) just as the patient is noted to lose consciousness will compress the esophagus, thereby preventing aspiration and passive regurgitation of gastric contents (Figure 20-17). Sellick’s maneuver should be maintained until the ETT has been inserted into the trachea, its position verified, and the cuff inflated. If Sellick’s maneuver is applied too early, the patient may find it uncomfortable or vomit. If the patient begins actively vomiting, Sellick’s maneuver should be discontinued, and the patient should be logrolled and suctioned. Cricoid pressure should also be applied when the victim requires positive-pressure ventilation before, during, or after intubation attempts. Positive-pressure ventilation, whether from rescue breathing or a BMV device, may lead to gastric distention, compromised diaphragmatic excursion, and an increased risk for emesis or gastric rupture. By employing Sellick’s maneuver during positive-pressure ventilation, air will be directed to the lungs rather than the stomach, thus avoiding these complications.
OA
The airway may be thought of as having three separate axes: oral, pharyngeal, and laryngeal. Proper positioning of the head before laryngoscopy can help to align these three axes, thereby improving visualization of the glottis and greatly increasing the likelihood of a successful intubation. In the neutral position, these axes are misaligned (Figure 20-18). Placing a small pillow or a similar-sized object under an adult’s occiput flexes the lower cervical spine relative to the torso and aligns the pharyngeal and laryngeal axes (Figure 20-19). Positioning the patient in the sniffing position with the extension of the head on the neck aligns all three axes (Figure 20-20). Patients with potential cervical spine injury should be maintained in the neutral position. Placement During RSI, administration of a paralytic agent will predictably lead to paralysis and apnea. With adequate preoxygenation, arterial oxygen saturations remain normal despite this apnea. Complete muscular paralysis can be confirmed by gently grasping the patient’s jaw and checking for flaccidity. Wait until the patient is completely relaxed before proceeding with intubation. With the laryngoscope in the left hand, gently open the mouth with the right hand. Insert the laryngoscope into the right side
OA PA
PA LA
LA FIGURE 20-18 Head on a bed, neutral position. LA, Laryngeal axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)
FIGURE 20-20 Head elevated on a pad, head extended on neck. LA, Laryngeal axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)
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CHAPTER 20 Emergency Airway Management
OA
PART 4 INJURIES AND MEDICAL INTERVENTIONS
of the patient’s mouth, and then sweep the tongue to the left. The curved (Macintosh) blade is slid into the vallecula; the straight (Miller) blade is positioned below the epiglottis. The handle is pushed along the axis of the handle at a 45-degree angle to the patient’s body. Care should be taken not to “crowbar” with the laryngoscope, because this may injure the patient’s teeth. If the glottic aperture is not readily visible, the intubator or an assistant may elect to perform the BURP maneuver: this involves placement of the right hand on the thyroid cartilage and is followed by application of backward, upward, rightward pressure to help to bring the glottis into view (Figure 20-21). The resulting displacement of the thyroid cartilage backward against the cervical vertebrae, upward or as superiorly as possible and laterally to the right, has been found to significantly improve the view of the glottis during laryngoscopy. When the glottis is clearly visible, use the right hand to gently insert the ETT until the cuff is about 2 to 3 cm past the vocal cords. For adult males, the 23-cm marker of the ETT should be located at the corner of the mouth; this should be 21 cm for adult women. When the ETT is in place, remove the stylet and inflate the cuff. An air leak should not be audible with a BMV. If the patient is adequately preoxygenated, the laryngoscopist may make multiple attempts at intubation before arterial oxygen desaturation occurs. If available, a dedicated team member should focus on the patient’s cardiac rhythm, blood pressure, and oxygen saturation, and he or she should alert the intubator to any abnormalities. After any unsuccessful intubation attempt, recheck the patient’s position, and make any necessary adjustments. It is important to “change something” (e.g., the size or type of laryngoscope blade) before taking a second look to ensure that the same mistake or problem is not encountered again. Proof (Confirmation of Endotracheal Tube Placement) Proper ETT positioning within the trachea needs to be confirmed after every intubation. Failure to recognize an inadvertent esophageal intubation can be disastrous for both the patient and physician. Sellick’s maneuver should not be released until after confirmation of correct ETT placement. Methods that are used to detect ETT placement include clinical assessment, pulse oximetry, end-tidal carbon dioxide (ETCO2)
FIGURE 20-21 The BURP maneuver (backward, upward, rightward pressure). (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Copyright Chris Gralapp. http://www.biolumina.com.)
404
detection, and aspiration techniques. Chest radiography assesses ETT position but does not confirm ETT placement within the trachea. Clinical Assessment Classic clinical observations that are used to confirm correct ETT placement include the following: (1) seeing the ETT passing through the vocal cords during intubation; (2) auscultation of clear and equal breath sounds over both lung fields; (3) absence of breath sounds when auscultating over the stomach; (4) observation of symmetric chest rise during ventilation; and (5) observation of “fogging” of the ETT during ventilation. All of these clinical findings are subject to failure and should not serve as the sole means for confirming ETT placement. Pulse Oximetry A drop in oxygen saturation after intubation should raise concern for an esophageal intubation; however, this drop may be delayed for several minutes if the patient was adequately preoxygenated. For certain patients (e.g., those with hypotension), oxygen saturation measurement may be unreliable or difficult to detect. Although pulse oximetry is important to assess after endotracheal intubation, it should not be the primary indicator of successful ETT placement. End-Tidal Carbon Dioxide Detection Detection of exhaled carbon dioxide is a highly reliable method for identifying proper placement of the ETT within the trachea. A colorimetric ETCO2 detector is a small disposable device that connects between the bag and the ETT. When this device detects ETCO2, its colorimetric indicator changes from purple to yellow; absence of this color change for six manual ventilations indicates that the tube is incorrectly placed in the esophagus. A falsepositive color change may occur if the tube is placed just above the glottis. A false-negative color change may occur (even with correct ETT placement) in some cases of cardiac arrest and profound circulatory collapse as carbon dioxide production and delivery to the lungs abruptly decline. Aspiration Devices Aspiration appliances (e.g., bulb and syringe aspiration devices) may also be used for confirmation of ETT placement. The bulb aspiration device is a round and compressible plastic globe (i.e., “turkey baster”) that is first compressed and deflated and then placed within the ETT and released. If the bulb reexpands rapidly, the ETT is likely in the trachea, whereas failure to reexpand or delayed reexpansion suggests that the ETT is in the esophagus. Syringe aspiration devices are large syringes (usually 30 mL [1 oz]) that are inserted into the ETT. The syringe plunger is then drawn back rapidly to allow for brisk aspiration of a large amount of air. The rapid and easy flow of air suggests tracheal intubation, whereas resistance suggests esophageal intubation. Postintubation Management After verification of correct ETT placement within the trachea, the tube should be secured (i.e., taped or tied) to prevent movement or migration. The patient’s blood pressure and other vital signs should be repeated. Bradycardia after intubation is worrisome for hypoxia and should prompt exclusion of an esophageal intubation. Hypertension after intubation suggests inadequate sedation. Hypotension after intubation may result from a tension pneumothorax, decreased venous return, the induction agent, or a cardiac cause. After intubation, consideration should be given to long-term sedation, analgesia, and paralysis. A benzodiazepine such as midazolam (0.1 to 0.2 mg/kg), diazepam (0.2 mg/kg), or lorazepam (0.05 to 0.1 mg/kg) may be given initially for sedation and repeated for any signs of awareness. An opioid agent such as fentanyl (3 to 5 mcg/kg) or morphine sulfate (0.1 mg/kg) may also be administered for additional patient comfort. Nondepolarizing NMBAs such as pancuronium (0.1 mg/kg) or vecuronium (0.1 mg/kg) may be used for long-term paralysis; a repeat dose that is one-third of the initial dose may be given after 45 to 60 minutes if any motor activity is detected.
There are certain clinical circumstances, such as the spontaneously breathing patient who presents with a difficult airway, in which RSI may not be advisable. In the patient with anatomic features that may pose a challenge to RSI and BMV, awake nasotracheal intubation (NTI) may provide a better alternative, because it can be performed while preserving the patient’s spontaneous respirations. Technique: 1. Prepare the mucosa to facilitate tube passage and to minimize the risk for epistaxis. Instill 2 to 3 drops of a topical vasoconstrictor agent such as phenylephrine hydrochloride (0.25%) or oxymetazoline (0.05%) in each naris. Anesthetize the nasal mucosa using a 4% cocaine pack or 2% lidocaine jelly. 2. Select a cuffed ETT that is sized 0.5 to 1.0 mm smaller than would be used for orotracheal intubation. The tube should be lubricated with a water-soluble lubricant to facilitate passage. 3. The patient may be seated or reclined while the clinician stands to the side of the patient. 4. The tube is inserted into the more patent of the two nares. The right side is preferable because the tube bevel will face the septum, thus avoiding Kiesselbach’s plexus. If going through the left nares, consider inserting the tube “upside down” and then rotating it so that the curve follows the posterior nasopharynx when the turbinates are passed. 5. Direct the tube straight back along the nasal floor toward the occiput, and rotate it 15 to 30 degrees with advancement. When the tube nears the glottis, listen for airflow within the tube with each breath. 6. When maximal airflow is heard, quickly and gently advance the tube. A cough will likely be heard with passage of the tube into the trachea. The tube should be advanced to 32 cm at the nares in the adult male and to 27 to 28 cm in the adult female. 7. Confirm the tube’s position with an ETCO2 detection device. Because the tube is placed blindly, it may also be misdirected into the esophagus, the piriform sinus, or the vallecula, although this is rare. When this occurs, withdraw the tube slightly, redirect it, and retry the procedure. If the tube FIGURE 20-22 Laryngeal mask airway (LMA). A, The LMA is an adjunctive airway that consists of a tube with a cuffed mask-like projection at the distal end. B, The LMA is introduced through the mouth into pharynx. C, When the LMA is in position, a clear and secure airway is present. D, During insertion, the LMA is advanced until resistance is felt as the distal portion of tube locates in the hypopharynx. The cuff is then inflated. This seals the larynx and leaves the distal opening of the tube just above the glottis to provide a clear and secure airway (dotted line). (Redrawn from American Heart Association, International Liaison Committee on Resuscitation: Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 3: Adjuncts for oxygenation, ventilation and airway control, Circulation 102:I95, 2000.)
becomes caught on the vocal cords, rotate the tube slightly to realign the bevel with the cords. Occasionally, externally manipulating the larynx posteriorly or laterally with one’s nondominant hand will facilitate successful passage. NTI is absolutely contraindicated in the apneic patient, because air movement is essential to placement of the ETT. NTI is also contraindicated in patients with the possibility of cribriform plate injury, basilar skull fracture, or midface fracture out of concern that the tube may enter the cranial vault. Patients with bleeding disorders or coagulopathy may develop massive epistaxis from NTI. Other contraindications include combativeness; increased intracranial pressure; neck hematoma; upper airway obstruction or anatomic alteration from trauma, edema, or infection; and the need for immediate airway management. Blind nasotracheal intubation is not generally recommended for patients with neck trauma; it can be especially dangerous when there is a possibility of dislodging a clot. In addition, the distorted anatomy leads to a higher failure rate for blind nasotracheal intubation. Epistaxis and nasal turbinate injury from blind NTI can be greatly reduced by pretreatment with vasoconstrictor agents and proper technique. Long-term complications (e.g., sinusitis, turbinate destruction) are uncommon and result from multiple intubation attempts or prolonged intubation.
Alternative Airway Adjuncts and Techniques In certain wilderness conditions and settings, tracheal intubation may be difficult or impossible. Under such circumstances, alternative airway adjuncts or techniques may be employed to provide an airway. Alternative airways that require blind passage of the device into the airway may be simpler to master than passing an ETT under direct vision. To achieve good outcomes with these devices and techniques, health care providers must maintain a high level of knowledge and skills through frequent practice and field use.
LARYNGEAL MASK AIRWAY The laryngeal mask airway (LMA) is a modified ETT with an inflatable oval cuff (i.e., the laryngeal mask) at its base (Figure 20-22). The LMA is blindly inserted into the pharynx and advanced
A
B
C
D 405
CHAPTER 20 Emergency Airway Management
NASOTRACHEAL INTUBATION
COMBITUBE The Combitube is a double-lumen, dual-cuffed airway; one lumen functions as an esophageal airway, whereas the other performs as a tracheal airway (Figure 20-23). The Combitube is typically blindly inserted and advanced until the victim’s teeth lie between two guide marks that are printed on the tube. The distal end of the tube most commonly finds its way into the esophagus. The pharyngeal and distal balloons are then inflated, thus isolating the oropharynx above the upper balloon and the esophagus or trachea below the lower balloon. The location (i.e., esophagus or trachea) of the distal orifice is then ascertained, and the victim is ventilated through the appropriate opening. One lumen contains ventilating side holes at the hypopharyngeal level and is closed at the distal end; the other lumen has a distal open end with a cuff that is similar to that of a tracheal tube. Advantages of the Combitube over BMV include isolation of the airway, reduced aspiration risk, and more reliable ventilation. Because laryngoscopy and visualization of the vocal cords are not necessary for insertion, use of the Combitube is easier to teach, learn, and practice compared with tracheal tube placement. In addition, ventilation and oxygenation with the Combitube compare favorably with those achieved with the use of a tracheal tube. Fatal complications with the Combitube may result from incorrect identification of the position (trachea or esophagus) of the distal lumen. For this reason, an ETCO2 or esophageal detector device should be used in conjunction with the Combitube. Another possible complication is esophageal trauma.
KING LT The King LT airway is a single-lumen, dual-cuffed airway with ventilation outlets between the pharyngeal and esophageal cuffs. The King LT is inserted blindly, and a single pilot balloon inflates both cuffs simultaneously. Although it is similar to the Combitube, the King LT is shorter, easier to insert, and easier to inflate. Ventilation capability seems to be similar to that of the Combitube and the LMA. The device’s airway seal may be lost after insertion and require deflation of the balloons and repositioning. The King LT airway is available in newborn through adult sizes.
VIDEO LARYNGOSCOPY Video laryngoscopes, which consist of a micro video camera and a modified laryngoscope, transmit images of the glottis to an external monitor to allow for intubation while looking at the video screen. As compared with traditional laryngoscopy, video laryngoscopes such as the GlideScope provide superior glottic views and greater airway anatomic detail without requiring alignment of the airway axes. As a result, the GlideScope is associated with high intubation success rates and less cervical spine movement. Although rigorous trials to assess performance are limited, clinical experience (including that of the author) indicates that these devices are highly effective. The GlideScope Ranger is a rugged, portable, battery-operated unit that is designed for field use.
FIBER-OPTIC INTUBATION Fiber-optic techniques for endotracheal intubation have emerged as invaluable tools for difficult airway management and include fiber-optic intubating bronchoscopes and rigid fiber-optic laryngoscopes. These devices may allow for awake intubation in select victims for whom RSI or insertion of a laryngoscope blade may be disadvantageous. Use of fiber-optic devices may be difficult in the setting of uncontrolled secretions or active bleeding, because visualization is impaired.
LIGHTED-STYLET INTUBATION By transilluminating the soft tissues of the neck, a lighted-stylet apparatus can be used to facilitate blind ETT placement within the trachea. Devices such as the Rusch Trachlight take advantage of the anterior location of the trachea relative to the esophagus. When the ETT and the lighted stylet correctly enter the glottic opening, a well-defined and circumscribed glow can readily be seen in the anterior neck. If the tip of the tube is correctly
.2 No No.1
A
Insertion
B
Esophageal placement
2 No. No.1
2 No. No.1
PART 4 INJURIES AND MEDICAL INTERVENTIONS
until resistance is felt as the distal portion of the tube locates in the laryngopharynx. Inflation of the collar provides a seal around the laryngeal inlet to facilitate tracheal ventilation. Although the LMA does not provide a definitive airway or ensure absolute protection against aspiration, studies have shown that aspiration is uncommon and that regurgitation is less likely with an LMA as compared with a BMV device. The LMA provides ventilation equivalent to that with the tracheal tube. The LMA may have advantages over traditional endotracheal intubation when access to the victim is limited, when the possibility of unstable neck injury exists, or when appropriate victim positioning for tracheal intubation is impossible. However, studies have shown that a small proportion of patients cannot be ventilated, even when the LMA is successfully inserted. An updated version of the original LMA called the intubating ILMA facilitates blind endotracheal intubation by allowing for the passage of an ETT through the device and into the trachea with a high degree of success.
C
Tracheal placement
FIGURE 20-23 Esophageal–tracheal Combitube. (Redrawn from Skinner D, Swain A, Peyton R, et al, editors: Cambridge textbook of accident and emergency medicine, Cambridge, UK, 1997, Cambridge University Press.)
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RETROGRADE INTUBATION Retrograde intubation is an invasive technique that involves needle puncture of the cricothyroid membrane followed by threading a guidewire retrograde through the vocal cords and into the mouth or nose. The wire is then used to guide the ETT through the glottis. Kits are commercially available. Retrograde intubation may play a role in difficult airways as a result of anatomic abnormalities, upper airway trauma, and victims with limited neck mobility caused by cervical spine immobilization.
DIGITAL INTUBATION Digital or tactile intubation is a technique in which the index and long fingers of the nondominant hand are used to identify the epiglottis and then manually direct an ETT into the larynx. It may be useful when poor lighting, poor positioning, copious airway secretions, or equipment failure make laryngoscopy difficult or impossible. Digital intubation requires a profoundly unresponsive victim and is relatively contraindicated in the semiconscious victim with intact oropharyngeal reflexes. Other relative contraindications include caustic ingestions, thermal burns, and upper airway foreign bodies.
Surgical Airway Management Surgical airway management involves creation of an opening directly into the trachea by surgical means and includes both cricothyrotomy and needle cricothyrotomy with percutaneous transtracheal ventilation.
CRICOTHYROTOMY Cricothyrotomy is the creation of a surgical opening through the cricothyroid membrane to allow placement of an ETT or cuffed tracheostomy tube. The proximal ends of these tubes can be connected to a BMV device for oxygenation and ventilation. The primary indication for cricothyrotomy is need for a definitive airway in the victim in whom orotracheal or blind NTI has failed, is contraindicated, or is extremely difficult. Clinical scenarios include the victim with severe facial trauma for whom conventional airway management is extremely complicated or unfeasible, the victim with severe laryngeal edema, or the victim with upper-airway foreign-body obstruction that cannot be alleviated with the Heimlich maneuver or direct laryngoscopy. The primary contraindication to cricothyrotomy is young age. As a result of anatomic considerations, the procedure is extremely difficult for children who are less than 10 to 12 years old, and is generally avoided in this population. Other contraindications to cricothyrotomy include preexisting tracheal or laryngeal pathology, anatomic obliteration of the landmarks (e.g., hematoma), coagulopathy, and operator inexperience with the procedure. Complications of cricothyrotomy include incorrect airway placement, hemorrhage, tracheal or laryngeal injury, infection, pneumomediastinum, subglottic stenosis, and voice change. Standard Surgical Cricothyrotomy Technique (Figure 20-24): 1. Identify the thyroid cartilage; this is the only V-shaped structure encountered when palpating the anterior neck. The cricothyroid space is the gap immediately caudad to the thyroid cartilage. 2. Prepare the neck in sterile fashion. With the nondominant hand holding the thyroid cartilage, make a vertical midline incision with a No. 11 scalpel from the thyroid cartilage caudad about 3 to 4 cm (1.18 to 1.57 inches) (A).
3. Place a tracheal hook through the cricothyroid space, and hold cephalad traction with the nondominant hand (B, C, and D). 4. Make a transverse incision across the exposed cricothyroid membrane (E and F). If time permits, insert silk stay sutures in the trachea (G and H). Dilate the space using the Trousseau dilator while maintaining traction with the hook (I, J, and K). 5. Place a Shiley cuffed tracheostomy tube through the cricothyroid membrane, initially aiming posteriorly then redirecting caudad once through the membrane (L). The tracheal hook may be removed before insertion of the tube to avoid damaging the tube. Rapid Four-Step Cricothyrotomy Technique: 1. From a position at the head of the victim, palpate and identify the landmarks, especially the cricoid and thyroid cartilages and the cricothyroid membrane (Figure 20-25). 2. Incise the cricothyroid membrane and the overlying skin simultaneously with a single horizontal 1.5-cm (0.6-inch) incision using a No. 20 scalpel. While maintaining the blade within the airway, slide a tracheal hook along the caudal side of the blade into the wound. 3. Orient the hook caudally, and place gentle traction on the cricoid ring; this typically widens the incision. Then remove the blade from the airway. 4. The ETT is then placed through the incision into the airway and secured. Improvised Cricothyrotomy For circumstances in which formal cricothyrotomy equipment is not available, a knife and a hollow device (as a substitute for the tracheostomy tube) may be used. An improvised cricothyrotomy could be performed using a modified intravenous macro drip chamber or the cut barrel of 1- or 3-mL syringe (see Chapter 23). Any small hollow object (e.g., a ballpoint pen casing, a sports-bottle straw) may be employed as the cricothyrotomy tube; however, devices with an internal diameter of at least 3 mm (0.12 inch) provide the best gas exchange.
NEEDLE CRICOTHYROTOMY WITH PERCUTANEOUS TRANSTRACHEAL (TRANSLARYNGEAL) JET VENTILATION An alternative surgical airway procedure is needle cricothyrotomy with percutaneous transtracheal jet ventilation (TTJV). With this technique, a transtracheal catheter is inserted through the cricothyroid membrane into the trachea and connected to a jet ventilation system that includes high-pressure tubing, an oxygen source at 50 psi, and an in-line one-way valve for intermittent administration of oxygen. One hundred percent oxygen is then delivered at 12 to 20 bursts/min. The inspiratory phase should last 1 second, and the expiratory phase should last 2 to 4 seconds. Advantages of this technique include simplicity, safety, and speed. There is typically less bleeding as compared with cricothyrotomy, and age is not a contraindication, thereby making this the preferred surgical airway technique for children who are less than 12 years old. During TTJV, the upper airway must be free of obstruction to allow for complete exhalation; otherwise, the victim is at risk for barotrauma from air “stacking.” All victims who are receiving TTJV should have an oral and nasal airway placed. Unlike cricothyrotomy, TTJV does not provide complete airway protection; therefore it should be considered a temporizing measure until a definitive airway can be established. Technique: 1. Stand to one side of the victim at the level of the neck. Expose the neck, and identify the landmarks, especially the cricoid and thyroid cartilages and the cricothyroid membrane. 2. Prepare the neck with an antiseptic solution, and provide local anesthesia if time permits. 407
CHAPTER 20 Emergency Airway Management
placed in the esophagus, the light glow is diffuse and not readily seen. Lighted stylets may have a role in management of difficult airways as a result of anatomic difficulties (e.g., restricted mouth opening), severe facial trauma, and victims with limited neck mobility. Despite the absence of absolute contraindications to using the lighted stylet, this device should probably be avoided in any victim with an unknown cause of upper airway obstruction.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Cricoid cartilage
Cricothyroid membrane Cricoid cartilage Thyroid cartilage
Cricothyroid space
A
B
C
E
F
Left hand takes trachea hook from right hand L R
L
R
Right hand picks up scalpel
R
D
L R Right hand takes trachea hook from left hand
L
G
J
H
I
K
L
R
Left hand picks up trachea spreader
L
FIGURE 20-24 Standard surgical cricothyrotomy. (Redrawn from Walls RM: Cricothyrotomy. In Rosen P, Chan TC, Vilke GM, et al, editors: Atlas of emergency procedures, St Louis, 2001, Mosby.)
408
A
B
C
D
3. Immobilize the larynx between your thumb and middle finger while your index finger identifies the cricothyroid membrane. 4. Attach a large-bore (12- to 16-gauge) over-the-needle catheter to a 20-mL syringe. Hold the needle and syringe in the dominant hand. Direct the needle caudally through the cricothyroid membrane at a 30-degree angle to the skin while maintaining negative pressure on the syringe. As soon as the needle enters the trachea, the syringe should fill easily with air. 5. Advance the catheter to the hub while simultaneously removing the needle. Reconfirm catheter position within the trachea. 6. Connect the catheter to the jet ventilation system. Commercial kits with cannulas that have been designed for cricothyrotomy or percutaneous translaryngeal ventilation are available. Several of these employ the Seldinger technique for catheter placement, whereas others rely on direct percutaneous placement of the airway device. These kits include Nu-Trake, PCK-Portex, Pertrach, QuickTrach, and the Melker emergency cricothyrotomy catheter. In terms of expedition kit portability, three transtracheal puncture emergency airway devices deserve special mention. LifeStat manufactures a keychain emergency airway set that consists of a sharp-pointed metal trocar introducer that fits through a straight metal cannula that screws into a metal extension with a universal 15-mm (0.6 inch) male adaptor. Lightweight and less than 7.6 cm (3 inches) long, the three-component apparatus is attached to a separate and detachable keychain (Figure 20-26). Cook Critical Care offers a 6-Fr reinforced-catheter emergency transtracheal airway catheter (order number C-DTJV-6.0-7.5-BTT) with a molded Luer-Lok connection for jet ventilation or the added assembly of a 15-mm (0.6 inch) adaptor for standard modes of positivepressure ventilation. Cook Critical Care also offers the Wadhwa Emergency Airway Device (order number C-WEAD-100). This lightweight and impact-resistant assembly disassembles to yield a 12-Fr Teflon-coated cricothyrotomy catheter with a removable metal stylet, a molded plastic Luer-Lok connection for oxygen or jet ventilation, and a flexible nasopharyngeal airway adhered to a molded plastic flange (Figure 20-27). Both the cricothyrotomy catheter and the NPA screw into the Wadhwa case to provide a low-resistance extension and a 15-mm (0.6 inch) male connection for standard positive-pressure ventilation equipment.
CHAPTER 20 Emergency Airway Management
FIGURE 20-25 Rapid four-step cricothyrotomy. A, Step 1: Palpation (location of the cricoid membrane externally). B, Step 2: Incision (horizontal incision of the skin and soft tissues through the cricoid membrane). C, Step 3: Traction (application of caudal traction to the cricoid ring). D, Step 4: Intubation (passage of the tracheal tube). (Redrawn from Brofeldt BT, Panacek EA, Richards JR: An easy cricothyrotomy approach: The rapid four-step technique, Acad Emerg Med 3:1060, 1996.)
For circumstances in which a jet ventilator is not readily available, the clinician in the wilderness may improvise by using a self-inflating bag-valve device to ventilate the victim through the transtracheal catheter. The bag-valve device may be connected to a 3.0-mm-ID ETT adapter that is inserted directly into the transtracheal catheter or to a 7.5-mm-ID ETT adapter that is inserted into a 3-mL (0.1-oz) syringe barrel and then into the transtracheal catheter (Figure 20-28). Ventilation using such an apparatus is temporary at best, but it may have usefulness in children who are younger than 5 years old.
Airway Equipment for the Wilderness Although it is neither practical nor possible to bring every type of airway device to the wilderness, the airway equipment listed in Box 20-1 is worth considering. Emergency medical kits with basic or advanced airway equipment (e.g., the StatKit) are commercially available.
Universal adaptor
Cannula Trochar FIGURE 20-26 LifeStat emergency airway device. (Redrawn from LifeStat product information.)
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PART 4 INJURIES AND MEDICAL INTERVENTIONS
15-mm adapter
Cricothyrotomy catheter
Nasopharyngeal airway catheter
Assembled airway device FIGURE 20-27 Wadhwa emergency airway device. (Redrawn from Cook Critical Care product information.)
Ventilation bag
BOX 20-1 Sample Contents of a Wilderness Airway
Management Kit
Standard endotracheal tube connector
Cricothyroid membrane
3-cc syringe barrel
14-gauge IV catheter-over-needle
Thyroid cartilage
Cricoid ring
FIGURE 20-28 A simple setup for translaryngeal ventilation with the use of standard equipment found in any emergency department. This setup is inadequate for adults. High-pressure (50-psi) ventilation systems are optimal. Even with the pressure relief valve on the bagvalve device turned off, only a suboptimal pressure can be developed. However this technique may be satisfactory for infants and small children. (Redrawn from Roberts JR, Hedges JR, editors: Clinical procedures in emergency medicine, ed 4, Philadelphia, 2004, Saunders.)
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Basic Airway Equipment Laerdal pocket mask CPR microshield barrier Nasal airway kit Oral airway kit Stethoscope Bulb suction device Advanced Airway Equipment Bag-mask ventilation device with pediatric and adult masks Manual suction device Endotracheal tubes with stylet Laryngoscope handles and blades Magill forceps Esophageal detector device Colorimetric end-tidal carbon dioxide detector Laryngeal mask airway, King LT, or Combitube Needle cricothyrotomy catheter or device Commercial cricothyrotomy kit Oxygen cylinder with toggle handle Nasal cannula, oxygen mask with strap, and nonrebreather bag Oxygen tubing Pulse oximeter
SUGGESTED READINGS Complete Suggested Readings used in this text are available online at www.expertconsult.com.
CHAPTER 21
Wilderness Trauma and Surgical Emergencies* KIRBY R. GROSS, BRYAN R. COLLIER, WILLIAM P. RIORDAN, JR., AND JOHN A. MORRIS, JR.
Purpose This chapter is written to provide physicians and health care practitioners with a concise, pragmatic approach to the management of trauma and surgical emergencies encountered in a wilderness environment. Our focus is directed primarily at the health care professionals responsible for the well-being of expedition members. Wilderness expedition health care providers will have varied capabilities and experience, but it is the environment (location, time from medical facilities, and conditions) and available resources that will most influence patient outcome. Complex interventions in the field are frequently impractical. With ongoing debate concerning issues ranging from the value of field resuscitation for internal hemorrhage to the method (if any) of closure of animal bite wounds, it remains clear that simple things, such as identifying injuries, establishing an airway, keeping the patient warm, and making expedient evacuation plans, most strongly influence survival.21,26,74 The key to successful management of wilderness emergencies is preparedness. Knowledge of the Advanced Trauma Life Support (ATLS) protocols provides a scaffold for preparation for wilderness travel. The simple, concise principles contained in ATLS concepts are well suited to management of wilderness emergencies, where resources are scant and prompt response is essential to victim survival. Newer training programs, such as Advanced Wilderness Life Support (AWLS), provide additional wilderness-specific learning opportunities. In addition to knowledge and skill, physicians in the wilderness environment should prepare by understanding their role in the expedition. Lessons from teamwork management have application to the wilderness environment as well as the sophisticated medical environment. The basic tenets of teamwork are those of (1) team structure, (2) application of problem-solving strategies, (3) communication, (4) execution, and (5) improving team skills.79 The provider in an expedition should fully understand his or her role during preparation. Is the physician a team member because he or she has medical training and expertise that has application to the specific environment and potential risks? Is the provider serving in a capacity in which he or she has been directed to become the responsible physician if needed? Or, is the provider in the wilderness to escape from professional responsibilities and enjoy an avocation that can only be appreciated in the austere environment? The medical director of an expedition takes on a significant responsibility in preparation for the trip. He or she must provide input to the expedition leader regarding local health threats and also assess risk. Screening participants for durability and comorbidities is important. The medical director must be knowledgeable in wilderness medicine protocols. For longer expeditions, diagnostic capability such as handheld ultrasound and point-ofcare testing should be considered. Also, establishing contact with evacuation assets before commencing the trip is prudent. The medical director must have a plan for transfer of information to
*The views expressed in this chapter are those of the authors and do not reflect the official policy or position of the Department of the Army, the Department of Defense, or the U.S. Government.
the next level of care. It may be as simple as recording findings on a piece of tape applied to an uninjured location on the casualty. Paper is a poor way to transfer information. In the evacuation process, paper will often be lost because of helicopter rotor wash and jostling during travel. Standard time designations should be used. The casualty may be evacuated across different time zones. Any times recorded for findings or interventions should have the appropriate time zone clearly designated. In any austere environment, physicians will commonly and immediately be thrust into a position of authority. The time to clarify structure and roles is before the expedition. Understanding the expectations for each provider permits appropriate team preparation. The physician in a position of responsibility would be wise to brief team members about contingencies before entering the austere environment. The specifics of wilderness preparation, equipment, and medical supplies are presented in Chapter 91.
Wilderness Trauma Emergencies OVERVIEW All three classic mechanisms of trauma (penetrating, blunt, and thermal) may be seen in the wilderness. Particularly in the austere environment, blunt trauma presents pitfalls, because the patient is at risk due to blunt mechanisms. Delayed diagnoses in victims of blunt trauma occur in highly sophisticated medical environments. The possibility of delayed diagnoses in the wilderness is even greater due to lack of diagnostic resources.
BACKGROUND The medical literature is limited regarding the incidence of injury incurred during wilderness-related activities. It is estimated that greater than 10 million Americans participate in wilderness backpacking and camping activities annually. A study by Gentile and colleagues33 documented the injury and evacuation patterns recorded by the National Outdoor Leadership School over a 5-year period. Injuries occurred at a rate of 2.3 per 1000 persondays of exposure, with orthopedic and soft tissue injuries most frequent. Montalvo65 analyzed case incident report files from eight California National Park Service parks and found an injury incidence of 9.2 nonfatal events per 100,000 visits, with 78 fatalities reported in a 3-year period. In a prospective surveillance study evaluating 38,940 days of wilderness exposure on the Appalachian Trail,12 foot blisters and diarrhea were the most common reasons that hikes were prematurely ended. Leemon and Schimelpfenig52 showed that over 50% of evacuated participants in the National Outdoor Leadership School were able to return and finish their courses. These studies document a low risk for injury but highlight the possible morbidity resulting from wilderness injury or illness and the need for rapid, uniform intervention. A 2001 study from the University of Arizona36 highlighted wilderness mortalities over the past 13 years. Alcohol was the most common causative factor, involved in 40% of the 59 unintentional trauma deaths. In addition, 80% of these victims died immediately or before evacuation could be completed. This again emphasizes the importance of sound judgment and preparedness as keys to maximizing care to rescuers and expedition members. 411
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ESTABLISHING PRIORITIES There are three immediate priorities in managing wilderness trauma: 1. Control oneself. It is normal to feel anxious when confronted with an injured victim. However, anxiety must not be transmitted to the victim or other members of the expedition team. One must be in control of oneself to take control of the situation. 2. Control the situation. The first priority in controlling the situation is ensuring the safety of uninjured members of the party. Expeditious evacuation of a victim requires that all expedition members function at maximal efficiency; even minor injuries to other members in the group can jeopardize physical strength, functional manpower, and success of the evacuation. Although the physician member of the team may not be the expedition leader, his or her position is automatically elevated during a medical crisis. However, this does not mean that the physician should dominate the evacuation process. Although the expedition leader must rely on the medical assessment provided by the physician, the leader is best prepared to plan the evacuation. 3. Obtain an overview of the situation. The victim’s general condition should be evaluated. Is the victim in immediate distress from a condition that requires relatively simple management, such as airway control? Is the victim in such a precarious environmental situation that he or she needs to be moved before resuscitation? Scene security may be integral to the safety of the injured and caregiver. Is the victim properly protected from the elements, including sun, wind, cold, and water? Hypothermia remains one of the most important contributors to trauma-related coagulopathies.91 In addition to these three priorities, McSwain and Kerstein62 have described the “golden principles” of prehospital trauma care. Although not intended for wilderness medicine, several key components are applicable: ensure scene and provider safety, use primary and secondary surveys, provide cervical spine immobilization, control external hemorrhage, keep the patient warm and use warm intravenous (IV) fluid resuscitation if possible, initiate early transport, and, above all, do no further harm. After the victim has been placed in the most stable and safe environment, the examining physician is ready to implement the ATLS-based five steps of wilderness trauma management:3 1. Primary survey 2. Resuscitation 3. Secondary survey 4. Definitive plan 5. Packaging and transfer preparation The purpose of the primary survey is to identify and begin initial management of life-threatening conditions by assessing the following (called the ABCDE’s of trauma care): • Airway maintenance and cervical spine stabilization • Breathing • Circulation, with control of significant external hemorrhage • Disability: neurologic status • Exposure/environmental control: completely undress the victim with careful attention to prevention of hypothermia After the primary survey is performed, resuscitation efforts are initiated. The level of resuscitation depends on the equipment and expertise available (see Chapters 23, 91, and 94). At a minimum, resuscitation consists of control of external hemorrhage and, when available, administration of oxygen and provision of warm IV fluids. The third step is the secondary survey, a head-to-toe evaluation of the trauma victim that uses inspection, percussion, and palpation techniques to evaluate each of the body’s five regions: head and face, thorax, abdomen, skeleton, and skin. A history should be taken at the same time as performance of the secondary survey. The specifics of the mechanism of injury, if unknown to the physician or caregiver, may be of vital importance. Loss of consciousness, head injury, the height of a fall, or the species of attacking animal may influence treatment and evacuation plans, as well as contribute to stability of the scene. The ATLS AMPLE method of rapid history taking is discussed later in detail 412
in the Secondary Survey section. After this survey, the examining physician should formulate a definitive plan. It is useful to document all observations if circumstances permit. Such data may prove of critical importance to field evacuation or hospital personnel. The first step in formulating a plan is to compile a list of the injuries. The next step is to determine if any injury warrants evacuation. A determination needs to be made as to the route of evacuation: air, land, or water. Aeromedical evacuation is expensive and, depending on the environment, may pose its own risk to both the victim and medical evacuation team. Aeromedical evacuation should be considered only for victims with potentially life- or limb-threatening injuries where the terrain and environment allow safe access, for the purpose of evacuation, to the patient. Packaging the victim for evacuation is the final step. The evacuation effort requires organization, coordination, and great effort on the part of the expedition team. Transfer protocols are discussed within the respective injury sections. Preparation for wilderness patient care should address the challenges associated with varying levels of personnel help, minimal medical resources, prolonged prehospital care, and difficult evacuation proceedings. However, with ATLS knowledge, improvisation, and an organized effort, the patient’s outcome can be maximized.
UNIVERSAL (BODY FLUIDS) PRECAUTIONS IN THE WILDERNESS A number of life-threatening viruses are transmitted through contact with bodily fluids. The Centers for Disease Control and Prevention (CDC) have established a set of standard precautions to be applied in all cases of contact with human body fluids: • Goggles • Gloves • Fluid-impervious gowns • Shoe covers and fluid-impervious leggings • Mask • Head covering Created in 1983 and revised in 1987, recommendations for universal precautions and use of the aforementioned equipment have undergone no additional changes over the past decade. Multiple types of body fluids (blood, semen, vaginal secretions, cerebrospinal, pleural, synovial, pericardial, peritoneal, and pericardial) can place a caregiver at risk. In the wilderness setting, the materials necessary for universal precautions are rarely available. However, every victim in the wilderness must be assumed to carry a communicable disease. Every effort should be made to approximate universal precautions, particularly covering the hands and eyes.
PRIMARY SURVEY Persons injured in the wilderness should be assessed and their treatment priorities established based on their mechanism of injury, vital signs, and specific injuries. The victim’s vital signs must be assessed quickly and efficiently, with restoration of lifepreserving vital functions. Airway The upper airway should be assessed for patency (see Chapter 20). This rapid assessment should include inspection for signs of airway obstruction, including foreign bodies and signs of facial or tracheal fractures that sometimes lead to airway obstruction. The chin lift or jaw thrust may be helpful in establishing an airway. If the victim can speak, the airway is likely not jeopardized, but this is not an absolute rule. Frequent repeated evaluation of the patient’s airway, breathing and circulatory status in the familiar ABC format is mandatory. In addition, a Glasgow Coma Scale (GCS) score of 8 or less indicates the possibility of a precarious airway and requires establishment of a definitive airway. Specific attention should be directed toward the possibility of cervical spine injury. The victim’s head or neck should never be
Breathing and Ventilation The victim’s chest should be exposed and chest wall movement observed. Because oxygenation and carbon dioxide elimination require adequate function of the diaphragm, chest and abdominal musculature, and ribs, any trauma sustained by these structures will alter normal pulmonary mechanics and increase the work of breathing. Establishment of an airway in the primary survey, although critical to patient survival, does not ensure adequate oxygenation or ventilation. All trauma victims must be continuously monitored for the signs and symptoms of hypoxemia and hypercarbia. Auscultation, observation, and palpation of the chest after establishment of the airway are integral parts of the primary survey. Absent breath sounds may indicate improper placement of an endotracheal tube. This can occur with inadvertent esophageal intubation or intubation of a single lung (right or left mainstem bronchial intubation). Diminished breath sounds or asymmetric chest wall movement can occur with pneumothorax (simple or tension), hemothorax, or tracheobronchial obstruction. Observation and palpation of the chest may identify thoracic injuries such as rib fractures, fractures with flail segments, or pneumothorax (by the presence of subcutaneous emphysema). Circulation Evaluation of circulation is divided into assessment of cardiac output and control of major external hemorrhage. Manometric blood pressure measurement is not easily performed in the field, although it may provide useful data. Important information regarding perfusion and oxygenation can be obtained rapidly by determining the victim’s level of consciousness, assessing peripheral and central pulses, looking at skin color, and evaluating capillary refill time. The pulse should be assessed first. Although the following are only general estimates and carry some inaccuracy, approximations of systolic blood pressure can be used if a palpable pulse is present: • Radial artery—80 mm Hg • Femoral artery—70 mm Hg • Carotid artery—60 mm Hg When circulating blood volume is reduced, cerebral perfusion pressure may be critically impaired, resulting in altered level of consciousness. Do not assume that altered level of consciousness is attributable to head injury. Altered levels of consciousness may be due to hypoperfusion of the brain. Peripheral perfusion can be assessed using skin color and capillary refill. Pressure applied to the thumbnail or hypothenar eminence causes underlying tissue to blanch. In a normovolemic person, color returns to the nail bed within 2 seconds. In a hypovolemic, poorly oxygenated person, capillary refill requires more than 2 seconds. There is no direct relation between blood pressure and capillary refill. Capillary refill reflects flow, which is more important than blood pressure. If hypovolemia is suspected on the basis of either absent pulses or prolonged capillary refill, the examiner should immediately assess the neck veins. Distended neck veins, although a nonspecific sign, may suggest tension pneumothorax or pericardial tamponade in the context of hypotension. Flat neck veins suggest hypovolemia and hemorrhagic shock. Major hemorrhage can occur in five anatomic areas: 1. Chest 2. Abdomen 3. Retroperitoneum 4. Thigh 5. External environment
Exsanguinating external hemorrhage should be identified and controlled during the primary survey. Blood loss should be controlled by direct pressure on the wound. Tourniquets should not be used to control external bleeding unless direct pressure fails to control the bleeding. Tourniquets may be considered in the situation where pressure cannot be applied as the patient is being transported. In this situation, a tourniquet may be applied temporarily. As soon as the operational situation permits, the tourniquet may be removed and direct pressure reapplied. The greatest challenge for extremity vascular injuries is hemorrhage, not ischemia. Recent military experience has demonstrated that tourniquets may be used with infrequent untoward consequences.50 Proper stabilization of long bone fractures (femur fractures specifically) minimizes blood loss into soft tissues. In the wilderness, little can be done about significant intrathoracic or intra-abdominal hemorrhage. In a modern trauma center, however, less than 5% of blunt trauma patients with intraabdominal or intrathoracic injuries require surgery to control bleeding. Consequently, even significant blunt injuries in the wilderness carry a real probability for survival if basic ATLS principles are followed. Rarely, large degloving injuries may be a source of significant blood loss. Hemostatic dressings have been developed to promote hemorrhage control in this type of wound. The hemostatic dressings require the benefit of pressure to be maximally effective. Several commercial products are available that promote clotting by different active agents. The hemostatic dressings are described in detail in Chapter 22. Disability and Neurologic Assessment The neurologic assessment of the injury victim conducted during the primary survey should be rapid and efficient. The victim’s level of consciousness should be established. In addition, pupillary size and reactivity should be assessed. Level of consciousness should be assessed using the GCS (Box 21-1). It is critical that the neurologic assessment be repeated hourly, particularly if evacuation is delayed. Deterioration in mental status portends a poor prognosis, although a variety of conditions other than intracranial injury can affect mental status. Hypoxia, hypovolemia, and hypothermia should be expeditiously corrected. Exposure and Environmental Control The victim should be fully undressed and exposed, if possible in a protected environment. Garments and gear should be removed if necessary by cutting them away, unless the garments can be dried and are essential for future protection from the environment. Wet clothing must be removed early to prevent BOX 21-1 Glasgow Coma Scale This scale evaluates the degree of coma by determining the best motor, verbal, and eye-opening responses to standardized stimuli. Eye Opening Spontaneous To voice To pain None
4 3 2 1
Verbal Response Oriented Confused Inappropriate words Incomprehensible words None
5 4 3 2 1
Motor Response Obeys command Localizes pain Withdraw (pain) Flexion (pain) Extension (pain) None Maximum Score
6 5 4 3 2 1 15
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CHAPTER 21 Wilderness Trauma and Surgical Emergencies
hyperextended, hyperflexed, or rotated to establish or maintain an airway. Approximately 10% of victims with head injuries or facial fractures have a concomitant cervical spine fracture. In one series of patients, 25% (29 of 116 patients) had unstable cervical fractures as defined by needing a halo or surgical intervention.23 Such a fracture should be assumed to exist in any person with a significant injury above the level of the clavicle. If a situation requires removal of immobilizing devices, in-line stabilization, not traction, must be maintained.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
hypothermia. It is mandatory to visualize the entire victim to document and assess injury. However, this step of the primary survey should be performed with caution. First, it is imperative to cover the victim immediately after removal of clothing. Hypothermia and its effects on mental status, cardiovascular function, and coagulation are among the most underappreciated entities in care of the trauma victim. The possibility of hypothermia should be entertained in all environments because it is most prevalent in the winter and summer months. Hypothermia reflects the inability of trauma victims to use available stored energy to carry on normal metabolic processes. A severely injured patient may become hypothermic in any ambient environment. Second, clothing and gear should not be removed from the victim unless complete immobilization of injuries can be achieved. Assessment of an area of injury should be performed, but clothing should be left to cover the patient to ensure body temperature is maintained. Expedition members may be wearing a variety of gear and clothing, including biking, skiing, or climbing helmets. Helmets should be removed with in-line stabilization of the cervical spine.
SHOCK The shock state has been defined in many ways. Essentially, shock describes the physiologic condition in which oxygen delivery to the tissues of the body is not adequate for the metabolic demands of those tissues. This results in cellular hypoxia, anaerobic metabolism, and, eventually, cell death. Shock was defined historically by John Collins Warren as “a momentary pause in the act of death.” Nowhere is this adage more applicable than in the wilderness setting. Any physician who cares for trauma victims has witnessed an apparently “stable” victim rapidly deteriorate and die. With only clinical acumen, the wilderness physician must be sufficiently astute to identify the subtle early signs of shock. The treatment for shock is resuscitation, which may be defined as any intervention that restores blood flow and cellular oxygenation. The power of the primary survey lies in the fact that it is essentially a form of resuscitation. Rapid identification and treatment of conditions leading to hypoperfusion facilitate their reversal. A key in resuscitation of the trauma victim is identification of and stopping ongoing hemorrhage.3 Rapid control of external hemorrhage is critical. External sources of hemorrhage can initially be managed with direct pressure. If direct pressure must be interrupted during extrication, other techniques may be used. Exsanguinating hemorrhage from the scalp can be managed with sutures. Tourniquets may be applied to extremities for temporary control.50 Although the majority of trauma victims exhibiting signs of shock in the wilderness have sustained acute blood loss, a nonhemorrhagic entity, such as a spinal cord injury or pneumothorax, may be responsible for shock. Hemorrhagic shock is classified according to the blood volume that has been lost. A central question in caring for victims of blood loss in the wilderness is the reliability of vital signs in quantifying degree of hemorrhage. Associated with each class of hemorrhage are clinical signs that allow a caregiver to quantify blood loss (Table 21-1). It is evident that assessing blood pressure alone is a poor way to predict impending deterioration. When hypotension is present, a normal individual has already lost 30% of his or her blood volume, and salvage may be impossible.
Resuscitation should be initiated at the first sign of shock, equating to class II hemorrhage, and evacuation planned accordingly.
VASCULAR ACCESS Vascular access must be obtained promptly. The standard method of obtaining access is by insertion of two large-bore (16-gauge or larger) catheters, preferably into peripheral veins of the upper extremity. Alternatives include using lower extremity veins and obtaining central venous access. If peripheral access cannot be secured, the femoral vein should be the next site attempted. Advantages of femoral vein access include ease of cannulation relative to jugular and subclavian access, and fewer complications.93 Depending on expertise, the internal jugular and subclavian veins may be accessed. Despite a higher incidence of complications compared with peripheral access, central access complication rates in trauma centers have been demonstrated to be less than 5% in most studies.93 If peripheral access is inadequate or unobtainable, it is clear that the next site attempted should be determined by the provider’s level of confidence and expertise. As a last resort, venous cutdown may be considered. Despite fewer complications than central access, cutdowns are experience and equipment dependent and not recommended in the wilderness environment. Intraosseous access is also to be considered in adults. Several commercially available products are available (Figure 21-1). The manubrium is the target for insertion of the FAST1 intraosseous device. The Bone Injection Gun (BIG) and EZ-IO can be used to access the bone in the proximal tibia and humerus. The FAST1 and BIG are impact-driven devices. The EZ-IO is a drill-based device. Skills to successfully place intraosseous venous access can be acquired with short training times.30 Children in the wilderness younger than 6 years of age in whom venous access cannot be obtained should undergo intraosseous resuscitation. This is accomplished by introducing a needle through the periosteum of the tibia just inferior to the tibial tuberosity. Needles that are 18- to 20-gauge are preferable, but any needle strong enough to penetrate the periosteum without bending can be used. Of the resuscitative therapies that potentially may be initiated in a well-prepared expedition, volume resuscitation deserves considerable attention. Fluid resuscitation in trauma has been a contentious topic, perhaps overly so, relative to fluid type and amounts used. A number of recent studies focusing on the prehospital administration of fluids in trauma victims not only rehashed the fluid composition debate but called into question the efficacy of prehospital resuscitation.74 Although further prospective trials are needed relative to fluid type and prehospital use, an impressive compilation of data has been amassed looking at resuscitative fluids in the trauma victim. Past studies have not only compared colloids with crystalloids89 but explored the use of blood and plasma substitutes and hypertonic saline. Detailed analyses of these studies is beyond the scope of this chapter, but a summary of fluid recommendations is in order. In small volumes, hypertonic saline has been shown to be an effective resuscitative fluid, and its efficacy in closed head injury is under evaluation. Currently, no improvement in survival has been demonstrated using hypertonic saline compared with
TABLE 21-1 Classes of Hemorrhagic Shock
Blood loss (mL) Blood loss (% blood volume) Pulse rate (beats/min) Blood pressure Pulse pressure (mm Hg) Respiratory rate (breaths/min) Urine output (mL/hr) CNS/mental status Fluid replacement (3 : 1 rule) CNS, Central nervous system.
414
Class I
Class II
Class III
Class IV
Up to 750 Up to 15 <100 Normal Normal or increased 14-20 >30 Slightly anxious Crystalloid
750-1500 15-30 >100 Normal Decreased 20-30 20-30 Mildly anxious Crystalloid
1500-2000 30-40 >120 Decreased Decreased 30-40 5-15 Anxious, confused Crystalloid and blood
>2000 >40 >140 Decreased Decreased >35 Negligible Confused, lethargic Crystalloid and blood
B
C
FIGURE 21-1 A, FAST1 intraosseous infusion system. B, Bone Injection Gun (BIG). C, EZ-IO.
crystalloid, and its use has been associated with hypokalemia, pulmonary edema, and dramatic increases in serum sodium and osmolarity.6 The significance of these reported complications in trained hands is questionable, and hypertonic fluids may have a future role in resuscitation. Further study is warranted on the use of hypertonic saline, but its use in the wilderness setting is not recommended at this time. Based on the current literature, it is clear that both colloids (including hetastarches and albumin) and crystalloids are efficient volume expanders.80 Larger volumes of crystalloids than of colloids are needed to achieve similar resuscitative end points, usually in a ratio of 3 to 1. However, no benefit in survival by using colloids has been demonstrated, and recent studies indicate that their use in critically ill patients may increase mortality.18,71 In addition, no proved detriment, including increased extravascular lung water, impaired wound healing, or decreased tissue oxygen diffusion, has been demonstrated with the use of large volumes of crystalloids. Crystalloids are safe, nonantigenic, easily stored and transported, effective, and inexpensive. Most experts in trauma care agree that crystalloid is preferable to colloid infusion in the prehospital, early resuscitative phase of trauma care. Accordingly, the resuscitative fluid recommended by ATLS protocol is normal saline. In expeditions in which weight and space are considerations, colloids may have an advantage. “Colloid fluids will achieve a given increment in plasma volume with only one-quarter to onethird the volume required of crystalloid fluids.”58 To restore circulating volume, colloids provide greater efficacy per weight/ volume trekked into the austere environment. For the expeditionist carrying resuscitation fluids in a backpack, 1 lb of colloid will provide about three times the volume expansion of 1 lb of crystalloid. Several animal studies and recent human clinical trials in trauma victims have found that treatment with IV fluids before control of hemorrhage resulted in increased mortality rates.8,60 Although these data are compelling, they have been accumulated in victims with penetrating injuries and short prehospital times, and the definition of prehospital resuscitation in these studies comprised widely varying volumes. Prehospital resuscitative protocols remain in evolution. However, application of these data to the wilderness setting at the current time is dangerous, for a number of reasons. First, the leading cause of death in wilderness trauma is head injury. Many multiple-trauma victims have a head injury, and it may be impossible to discern whether an intracranial lesion is present. Although under continued study, the current approach to management of head injury is aggressive maintenance of cerebral perfusion pressure to control intracranial pressure (ICP). Underresuscitation in the context of an intracranial injury could be catastrophic. Second, the multisystem-injured victim frequently presents with associated orthopedic injuries. A victim with closed extremity fractures with significant contained hemorrhage benefits from fluid resuscitation. Third, a victim with significant external hemorrhage that can be controlled before evacuation benefits from intravascular repletion.
In summary, resuscitation with IV fluids should be initiated in the field, particularly in victims with head injury and unquantified multiple trauma. Victims should have vascular access secured and resuscitative fluids given in the form of normal saline as dictated by severity of injuries and hemodynamics. In patients in whom urinary catheterization can be performed, a target of 30 mL/hr is a good target. In those patients in whom hourly urine output cannot be determined, other measures of perfusion, such as heart rate, blood pressure, and mental status, can determine the efficacy of resuscitation.
SECONDARY SURVEY The secondary survey is an extension of the primary survey and should not be undertaken until the primary survey is complete and the victim has been stabilized. In addition, resuscitative regimens, if available, should have been initiated. The secondary survey is a head-to-toe assessment of the victim, including history and physical examination. The face, neck, chest, abdomen, pelvis, extremities, and skin should be examined in sequence. A more detailed neurologic examination should be completed, including reassessment of the GCS. The neck should be examined independently of the thoracolumbar spinal cord. Examination of the pelvis should not include the traditional “rocking” to determine stability, because in the presence of pelvic fractures, this action may exacerbate existing comminution. The detailed secondary survey should not delay evacuation packaging. As in the nonwilderness setting, it is imperative to repeat the primary survey as the victim’s condition warrants. Specific examinations are discussed in the sections covering regional injuries. History The victim’s history should be assessed during the secondary survey. Knowledge of the mechanism of injury and any comorbid medical conditions or allergies may enhance understanding the victim’s physiologic state. The ATLS “AMPLE” history is a useful and rapid mnemonic for this purpose: Allergies Medications currently used Past medical history/Pregnancy Last meal Event or Environment related to the injury Adjuncts Resuscitation should be initiated simultaneously with the primary survey. The degree of resuscitation depends on available resources, experience of the rescuer(s), and environmental conditions. Under the best circumstances, initial management of the wilderness trauma victim provides for airway control, adequate oxygenation and ventilation, appropriate fluid resuscitation, and stabilization of cardiac function while continuing to monitor and reassess the patient’s vital signs. As adjuncts to the secondary survey, it also 415
CHAPTER 21 Wilderness Trauma and Surgical Emergencies
A
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includes placement of a urinary catheter and nasogastric (NG) tube. This degree of resuscitation will be almost universally unavailable in the wilderness setting. Here, resuscitation may be limited to oral administration of warm, high-calorie fluids and maintenance of victim comfort and body temperature. An NG tube and indwelling urinary (Foley) catheter should be placed if available and appropriate. Aspiration of gastric contents can be catastrophic in terms of patient survival after trauma. Gastric decompression with an NG tube may help prevent this type of adverse event in patients with a depressed level of consciousness. It should be remembered that children can exhibit significant hemodynamic consequences secondary to massive gastric distention. In this setting, decompression becomes critical. If possible, NG tubes should be placed in persons who are endotracheally intubated in the field. The tube can be aspirated sequentially with a syringe or left open to gravity drainage. Any suspicion of facial fracture should deter attempts to place an NG tube, and orogastric decompression should be chosen instead. A Foley catheter can assist in volume assessment and hemodynamic status determination in a critically injured victim. Hourly urine output typically does not decrease until the onset of class III hemorrhagic shock, with loss of 30% to 40% of blood volume. Contraindications to urinary catheter placement in the field are blood at the urethral meatus, high-riding prostate, scrotal hematoma, and personnel not experienced in placement. Injuries to the Head, Face, and Neck The secondary survey begins with examination of the entire head and scalp for evidence of skull or facial fractures, ocular trauma, lacerations, and contusions. The scalp is thoroughly palpated for tenderness, depressions, and lacerations. The bones of the face, including the zygomatic arch, maxilla, and mandible, are palpated for fractures. Elements of the GCS are repeated. The wilderness eye is discussed in detail in Chapter 28, but general examination principles are simple. Significant periorbital edema may preclude examination of the globe, so assessment should be carried out early. The globe should be evaluated for visual acuity, pupillary size, conjunctival hemorrhage, lens dislocation, and entrapment. Persons with significant facial trauma have a high incidence of associated ocular or orbital injuries.77 Recent studies of ocular injuries in trauma victims have emphasized underappreciation by many disciplines of ocular and periocular signs indicative of significant underlying injury.73
HEAD INJURIES Approximately 500,000 to 2 million cases of head injury occur in the United States yearly.34 Of these, approximately 10% result in the patient’s prehospital death.3 Long-term disability associated with head injury is significant, with more than 100,000 persons suffering varying degrees of permanent impairment. Because of the high-risk nature of traumatic brain injury (TBI) and the impact of initial management on disability and survival, clinical management objectives must address both immediate survival and longterm outcome. Management guidelines for head injuries in a wilderness do not exist, and a wide range of clinical approaches are used in hospital settings.34 However, the literature suggests that morbidity and mortality can be reduced by means of a protocol that includes early airway control with optimization of ventilation,40 prompt cardiopulmonary resuscitation, and rapid evacuation to a trauma care facility. Initial management of head injury in the wilderness should follow established ATLS protocols. Prompt attention must then be given to victim triage, evacuation strategies, and ongoing resuscitative needs to prevent or minimize secondary brain injury. Expeditious evacuation to a neurosurgery-capable trauma center is essential. Multiple clinical and experimental studies have demonstrated the detrimental effects of hypoxia on the injured brain. A definitive airway should be established if any degree of neurologic or respiratory compromise exists. Cervical spine injuries are common in patients with TBI. Therefore cervical spine immobilization is paramount in the prevention of further devastating neurologic injury. 416
After immobilization, attention is directed to the prevention of secondary brain injury. The purpose of the wilderness head injury protocol is to allow individuals with widely varying levels of experience and expertise to identify signs of significant head injury, begin proper resuscitation in the context of prevention of secondary brain injury through airway maintenance and hemodynamic support, and evacuate appropriately. Anatomy The scalp comprises five layers of tissue that cover the calvaria: skin, connective tissue, galea aponeurotica, loose areolar tissue, and periosteum of the skull. The galea is a fibrous tissue layer with important ramifications in closure of scalp wounds, discussed later in this chapter. Loose areolar tissue beneath the galea represents the site of accumulation of blood in scalp hematomas. A rich vascular network located between the dermis and the galea supplies the scalp. When lacerated, these vessels can be a significant source of hemorrhage, which may be important if evacuation is impossible or delayed. The skull is composed of two groups of bones that form the face and cranium. Cranial bones are divided into the calvaria and skull base. The calvaria is composed of frontal, ethmoid, sphenoid, parietal, and occipital bones. Within the skull, the brain is covered by three membranous layers that may be of pathophysiologic importance after injury. However, in the wilderness environment, these layers have little clinical relevance (except in terms of defining an open versus closed brain injury). Pathophysiology of Traumatic Brain Injury TBI can be divided into primary and secondary brain injuries. Primary injury consists of the physical or mechanical insult at the moment of impact, and the immediate and permanent damage to brain tissue. Little can be done in the wilderness setting relative to primary brain injury. Secondary brain injury is the biochemical and cellular response to the initial mechanical trauma and includes physiologic derangements that may exacerbate effects of the primary trauma. Such pathophysiologic alterations include hypoxia, hypotension, and hypothermia. Compounding these pathophysiologic alterations is elevation of ICP after TBI. Increased ICP increases cerebral ischemia and exacerbates secondary brain injury. Many forms of head injury result in elevated ICP, the duration of which is significantly correlated with poor outcome. The Monro-Kellie doctrine states that the volume of intracranial contents must remain constant because the cranium is a rigid container. The normal compensatory response to increased intracranial volume is to decrease venous blood and cerebrospinal fluid (CSF) volume within the brain. If this normal response is overwhelmed, small increases in intracranial volume result in exponential increases in ICP. A rigid bony cranium cannot expand to accommodate increases in brain volume and the resultant increase in ICP. Brain parenchyma becomes compressed and eventually displaced from its anatomic location. In the most devastating circumstances, the brain parenchyma herniates toward the brainstem through the largest cranial opening (the foramen magnum) and death rapidly follows. The volume– pressure curve in Figure 21-2 relates the small, but critical, time period between neurologic symptoms, hemodynamic decompensation, and brainstem herniation. Elevation in ICP directly correlates with secondary brain injury. Therefore the field provider must attempt to minimize ICP of head-injured patients to the greatest extent possible. The most important priority in minimizing secondary brain injury in the field is optimizing cerebral perfusion pressure (CPP). CPP is related to ICP and mean arterial pressure (MAP) as follows: CPP = MAP − ICP A CPP less than 70 mm Hg after head injury correlates with increased morbidity and mortality.3,39 Cerebral blood flow (CBF) should be maintained at approximately 50 mL/100 g brain tissue per minute.57 At 5 mL/100 g per minute, irreversible damage and potential cell death occur.3 Study data have shown a correlation between low CBF and poor outcome.57 At a MAP between 50 and 160 mm Hg, cerebral autoregulation maintains CBF at relatively constant levels. Not only is autoregulation disturbed in
Herniation
60 55 50 ICP (mm Hg)
45 40 35 30 25 20 15 10 5
Point of hemodynamic decompensation Volume of mass
FIGURE 21-2 Critical time period between decompensation and brainstem herniation after traumatic brain injury.
injured regions of the brain, but a precipitous fall in MAP can further impair autoregulatory function, decreasing CBF and exacerbating ischemia-induced secondary injury. The field provider is able to combat a rise in ICP by simply optimizing MAP through aggressive IV fluid resuscitation. Diagnosis The three useful descriptions of head injury that may be applied to field recognition are history, severity, and morphology. History includes mechanism of injury, timing of the event, and related circumstances. This knowledge assists in the decision-making process with regard to resuscitation and evacuation.3 Mechanism of injury is identified as blunt or penetrating trauma. The anatomic demarcation between blunt and penetrating injury is traditionally defined by violation of the outer covering of the brain (dura mater). Blunt injuries in the wilderness setting most often result from falls, falling objects, or assaults. Penetrating injuries are most commonly gunshot or other projectile wounds. Severity of injury can be estimated by quantifying the GCS and pupillary response. The generally accepted definition of coma is a GCS score less than or equal to 8; these patients often require endotracheal intubation. Although GCS score does not directly correlate with the need for intubation, it is essential that all head-injured patients be provided a stable, secure airway by the most appropriate means available. It is important to note the TBI victim’s best initial motor response because this is most predictive of long-term neurologic outcome. Any victim with a GCS score less than 15 who has sustained a head injury should be evacuated if possible. A low or declining GCS score suggests increasing ICP. Abnormal pupil size or asymmetric pupillary responses suggest increased ICP. These clinical deteriorations demand the rapid attention of rescue or evacuation personnel to optimize MAP and CPP, minimize secondary brain injury, and prevent brainstem herniation. Injury morphology may be difficult to assess in the wilderness setting and relies on level of suspicion and clinical signs and symptoms. After attention to the primary survey, including airway provision and spinal immobilization, the physical examination component of the secondary survey is imperative and can provide information about the presence of a TBI. Injury Classification Intracranial injuries range from concussion to massive subdural hematoma. Subdural hematomas are more common than are epidural hematomas, constituting 20% to 30% of mass lesions. “Subdurals” result from torn bridging veins between the cerebral cortex and draining venous sinuses. Their prognosis is worse than that of “epidurals,” although prompt recognition and drainage improve patient outcome. Epidural hematomas are most commonly located in the temporal region and result from injury to the middle meningeal artery, often associated with a fracture.
These patients may present with loss of consciousness, followed by a lucid interval and subsequent rapid neurologic deterioration. This sequence, however, is not frequently observed. Hemorrhagic contusion is also quite frequent, constituting 35% of traumatic injuries, and has the propensity to significantly increase ICP. Diffuse axonal injury (DAI) is the term used to describe prolonged post-traumatic coma not resulting from a mass lesion or ischemic insult. Similar to hemorrhagic contusion, diffuse axonal injury may result in elevated ICP. Physical Examination After the primary survey and initial attempts to resuscitate the victim, a more complete physical examination should be done. However, this examination should not delay patient evacuation. A hallmark of TBI is altered level of consciousness. Determination of the GCS score aids in recognition of TBI and should be regularly reassessed to provide a mechanism for quantifying neurologic deterioration. Physical signs that may denote underlying brain injury include significant scalp lacerations or hematomas, contusions, facial trauma, and signs of skull fracture. Findings specific for basilar skull fracture include ecchymosis behind the ears (Battle’s sign) and periorbital ecchymosis (raccoon eyes). Blood behind the tympanic membrane on otoscopic examination (hemotympanum), frank bleeding from the ears, and CSF rhinorrhea/otorrhea also suggest skull fracture and underlying TBI. The pupillary examination may provide valuable data in assessing underlying TBI. Herniation of the temporal lobe of the brain may be heralded by mild dilation of the ipsilateral pupil with sluggish response to light. Further dilation of the pupil followed by ptosis (drooping of the upper eyelid below its normal level), or paresis of the medial rectus or other ocular muscle, may indicate third cranial nerve compression by a mass lesion or herniation. Table 21-2 relates pupillary examinations to possible underlying brain lesions. Most dilated pupils (mydriasis) are on the ipsilateral side to the mass lesion. With direct globe injury, traumatic mydriasis may result, making evaluation of TBI more difficult. In addition, 5% to 10% of the population has congenital anisocoria (a normal difference in pupillary size between the eyes). Casual inspection may overlook a prosthetic eye, which is mistaken for a fixed pupil. Neither direct trauma nor congenital anisocoria should be assumed in a head-injured victim exhibiting mental status change in the wilderness. After quantification of GCS score, pupillary examination, and examination of the head and face for signs of external trauma, a concise neurologic examination should be performed. The goal of the field neurologic examination is to identify motor or sensory focal deficits suggestive of intracranial injury. Sensory deficits follow the general dermatome patterns shown in Figure 21-3. Unilateral hemiplegia may signify uncal herniation resulting from mass effect in the contralateral cortex because of compression of the corticospinal tract in the midbrain. Ipsilateral pupillary dilation associated with contralateral hemiplegia is a classic and ominous sign of tentorial herniation. Deep tendon reflex changes in the absence of altered mental status are not indicative of TBI. TABLE 21-2 Interpretation of Pupillary Findings in
Head-Injured Victims
Pupil Size
Light Response
Interpretation
Unilaterally dilated
Sluggish or fixed
Bilaterally dilated
Sluggish or fixed
Unilaterally dilated or equal Bilaterally constricted
Cross-reactive (Marcus Gunn) Difficult to determine; pontine lesion Preserved
Third nerve compression secondary to tentorial herniation Inadequate brain perfusion; bilateral third nerve palsy Optic nerve injury
Bilaterally constricted
Opiates Injured sympathetic pathway
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CHAPTER 21 Wilderness Trauma and Surgical Emergencies
VOLUME-PRESSURE CURVE
PART 4 INJURIES AND MEDICAL INTERVENTIONS
C2 C2 C3 C4 C5 T1 T2 T3 T4 T5
C6
Posterior cervical rami Posterior thoracic rami Supraclavicular (C3,4) Axillary (C5,6) Medial brachial cutaneous (C8–T1) Radial (C5,8) Anterior thoracic rami Lateral thoracic rami
T6 T7 T8 T9 T10 T11 T12 L1 L2 L3
L4
Musculocutaneous (C5,6) Medial antebrachial cutaneous (C8, T1) Iliohypogastric (L1) Posterior sacral rami Radial (C6–8) Ulnar (C8,T1)
S2 Ilioinguinal (L1)
Median (C5–8)
Lateral femoral cutaneous (L2,3) Obturator (L2,3,4) Anterior femoral cutaneous (L2,3)
C3 C4 C5 C6 C7 C8 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2 S3
L3 Posterior lumbar rami
S2 L1 L2
Posterior femoral cutaneous (S1,2,3)
L5
Common peroneal (L4,5,S1) Saphenous (L3,4)
S1 Superficial peroneal (L4,5,S1)
Sural (S1,2) Superficial peroneal (L4,5,S1) Deep peroneal (L4,5)
Dermatomes–anterior
CUTANEOUS NERVES
Dermatomes–posterior
FIGURE 21-3 Dermatome pattern, showing the skin area stimulated by spinal cord elements. Sensory deficits follow general dermatome patterns.
Detailed evaluation of brainstem function cannot be undertaken in the wilderness setting. Performance of gag and corneal reflex evaluations may provide some information helpful in triage and evacuation planning, but their presence would not automatically obviate the need for prompt evacuation. Resuscitation Resources and circumstances permitting, resuscitation should be initiated as an adjunct to the primary survey. The primary focus for the head-injured victim, similar to any traumatized victim, is the airway. During the primary survey and performance of the ABCDE sequence, IV access should be established. If IV resuscitation is impossible, it is not advisable to administer fluids orally to the victim with head injury because of the likelihood of vomiting, airway compromise, and aspiration. Individuals sustaining head trauma have a high incidence of concomitant injuries. Up to 32% of persons with severe head injury have a long bone or pelvic fracture, 20% to 25% a chest injury, and 10% an abdominal injury. A victim who does not have a palpable femoral pulse or presents with other signs of hypotension in the context of suspected head injury must not be assumed to have a neurogenic etiology of shock, so other etiologies must be thoroughly and aggressively investigated. Resuscitation is critical in the setting of head injury for multiple reasons. Management of a head injury should be secondary to other life-threatening injuries, which, if not addressed, may preclude survival. As previously discussed, maintenance of MAP (and thus CPP) is critical in preventing secondary brain injury. The type of resuscitative fluid administered to trauma victims continues to be controversial. Previously, recommendations warning of the dangers of overhydration in head injury led to 418
recommendations restricting fluids. Restriction of fluid has not been shown to reduce ICP or edema formation in laboratory models of TBI. Theories about limiting cortical free water content in TBI by using hypotonic IV solutions have not been borne out in animal studies.88 The need for resuscitation and intravascular volume support has been well established. Possible resuscitative fluids include isotonic crystalloids, hypertonic crystalloids, or colloid solutions. There is convincing evidence that hypotonic fluids are not appropriate in TBI secondary to an increase in whole-brain water content and subsequent elevation in ICP. Recent data from animal studies of TBI suggest that colloid solutions offer no advantage over isotonic crystalloids, such as lactated Ringer’s solution, in terms of augmenting CBF or preventing cerebral edema.97 As previously noted, no prospective trial has clearly documented an advantage of colloid over crystalloid administration in the victim with multiple systemic injuries. Evidence is accumulating that hypertonic solutions, particularly hypertonic saline, may be beneficial in TBI.90,94 However, an advantage has not been demonstrated in trauma victims overall, and expertise is necessary for their use. The recommended resuscitative fluid for the head-injured victim in the wilderness setting is isotonic crystalloid, with a target MAP of 85 to 95 mm Hg based on cuff blood pressure determinations or extrapolation from distal pulses evaluation. Further Management Numerous adjuncts exist in the management of the head-injured victim, few of which are applicable in the wilderness setting. Once the primary and secondary surveys are complete, the airway is secured, resuscitation has been initiated, and spine immobilization has been achieved, the victim should be placed
Skull Fracture Skull fracture in the wilderness mandates evacuation. Therapeutic options in the field are few, with intervention limited to identifying the injury and arranging rapid transport. Skull fractures may be open or closed, linear or stellate, and may occur in the vault or skull base. These fractures are associated with a high incidence of underlying intracranial injury. Skull fractures with depression greater than the thickness of the skull may require elevation. No attempt at elevation should be made in the field. Any exposed brain surface should quickly be covered with the most sterile covering available, preferably moistened with crystalloid solution. Loose bone or brain fragments should not be manipulated. If a broad-spectrum antibiotic is available, it should be administered. After attention to the wound and stabilization of associated injuries, the victim should be rapidly evacuated. Penetrating Head Injuries The majority of penetrating head injuries in the wilderness are gunshot wounds, although knives and arrows may penetrate the cranium. Such penetrating injuries are usually catastrophic. However, examples of survival exist with small-caliber, lowvelocity injuries and tangential wounds.59 As with closed head injury, management priorities consist of maintenance of airway, prevention of secondary brain injury, and rapid evacuation. If the cranium has been violated, the victim should receive antibiotics and tetanus immunization in the same manner as for open skull fracture. In the rare instance that the projectile is embedded
in the skull, no attempt at removal should be undertaken. If the length of the projectile makes immobilization or transport cumbersome, excess length may be removed, but only if this can be done without displacement of the intracranial segment. Evacuation Survival and outcome of head injury in the wilderness correlate directly with rapidity of evacuation. Certain situations dictate immediate evacuation. Any person with evidence of an open or closed skull fracture should be evacuated. The incidence of TBI associated with skull fracture is variable but significant throughout the literature. Recent data predict that 30% to 90% of persons with raccoon eyes or Battle’s sign will show abnormalities on computed tomography (CT) scan.11,17 Similarly, any person who sustains a penetrating injury should be evacuated. Decisions concerning evacuation of victims who have sustained closed head injuries can be simplified by dividing the victims into three groups based on probability of injury. A high-risk group, defined as patients with a GCS score of 13 or less, focal neurologic signs, or evidence of decreasing level of consciousness, requires evacuation. The low-risk group includes persons who have suffered a blow to the head but are asymptomatic, did not lose consciousness, and complain only of mild headache or dizziness. Data from recent studies suggest that persons who meet low-risk criteria (including a GCS of 15, no loss of consciousness, minimal symptomatology, and unlikely mechanism) have a minimal chance of having significant TBI and may be closely observed.11,17 This group includes patients who have suffered a concussion. The Quality Standards Subcommittee of the American Academy of Neurology78 defines concussion as a trauma-induced alteration in mental status that may or may not involve the loss of consciousness. The neurologic impairment is short-lived and resolves spontaneously without any structural injury to the brain. Close observation includes awakening the patient from sleep every 2 hours and avoidance of strenuous activity for at least 24 hours. The following signs indicate more advanced medical care is necessary: (1) inability to awaken the patient; (2) severe or worsening headaches; (3) somnolence or confusion; (4) restlessness, unsteadiness, or seizures; (5) difficulties with vision; (6) vomiting, fever, or stiff neck; (7) urinary or bowel incontinence; and (8) weakness or numbness involving any part of the body.51 No prospective validated guidelines for return to activity have been established. Generally, one should not return to an environment in which concussion is a risk (e.g., contact sports) until symptoms have been absent for 7 days. Patients with a predisposition to bleeding need a much more aggressive approach requiring evacuation and evaluation at a higher level of care. The group for which the evacuation decision is most difficult is the moderate-risk group. These persons have a history of brief loss of consciousness or change in consciousness at the time of injury, or a history of progressive headache, vomiting, or posttraumatic amnesia. If any of these signs is present in the face of concurrent systemic injury, the victim should be evacuated immediately. Studies associating clinical variables and abnormal results on CT scan have demonstrated the significance of decreased GCS score, symptoms, and loss of consciousness. If these signs are present in isolation and the evacuation can be completed in less than 12 hours, the evacuation should proceed. If the evacuation is impossible or will require longer than 12 hours, the victim should be closely observed for 4 to 6 hours. If the examination improves to normality during the observation period, it is reasonable to continue observation.
NECK INJURIES Blunt Neck Injuries Injuries to the neck may be classified as blunt or penetrating. Significant blunt injuries include cervical spine injuries and laryngotracheal injuries. Seventy-five percent of injuries to the trachea are confined to the cervical region.72 Fracture of the larynx and disruption of the trachea usually require surgical intervention unavailable in the wilderness. The sooner laryngeal repair is accomplished, the better the outcome with respect to phonation.20 Victims present with a history of a significant blow to the 419
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in a 30-degree head-up position. This position assists in control of ICP, and thus CPP, through augmentation of venous outflow. This maneuver should not be attempted if the spine cannot be adequately immobilized. If endotracheal intubation is possible, ventilation should be optimized without hyperventilating the victim. Hyperventilation has been used aggressively in the past to promote hypocarbiainduced cerebral vasoconstriction, theoretically to decrease brain swelling. However, if the PaCO2 falls below 25 mm Hg, severe vasoconstriction ensues, effectively reducing CBF, promoting ischemia, and possibly augmenting secondary brain injury. Studies have demonstrated worse outcomes in victims with severe head injury who were hyperventilated.67 Inability to measure or titrate PaCO2 in the wilderness mandates that res piration be controlled to approximate near-normal minute ventilation. All bleeding from the scalp or face should be controlled with direct pressure. Scalp hematomas, regardless of size, should not be decompressed. Open wounds, particularly skull fractures, should be irrigated and covered with the most sterile dressing available. Fragments of displaced cranium overlying exposed brain tissue should not be replaced. If signs of skull fracture are present, broad-spectrum antibiotic prophylaxis and immunization against tetanus are recommended as soon as possible. Although diuretics have been widely used in the intensive care management of intracranial hypertension, no rationale exists for their use in the field. The wilderness trauma victim may have many injuries that are impossible to evaluate fully in the field. In this setting, particularly in the presence of hemorrhagic shock, attempts to induce osmotic diuresis to decrease ICP may be lifethreatening. Diuretics such as furosemide or mannitol may exacerbate hypotension, cause metabolic alkalosis, and induce renal complications in the absence of physiologic monitoring.2 Corticosteroids have no role in head injury in the field or intensive care unit. Studies have documented no beneficial impact on ICP or survival. Attempts at brain preservation by slowing metabolic rate and oxygen consumption have no role in the wilderness setting. Barbiturates have been used for elevated ICP refractory to other measures, but may induce hypotension, depress myocardial function, and confound the neurologic examination.2 Compared with minimizing ICP, these interventions offer no significant benefit.39 Approximately 15% of persons with severe head injury experience post-traumatic seizures. Phenytoin, if available, can be safely administered in the field, but only after a witnessed seizure. Prophylactic administration has not been shown to decrease long-term seizure activity.
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anterior neck. Physical examination findings include difficulty with phonation, subcutaneous emphysema that may extend as far inferiorly as the abdominal wall, stridor, odynophagia, and often acute respiratory distress. Treatment is focused on establishing and maintaining an airway until evacuation can occur. Frequently the airway is in jeopardy. Because of the propensity for injuries of this type to result in significant and progressive edema, endotracheal or nasotracheal intubation is often necessary. If these options are unavailable, airway maintenance techniques, as described in the Primary Survey section, should be used. In the event of intubation failure or lack of availability with impending hypoxic death, a surgical cricothyrotomy may be needed. A recent study of prehospital cricothyrotomy demonstrated that success rates were high regardless of medical specialty as long as previous training had been accomplished.53 For further descriptions of airway management, refer to Chapter 20. Background. Vertebral column injury, with or without neurologic deficits, must be identified in any wilderness multipletrauma victim. Fifteen percent of victims sustaining an injury above the clavicles and 5% to 10% of persons with a significant head injury have a cervical spine injury. In addition, 55% of spinal injuries occur in the cervical region.59 In the wilderness setting, fractures or dislocations of the cervical spine are a result of falls from significant heights or of high-velocity ski or vehicular injuries. Twenty-eight percent of persons with cervical spine fractures have fractures elsewhere in the spine.10 Anatomy. The cervical spine consists of seven vertebrae. The anteriorly placed vertebral bodies form the weight-bearing structure of the column. The bodies are separated by intervertebral disks and held in place anteriorly and posteriorly by longitudinal ligaments. The paraspinal muscles, facet joints, and interspinous ligaments contribute as a whole to the stability of the spine. The cervical spine, based on its anatomy, is more susceptible to injury than are the thoracic and lumbar spine. The cervical canal is wide from the foramen magnum to C2, with only 33% of the canal constituting the spinal cord itself. The clinically relevant tracts in the spinal cord include the corticospinal tract, spinothalamic tract, and posterior columns. Classification and Recognition. Fractures of the cervical spine may result in neurologic deficit, with total loss of function below the level of injury.49 Spinal cord injuries should be classified according to level, severity of neurologic deficit, and spinal cord syndrome. Fractures of the C1-C2 complex generally result from axial loading (a C1 ring fracture, or Jefferson’s fracture) or an acute flexion injury (a C2 posterior element fracture, or hangman’s fracture). Approximately 40% of atlas (first cervical vertebra) fractures have an associated fracture of the axis (second cervical vertebra). The atlas fracture, if survived, is rarely associated with cord injury but is unstable and requires strict immobilization. Usually a complete neurologic injury at this level is unsurvivable owing to paralysis of respiratory muscle function. One-third of victims sustaining a severe upper cervical spine injury die at the scene. The severity of cervical spine fractures is a result of the neurologic compromise incurred. The most common mechanism of injury is flexion, and the most common level of injury is C5-C6.10 Fractures and dislocations may result in partial or complete neurologic injury distal to the fracture or in no neurologic injury at all. Partial injuries to the spinal cord result from typical patterns of injury. Because flexion injuries are the most common type of injury to the cervical spine, the anterior cord syndrome (see later) is the most commonly seen serious neurologic picture. A careful neurologic examination in the field to grade motor strength and document sensory response to light touch and pinprick yields important information that should be documented and reported to the treating physician at the definitive care facility. When appropriate resources are available, a rectal examination should be performed. Complete lack of tone and failure of the sphincter muscles to contract when pulling on the penis or clitoris (the bulbocavernosus reflex) indicate the presence of spinal cord injury. 420
When individuals with cervical spine fractures or dislocations are transported, the neck must be stabilized to prevent further injury to the spinal cord or nerve roots at the level of the fracture or dislocation. Approximately 28% of persons with cervical spine fractures have fractures elsewhere in the spine10; therefore the entire spine must be protected during transport. Occasionally a pure flexion event can result in dislocation of one or both of the posterior facets without fracture or neurologic injury. The victim may complain only of neck pain and limitation of motion. If so, the victim should be transported with the neck rigidly immobilized. With this injury, posterior instability is present (because the interspinous ligament is ruptured), and any further flexion stress could produce a spinal cord injury. Physical Examination. A thorough neurologic examination should be performed. Initial documentation of deficits and frequent repeat examinations are critical to follow-up care. The classification of injury in the field begins with determination of the level of injury. Knowledge of sensory dermatomes (see Figure 21-3) and motor myotomes is invaluable. The sensory level is the lowest dermatome with normal sensation and may differ on each side of the body. C1 to C4 are variable in their cutaneous distribution, so assessment should begin at C5. The examiner should not be confused by the occasional innervation of the pectoral skin by C1 to C4, known as the “cervical cape.” Light touch and pinprick should be assessed. Motor function should be assessed by the myotomal distribution listed in Box 21-2. Each muscle should be graded on a sixpoint scale: 0—Total paralysis 1—Palpable or visible contraction 2—Full range of motion without gravity 3—Full range of motion against gravity 4—Full range of motion with decreased strength 5—Normal strength Each muscle must be tested bilaterally and documented. The reflexes alluded to in the classification section, as well as anal sphincter tone, must be tested. Syndromes. There are three clinically useful spinal cord syndromes: Central cord syndrome is characterized by a disproportionate loss of motor power between the upper and lower extremities, with greater strength retained in the lower extremities. Sensory loss is variable. The mechanism of injury usually involves a forward fall with facial impact and hyperextension of the spine. Anterior cord syndrome is characterized by paraplegia and loss of pain and temperature sensation. It is the most common manifesting syndrome caused by cervical spine injury and carries a poor prognosis. Brown-Séquard syndrome results from hemisection of the cord. It consists of ipsilateral motor loss and position sense with contralateral sensory loss two levels below the level of injury. It is usually secondary to penetrating injury. Immobilization. After identification of injury, the caregiver faces a critical decision with important ramifications—whether to immobilize.29 Victims who would as a matter of course be immobilized in an urban setting might not be appropriate candidates for immobilization in the wilderness. The decision to immobilize converts an otherwise ambulatory victim who can actively participate in his or her own evacuation to one requiring more involved evacuation procedures. The subsequent evacuation can be dangerous to the victim and rescuers and demands significant expense and resource utilization. Risk criteria for cervical spine injury and the need for immobilization have been defined.43,56 All criteria for the exclusion of immobilization must be satisfied. These include normal mental status without chemical influence; lack of distracting injury; normal neurologic examination; and a reliable neck examination without midline neck pain, deformity, or tenderness. Figure 21-4 presents an evidence-based algorithm for determining need for immobilization. Although the need for immobilization poses hazards for the evacuation process, if criteria are met, immobilization takes
Sensory C5: Area over deltoid C6: Thumb C7: Middle finger C8: Little finger T4: Nipple T8: Xiphisternum T10: Umbilicus T12: Symphysis pubis L3: Medial aspect of thigh L4: Medial aspect of leg L5: First toe web space S1: Lateral foot S4 and S5: Perianal skin FIGURE 21-5 Proper spine immobilization.
Motor C5: Deltoid C6: Wrist extensors C7: Elbow extensors C8: Finger flexors, middle finger T1: Small finger abductors L2: Hip flexors L3: Knee extensors L4: Ankle dorsiflexors L5: Great toe extensors S1: Plantar flexors
precedence over ease of evacuation.63 A difficult balance must be struck in the wilderness between the likelihood of true injury and the danger to the expedition members and rescuers that may ensue when the victim is immobilized. If a rigid litter is not available, the victim should be maintained on the flattest surface possible. A rigid cervical collar should be placed. All collars allow some degree of movement, particularly rotation. Soft collars offer the least immobilization.28 The Philadelphia collar has been shown to allow 44% of normal rotation and 66% of normal lateral bending.59 To achieve 95% immobilization, a halo and vest are necessary. Any number of materials may be used to improvise an immobilizing device (see Chapter 23). Restriction of flexion, extension, and rotation must be achieved to the greatest degree possible. Optimal immobilization consists of a long spine board or litter, rigid collar, bolsters to the sides of the head, and tape or straps restricting movement (Figure 21-5). Treatment. The issue of pharmacotherapy for spinal cord injury is under continuous study. Currently, based on data accumulated by the National Acute Spinal Cord Injury Study Group,
documented blunt spinal cord injury should be treated with a bolus of 30 mg/kg of methylprednisolone within 8 hours of injury followed by a continuous infusion of 5.4 mg/kg/hr over the next 23 hours.14 Corticosteroids are not recommended in the field unless a victim clearly presents with a spinal cord injury in the absence of head injury. Because little definitive treatment for cervical spine injury can be accomplished in the field, survival and outcome depend on speed of transport and maintenance of airway. This is particularly true considering the association of cervical spine injury with head injury and major systemic trauma. Transport all victims with proven or suspected cervical spine injury to a definitive care facility. Penetrating Neck Injuries Similar to penetrating head injury, penetrating neck injury is usually due to gun or knife wounds. Most penetrating injuries do not confer bony instability; however, stability should not be assumed. Neurologic deficits, if present, can progress with further movement of an unstable spine. Projectiles should not be removed if embedded in the neck. Penetrating injuries to the neck may not directly injure the spine, but neurologic sequelae may result from blast effect. The same immobilization criteria should be implemented as when dealing with blunt injuries. Penetrating injuries to the neck are classified according to anatomic zones of injury (Figure 21-6). Zone I injuries extend from the clavicles to the cricoid cartilage. Zone II injuries occur between the cricoid cartilage and the angle of the mandible. Zone III injuries occur superior to the angle of the mandible. Historically, treatment has been based on penetration of the platysma muscle. In the wilderness setting, if the examiner is confident that platysmal penetration has not occurred, the victim may be observed and the wound considered a laceration. Much
Mechanism of injury suggestive of cervical spine injury? Yes/unknown Alert and oriented, no distracting injury, not intoxicated? Yes
III
II
Tenderness, pain spontaneously or with movement? No
I
Normal neurologic exam? Yes Immobilization unnecessary? FIGURE 21-4 Clinical assessment of cervical spine stability. Failure of any criterion suggests need for immobilization.
FIGURE 21-6 Zones in penetrating neck trauma (see text).
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BOX 21-2 Sensory and Motor Deficit Assessment
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debate has occurred over management of platysmal penetration within respective topographic zones, with treatment arms con sisting of surgical exploration versus radiographic evaluation. In the wilderness setting, such considerations remain relevant. A penetrating injury violating the platysma muscle indicates the possibility of significant neurovascular, esophageal, or tracheal injuries, so the victim should be evacuated with close attention to the airway.
INJURIES TO THE THORAX Background The mortality rate from thoracic trauma is approximately 10%. Approximately 25% of all trauma deaths in the United States are attributable to chest injury.3 However, only 15% of persons with penetrating thoracic trauma require thoracotomy. In the wilderness environment, blunt thoracic injuries usually result from falls or direct blows to the chest. Penetrating injuries result from gun, knife, or arrow wounds, or from impalement after a fall. Immediate, life-threatening thoracic injuries include airway obstruction, tension pneumothorax, flail chest, and cardiac tamponade. Pathophysiology Chest injuries often result in hypoxia, hypercarbia, and acidosis. The tissue hypoxia of thoracic trauma can be multifactorial. Inadequate delivery of oxygen can be from hemorrhagic shock, direct lung injury with ventilation–perfusion mismatch (pulmonary contusion, atelectasis, hematoma), or changes in normal intrathoracic pressure dynamics (tension or open pneumothorax). Hemodynamic instability and inadequate oxygen delivery may also result from cardiac tamponade or contusion. The expedition team member should report to any air crew the consideration of pneumothorax in the evacuated patient. Many wilderness expeditions involve travel to different altitudes. Flight medics are well trained in the impact of altitude on air in closed spaces. Flight medics may be better equipped and prepared to deal with chest injuries than is the expedition team. The air crew will also know the flight path and anticipated elevations to traverse to reach the next level of care. Physical Examination Thorough physical examination begins with visualization and inspection of the chest. Exposure of the chest should be completed in the primary survey. The airway is assessed for patency and air exchange, and the pattern of breathing is noted. In the immediate postinjury period, most trauma victims are tachypneic, partly from pain and anxiety. Dyspnea, cyanosis, the use of accessory muscles of respiration, and intercostal muscular retraction are abnormal and may give clues to the underlying injury. Chest wall movement during respiration should be symmetric. Paradoxical chest wall movement is associated with flail chest. The chest wall should be inspected for contusions and abrasions, which may herald underlying bony or visceral injury. Distention of the external neck veins in a person who has just suffered thoracic trauma and is hypotensive or tachycardic (heart rate greater than 130 beats/min) suggests impaired venous return to the heart. This finding may be seen in situations of increased intrathoracic or intrapericardial pressure and is associated with tension pneumothorax and pericardial tamponade. In tension pneumothorax, deviation of the trachea is in a direction opposite the lesion. One technique to identify the deviated trachea is to place the index finger in the suprasternal notch. Dyssymmetry of the space between the trachea and the lateral margins of the suprasternal notch facilitates identification of tracheal deviation. However, a recent review suggests the tracheal deviation should be de-emphasized as an indicator of tension pneumothorax because tracheal deviation was observed in less than 5% of two series of patients with pneumothorax.54 Significant sternal bruising may herald fracture or cardiac contusion. The thorax should be palpated systematically for bony tenderness, starting at the distal clavicles and working medially toward the sternum. The sternum is divided into the manubrium, 422
gladiolus (body), and xiphoid cartilage. The manubrium is joined to the gladiolus by fibrocartilage, but mobility at this joint is minimal. Each rib should be palpated individually. Ribs 1 to 7 are vertebrosternal; their costal cartilages join the sternum. Ribs 8 through 10 are vertebrochondral, with each costal cartilage commonly joining the cartilage of the rib above. Ribs 11 and 12 are vertebral ribs without attachment to the sternum. Point tenderness over a rib can be associated with contusion or fracture. Displaced fractures can be palpated; occasionally, bone grating can be palpated during respiration. Subcutaneous emphysema may extend up into the neck and down to the level of the inguinal ligaments. In the trauma situation, subcutaneous emphysema is invariably associated with pneumothorax. Vocal fremitus describes palpation of vibrations transmitted through the chest wall. During speech, the victim’s vocal cords emit vibrations in the bronchial air column that are conducted to the chest wall. Diminished vocal fremitus is associated with pneumothorax or hemothorax. To test for vocal fremitus, the examiner applies the palmar arch of the examining hand against the person’s anterior chest wall. The person is asked to repeat “one, two, three,” using the same pitch and intensity of voice with each repetition. If the vibrations are not well perceived, the patient is asked to lower the pitch of the voice. The chest should be symmetric, left to right. Percussion is used to detect changes in the normal density of an organ. Percussion of the chest is performed by placing the examining fingertips on the chest wall and sequentially striking the fingertips with the tip of the index or middle finger of the other hand. In the trauma victim, dullness replacing resonance in the lower lung suggests hemothorax. Hyperresonance or tympani replacing resonance occurs only with a large pneumothorax or tension pneumothorax. If a stethoscope is not available, primitive chest auscultation can be performed using a rolled piece of cardboard or paper. Any cylinder that can transmit sound through a column of air accentuates breath sounds when placed against the chest wall. The absence of sounds normally produced by the tracheobronchial air column indicates blockage in the airways or abnormal filtering of sound by fluid in the pleural cavity. In the trauma victim, this is invariably associated with pneumothorax or hemothorax. Ultrasound may be considered as an extension of the physical examination. Portable ultrasound systems are lightweight and durable. Ultrasound can be used to identify pneumothorax with greater sensitivity than physical examination. A pneumothorax can be identified by loss of the “comet tails” or pleural sliding. In a study using CT as the gold standard for identification of pneumothorax in 176 victims of blunt trauma, the sensitivity and specificity for ultrasound were 98.1% and 99.2%, respectively. This compared with the sensitivity and specificity for chest radiography of 75.5% and 100%, respectively.9 Six articles on the use of ultrasound to identify hemothorax concluded that ultrasound is a sensitive and specific method to identify hemothorax in trauma patients.61 Chapter 92 addresses the use of ultrasound and telemedicine in the wilderness. Blunt Chest Trauma Blunt chest trauma in the wilderness is most often associated with either a direct blow or a deceleration injury. The mechanism usually relates to a fall from a height. Compression of the chest wall by moving or falling debris may also contribute to intrathoracic injuries, as may be seen in traumatic asphyxia associated with burial in an avalanche or earthquake. Rib Fractures. Rib fractures range in severity from an isolated nondisplaced single fracture, which causes minor discomfort, to a major flail segment, which can be associated with an underlying hemopneumothorax and pulmonary contusion. Rib fractures are characterized by painful respiration, most severe on inspiration. Victims often breathe in a characteristically rapid, shallow pattern. Point tenderness is palpated over the fracture, and displacement can occasionally be detected. Rib fractures are detected with a compression test, in which pressure is exerted on the sternum
Costochondral Separation. It is difficult to distinguish between a rib fracture and costochondral separation. With the latter, pain is more likely to be predominantly anterior over the costochondral junction. Pain increases with inspiration and worsens with direct palpation. Costochondral separation also responds to intercostal nerve block and oral and IV analgesics. Sternal Fracture. A sternal fracture is usually associated with a direct blow to the anterior chest wall. The injury is characterized by severe, constant chest pain that worsens with direct palpation. Sternal instability is unusual and can be associated with a significant underlying visceral injury, including pulmonary or myocardial contusion. If the sternum is unstable, the victim should immediately be evacuated by litter or helicopter. Pneumothorax. Simple pneumothorax can occur from an injury that allows air to enter through the thoracic wall or, more frequently, from an injury to the lung that permits air to escape into the pleural space. Symptoms include tachypnea, dyspnea, resonant hemithorax, absence of breath sounds, and tactile fremitus. A person with chest pain after a blunt blow to the chest, particularly with accompanying rib fracture, should be suspected of having a pneumothorax. Treatment of pneumothorax involves decompression of the pleural space. In the wilderness environment, tube thoracostomy is rarely possible. Fortunately, although victims with isolated pneumothorax may complain of chest pain or dyspnea, they are not completely disabled. With analgesia to control pain, ambulation facilitates evacuation. It may be easier and more prudent to set a slow pace with frequent rest periods than to perform an unnecessary litter evacuation. If resources and expertise allow placement of a thoracostomy tube, it should be performed only when clinically indicated. Considering possible morbidity in a remote area, prophylactic decompression should never be undertaken. Suspicion of a pneumothorax alone on physical examination does not warrant a catheter or chest tube. When a high index of clinical suspicion is accompanied by incapacitating symptoms, such as shortness of breath, decompression should be considered. The key to saving a victim’s life is understanding that a condition exists that can rapidly progress from a nondisabling condition to a lifethreatening condition. Once the diagnosis of pneumothorax is entertained, vigilant observation and a high index of clinical suspicion are necessary in the event of progression to a tension pneumothorax. Symptoms should be closely monitored, and frequent repeat examinations should be performed. Tension Pneumothorax. A tension pneumothorax develops when a one-way air leak follows lung rupture or chest wall penetration. Air is forced into the thoracic cavity with no means of escape, and pressure mounts within the hemithorax. With sufficient increases in intrathoracic pressure, the mediastinum is shifted to the contralateral side, which impedes venous return from both the superior and inferior venae cavae. Cardiac output is diminished, and the victim soon exhibits signs and symptoms
of shock. Victims with tension pneumothorax present with distended neck veins and tracheal deviation away from the side of the lesion. There is unilateral absence of breath sounds, and the hemithorax is hyperresonant or tympanitic. Respiratory distress, cyanosis, and frank cardiovascular collapse may occur. Tension pneumothorax is life threatening and frequently associated with additional serious injuries. It mandates rapid chest decompression, followed by evacuation to a medical facility. Decompression is performed by inserting a needle or catheter into the chest and converting the tension into an open pneumothorax. Ideally, a 14-gauge catheter is inserted percutaneously over the second rib in the midclavicular or over the fifth or sixth intercostal space along the anterior axillary line (Figure 21-7). Once the rib is identified with the tip of the needle, the needle is marched over the anterior superior surface of the rib and inserted through the intercostal muscles and pleura into the thoracic cavity. As the pressure within the hemithorax is released, a distinct rush of air is heard. The plastic catheter is advanced over the tip of the needle, the needle withdrawn, and the catheter left in place to ensure continued decompression. The needle should not be reintroduced into the catheter because it may damage or sever the catheter. Because tension pneumothorax is commonly associated with severe injury, the victim should be evacuated to a medical facility as rapidly as possible. A rubber glove or a finger cot can be attached to the external catheter opening to create a unidirectional flutter valve that allows egress of air from the pleural space. The Asherman chest seal (Figure 21-8) can be applied directly over the 14-gauge catheter and serves as a one-way valve to permit evacuation of pleural air. The Asherman chest seal can also be applied to sucking chest wounds to permit more normal chest dynamics (see Penetrating Chest Trauma). If resources are limited and treatment is needed, any number of devices can be used to decompress the chest. A sharp instrument and hollow tube sterilized as well as possible are all that is needed. Rapid cleansing of the skin surface is accomplished with antiseptic, alcohol, or water. A Heimlich valve kit is ideal for decompression and represents a valuable addition to the expedition first-aid arsenal. If resources permit placement of a thoracostomy tube, adequate anesthesia and expertise are required. The skin should be sterilized if possible, and local anesthetic should be infiltrated
Fifth rib Intercostal vessels and nerves Air escaping from pleural space
Lung
Sixth rib
Parietal pleura
Pleural space
Visceral pleura
FIGURE 21-7 Needle decompression of tension pneumothorax. This procedure is performed only for tension pneumothorax in patients with hemodynamic instability.
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while the victim lies supine. This will elicit pain over the fracture site. Most patients with rib fractures can be managed with oral analgesics and rest. Thoracic taping and splinting are contraindicated. Multiple rib fractures are significant because of the potential seriousness of associated injuries and increased pain. However, if extreme and compromising respirations, this pain responds well to an intercostal nerve block. Victims with multiple rib fractures need to be evacuated as conditions permit. After administration of an intercostal block, a person may regain the ability to hike out of the wilderness. The morbidity of rib fractures relates to decreased inspiratory tidal volume secondary to pain and splinting. In the wilderness setting, management must focus on pain control and pulmonary toilet. If oral analgesia is insufficient to control pain, an intercostal block is ideal. Depending on the anesthetic used, varying durations of analgesia can be attained, perhaps allowing transient ambulation for evacuation. Deep breathing should be encouraged at a rate of 10 times hourly to help prevent atelectasis.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
flail segment only to control unnecessary motion and pain may provide minimal relief from the discomfort.
FIGURE 21-8 Asherman chest seal.
into the skin and periosteum of the rib. Insertion is most effectively accomplished through the fifth intercostal space at the anterior axillary line. A small incision is made and the subcutaneous tissue bluntly separated with a finger or clamp. A blunt instrument, preferably a clamp, is forcefully inserted into the pleural space closely adhering to the superior surface of the rib to avoid the inferiorly located intercostal neurovascular bundle. Once the pleural space is entered, a tube (36F or greater in size) is inserted apically and posteriorly. The tube should then be secured with suture or tape and 10 to 20 cm H2O suction or underwater seal applied. A tube open to the atmosphere can accomplish decompression. The end of the tube can be covered with a rubber glove, finger cot, or plastic bag modified to permit unidirectional flow of air. One-way flow evacuating the chest is the goal. This procedure is not without morbidity and should be used only by trained personnel under optimal conditions. Antibiotics with grampositive coverage should be initiated if the pleural space is penetrated with an indwelling catheter or tube. Hemothorax. Hemothorax is usually associated with multiple rib fractures resulting from a direct blow to the chest. The primary cause of a hemothorax is laceration of the lung, intercostal vessel, or internal mammary artery. The victim complains of chest pain, tenderness associated with rib fractures, inspiratory pain, and dyspnea. Vocal fremitus is absent, percussion may be flat or dull, and breath sounds are diminished or absent. A chest tube for hemothorax is rarely required in the wilderness setting but may be placed if proper equipment is available, the patient is symptomatic, and evacuation will be prolonged. Needle aspiration of a hemothorax is unnecessary in the immediate postinjury period and may precipitate a pneumothorax. Flail Chest. When a series of three or more ribs is fractured in both the anterior and posterior planes, a portion of the chest wall may be mechanically unstable. As negative intrathoracic pressure develops during inspiration, the unstable segment paradoxically moves inward and inhibits ventilation. A flail segment indicates a severe direct blow to the chest wall with associated multiple rib fractures and decreased tidal volumes, often with associated underlying pulmonary contusion. The contusion can be expected to progressively impair ventilation and oxygenation over the succeeding 48 hours. Victims often tolerate a flail segment for the first 24 to 48 hours, after which they require mechanical ventilation. Any victim with a flail segment should be rapidly evacuated. Because the victim is usually incapable of participating in evacuation, a litter should be prepared or aeromedical evacuation considered. Intercostal nerve block may assist in short-term management of pain and pulmonary toilet. Restrictive (to chest wall expansion during inhalation) external chest wall supports, including taping or extensive stabilization with sandbags, are contraindicated. These measures hinder chest wall movement, decrease vital capacity, and are less effective than intercostal nerve block in pain control. However, focal stabilization or cushioning of the 424
Blunt Cardiac Injuries. Blunt cardiac injuries leading to pericardial tamponade or cardiac contusion are rare. Pericardial tamponade is life threatening. The pericardial sac is fibrous and expands little. A small amount of intrapericardial blood can severely restrict diastolic function. Blunt injury resulting in tamponade is usually from chamber rupture and rarely survivable, particularly in a remote setting. The diagnosis of tamponade can be difficult, particularly in the wilderness. Beck’s triad, which consists of distended neck veins, hypotension, and muffled heart sounds, is present in less than 33% of cases of tamponade and is particularly difficult to ascertain under nonoptimal conditions. Pulsus paradoxus, an increase in the normal physiologic decrease in blood pressure with inspiration, may be indicative of tamponade. Kussmaul’s sign, or a rise in venous pressure with spontaneous inspiration, is possible to assess outdoors. Once pericardial tamponade is diagnosed, immediate evacuation is required. Treatment consists of median sternotomy in a hospital operating room. The only temporizing measure pending evacuation is pericardiocentesis. This procedure can be lifesaving, particularly if a cardiac injury with a slow leak exists. However, its application in the wilderness setting should occur only if there is a high index of suspicion, coupled with shock and impending death unresponsive to resuscitative efforts. A long (approximately 15 cm [6 inches]), 16- to 18-gauge needle with an overlying catheter is introduced through the skin 1 to 2 cm (0.5 to 0.75 inches) below and to the left of the xiphoid. The needle is advanced at a 45-degree angle with the tip directed at the tip of the left scapula. When the pericardial sac is entered, aspiration with a syringe follows. The catheter is left in place and secured for possible repeat aspirations as the victim’s condition warrants. Immediate evacuation should follow. Cardiac contusion is a rare condition resulting from a severe blow to the precordium. An overlying sternal contusion or fracture may be present. The diagnosis should be suspected in an isolated high-velocity blow to the precordium with unexplained evidence of increased venous pressure, arrhythmias, and hemodynamic instability. Chest pain is invariably present, usually resulting from musculoskeletal contusion. Morbidity results from ensuing arrhythmias. Diagnosis can be definitively made only at autopsy. Electrocardiographic abnormalities after injury have correlated with subsequent arrhythmias.55 In the wilderness setting, any person who is unstable or symptomatic from an arrhythmia should be evacuated. If evacuation is not possible, it is noteworthy that fatal arrhythmia potential decreases significantly after 24 hours. Traumatic Asphyxia. Traumatic asphyxia is a rare syndrome of craniocervical cyanosis, facial edema, petechiae, subconjunctival hemorrhage, and occasional hypoxemia-related neurologic symptoms that results from severe thoracic crush injury. In the wilderness environment, it is associated with landslides or mud slides, avalanches, or falling debris. Any significant blunt compressive force to the thorax can result in the syndrome. Children are particularly susceptible because of high compliance of the chest wall.15 Traumatic asphyxia is associated with a high incidence of serious associated injuries,1,70 and the mortality rate in natural disasters is consequently high.32 A significant crush injury component may accompany traumatic asphyxia.32 Crush injuries and rhabdomyolysis are discussed later in the Extremity Trauma section of this chapter. The pathophysiology of traumatic asphyxia involves two elements. The crush injury results in acute increases in intrathoracic pressure and thus inferior and superior vena caval pressures. Venous flow is reversed in the veins of the head, which contain no valves. Venous hypertension leads to capillary rupture and the characteristic facial edema and petechiae. Recognition of the physical findings is imperative in diagnosing the syndrome and identifying concomitant injuries (Figure 21-9). Treatment consists of carefully extracting and, if necessary, immobilizing the victim. Rapid extrication is the single most important factor in improving survival. Establishment and
FIGURE 21-9 Typical clinical facial appearance of traumatic asphyxia.
maintenance of an airway is critical because significant facial and laryngeal edema may rapidly develop. Associated injuries should then be addressed in the primary survey. Subsequent care is supportive, consisting of airway control, administration of oxygen, head elevation of 30 degrees, treatment of associated injuries, and possible evacuation. The mortality rate is low in civilian environments but higher in wilderness disaster settings. Mortality is due to pulmonary dysfunction and associated injuries. Morbidity is secondary to neurologic damage; however, the majority of neurologic sequelae clear within 24 to 48 hours. If the victim survives, long-term sequelae are rare. Penetrating Chest Trauma Penetrating chest trauma above the nipple line is associated with hemopneumothorax and may also be associated with significant visceral injury. A victim with penetrating chest trauma below the nipple line often has intra-abdominal penetration in addition to possible thoracic injury. Such a victim requires immediate rapid evacuation. The open (“sucking”) chest wound produces profound intrathoracic physiologic alterations. Normal chest expansion creates negative intrathoracic pressure, which pulls air into the trachea and allows the lungs to expand. When the diaphragm and chest wall relax, positive pressure creates expiration. If the chest wall sustains an injury approximately two-thirds the tracheal diameter, negative intrathoracic pressure for inspiration is lost, the ipsilateral lung collapses, and loss of negative intrathoracic pressure affects the good lung. Consequently, it is important to rapidly reconstruct chest wall integrity. Initially this is most easily done by placing a hand over the sucking chest wound. Field treatment includes placing petrolatum gauze on top of the wound, covering it with a 4 × 4 gauze pad, and taping it on three sides (Figure 21-10). The untaped fourth side serves as a relief mechanism to prevent tension pneumothorax. Persons with sucking chest wounds should be rapidly evacuated to sophisticated medical care. Alternatively, an Asherman chest seal could be applied over the wound.
Anatomy. For descriptive purposes, the abdomen may be divided into thoracic, true, and retroperitoneal compartments. The thoracic abdomen contains the liver, spleen, stomach, and diaphragm. The liver, spleen, and, more rarely, stomach may be injured by direct blows to the ribs or sternum. Twenty percent of persons with multiple left lower rib fractures have a ruptured spleen. A direct blow to the epigastrium may result in increased intra-abdominal pressure with subsequent rupture of the liver or diaphragm. The true abdomen contains the small bowel, large bowel, and bladder. Isolated bowel injuries are rare in the wilderness setting. Blunt bladder or rectal injury usually occurs in conjunction with severe pelvic fracture and carries high mortality. The retroperitoneal abdomen contains the kidneys, ureters, pancreas, and great vessels. It is notoriously difficult to evaluate by physical examination. Life-threatening hemorrhage can occur into the true abdomen or retroperitoneal space. Diagnosis. The wilderness physician must have a high index of suspicion and perform a superlative history and physical examination. Physical Examination. The physician should look for signs of early shock: tachycardia, tachypnea, delayed capillary refill, weak or thready pulse, and cool or clammy skin. Physical examination of the abdomen begins with visualization and inspection. Contusions and abrasions may be the only harbingers of occult visceral injury. Periumbilical ecchymosis associated with abdominal hemorrhage (Cullen’s sign) is virtually never present in a victim with acute abdominal trauma. Abdominal distention secondary to hemorrhage is a very late sign and never present before shock and cardiovascular collapse. Abdominal inspection should survey the flanks, lower chest, and back. Inspection of the back should follow palpation of the spine while the victim is supine. The victim should be very carefully logrolled if there is any suspicion of spinal injury. Looking for muscle guarding, the examiner gently palpates the abdomen in all four quadrants. Any persistent guarding or tenderness after wilderness trauma mandates rapid evacuation. Percussion tenderness is an indicator of peritoneal irritation, also mandating evacuation. The presence or absence of bowel sounds has little prognostic significance. Bowel sounds may be present in the face of significant intra-abdominal hemorrhage or, conversely, absent in victims when extra-abdominal injuries induce ileus. Referred pain to the left shoulder (Kehr’s sign) strongly suggests the presence of a ruptured spleen. This pain is often exaggerated by placing the victim in the Trendelenburg position,
INJURIES TO THE ABDOMEN Intra-abdominal injuries in the wilderness setting are difficult to recognize. However, if recognized, all intra-abdominal injuries require rapid resuscitation and immediate evacuation. The abdomen represents the most frequent site of life-threatening hemorrhagic shock; however, in the wilderness setting, few diagnostic and treatment options exist. Blunt Abdominal Trauma Blunt intra-abdominal injury is commonly associated with falls. Abdominal injuries are often associated with fractures or closed head injuries. Often the decision for evacuation is made on the basis of other injuries; however, the wilderness physician must
Petrolatum gauze and 4˝ x 4˝ gauzepad
FIGURE 21-10 Treatment of a sucking chest wound. Sealing the wound with a gel defibrillator pad works best because this pad adheres to wet or dry skin. Petrolatum gauze or plastic wrap also works well. Note that one side is not sealed to allow egress of air.
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CHAPTER 21 Wilderness Trauma and Surgical Emergencies
be attuned to the potential for intra-abdominal hemorrhage as an occult injury.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
increasing the amount of left upper quadrant blood irritating the diaphragm. Pain from the retroperitoneal abdomen associated with injuries to the kidneys or pancreas may be referred to the back. However, referred pain is usually a late finding and not helpful in the evaluation of acute trauma. Gross hematuria that does not clear immediately or is coupled with an associated injury, such as pelvic fracture or abdominal or back pain, requires immediate evacuation. To minimize blood loss, the victim should be kept stationary and the evacuation team brought as close to the victim as possible. In a wilderness setting, rectal and vaginal examinations add little to the evacuation decision when evaluating for abdominal trauma. The unstable pelvic fracture associated with rectal and vaginal injuries is usually the determinant for evacuation. Diagnostic modalities in the austere environment are limited. Plain imaging, CT scans, and diagnostic peritoneal lavage have a very limited role. Ultrasound can be used to identify fluid in the peritoneum. Penetrating Abdominal Trauma Penetrating intra-abdominal injuries may result from gunshot, stab, or arrow wounds. The social context in which these injuries occur (accidental, intentional, or self-inflicted) makes little difference in the wilderness setting. Recrimination, guilt, and blame only interfere with the paramount goal of immediate evacuation. Gunshot Wounds. Low-caliber gunshot injuries often manifest with small entrance and no exit wounds. High-caliber, highvelocity gunshot injuries may have relatively innocuous entrance wounds but may be associated with large, disfiguring exit wounds and extensive internal injuries. No matter what the caliber or trajectory and no matter where the entrance and exit, all gunshot wounds from the nipple line to the inguinal ligament should be presumed to have penetrated the abdominal cavity and created an intra-abdominal injury. These injuries mandate immediate surgical intervention. A victim of gunshot wounds to the head, neck, chest, abdomen, or groin should undergo immediate evacuation accompanied by the administration of a single-agent broad-spectrum antibiotic, such as an oral fluoroquinolone (e.g., ciprofloxacin, 750 mg orally [PO]). Hunting injuries are discussed in Chapter 24. Shotgun Injuries. Shotgun injuries to the torso are managed in the same manner as gunshot wounds. Shotgun injuries have a potentially lower incidence of underlying visceral injury than gunshot wounds, but there is often extensive soft tissue damage requiring surgical debridement. The potential exists for delayed development of peritonitis from a single penetrating pellet to the viscera. Consequently, shotgun injuries should also be treated with emergency evacuation and a broad-spectrum antibiotic, as recommended previously for gunshot wounds. Occasionally, a close-range shotgun blast results in a soft tissue defect large enough for the injured bowel to extrude through the wound. The injured bowel should not be placed back into the abdomen. Injured bowel displaced from the abdominal cavity conceptually should be treated as though it were an enterocutaneous fistula. Because evacuation is often delayed in the wilderness, it is better to have fecal contents outside, rather than inside, the peritoneal cavity. The exteriorized bowel should be kept moist and covered at all times. Uncovered bowel outside the peritoneal cavity rapidly desiccates and becomes nonviable, mandating later surgical resection. Exposed bowel should be covered with an abdominal pack or cloth moistened with sterile saline at best, or at worst with potable water. The dressing should be checked and remoistened at least every 2 hours. Stab Wounds. The penetrating object is usually a knife but may be as varied as a piton, ski pole, or tree limb. Any deep skin laceration from the nipple line to the groin should be considered to have damaged an intra-abdominal organ. Whereas the odds of an abdominal gunshot wound injuring a visceral organ exceed 85%, the odds of a stab wound injuring a visceral organ are less than 50%. 426
In certain urban hospitals, the high incidence of negative surgical explorations for stab wounds had led to a more selective approach toward patients with abdominal stab wounds.68 This approach uses local wound exploration and frequent physical examination. Although there are no data addressing the management of stab wounds in the wilderness environment, the following approach is practical and reasonable. If the wound extends into the subcutaneous tissue, the evacuation decision depends on local wound exploration. This procedure is simple to perform, even in the wilderness environment. The skin and subcutaneous tissue are infiltrated with local anesthetic, and the laceration is extended several centimeters to clearly visualize the underlying anterior fascia. It is helpful to use lidocaine (Xylocaine) 1% with epinephrine to minimize slight but annoying bleeding that can impair visualization. The wound should never be probed with any instruments, particularly if overlying the ribs. Wound exploration is confined to the area from the costal margin to the inguinal ligament. Local wound exploration is contraindicated in wounds that extend above the costal margin, because it is possible for such exploration to communicate with a small pneumothorax, potentially exacerbating respiratory distress. If thorough exploration of the wound shows no evidence of anterior fascial penetration, and if the victim demonstrates no evidence of peritoneal irritation, the wound can be closed with tape (Steri-Strips) or adhesive bandages, dressed, and the evacuation process delayed. Physical examination should be performed every few hours for the next 24 hours. If no peritoneal signs develop and the victim feels constitutionally strong, a remote expedition may resume with caution and an eye to evacuation should the victim become ill. In the wilderness environment, it is prudent to have a low threshold for evacuation because of technical difficulties in performing wound exploration, such as insufficient light and inadequate instruments. Persons who have been impaled by long objects, such as tree limbs or ski poles, should have the object left in place and carefully shortened, if possible, to facilitate transport.
PELVIC TRAUMA In the wilderness setting, fractures of the pelvis are generally associated with falls from significant heights, high-velocity ski accidents, or vehicular trauma. Pelvic fractures can be lethal. With opening of the pelvic ring, there may be hemorrhage from the posterior pelvic venous complex and occasionally from branches of the internal iliac artery. For hemodynamically unstable victims with severe pelvic fractures, resuscitative efforts should be instituted. In addition, simple techniques to reduce increased pelvic volume through the application of sheets or slings may slow bleeding. Several pelvic binders are available commercially and all provide circumferential pressure to minimize the pelvic volume (e.g., T POD [www. pyng.com], SAM Pelvic Sling II [www.sammedical.com]). The key factor in initial management of pelvic fractures is identification of posterior injury to the pelvic ring. Posterior ring fractures or dislocations are associated with a greater incidence of significant hemorrhage, neurologic injury, and mortality than are other pelvic fractures. The diagnosis of a posterior ring fracture is based on instability of the pelvis associated with posterior pain, swelling, ecchymosis, and motion at the sacroiliac joints with application of manual pressure at the anterior superior iliac spines. Persons with posterior ring fractures must be immediately evacuated on backboards, with care taken to minimize leg and torso motion. The flank, scrotum, and perianal areas should be inspected for blood at the urethral meatus, swelling or bruising, or a laceration in the perineum, vagina, rectum, or buttocks suggestive of an open pelvic fracture. The pelvis should be examined carefully once, without any aggressive rocking motion. The first indication of mechanical disruption is leg length discrepancy or rotational deformity in the absence of an obvious leg fracture or hip location. For more information on pelvic fracture, see Chapter 27.
BOX 21-3 Vascular “Hard Signs”
The majority of wilderness-related extremity injuries involve fractures and sprains, which are discussed in Chapter 27. This section focuses on the general field management of significant extremity vascular injury, traumatic amputation, and recognition and treatment of rhabdomyolysis.
Pulsatile bleeding Palpable thrill Audible bruit Expanding hematoma Six “P’s” of regional ischemia Pain Pulselessness Pallor Paralysis Paresthesia Poikilothermia
Vascular Injuries Injury to the major vessels supplying the limbs can occur with penetrating or blunt trauma. Fractures can produce injury to the vessels by direct laceration (rarely) or by stretching, which produces intimal flaps. Penetrating injuries can be devastating if transection of a vessel occurs. Significant vascular injuries, from both penetrating and blunt causes, can result in multiple vessel injury subtypes, each of which may be limb-threatening. Injury subtypes include laceration, transection, contusion with spasm, thrombosis, or aneurysm formation (true and false), external compression, and arteriovenous fistula. An accurate history, expeditious physical examination, and prompt evacuation are the keys to life and limb salvage. Significant vascular injuries result in one of two clinical presentations—hemorrhage or ischemia. The greatest priority is cessation of hemorrhage. The victim of trauma may die in short order from a major vascular injury. Stop the bleeding. Ideally, control of hemorrhage can be accomplished without resultant ischemia of the distal extremity. The vast majority of times, hemorrhage from an extremity wound can be controlled with pressure dressings and direct pressure. These measures permit circulation to and from the extremity outside the area of pressure application. In the very rare circumstance, a tourniquet may be required. History. A complete history of the time and mechanism of injury is invaluable in planning further management. Although no absolute ischemia time has been established, a goal of less than 6 hours to reperfusion is prudent.28 The amount of blood present at the scene should be quantified. A history of bright pulsatile blood that abates suggests arterial injury. Thirty-three percent of victims with arterial injuries have intact distal pulses. Physical Examination. Vascular examination in the field can be highly variable. Hypovolemia, hypothermia, and hostile conditions make accurate examination challenging. Skin color and extremity warmth should be first assessed. Distal pallor and asymmetric hypothermia suggest vascular injury. Pulses should be palpated. In the upper extremity, the axillary, brachial, radial, and ulnar pulses should be assessed. In the lower extremity, the femoral, popliteal, posterior tibial, and dorsalis pedis pulses should be assessed. Location and direction of the wound, amount of hemorrhage, and presence of hematomas or palpable thrill should be noted. A neurologic examination that quantifies motor and sensory deficits is critical. Because of the high metabolic demands of peripheral nerves, disruption of oxygen delivery makes neuronal cells highly susceptible to ischemic death. Conversely, skeletal muscle is relatively resistant to ischemia. Loss of sensation or limb paralysis is an alarming sign of impending anoxic necrosis. Treatment of Vascular Injuries. All external hemorrhage should be identified during the primary survey and controlled with direct pressure at the site of injury. Tourniquets should be applied only when direct pressure fails to control bleeding or when direct pressure cannot be applied (such as while a casualty is being evacuated by hoist to an aircraft). In the civilian experience, the need for tourniquets should be uncommon, because direct pressure is the preferred technique. Tourniquets should be released every 5 to 10 minutes to attempt to limit ischemia, unless severe hemorrhage continues when the tourniquet is loosened. In this case, it should be left tightened. Efforts to control bleeding with pressure should be undertaken. Direct pressure permits collateral flow to provide some perfusion to the distal extremity. Hematomas should never be explored or manually expressed without surgical capability readily available. Attempts to clamp or ligate vessels are not recommended. Frequent repeat neurovascular examinations are mandatory.
Once bleeding is controlled and the wound is covered with a sterile but nonconstrictive dressing, completion of the primary survey, identification and stabilization of associated injuries, and appropriate resuscitation with normal saline should follow. After hemostasis is achieved, a nonconstrictive dressing will obviate the chance for unintended venous outflow obstruction. The extremity should be splinted to prevent movement. The need for evacuation depends directly on the results of the physical examination. Examination results can be grouped into “hard signs,” indicative of ischemia or continued hemorrhage, and “soft signs” that are suggestive but not indicative of ischemia (Boxes 21-3 and 21-4). All victims with hard signs should be evacuated emergently. Based on current data, an isolated soft sign may warrant observation alone, depending on the remoteness of the expedition and the risks of evacuation. The data for observation of soft signs have emerged from hospital settings and must be applied with great caution in the wilderness. If soft signs are present, clinical suspicion is high, and evacuation can be accomplished safely, the victim should be transported and observed in a medical facility. Traumatic Amputation In the wilderness environment, amputation victims require immediate evacuation. Hemorrhage is controlled during the primary survey with direct pressure, and resuscitation is instituted. Tourniquets are rarely required. The victim should be kept warm and calm. Reassurance and analgesics should be administered. Amputations should be completed only if minimal tissue bridges exist and it is clear that the neurovascular supply has been interrupted. Amputation of a mangled extremity, defined as an extremity with high-grade open fracture and soft tissue injury, should not be carried out in the wilderness except to free a trapped victim to avoid further severe injury or even death, or in the case of uncontrollable hemorrhage threatening the life of the victim, and then only by experienced surgical personnel. All other severely injured extremities should be wrapped in available sterile materials, splinted, and kept moist. Amputated extremities should be cooled if possible, optimally in a plastic bag in ice or ice water. Avoid placing the extremity in direct contact with ice. Without cooling, the amputated extremity remains viable for only 4 to 6 hours; with cooling, viability may extend to 18 hours. The amputated extremity should accompany the victim throughout the course of the evacuation. Crush Injuries and Rhabdomyolysis Rhabdomyolysis is a potentially fatal syndrome that results from lysis of skeletal muscle cells. In its fulminant form, BOX 21-4 Vascular “Soft Signs” Injury in proximity to major vessel Diminished but palpable pulses Isolated peripheral nerve deficit History of minimal hemorrhage
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CHAPTER 21 Wilderness Trauma and Surgical Emergencies
EXTREMITY TRAUMA
PART 4 INJURIES AND MEDICAL INTERVENTIONS
rhabdomyolysis can affect multiple organ systems. Compartment syndrome, renal failure, and cardiac arrest represent the major complications. Any condition resulting in significant acute or subacute striated muscle damage can precipitate rhabdomyolysis. Crush injuries of the extremities and pelvis, revascularization of ischemic tissue, ischemic extremities, animal bite and snakebite,16,22 frostbite, and traumatic asphyxia32 can all result in rhabdomyolysis in a wilderness setting. Crush injuries are frequently results of avalanches, falls from heights, or rock slides. The pathophysiology of rhabdomyolysis remains controversial. The exact mechanism of muscle injury appears not to be simple direct force or isolated ischemia and is probably multifactorial.32 The common cellular derangement is interference of the normal function of muscle cell membrane sodium-potassium adenosine triphosphatase (ATPase) with intracellular calcium influx and cell death.76 After cell death, multiple intracellular constituents, including myoglobin, creatine kinase, potassium, calcium, and phosphate, are released into the systemic circulation. The metabolic derangements of rhabdomyolysis depend directly on release of intracellular muscle constituents. Myoglobinemia, hypercalcemia, hyperphosphatemia, hyperkalemia, hyperuricemia, metabolic acidosis, coagulation defects, and contracted intravascular volume result. The clinical presentation of rhabdomyolysis may include muscle weakness, malaise, fever, tachycardia, abdominal pain, nausea and vomiting, or encephalopathy. Symptoms may mimic those of persons with spinal cord injury.7 The danger of the syndrome lies in the cardiovascular effects of electrolyte disturbances and renal failure69 secondary to changes in renal perfusion and direct toxicity of myoglobin to tubular cells. Successful treatment relies on prompt diagnosis based on clinical signs and urinalysis, aggressive hydration, and forced diuresis. Myoglobin turns urine tea-colored, which is an important indicator of significant muscle death and need for aggressive treatment. Normal saline should be administered IV at 1 to 2 L/hr to achieve a urine output of 100 to 300 mL/hr. Signs for fluid overload should be monitored. Victims who are trapped in rubble should have resuscitation initiated before extrication, if possible. The addition of agents to alkalinize the urine and promote diuresis has been shown to improve clearance of myoglobin but not to alter survival. In addition, diuretics may be detrimental in multisystem trauma victims who are hypovolemic. All victims demonstrating myoglobinuria should be evacuated.
Wilderness Surgical Emergencies THE ACUTE ABDOMEN In the wilderness, the critical distinction between the surgical and nonsurgical abdomen determines whether the victim should be evacuated. A myriad of nonsurgical conditions mimic a surgical abdomen. It has been extensively reported that the bite of the black widow spider, Latrodectus mactans, can induce abdominal pain indistinguishable from a surgical acute abdomen,48 and mushroom ingestion can cause severe gastroenteritis.83 Pain, anorexia, nausea, vomiting, and fever are characteristic manifestations of an acute abdominal disorder. Tenderness and guarding are the hallmarks of peritoneal irritation and suggest that surgery is indicated. The approach to someone with abdominal pain begins with a detailed history that includes age, gender, systemic symptoms, and past medical history. This information provides a framework for more detailed questioning about the character of the pain, its mode and time of onset, severity, and precipitating and palliating factors. In persons 15 to 40 years of age, women are more likely to have abdominal pain, but men have a higher incidence of surgical disease. Common genitourinary causes for abdominal pain in men include epididymitis, renal colic, urinary retention, and testicular torsion. Common causes in women include pelvic inflammatory disease (PID), urinary tract infection (UTI), dysmenorrhea, ruptured ovarian cyst, and ectopic pregnancy. Pain is the hallmark of a surgical abdomen (Table 21-3). It can be characterized by nature of onset, severity, location, and precipitating factors. The onset of abdominal pain can be explosive, rapid, or gradual. The person who is suddenly seized with explosive, agonizing pain is most likely to have rupture of a hollow viscus into the free peritoneal cavity. Colic of renal or biliary origin may also be sudden in onset, but seldom causes pain severe enough to prostrate the victim. If someone has rapid onset of pain that quickly worsens, acute pancreatitis, mesenteric thrombosis, or small bowel strangulation should be suspected. The person with gradual onset of pain is likely to have peritoneal inflammation, such as that accompanying appendicitis or diverticulitis. Severity of the pain may be characterized as excruciating, severe, dull, or colicky. Excruciating pain unresponsive to narcotics suggests an acute vascular lesion, such as rupture of an abdominal aneurysm or intestinal infarction. Both conditions are
TABLE 21-3 Differential Diagnostic Features of Abdominal Pain Disease Acute appendicitis Intestinal obstruction Perforated duodenal ulcer Diverticulitis Acute cholecystitis Renal colic Acute pancreatitis Acute salpingitis
Ectopic pregnancy
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Location of Pain and Prior Attacks
Mode of Onset and Type of Pain
Associated Gastrointestinal Problems
Periumbilical or localized generally to right lower abdominal quadrant Diffuse
Insidious to acute and persistent
Anorexia common; nausea and vomiting in some
Sudden; crampy
Vomiting common
Abrupt; steady
Anorexia; nausea and vomiting Diarrhea common
Epigastric; history of ulcer in many Left lower quadrant; history of previous attacks
Gradual; steady or crampy
Epigastric or right upper quadrant; may be referred to right shoulder Costovertebral or along course of ureter Epigastric penetrating to back Bilateral adnexal; later, may be generalized
Insidious to acute
Anorexia; nausea and vomiting
Sudden; severe and sharp Acute; persistent, dull, severe Gradually becomes worse
Frequently nausea and vomiting Anorexia; nausea and vomiting common Nausea and vomiting may be present
Unilateral early; may have shoulder pain after rupture
Sudden or intermittently vague to sharp
Frequently none
Physical Examination Low-grade fever; epigastric tenderness initially; later, right lower quadrant Abdominal distention; high-pitched rushes Epigastric tenderness; involuntary guarding Fever common; mass and tenderness in left lower quadrant Right upper quadrant pain Flank tenderness Epigastric tenderness Cervical motion elicits tenderness; mass if tubo-ovarian abscess is present Adnexal mass; tenderness
General Field Treatment Principles When evaluating someone with a possible emergent surgical condition in the wilderness, correctly identifying the etiology of a given condition is less important than identifying peritoneal inflammation and the need for operation. When dealing with a surgical abdomen or other condition requiring evacuation, adjuncts to definitive hospital treatment can be initiated in the field. Dehydration and intravascular volume depletion accompany many surgical conditions, particularly when the disease process has progressed and evacuation is delayed. Crystalloid resuscitation in the field is beneficial for patients who have developed or have the potential to develop septic or hypovolemic shock. Dehydration is common in the wilderness, and frank hypovolemia can result from vomiting associated with gastroenteritis, appendicitis, renal colic, and small bowel obstruction. Perforated viscus, pancreatitis, cholecystitis, small bowel obstruction, PID, and necrotizing soft tissue infections all may feature volume depletion. The goal in the wilderness setting is to recognize the signs of hypovolemia and initiate resuscitation to decrease perioperative morbidity. Nasogastric tube decompression of the stomach may help alleviate emesis secondary to abdominal pain or obstruction. Large-bore (i.e., 18F) catheters are best and can be easily aspirated with a syringe. Placement should be confirmed by aspiration of gastric contents or auscultation of gastric air on insufflation of the stomach. Foley catheters are becoming increasingly more available in wilderness first-aid kits (Figure 21-11). Recording urine output provides an effective estimate of intravascular volume status. Foley catheter placement should never hinder the possibility of ambulatory evacuation. Radiographic imaging techniques will not be available. Some expeditions will have the availability of portable ultrasound and the professional expertise to use this modality. A team of three emergency medicine physicians described their application of ultrasound in the austere environment following mud slides in Guatemala. In a series of 99 patients, ultrasound was used to identify an emergent problem in 6% of patients and rule out an emergent problem in 42% of patients.19 Appendicitis Acute appendicitis is the most common cause of a surgical abdomen in persons younger than 30 years of age. Acute appendicitis is more than a single disease entity. In terms of physical signs and symptoms, appendicitis proceeds from inflammation to obstruction to ischemia to perforation, all within approximately 36 hours. Symptoms reflect the stage of the disease. Unfortunately, the time frame for the progression of clinical events is highly variable.
The differential diagnosis of appendicitis includes gastroenteritis and mesenteric adenitis, the most common inflammatory disorders in adults. The first symptom of gastroenteritis is typically vomiting, which precedes the onset of pain and is often associated with diarrhea; it is rarely associated with localizing signs or muscular spasm. Bowel sounds are usually hyperactive. A rectal examination rarely shows abnormalities in gastroenteritis but frequently does in adults with appendicitis. Mesenteric adenitis is often preceded by an upper respiratory infection and is associated with vague abdominal discomfort that often begins in the right lower quadrant. Abdominal examination reveals only mild right lower quadrant tenderness that is often poorly localized. The incidence of PID in young women with abdominal pain confounds the diagnosis of appendicitis. Some clinicians have documented a connection between menses and onset of pain. If abdominal pain occurs within 7 days of menses, the incidence of PID is twice that of appendicitis. If onset of pain occurs greater than 8 days from menses, appendicitis is twice as likely as PID. This history with a pelvic examination may enable the examiner to differentiate between the two entities. Acute appendicitis mandates evacuation, because untreated perforation is associated with significant mortality. Recent literature has supported nonoperative management of acute appendicitis.5,41,92 However, in these series, patients who do not improve promptly with antibiotics proceed to appendectomy. The prudent medical director of an expedition would seek to evacuate the patient with presumed appendicitis to ensure surgical capability is available. Broad-spectrum antibiotics (if IV capability, cefotetan [Cefotan] 2 g IV every 12 hours, or as an alternative, piperacillin/ tazobactam [Zosyn] 3.375 g IV every 6 hours; if only oral antibiotic capabilities, a fluoroquinolone, such as ciprofloxacin [Cipro] 750 mg PO twice a day) should be initiated, attempting coverage against gram-negative and anaerobic organisms. IV crystalloid resuscitation should be initiated, particularly if the victim is older or perforation is suspected, and the victim should be placed on bowel rest. Acute Cholecystitis and Biliary Colic Biliary colic refers to pain induced by obstruction of the cystic duct, usually by gallstones. The label of this condition as “colic” is a misnomer because the pain is usually constant. The condition is rarely seen before adulthood and is several times more common in women than in men. A sufferer often relates a past history of gallstones and previous episodes of similar pain, which is described as constant right upper quadrant or epigastric pain, radiating to the right scapula and back. Onset ranges from insidious to acute and frequently follows a meal. The episode usually lasts 15 minutes to 1 hour and then abates.66 If pain is severe, nausea and vomiting may be present (60% to 70%). Acute cholecystitis is an infection of the gallbladder secondary to cystic duct obstruction, usually from gallstones. In the wilderness setting, it is useful to think of these interrelated conditions as a continuum of one unified disease process. Both biliary colic and cholecystitis manifest with right upper quadrant pain; however, biliary colic has the potential to be self-limited and may not require evacuation. Not all persons with biliary colic develop cholecystitis, and signs of infection should be excluded. Cholecystitis symptoms typically escalate in severity. Pain that persists for more than 1 to 2 hours is suspect for cholecystitis, particularly when accompanied by fever, more significant nausea and vomiting, and right upper quadrant tenderness. Studies have shown that fever may be an unreliable predictor of severity of infection.38 Acute cholecystitis mandates hospitalization, and evacuation plans should be instituted. The disease can progress to gangrenous changes in the gallbladder wall, leading to perforation and death if untreated. The definitive treatment of cholecystitis is cholecystectomy. In the field, IV antibiotics (ampicillin/sulbactam [Unasyn] 3 g IV every 6 hours) or an oral alternative (ciprofloxacin 750 mg PO twice a day) should be given, directed at common biliary organisms, including Escherichia coli and Klebsiella, Bacteroides, Enterobacter, Streptococcus, and Proteus species. Oral antibiotics with optimal bioavailability should be initiated in the absence of parenteral forms, ensuring the broadest spectrum of coverage 429
CHAPTER 21 Wilderness Trauma and Surgical Emergencies
unusual in the wilderness environment. Severe pain readily controlled by medication is characteristic of peritonitis from a ruptured viscus or acute pancreatitis. Dull, vague, and poorly localized pain suggests an inflammatory process and is a common initial presentation of appendicitis. Colicky pain characterized as cramps and rushes is suggestive of gastroenteritis. The pain from mechanical small bowel obstruction is also colicky but has a rhythmic pattern, with pain-free intervals alternating with severe colic. The peristaltic rushes associated with gastroenteritis are not necessarily coordinated with colicky pain. Physical examination of the abdomen is initiated by inspection. Valuable clues to the underlying condition that may be obtained in this manner include stigmata of cirrhosis, distention, hyperperistalsis, or incarcerated hernia. The victim may not be able lie still, which is indicative of renal or biliary colic. Persons lying perfectly still frequently have peritoneal inflammation. Auscultation is helpful if the classic “rushes and tinkles” of small bowel obstruction are present. Palpation in the wilderness setting is most helpful in documenting the presence or absence of peritoneal signs. Shake or percussive tenderness, particularly in the context of fever, nausea, and/or vomiting, indicates a need for evacuation. Rectal and vaginal examinations should be performed as dictated by the clinical presentation and setting.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
available. As with most abdominal infections, IV hydration should be started in the field. If significant nausea and vomiting are present, NG decompression may improve comfort and prevent aspiration. Peptic Ulcer Disease The incidence of peptic ulcer disease (PUD) is decreasing in the United States. With the advent of treatment of Helicobacter pylori infections and the variety of acid-reducing agents available, PUD is now rarely seen by surgeons. The exception is perforation of a gastric or duodenal ulcer, which should be considered in the differential diagnosis of acute abdomen in the wilderness. Victims frequently relate a history of PUD and need for medication. This history, in combination with acute onset of unrelenting epigastric pain radiating to the back, is suspect for perforation of an ulcer. The physical examination greatly assists in differentiation between simple ulcer disease symptoms and perforation. Pain may be severe. Gastric secretions are caustic to the peritoneum and, as a result, the abdomen frequently displays a rigid, boardlike character with associated diffuse peritoneal signs. History and examination consistent with gastric or duodenal perforation mandate evacuation. Dehydration may be significant. IV resuscitation should be started and the victim placed on bowel rest. Diverticulitis Diverticulitis is localized infection of a colonic diverticulum. Impacted material in the diverticulum, usually feces, leads to a localized inflammatory process that can lead to abscess formation and perforation. Diverticulitis manifests over a wide range of severity, from mild, localized infection to an intra-abdominal catastrophe. It is more common in middle age; one-third of the population older than 45 years of age has diverticula, 20% of whom will develop diverticulitis.81 Victims often relate a history of previous attacks. Pain is typically described as gradual in onset and localized in the left lower quadrant of the abdomen, although right-sided diverticulitis can occur. Diarrhea and fever are frequently associated complaints. Examination findings range from mild left lower quadrant abdominal tenderness to frank peritonitis, depending on the severity of the underlying infection. Treatment in the wilderness setting consists of hydration, bowel rest, antibiotics, and evacuation. If evacuation is impossible or significantly delayed, oral broad-spectrum antibiotics may be effective. Mild cases of diverticulitis are frequently treated on an outpatient basis with broad-spectrum oral antibiotics,81 such as ciprofloxacin 750 mg PO twice a day. Antibiotic therapy is directed primarily at gram-negative aerobic and anaerobic bacteria, and single-agent therapy covering these organisms has been demonstrated to be as effective as multiple-agent regimens.47 Because of unpredictability of response to antibiotic treatment, evacuation is indicated. Mechanical Small Bowel Obstruction Small bowel obstruction is a true emergency in the wilderness. When the obstruction is complete, expedient surgery is the only treatment. Small bowel obstruction in the United States is almost invariably the result of adhesions from previous laparotomy or incarceration of abdominal hernias. Victims complain of sudden onset of diffuse, crampy abdominal pain associated with vomiting and obstipation. With progression of the process to strangulation and infarction of bowel, fever and tachycardia develop. Late physical examination findings reveal a distended, tympanitic abdomen. Although variable, high-pitched tinkling bowel sounds suggest obstruction. A thorough inspection for hernias should be performed. Progression of examination findings to frank peritonitis is alarming and suggests ischemic bowel. The adage, “Don’t let the sun set on a small bowel obstruction,” is sound advice in the wilderness setting. All persons suspected of having a small bowel obstruction should be evacuated immediately. In the interim, the stomach should be decompressed with an NG tube to relieve vomiting and abdominal distention, and aggressive IV hydration should be started. 430
Incarcerated Abdominal Wall Hernias Abdominal wall hernias are common. Hernias can become incarcerated or strangulated, which constitutes a surgical emergency. Seventy-five percent of hernias occur in the groin84; the majority of incarcerated hernias manifesting in the wilderness setting are inguinal hernias. Other common hernias with the capacity for incarceration are incisional and umbilical hernias. Many people live with bulging asymptomatic hernias. Others manually reduce symptomatic hernias. New painful hernias or known hernias that can no longer be reduced are concerning. The pain of inguinal hernias is usually intermittent. A description of constant pain is suspect for incarceration. Associated symptoms of fever, tachycardia, nausea, and vomiting are indicative of possible incarceration or strangulation. On physical examination, a mass should be sought along the course of the spermatic cord. Masses may manifest from the external inguinal ring to the scrotum. The differential diagnosis for painful inguinal or scrotal masses includes lymphadenopathy, testicular torsion, and epididymitis. Associated tenderness of the spermatic cord may be present. A painful mass at the umbilicus, a previous incision site, or below the inguinal ring could represent an incarcerated umbilical, incisional, or femoral hernia, respectively. Bowel within an incarcerated hernia sac can become gangrenous in as little as 4 to 5 hours64; therefore it is important to determine the time of incarceration. The decision to evacuate is influenced by the presence of contraindications to manual reduction (see later), which are essentially physical signs that suggest progression to strangulation. Femoral hernias should not be reduced. The danger is en masse reduction of compromised or gangrenous bowel. Contraindications to reduction include associated signs of toxicity, such as fever, tachycardia, or evidence of bowel obstruction in association with a painful, irreducible mass. If the hernia itself is exquisitely tender to palpation and the overlying skin is erythematous and warm, the hernia should not be reduced. Victims with incarcerated hernias with signs of systemic or local toxicity should be evacuated. Similarly, victims with irreducible hernias—which require emergent surgery—should be evacuated. A newly incarcerated hernia without contraindications to reduction may be reduced by personnel experienced in such techniques. Gentle pressure is exerted on the hernia mass toward the inguinal ring, optimally with the victim flat and hips elevated. Analgesia and sedation may aid in reduction. Gangrenous bowel can rarely be reduced by this method.64 If successful, the victim should be closely observed for signs of recurrence or abdominal pain.
UROLOGIC EMERGENCIES Renal colic describes a symptom complex resulting from acute obstruction of the urinary tract secondary to calculus formation. The goal of the wilderness physician is to recognize the symptom complex and institute treatment. After obstruction of the urinary tract, the pain crescendo of renal colic begins in the flank. The pain progresses anteriorly over the abdomen and radiates to the groin and testes in men and the labia in women. Because the autonomic nervous system transmits visceral pain, many abdominal complaints may manifest. Nausea and vomiting are common. With severe colic, the victim writhes in pain and is unable to find a comfortable position. Physical findings are less revealing than is the review of systems. Tenderness to deep palpation of the region of obstruction or to percussion of the flank is present. Diagnosis in the wilderness is assisted by the presence of gross hematuria. Management of ureteral colic is pain control. Although almost universally deployed, forced diuresis may reduce ureteral peristalsis. Thus, forced oral fluids or aggressive IV hydration are of questionable benefit.96 The majority of calculi pass spontaneously in 4 to 6 hours. The goal of management is to control pain until passage of the stone has occurred. A number of pharmacologic approaches may be used. Nonsteroidal antiinflammatory drugs, such as ibuprofen and ketorolac, have been shown to be effective in the management of renal colic.96 For symptoms
Urinary Retention Urinary retention is a painful experience that requires immediate medical, and often surgical, intervention.13 The etiology of urinary retention ranges from prostatism45 in men to atonic bladder in women. In general, causes have been broadly divided into four groups: obstructive, neurologic, pharmacologic, and psychogenic.95 Twenty-five percent of men reaching 80 years of age will experience acute retention,13 which has been shown to increase prostate surgery perioperative mortality rates.75 Acute urinary retention can lead to incapacitating symptoms in the wilderness; prompt recognition and intervention are necessary. Principal symptoms are bladder distention and pain that may mimic acute abdomen, overflow incontinence, dribbling, and hesitancy. Physical examination findings include prostatic enlargement in men and lower midline abdominal tenderness and distention. If painful distention of the bladder is present, decompression should be undertaken. Medical therapy may be considered before complete obstruction to urinary flow. Tamsulosin (Flomax CR) is a third-generation α-blocker that may provide some relief. The α-blockers promote bladder neck and prostatic urethral relaxation.35 Bladder decompression should be initially attempted with a standard Foley catheter. In men with prostatic hypertrophy, passage of the catheter may be challenging, and a large catheter or coudé catheter should be used if a standard Foley catheter cannot be passed. Instrumentation of the urethra with hemostats or dilators is dangerous and should not be attempted in the field. The OPTION-vf (female) (see Figure 21-11, A) and OPTIONvm (male) (see Figure 21-11, B) are valved urinary catheters
A
B FIGURE 21-11 A, OPTION-vf (female) catheter. B, OPTION-vm (male) catheter. (Courtesy Opticon Medical, Dublin, Ohio.)
that eliminate the need for urine drainage bags and connecting tubes normally required with Foley catheters. These catheters incorporate a manually activated valve at the end of the catheter that allows the patient to store urine in the bladder and to mimic normal voiding behavior. The catheters may be used with a continuous drainage adapter when appropriate, so that a bag may be placed and urination rate and volume assessed. If multiple attempts are unsuccessful and symptoms are severe, needle decompression is indicated. The skin of the suprapubic region should be anesthetized, if possible. The distended bladder is palpated to guide aspiration. A 22-gauge needle attached to a syringe is introduced through the skin of the lower abdomen two finger breadths above the pubic symphysis and directed at the anus. The needle is advanced with simultaneous aspiration of the syringe until free-flowing urine is visualized. Palpation of the bladder in combination with adherence to this technique should lead to successful decompression. Complications related to decompression can occur.82 Drainage of greater than 300 mL/hr can induce mucosal hemorrhage. In addition, 10% of victims develop postobstructive diuresis that may lead to dehydration, in which case aggressive oral hydration or crystalloid repletion should be undertaken. Finally, surgical decompression is temporizing, and retention will recur. Treatment may need to be continued or repeated. Drainage of the bladder acutely relieves symptoms and may allow ambulatory evacuation, but the underlying etiology must be addressed in a medical facility. The Acute Scrotum Acute onset of scrotal pain and swelling requires immediate attention. Etiologies are multiple, but incarcerated hernia and testicular torsion are the most clinically significant in the field. Although any one aspect of the history and physical examination may not be diagnostic, when taken as a whole, they frequently suggest the etiology of the scrotal pathology.46 Testicular torsion can occur at any age, but it is more likely near puberty. The likelihood of testicular salvage is inversely proportional to elapsed time from torsion; this is a true surgical emergency. Acute onset of severe testicular pain is the hallmark. Mild to moderate pain is more suggestive of torsion of a testicular appendage or epididymitis. It has been stated that victims who can ambulate with minimal pain are less likely to have testicular torsion. In addition, nausea and vomiting may accompany torsion, whereas fever, dysuria, and frequency are associated with epididymitis. Physical examination reveals a patient in extreme discomfort with a swollen scrotum and a tender testicle; the affected testicle may be higher than normal and have a horizontal lie.46 Scrotal skin may be edematous and discolored. Unilateral scrotal swelling without skin changes is more indicative of a hernia or hydrocele. In testicular torsion, the affected testis is often larger than the unaffected testis. Testicular torsion can be somewhat differentiated from acute epididymitis by Prehn’s sign,86 which is relief of pain accomplished by elevation of the testicle. Because torsion twists the spermatic cord and elevates the testicle, pain is not relieved by elevation (negative Prehn’s sign). Conversely, pain is relieved in epididymitis with elevation (positive Prehn’s sign). This maneuver has low sensitivity in distinguishing the two conditions, but may be helpful in conjunction with other findings.86 Treatment consists of surgical detorsion, which should be accomplished within 12 hours of torsion.46 Manual detorsion is not the treatment of choice; however, remoteness of the wilderness environment may mandate manual attempts. Studies of manual detorsion are scant and the cohorts small.42 If manual detorsion is necessitated, the victim should be placed supine. Because testicular torsion typically occurs in the medial direction, detorsion is initially attempted with outward rotation of the testis (toward the ipsilateral thigh). Simultaneous rotation in the caudal to cranial direction may be necessary to release the cremasteric muscle.31 The surgical treatment of testicular torsion includes pexing the testis to prevent recurrent torsion. Thus, although detorsion may temporize an acute situation in the field, all victims must be evacuated for definitive treatment. 431
CHAPTER 21 Wilderness Trauma and Surgical Emergencies
uncontrolled by antiinflammatory agents, narcotics may be added. Narcotic analgesics are most effective given parenterally; however, agents such as meperidine (Demerol), codeine, and hydromorphone (Dilaudid) may be given orally. Antiinflammatory agents and analgesics can be combined. An antiemetic may be added to relieve nausea. When administering pain medication in the field, particular attention should be given to airway maintenance and induced nausea and vomiting. Any person whose symptom complex cannot be controlled must be evacuated. Additional indications for evacuation include calculus anuria and evidence of obstruction-induced infection.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Prostatitis A number of forms of prostatitis have been defined, including viral, bacterial, nonbacterial, and chronic forms. The acute bacterial form may potentially lead to severe infection. Bacterial prostatitis is an infection of the prostate caused primarily by gram-negative bacteria, with 80% attributable to E. coli. It is an acute, febrile illness characterized by perineal pain radiating to the low back, chills, malaise, and voiding symptoms, such as urgency, frequency, and dysuria. Urinary retention is common, and cystitis frequently accompanies the infection. On rectal examination, the prostate gland is usually boggy, warm, and tender and enlargement is variable. In an ideal situation, treatment is individualized to the cause, which may be difficult to discern in the wilderness. The infection may respond to an oral antibiotic such as ciprofloxacin (750 mg PO twice a day), ampicillin (500 mg PO 4 times a day), or tri methoprim (160 mg with sulfamethoxazole 800 mg PO twice a day). Penetration of prostatic secretions has been shown to be best achieved by trimethoprim/sulfamethoxazole (TMP/SMX). The chosen antibiotic should be administered for 30 days. If retention is present, catheterization or suprapubic aspiration should be undertaken. Acute bacterial prostatitis can escalate in severity to systemic toxicity. Persons with evidence of systemic toxicity unresponsive to a trial of oral or parenteral antibiotic therapy should be evacuated. Urinary Tract Infection UTIs are extremely common and include episodes of acute cystitis and pyelonephritis occurring in otherwise healthy individuals. These infections predominate in women; approximately 25% to 35% of women 20 to 40 years of age report having had a UTI.44 Conversely, men between the ages of 15 and 50 years rarely develop a UTI. Despite the striking difference in prevalence, symptoms are similar between men and women. The symptoms may represent urethritis, cystitis, or an upper UTI; the distinction is often difficult. Common symptoms include frequency, urgency, dysuria, suprapubic pain, flank pain, and hematuria. Flank pain with tenderness to percussion suggests pyelonephritis. On urinalysis, pyuria is nearly invariably present, and hematuria may assist in the diagnosis. Definitive diagnosis is based on significant bacteriuria. The leukocyte esterase test has a screening sensitivity of 75% to 96% and a specificity of 94% to 98% in detecting greater than 10 leukocytes per high-power field.44 Treatment in the wilderness setting for both men and women should be directed at the most common causative agents, although 50% to 70% of cases resolve spontaneously if untreated. Causative bacteria include E. coli (70% to 95%); Staphylococcus species (5% to 20%); and, less frequently, Klebsiella, Proteus, and Enterococcus. Fortunately, oral antibiotics are highly effective. Although resistant E. coli strains are being reported, trimethoprim/ sulfamethoxazole (Bactrim DS) is an excellent first-line drug. Alternative regimens include nitrofurantoin, a fluoroquinolone, or a third-generation cephalosporin. A 3-day course of therapy has been shown to be more effective than single-dose therapy.44 For pyelonephritis, a similar antibiotic in a 10- to 14-day course is an acceptable initial treatment. Evacuation should be reserved for systemic toxicity unresponsive to oral antibiotics.
SKIN AND SOFT TISSUE INFECTIONS Poor hygiene, superficial skin wounds, blisters, dermatologically significant plants, and insect bites contribute to disruption of the skin barrier. Most often seen are superficial pyodermas that do not extend beyond the level of the skin. These include erysipelas, impetigo, folliculitis, furunculosis, and carbunculosis. The majority of superficial skin infections are self-limited. However, with less than optimal hygiene and limited resources, skin infections may progress to deep soft tissue infections. Cellulitis Cellulitis is acute infection of the skin involving subcutaneous tissue. The superficial form of cellulitis, erysipelas, is identified 432
by well-demarcated, warm, and erythematous plaques with raised borders. The face, scalp, hands, and lower extremities are most often affected. Cellulitis is frequently preceded by a superficial wound. In the wilderness setting, there are ongoing infection risk factors. Members of expeditions may be physically stressed and nutritionally depleted. High altitude is associated with immunosuppression. Clostridium species and other pathogens are ubiquitous in the soil, and proper initial wound care may be suboptimal. Under such conditions, cellulitis can progress to abscess formation and tissue necrosis, leading to septicemia. Wounds that develop erythematous, warm, and boggy margins should be treated with antibiotics and closely observed. The margins of erythema should be marked to gauge progression. Treatment consists of proper wound hygiene and antibiotic therapy. Local wound measures include elevation, application of moist heat every 4 to 6 hours, and immobilization. Antibiotic therapy is directed at common causative pathogens. Group A streptococci and Staphylococcus aureus are most commonly implicated. If complications occur and the cellulitis appears to be progressing, a mixed infection is likely. Because Gram’s stain and culture-directed therapy are not possible, the most broad-spectrum antibiotic available should be administered. Parenteral antibiotics are indicated for serious or mixed infections. Penicillin G (1 to 2 million units every 4 to 6 hours) is recommended, with first-generation cephalosporins as an alternative. Because oral antibiotics may be the only available therapy, they should be initiated early in the field. Suggested agents include erythromycin (for the penicillin-allergic victim); cephalexin; a macrolide, such as clarithromycin; or a fluoro quinolone, such as ciprofloxacin or levofloxacin. Methicillinresistant S. aureus is present in wilderness settings. If infection with this organism is suspected, appropriate antibiotics should be used. Lymphangitis Acute lymphangitis is an infectious process involving subcutaneous lymphatic channels. Its recognition in the wilderness setting is important relative to its propensity to follow puncture wounds, hand wounds, infected blisters, and animal bite wounds. Clinical presentation involves linear erythematous streaks that originate in the lymphatic drainage basin of the wound and “point” to the draining nodal group. Causative agents are similar to those common for cellulitis, with the addition of Pasteurella multocida from animal bite wounds. Treatment consists of antibiotics; warm, moist soaks every 4 to 6 hours; and immobilization and elevation of the extremity. Optimal treatment consists of parenteral antibiotics, but as with cellulitis, oral agents should be initiated if parenteral drugs are not available. Broad-spectrum agents with good oral bioavailability and gram-positive coverage are recommended.85 Abscess Formation When untreated, many superficial skin infections convert to abscesses. Development of a raised, fluctuant mass with overlying warmth and erythema should raise suspicion that surgical drainage is necessary. Frequently, the lesion will “point” when purulent fluid has amassed below the dermis and rupture is impending. Warm soaks and observation are recommended by some clinicians, particularly if the presence of drainable pus is uncertain. However, the definitive treatment is drainage. Antibiotics are recommended if significant associated cellulitis is present, but penetration may be poor. Local anesthesia should be administered before incision. The lesion should be incised in line with tissue planes over the point of maximum fluctuance. The value of cruciate incisions over linear incisions is debatable; the important feature is assurance of adequate drainage to prevent recurrence. If drainage is undertaken, the incision must be large enough to adequately drain the cavity. All purulent material should be evacuated and the cavity copiously irrigated with saline or water. Packing is unnecessary if continued drainage is ensured. The wound should be covered with a sterile dressing, changed two to three times per day with concurrent irrigation, and closely observed for reaccumulation of purulence.
Necrotizing skin and soft tissue infections are life-threatening conditions caused by virulent, toxin-producing bacteria. Depth of tissue involvement is variable and may involve skin, fascia, or muscle. The etiology of necrotizing infections is related to breaks in normal cutaneous defenses associated with some form of injury. Although rare, such infections are of importance to the wilderness physician because of the array of documented inciting injuries and the reduction in mortality possible if diagnosis and treatment are rapid.27 Necrotizing infections have developed after innocuous-appearing injuries, including simple scratches, insect bites, ankle sprains, and sore throats.37 The incidence of necrotizing soft tissue infections is unknown, and there is no age or gender predilection. They most commonly occur on the extremities, abdominal wall, and perineum, within 1 week of the inciting event. Common pathogens include Streptococcus species, Staphylococcus, Vibrio species, Clostridium, Pseudomonas, Aeromonas, Enterobacter, and fungi. Many infections become polymicrobial. The clinical manifestations can be subtle. An area of cellulitis is commonly the first indication of infection. Pain is often excruciating, and fever is usually present. The infection then progresses to spreading erythema, induration, blue-black discoloration, and blister formation. Necrosis of skin, subcutaneous fat, muscle, or fascia follows, depending on the organism involved. Necrotic tissue exudes a foul-smelling, watery “dishwater” fluid. Subcutaneous emphysema may be present, particularly with clostridial infections, although enteric organisms may also produce air in tissues. Unfortunately, treatment is limited in the wilderness environment. Debridement of infected tissue should be carried out to the greatest degree humanely possible, but further debridement in a hospital setting is invariably necessary. The extent of debridement necessary is often striking. After debridement, parenteral antibiotics are necessary. Vancomycin and gentamicin are appropriate first-line agents. The most broad-spectrum oral antibiotic available should be initiated, and the victim expeditiously evacuated. Time is of the essence because the infection can be halted only by aggressive surgical intervention.
FIELD OPERATING ENVIRONMENT On a rare occasion, surgical procedures must be performed in the austere environment. By definition, the austere environment is not the ideal situation in which to conduct any invasive procedure. Site security is a consideration. The circumstances responsible for the injury must not continue to exist. Otherwise, the caregivers may be at risk for suffering the same fate as the casualty. The medical expeditionist will need to select a location that provides optimal illumination, yet protection from the elements. Sterility in the Austere Environment One of the major disadvantages of operative procedures in the austere environment is the inability to establish a sterile field. The goal will be to decrease the risk for bacterial contamination to as little as possible. Antiseptics are agents that are used to decontaminate the skin. Chlorhexidine is an antiseptic with excellent antimicrobial activity and prolonged length of activity. In many health care facilities, chlorhexidine has replaced iodophors as the antiseptic of choice. Isopropyl alcohol may be used if no other antiseptics are available. Isopropyl alcohol is commonly available, but it is particularly ineffective on dirty skin and it has little persistent activity. If nothing is available, soap and water may be of benefit. Soaps
will remove the bacteria on the surface of the skin that are not attached, but will do nothing for adherent bacteria. Sterile irrigation may not be available for wound irrigation. If no sterile fluid is available, potable water may be used. Water could be boiled before irrigation, but boiling does not rid the water of spores. If water is to be treated by boiling, the boiling should be at a rolling boil for 20 minutes to be effective. Any irrigation that is used should be removed from the wound as best possible. Wounds should be managed to ensure that no devitalized tissue or foreign bodies remain to minimize the chance of infection. Should an expedition make preparations for the possibility of surgical procedures, instruments taken into the field should be packed sterile in durable containers. Paper wrappers can become perforated, permitting contamination. The term disinfectant means an agent to decontaminate inanimate objects. If surgical instruments are not sterile, disinfectants can be used to decrease the bacterial count on the surface. Of course, all instruments should be clean of debris. Unfortunately, many of the disinfectants used in health care facilities are not practical for the austere environment. Ortho-phthalaldehyde (Cidex OPA), peracetic (Nu-Cidex, Perasafe), and glutaraldehyde (Cidex) are agents that are effective disinfectants, but hazardous for personnel and the environment and impractical in the field environment.24 The antiseptic chosen for skin preparation may be applied to the instruments in the absence of a disinfectant. Placing the instruments into boiling water will decrease the bacterial count, but will not completely eliminate bacterial spores. Applying flame to the instruments may kill bacteria but may leave products of combustion on the instruments that are then left in the wound as foreign material. The U.S. Army has developed a field sterilization system that is lightweight and does not require an external energy source. The system is the size of a suitcase and has the capacity to accommodate a surgical tray. A mixture of water and dry reagents controllably generates chlorine dioxide. The chlorine dioxide kills all vegetative cells and bacterial spores within one-half hour.24 Anesthesia Local and regional anesthesia will be the techniques of choice to provide comfort during minor operative procedures. General anesthesia should not be considered without a full complement of trained personnel and equipment. Procedural sedation and analgesia may be used with the availability of adequate monitoring, and the capability to establish a definitive airway should be immediately available. Common agents to supplement local or regional anesthesia are opioids and benzodiazepines. Should these agents be used, reversal agents of naloxone and flumazenil should be available. Another consideration would be the use of ketamine to provide dissociative sedation.4 Chapter 17 discusses pain management more specifically. Any operative interventions performed in the wilderness should keep in mind “damage control” principles. The general concept of damage control is to manage immediately lifethreatening problems, such as hemorrhage and gross contamination. Definitive management is delayed. Resuscitation continues during this period of time.87 Damage control principles should be kept in mind before considering any procedure in the austere environment. Generally, the approach in the wilderness should be temporizing with resuscitation or lifesaving or limb-saving procedures before contemplating definitive management.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
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CHAPTER 21 Wilderness Trauma and Surgical Emergencies
Necrotizing Infections
CHAPTER 22
Wound Management RAMIN JAMSHIDI
Management of wounds sustained in remote and wilderness environments requires special preparation and knowledge. The basic elements of wound care can be outlined so that a provider in a remote, austere, or wilderness environment can safely manage the immediate wound and thereby limit secondary injury. In the care of acute injuries, attention is frequently focused on wound closure. In truth, most traumatic wounds would fare well if left open to heal by secondary intention.17 However, open wounds incur prolonged time to complete healing, discomfort of wound care, vulnerability to further injury, and larger scars. The critical goals of immediate wound care are to stop hemorrhage and limit morbidity related to infection. Secondary goals are to promote rapid healing and optimize cosmetic outcome.44
Types of Wounds and Definitions Abrasions result from tangential (shearing) forces. Although abrasions are most commonly superficial, they can be extensive and involve deep tissues. Superficial abrasions pose no threat to the patient but may require use of analgesics. Deep abrasions that have completely obliterated skin and denuded underlying fascia are at increased risk for infection and must be kept clean. By virtue of the mechanism of injury, abrasions involve more surface area than they do depth. As a consequence, they are not amenable to suture closure. Abrasions are treated by extensive irrigation to remove all debris (often dirt or gravel) and application of nonadherent dressings. Topical antiseptic solutions are not necessary but are useful adjuncts in preventing gauze dressings from adhering to raw tissue. Such dressings should be changed once daily or more frequently as needed for soiling or adherence (“drying out”). Abrasions do not form abscesses because they have no deep spaces to contain infection. They may become superinfected and develop cellulitis; although this is generally rare, the possibility is more real in the exposed wilderness environment. Diagnosis and management of cellulitis are discussed later in this chapter. Burns (see Chapter 13) may result from thermal or chemical insults. These injuries span a spectrum from trivial sunburn to deep tissue necrosis. The first principle of management is to limit further injury by extinguishing the source, seeking shade, washing out chemicals, and so on. For chemical exposures, voluminous irrigation is the key to limiting further injury. This should be done with clean (not necessarily sterile) water, and the run-off irrigant should be prevented from injuring more skin.7,15,34 Chemical quenchers (i.e., alkaline solution for an acid burn) should never be used because the resulting exothermic reaction will cause secondary injury. Once the burning process is arrested, burn care must focus on antisepsis because infection poses the single most important immediate threat. Burn wounds should be fastidiously cleaned to remove all foreign material and devitalized skin. Depth was formerly described as first, second, or third degree, but modern description relies on the descriptors partial thickness and full thickness (Figure 22-1). Blisters should be left intact unless they interfere with function. There is some debate about the management of blisters, but in a wilderness environment, the “biologic bandage” provided by an intact blister supersedes any academic debate about the presence of inflammatory mediators in the blister fluid. Blisters over the palms or joints are exceptions to this rule, because their presence will significantly limit motion and potentially engender contraction or decrement in function. One school of thought is that these blisters should be unroofed and gently scrubbed away with a moistened gauze or trimmed with scissors. 434
Once cleaned, burns should be dressed and kept clean. Topical antiseptic agents should be applied to burns with invasion deep enough to result in blistering or erosion through the skin to white tissue or burned muscle underneath. Silver sulfadiazine is an excellent agent, and can be reapplied once or twice daily to prevent the wound from desiccating. In the absence of silver sulfadiazine (and for burns <1% of body surface area), antibiotic or antiseptic ointment (e.g., bacitracin), can be employed. Lacerations can be deep or superficial, simple or irregular (Figure 22-2). Generally, lacerations are amenable to primary repair (i.e., closure at the time of injury). Closure simplifies wound care and optimizes cosmetic outcome. Much of the following discussion is dedicated to management of lacerations. Punctures are lacerations with very small entry site injury, but extended depth. Generally these injuries should not be closed because they cannot be adequately cleansed. There is little cosmetic benefit to closure, whereas there is significant risk for trapping infectious agents deep within them because of the inherent difficulty of properly irrigating the tract.
Clinical Presentation Immediate evaluation of traumatic wounds should include determination of the type of injury. Focused assessment includes determination of surface area and apparent depth. Distal sensation and passive and active range of motion must be assessed to elucidate any associated nerve injury, tendon disruption, or fracture. Nerve and tendon injuries will not affect acute management but are important as a baseline examination. Fractures require immobilization, which is discussed in Chapter 27. Distal perfusion must be assessed to determine likelihood of vascular injury. If there is suspicion of vascular injury based on examination, depth of the wound, or blood at the scene, the wound should not be probed (nor blood clots dislodged) until one is prepared to place direct pressure to control hemorrhage and potentially ligate or suture the injured vessel. Time since injury is very important when considering wound closure. Within several hours of injury, traumatic wounds become colonized with bacteria. Even without frank infection, heavy colonization impedes proper wound healing.17,23,45 A bacterialaden wound that has its edges approximated will generally not heal and has increased risk for developing an abscess. Various investigators have tried to establish a firm time limit beyond which traumatic wounds should not be closed, but results are inconsistent.3,28,49 With copious irrigation and removal of foreign bodies, most wounds that are otherwise suitable for closure (see earlier discussion) can be closed if this is accomplished within 6 hours of injury.21 This deadline may be extended in the hospital setting, where thorough sharp debridement can be undertaken and the environment controlled. In some circumstances, wounds may even be closed days or even weeks after initially generated, but this involves sophisticated surgical care.29 This situation should not be confused with an acute wound in the wilderness, which in all circumstances should be thoroughly irrigated, foreign bodies removed, and dressings applied. Acute wounds in the wilderness should be closed only if they are clean, suitable materials and instruments are at hand, and less than 6 hours have passed since the injury.
Treatment Personal protective equipment should be donned before interrogating, preparing, possibly closing, and dressing a wound. Eye
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CHAPTER 22 Wound Management
FIGURE 22-1 Campfire burns, mostly partial thickness with both intact and ruptured blisters. The distal forearm is pale white without capillary refill, representing full-thickness injury. (Courtesy Ramin Jamshidi, MD.)
FIGURE 22-2 A deep and irregular laceration that is suitable for irrigation and multi-layer closure with interrupted mattress sutures (see text). (Courtesy Ramin Jamshidi, MD.)
shields and gloves are considered mandatory equipment. Eye shields are particularly important in preventing exposure of mucous membranes to bodily fluids. Gloves are essential and should be made of a nonlatex material and contain no talcum or other lubricant. Talcum, calcium carbonate, and cornstarch are common glove lubricants, and all have been shown to cause wound granulomas, foreign body reactions, adhesions, and chronic sinuses. Sterile gloves are less cumbersome to work with but are not required because they do not reduce the incidence of infection in an austere setting.37 Use of a mask has also not been demonstrated to reduce rates of acute wound infection but certainly provides a protective barrier for the care provider. Hair coverings are not necessary, because studies have failed to demonstrate reduction in wound infection rates.
possible, an antiseptic ointment can be used to paste the hair down away from the wound. Water should be used to clean the wound. There is no demonstrated benefit to use of saline solutions, and there is no absolute need for the irrigant to be sterile.7,15,34 Although some persons mention use of dilute (1%) povidone-iodine as an irrigant, this is not proved to be more efficacious. Whatever method is available to generate potable water (e.g., iodine tablets, mechanical filter, irradiation, boiling) is sufficient to generate irrigation fluid for wound care. Hydrogen peroxide is injurious to deep tissues and should not be used as an irrigant. The greatest impact on wound cleanliness is gained from volume of irrigant and simple mechanical debridement. Debridement is achieved by removal of obvious foreign material (as with forceps) and also by pulsing irrigant at the wound (the fluid agitation is an effective debrider) (Figure 22-3).30 The available volume should be used in successive bursts rather than a single “gush,” because dilution of wound contaminants is far superior with small serial volumes. Although the matter has not been systematically researched, a guideline that is often used is a minimum of 100 mL per centimeter of wound length. Optimal stream pressure has been determined to be 5 to 10 psi, but in a remote setting, use of pressure gauges or regulators is unnecessarily cumbersome; it is sufficient to realize that excessive pressures are not required.43,49 A large (20 to 60 mL) syringe attached to a 19- or 20-gauge needle or catheter is an effective instrument for this purpose. Alternatively, holes can be punched into the cap of a squeezable water bottle to generate the same effect. A splash shield at the tip of the
Cleansing Techniques Cleansing involves removing devitalized tissue, clearing debris, and copiously irrigating the area.21 This may involve vigorous manipulation of painful and sensitive tissues, so if oral analgesics are available, they should be used. Constricting jewelry and equipment should be removed from the affected area (e.g., rings, piercings). Ideally, hair around the wound is trimmed because the roots harbor bacteria. Hair should be trimmed to a few millimeters in height because shaving at the surface increases wound infection rates by causing superficial skin trauma.2 Eyebrow hair is an important exception, because trimming or shaving can result in permanent abnormal hair growth. If hair trimming is not
A
B
C
FIGURE 22-3 A, Irrigation of a deep inguinal wound to remove debris. B, Placement of an interrupted vertical mattress suture to approximate the deep tissue defect with eversion of the edge and relief of tension. C, Completed interrupted closure. (Courtesy Ramin Jamshidi, MD.)
435
PART 4 INJURIES AND MEDICAL INTERVENTIONS
instrument decreases personal exposure risk. If not available as a specific commercial product for this purpose, one can easily be fashioned from a paper or plastic plate, or base of a disposable water bottle or drinking cup. Preparing for the actual wound closure, the skin edges may be prepared with an iodine, povidone-iodine, chlorhexidine, hydrogen peroxide, or isopropyl alcohol solution, but these antiseptic agents should not be used within the wound itself because of potential toxicity. If concentrated ethyl alcohol (i.e., liquor) is available, it may be effective in reducing wound contamination, but this has not been systematically evaluated. These agents should be used to cleanse the skin surrounding the wound, using a gauze soaked with the liquid to paint an overlapping spiral from the wound outward to a distance of approximately 5 cm. The cleansed skin must be allowed to dry to achieve full effect; this takes 3 to 5 minutes at 20° C (68° F). Honey instilled into a wound has demonstrated certain antimicrobial properties, but conflicting research exists on this topic. Although it is recommended by some as an improvisational technique, it cannot be recommended as a routine adjunct at this time.
Vascular Injuries Evaluation of hemorrhage is a major component of acute wound management; even if bleeding has stopped, there may be a risk for delayed rebleeding. The wound should be irrigated vigorously so that if bleeding is to occur, it happens while the wound is being interrogated and one is poised to address it. Inadequate hemostasis during initial treatment engenders avoidable delayed blood loss. Bleeding from wounds can almost always be controlled with direct pressure. The most common reason for failure of direct pressure to control bleeding is too short a compression time. Initial pressure should be applied for 5 minutes (checked with a timepiece to ensure accurate timing). If bleeding persists, either pressure should be reapplied for 10 minutes, or pressure should be applied at both the wound and a proximal inflow point (e.g., popliteal, femoral, or brachial artery).24 The second most common reason for failure of direct pressure is that pressure is not applied in a focused manner over the site of bleeding. A broadly applied towel over a large wound will not be as effective at controlling bleeding as will finger-point pressure applied over the actual site of greatest bleeding. In the face of profuse diffuse bleeding (as from a large raw wound), topical adjuncts are available to promote thrombosis.4 QuikClot is a granular coagulant that was originally designed to be poured onto wounds to stop diffuse bleeding. The mechanism of action of the original product is adsorption of water onto zeolites, which activates factor XII and catalyzes platelet aggregation. However, the granule form of this material is difficult to use for two reasons: the poured material is unwieldy and difficult to control in windy situations; and the reaction is exothermic, causing pain and risking burn injury. QuikClot has now been modified and integrated into a gauze dressing (also marketed as Combat Gauze). The active element is now kaolin, an alumina silicate that activates and accelerates the enzymatic clotting cascade. The solid consistency of Combat Gauze is more manageable and generates no heat on application. Celox gauze is based on chitosan, a natural product derived from shellfish. Initial versions of this product were granules to be poured into a wound, but it is now embedded into an actual gauze dressing and also has no exothermic properties. HemCon bandages are also chitosan based and not exothermic. These agents are all designed to be applied directly to bleeding wounds and compressed with direct pressure. Before wound closure, these dressings must be removed and bulky gelatinous deposits in the wound irrigated out (although mild residual coatings are reportedly safe to leave in place). All of these agents are supported by anecdotal reports of success and are clearly superior to simple gauze dressings, reducing bleeding by nearly an order of magnitude. However, head-to-head studies published to date have been underpowered and are difficult to interpret. Ongoing development of these products and comparative evaluation are the most active areas of acute wound care research and development. 436
FIGURE 22-4 Severe complex crush injuries of both legs. These wounds mandate immediate evacuation, but profound hemorrhage may require tourniquet placement to prevent exsanguination until advanced surgical care is available. (Courtesy Ramin Jamshidi, MD.)
In contrast to the above products, which are designed to control gross hemorrhage, there are adjuncts intended to assist with lower volume bleeding within the wound. Surgicel products are procoagulant materials composed of a scaffold of cellulose polymer. They have been in clinical use for more than 60 years and are manufactured in fibrillar consistency as well as woven sheets. The major benefit of these agents is that they are totally absorbable, so they can be left on or within the wound, even suturing the wound closed over them. Gelitacel is a procoagulant dressing that is similar to Surgicel. It is a knitted sheet of resorbable cellulose that boasts complete dissolution in as short as 96 hours (more rapidly than Surgicel, thus theoretically less likely to result in an encapsulated collection within the wound). Tourniquets may be considered as a last resort to stop lifethreatening hemorrhage. Great debate exists over the use of tourniquets and who should be allowed to apply them (laypersons, emergency first responders, midlevel health care providers, physicians, or even specialty-specific physicians). The more proximal a tourniquet is applied, the greater the risk for devastating tissue/limb loss. The best potential use of a tourniquet may be for a traumatic amputation in which there is copious diffuse bleeding at the open end. In this case, a tourniquet can be firmly applied just proximal to the open wound so that little distal ischemic tissue is created (Figure 22-4). Commercial tourniquets such as the Combat Action Tourniquet are available, but a blood pressure cuff is often an effective instrument. Whatever device is employed, it should be applied and intensified until pressure exceeds arterial pressure and then increased at least another 20 mm Hg or until bleeding stops. If transport to advanced surgical care is expected to be prolonged (more than 1 hour), the tourniquet should be slowly released every 45 to 60 minutes and allowed to gently bleed (i.e., so long as bleeding is not torrential) for 3 to 5 minutes. This allows intermittent perfusion of tissue and can gradually induce ischemic conditioning of the affected tissue to lessen the effects of ischemia and reperfusion. However, this is controversial, and some authorities do not advocate intermittent loosening to avoid dangerous hemorrhage. When a tourniquet is released, it should be done slowly over a minute or two, because recirculation of stagnant, acidic, and hyperkalemic blood from the nonperfused distal limb can lead to hemodynamic instability. If dysrhythmia is noted, the tourniquet should not be released further until the patient stabilizes. Hypotension and even cardiac arrest may result when a tourniquet is released; these dangers are frequently overlooked and can cause tragic outcomes. Although profuse external hemorrhage is easy to localize, ischemic complications of vascular injuries are more subtle and sometimes overlooked. Examination findings are classically divided into “soft” and “hard” signs of vascular trauma, indicating the relative likelihood of a significant vascular injury (Table 22-1).24 Presence of a hard sign is more than 90% predictive of need for vascular intervention. Only about one-third of patients with a single soft sign have an abnormality on arteriography, and
“Hard Signs”
“Soft Signs”
Active or pulsatile hemorrhage Pulsatile or expanding hematoma New thrill or bruit Limb ischemia/compartment syndrome Diminished/absent distal pulse
Hypotension/shock Neurologic deficit immediately following injury Stable, small, nonpulsatile hematoma Proximity of wound to major vessels
few of these require emergent intervention. Any patient with a hard sign of vascular injury requires immediate evaluation by a surgeon.
Anesthesia Manipulation of traumatic wounds can be painful and anxiety provoking. Studies have demonstrated that music can reduce procedural anxiety.32,42 For most patients, explaining the steps involved can improve tolerance by guiding expectations.54 If vigorous debridement or suture closure is to be attempted, infiltration of local anesthetic can provide tremendous comfort for the patient and thus facilitate technically superior closure. Anesthetic solutions can be applied locally within tissue, as topical agents, or as regional nerve blocks. Direct intradermal or subcutaneous injection is the most common technique of local anesthetic use. These agents are synthesized in two related chemical classes: aminoamides (lidocaine, bupivacaine, dibucaine, etidocaine, mepivacaine, prilocaine, and ropivacaine) and aminoesters (chloroprocaine, procaine, tetracaine, and cocaine ). Characteristics of the most commonly used local agents are listed in Table 22-2. Inclusion of epinephrine in the solution effects local vasoconstriction by α1-adrenoceptor agonism and nearly doubles the duration of the local effect of the medication. By slowing systemic absorption of the anesthetic, it also increases the maximum allowable total dose. Inclusion of epinephrine in the anesthetic solution is believed by some to improve local hemostasis, but this is a minor contribution relative to the effect of increased tissue turgor from infiltration of the solution. Conventional teaching is that epinephrine-containing local anesthetic solutions should not be used in TABLE 22-2 Properties of Select Local Anesthetics Name* Amide Class Lidocaine with epi Bupivacaine with epi Ester Class Chloroprocaine with epi
Maximum Dose
Weight-Based Dose
30-60 min 60-120 min 90-240 min 180-360 min
300 mg 500 mg 175 mg 225 mg
5 mg/kg 7.5 mg/kg 2 mg/kg 3 mg/kg
15-30 min 30-60 min
800 mg 1000 mg
Duration
7 mg/kg 10 mg/kg
*With epi, epinephrine 1 : 200,000 (5 mcg/mL).
end-vascular beds such as the nose, fingers, toes, and penis because of concern for ischemia. However, there is literature to support safe use of these solutions for digital blocks.46,51 Using anesthetics without epinephrine allows maximum flexibility in terms of allowable location of use. Pain of injection for any local anesthetic can be attenuated by mixing 1 mEq of sodium bicarbonate with each 9 mL of anesthetic to buffer the solution. It should be noted that this delays the onset of action by approximately 5 minutes. The most common reasons for apparently ineffective local anesthetic effect are use of an insufficient dose and inadequate time allowed for onset of effect. Time to onset depends on the agent’s ability to cross cell membranes, which is determined by the compound’s intrinsic pKa. In general, a minimum of 3 minutes is required for onset of effect (as with lidocaine), but sometimes as much as 15 minutes is required (as with bupivacaine). This chemistry explains the delayed onset of action when the anesthetic is mixed with bicarbonate. For all agents, intravascular administration or overdose will first cause agitation, tremor, and tinnitus, then seizures, and finally, cardiac arrest through aberrant conduction.19 These risks are particularly important to consider in children, in whom toxicity occurs at lower doses. Table 22-2 lists maximum doses of commonly employed local anesthetics, along with weight-based guidelines for children. Although ample anesthetic should be administered, caution must be exercised to ensure that no intravascular administration occurs and to avoid nearing the maximum dose. This principle is complicated by the fact that maximum doses are ill defined and are set at different levels in different nations.38 Of note, patients with liver disease and those taking medications (such as systemic antifungals) interfering with cytochrome P-450 metabolism will have decreased capacity to metabolize aminoesters. In patients with renal failure, the metabolism of bupivacaine is altered, which requires a dose reduction of 15% to 20%. Concern frequently arises over administration of epinephrine-containing local anesthetics to patients with heart disease. However, these dilute local/regional doses do not cause significant systemic hemodynamic effects. Local anesthetics can be applied topically as well and have demonstrated efficacy in numbing the skin, although 20 to 30 minutes is required for onset. Topical anesthetics are particularly useful for superficial wounds over a large surface, such as burns and abrasions.26 A variety of formulations are available: TAC (0.5% tetracaine, 0.027 epinephrine, 11.8% cocaine), LET (4% lidocaine, 0.1% epinephrine, 0.5% tetracaine), and EMLA (2.5% lidocaine, 2.5% prilocaine in a eutectic mixture containing a thickener, emulsifier, and distilled water buffered to pH 9.4), and 5% lidocaine jelly. Characteristics of these agents are summarized in Table 22-3. Care must be taken to avoid application near mucous membranes because of the potential for systemic absorption and toxicity. Compared with TAC, LET has less potential for toxicity, is not a controlled substance, and is less expensive.1 LET should be stored in a light-resistant container and is stable for 6 months refrigerated and 4 weeks at room temperature. It should be discarded if the solution becomes discolored. Near mucous membranes, 3 mL of LET solution can be combined with 150 mg methylcellulose (4000 cps) by stirring for a few minutes, to create a gel preparation that should be used immediately. This lessens the likelihood of having the topical preparation run onto the mucous membranes.
TABLE 22-3 Properties of Topical Anesthetics
TAC LET EMLA LMX 4 or 5
Composition
Time to Onset
Notes
0.5% tetracaine 0.057 epinephrine 11.8% cocaine 0.5% tetracaine 0.14 epinephrine 4% lidocaine 2.5% lidocaine 25% prilocaine 4 or 5% liposomal lidocaine
30 min
Seizures and cardiac arrest reported; controlled substance; avoid mucosal surfaces
15-30 min
Inactivated by extensive light exposure
30-120 min
Longer duration; requires occlusive dressing; methemoglobinemia reported; do not place over open wound
15-40 min
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CHAPTER 22 Wound Management
TABLE 22-1 Relative Indicators of Vascular Injury
PART 4 INJURIES AND MEDICAL INTERVENTIONS
True IgE-mediated allergic reactions to local anesthetics are very rare, particularly with aminoamide anesthetics.12,19,38 Typically these reactions are actually caused by preservatives such as methylparaben in multidose vials. One alternative is to use an aminoester anesthetic such as chloroprocaine. However, the principal metabolite of the aminoesters is para-aminobenzoic acid, which is chemically similar to methylparaben and can induce the same reactions. A reasonable approach to a reported allergy to a particular anesthetic is to use a preservative-free anesthetic of the other class. Use of diphenhydramine has been described as an alternative to traditional local anesthetics.36 At 1% concentration, it can be injected subcutaneously or subdermally but causes more pain from injection than do the classic anesthetics, and this pain is not diminished by dilution or mixing with bicarbonate.39 More importantly, diphenhydramine injection can result in vesicle formation and tissue necrosis.18 Because of these characteristics, it is not recommended as a local anesthetic. In the absence of any pharmacologic anesthetics, ice may be applied around the wound edges for 5 minutes to diminish sensation. Regional anesthetic techniques can be very useful for dealing with extremity wounds or fractures. This involves infiltrating the anesthetic around the nerve(s) innervating the affected region.52 These techniques rely on specific anatomic landmarks and are beyond the scope of this chapter.
Wound Closure Techniques The first determinant of whether or not to close a wound is the type of trauma sustained. The next is the degree of contamination and time since injury. If the wound clearly has foreign material that cannot be removed or devitalized tissue that cannot be completely debrided, then the wound should be left open to heal by secondary intention. Critical factors are the experience of the health care provider and availability of instruments. Wound closure is almost never so necessary that an untrained provider should attempt it. A variety of materials and approaches may be taken to close wounds. Sutures are generally required to approximate deep tissues, but the superficial aspects of wounds can be addressed with adhesive strips, sutures, glues, staples, or some combination thereof.22 Small superficial lacerations in areas with modest skin tension may be amenable to reapproximation with dressing strips such as Steri-Strips, Leukostrips, or Episeal. This can also be achieved with clean, semiporous medical paper tape. These strips of tape are laid perpendicular to the direction of the wound while holding the edges together. Small gaps should be left between strips to ensure ventilation. Different manufacturers boast superior adhesiveness, but the greatest impact on tape adherence is the use of liquid adhesive on the skin before applying the tape. Tincture of benzoin and Mastisol are equally effective for this purpose as long as they are allowed to dry for a minute before applying the strips. Modern genesis of these products was application of plastic medical tape to approximate wounds in remote locations when providers found the skin too thin or delicate to retain sutures. Modern adhesive strips can still be used for this purpose, or even in a hybrid fashion; strips can be placed along wound edges to reinforce the skin and help it “hold” suture. This practice actually dates back to the 16th century, when Ambroise Paré pasted linen strips to wound edges to reinforce suture closure. Modern cyanoacrylate skin glues are effective, affordable, and more versatile than adhesive strips.8,22,40 They boast the added benefit of sealing the incision, which may be particularly useful in a wilderness setting involving exposure to the elements. Cyanoacrylate glues are popular. These include Dermabond, Indermil, and SurgiSeal. Each of these differs slightly in time to drying, maximum tensile strength, and viscosity, but the clinical variability is minor; selection should be based on availability and cost. Although many are stable at lower than 30° C (86° F), it should be noted that storage of Indermil for longer than 4 weeks requires refrigeration. Another technique to close a wound if only tape, needle, and thread are available is accomplished as follows. Cut two strips of adhesive tape 2.5 cm (1 inch) longer than the wound. Fold 438
FIGURE 22-5 Folding a longitudinal piece of tape to prepare for a suture anchor strip.
one-quarter of each strip of tape over lengthwise (sticky to sticky) to create a long nonsticky edge on each piece (Figure 22-5). Attach one strip of the tape on each side of the wound, 0.6 to 1.3 cm (0.25 to 0.5 inch) from the wound, with the folded (nonsticky) edge toward the wound. Using a needle and thread, sew the folded edges together, cinching them tightly enough to bring the wound edges together properly (Figure 22-6). The tape will stick much better if you first apply a thin layer of benzoin to the skin.5 Sutures are the workhorse of wound closure because of durability and versatility; summary characteristics of the most versatile sutures for acute traumatic wounds are listed in Table 22-4.13,16,41 When suturing deep tissue, intermediate-durability absorbable materials such as polyglactin (e.g., Vicryl) or copolymeric glycolic and lactic acids (e.g., Polysorb) should be used. At 2 weeks, these materials retain approximately three-quarters of their original strength.11,14 Nondyed varieties are preferred within 5 mm (0.2 inch) of the skin surface to avoid wound tattooing. For mucosal lesions (such as within the mouth), rapid-absorbing gut suture is the most suitable.9 In all these cases, a tapered-tip needle should be used so that deep tissue is not lacerated. Ideally, skin suturing should be done with monofilament nonabsorbable material attached to a cutting needle. Nylon (e.g., Ethilon, Dermalon) and polypropylene (e.g., Prolene) are typical nonabsorbable sutures. Polypropylene is blue but does not tattoo skin as noted above for absorbable sutures. If proper materials are not available, nondyed absorbable suture with a tapered needle can be used on the skin, but nonabsorbable suture should not be buried within the wound; in this case, deep mattress sutures should be placed so that deep tissue is approximated but the suture can still be removed once healing is complete. Size selection is based on visibility and the degree of tension expected on the wound. For skin approximation, recommended sizes are: 5-0 or 6-0 for the face/neck/ears; 5-0 or 4-0 for fingers/hand; 4-0 or 3-0 for scalp/arm/leg/feet/chest/abdomen; and 3-0 or 2-0 on the back or over a major joint. Deeper layers (below the skin) generally require suture one size larger than or the same as is being used for the skin (e.g., deep upper arm laceration receives 4-0 absorbable suture to approximate deep layer, followed by 4-0 for skin). The goals of deep tissue closure are to take tension off the skin closure and to obliterate the gap in deep tissue so that seroma or abscess is less likely to form.13,16,41 Muscle sheaths (i.e., fascia) should be reattached, and subcutaneous tissues should be
FIGURE 22-6 Sewing the tape suture strips together to close the wound.
Name
Material
Structure
Tensile Strength
Absorption
Uses
Chromic gut
Bovine intestinal serosa and chromium acid Glycolide and dioxanone Polyglactic acid
Monofilament
0% at 2 wk
21 days
Mucosal repair
Monofilament
90-110 days
Skin
55-70 days
Glycolic and lactic acid copolymer Polypropylene
Braided
75% 40% 75% 50% 80% 30%
Monofilament
Long-term hydrolysis
55-70 days complete absorption Not absorbed
Deep tissue, including ligation of small bleeding vessels Deep tissue, including ligation of small bleeding vessels
Nylon
Monofilament
Long-term hydrolysis
Not absorbed
Nylon
Braided
Long-term hydrolysis
Not absorbed
Silk
Braided
Poorly defined
Permanent
Biosyn Vicryl Polysorb Prolene, Surgipro, Surgilene Ethilon, Dermalon, Monosof Nurolon, Surgilon Sofsilk
Braided
sutured together in interrupted fashion. A deep wound may require multiple layers of suture before skin closure, but usually one or two suffice. Each “layer” of suture is indicated not by the absolute depth of tissue, but by the presence of distinct anatomic “planes” (e.g., separate fascial sheaths) that must be approximated. If significant muscle, tendon, or nerve injuries are recognized, suture repair should not be attempted in the acute setting, but written notes should be recorded for long-term follow-up (Figure 22-7). If required later, these repairs are performed in an elective setting after healing has occurred and functional deficits are delineated. Traumatic wounds are typically irregular in shape and thus lend themselves to closure by interrupted technique. Running closure may be employed if there is a truly linear laceration. A straight or smoothly curved incision may be closed with a running suture to save time. An irregularly shaped wound should be closed with interrupted sutures to achieve optimal alignment (Figure 22-8, A; see Figure 22-3, B and C). Mattress techniques can be applied in deep wounds, thin skin, or those under tension.41,55 Vertical mattress sutures approximate the wound at two depths and evert wound edges for optimal healing (Figure 22-8, B). Horizontal mattress sutures close a single depth, evert wound edges, and distribute tension along the length of the incision (Figure 22-8, C ). More complex wounds can benefit from application of advanced techniques, such as local rotational or advancement flaps.48,50 Mechanical clips can be applied more rapidly than can sutures. Ancient Hindus used ant mandibles to pinch skin edges together, then twisted off their bodies.53 Modern skin staplers are made by various manufacturers and are useful for rapid closure of wounds
A
B
2 3 2 3 2 3
wk wk wk wk wk wk
Skin or full-thickness wound; major vessel ligation/repair Skin or full-thickness wound Skin or full-thickness wound (holds knots better than monofilament nylon) Can be used to ligate vessels, but falling out of use because of high tissue reactivity
on thick skin such as the scalp or back. They can be particularly effective for rapidly achieving hemostasis in the scalp, which is richly perfused and frequently rebleeds after direct pressure is released. Wounds of the abdomen and chest have the potential to involve the viscera. If air is felt, heard, or seen emanating from
FIGURE 22-7 Deep laceration over the wrist that is likely to involve nerve, tendon, and vascular injury. There is no role for attempting tendon or nerve repair in the field; care should focus on irrigation, control of hemorrhage, and aseptic aftercare. (Courtesy Ramin Jamshidi, MD.)
C
FIGURE 22-8 A, Interrupted simple sutures. B, Interrupted vertical mattress sutures. C, Interrupted horizontal mattress sutures.
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CHAPTER 22 Wound Management
TABLE 22-4 Properties of Select Sutures
PART 4 INJURIES AND MEDICAL INTERVENTIONS
a chest wound, or if the patient is complaining of shortness of breath, some form of pneumothorax must be present. The wound should not be closed tightly, but rather covered with a nonocclusive dressing. This will minimize contamination while allowing outflow of air so that tension pneumothorax does not develop. If intestine or omentum protrudes from an abdominal wound, there is considerable likelihood of visceral injury (Figure 22-9). Such a wound should be covered with a moist, secure dressing and not be sutured. Both of these conditions require prompt evaluation by a surgeon. Scalp wounds occur frequently, can be very bloody, and have unique management options. The scalp is richly perfused, so even superficial lacerations can bleed profusely. Initial care should include firm direct pressure for several minutes. If bleeding does not abate, then secure scalp closure is necessary to assist in local pressure and minimize the potential space for hematoma formation. If the galea aponeurotica is lacerated and suture is available, it should be primarily repaired to further limit the space available for hematoma expansion. For skin closure, staplers are excellent in this circumstance because staples are rapidly applied and effective, and the scars are less noticeable on the scalp. Sutures may be used but are not necessary. If a scalp wound is bleeding and needs to be closed but no instruments are available, a hair tie may be performed. Hair is parted along the incision and twisted into cords on either side of the incision. Cords opposing one another across the laceration are then tied together to approximate the wound edges5,25 (Figure 22-10). Timing of skin suture and staple removal depends on the individual wound. Healing and wound remodeling are gradual processes—at 1 week after injury, a typical wound has just 5% to 10% of the original tensile strength. The majority of healing takes place over the first 6 weeks, at which point tensile strength reaches 70% of baseline.17,44 Leaving skin closure material in place longer keeps tension off the wound but increases the likelihood of visible scar from the suture or staple itself. Therefore timing of removal varies based on durability and visibility of the affected area. On the face/neck, sutures are removed at 3 to 5 days, fingers/hand at 5 to 7 days, scalp/leg/chest/abdomen at 7 to 10 days, back/arm/feet at 10 to 14 days, and 14 days across any major joint. For each site, sutures should be left in place longer if scar integrity seems poor, malnutrition has been involved, or if the orientation of the wound subjects it to excessive tension. Sutures are removed with scissors, and staples are removed with a staple remover or by laterally spreading a hemostat between skin and staple. Once the sutures or staples are removed, the healing wound may be reinforced with adhesive strips or skin glue (as described earlier) to minimize tension while healing continues, especially in a wilderness environment where vigorous activity may strain the wound. Visibility of the resulting scar is minimized by keeping it out of direct sunlight, particularly for the first 3 months following injury.
FIGURE 22-9 Abdominal laceration with omentum emanating from the wound. This signifies the possibility of serious visceral injury and mandates immediate surgical evaluation. (Courtesy Ramin Jamshidi, MD.)
440
FIGURE 22-10 String and hair-tying method for closing a scalp wound.
Dressings and Aftercare Wounds should be kept as clean as possible. Any wounds addressed in austere environments are at increased risk for infection and should be carefully monitored for cellulitis or abscess (see Complications). Incidence of infection obviously depends on the specific wound characteristics, anatomic location, and context of injury. Although up to 25% of acute wounds reveal Streptococcus, Staphylococcus, or Escherichia when cultured, most studies have revealed just a 5% rate of infection. Weighing this against the risk for adverse reactions and effect of selecting resistant species, antibiotics are not prescribed for all traumatic wounds.33 The decision to administer prophylactic or empiric antibiotics must be individualized to each situation. Patient factors that should encourage consideration of antibiotics include poorly controlled diabetes mellitus, malnutrition, recent chemotherapy, prosthetic valve or organ transplant recipient, peripheral vascular disease, renal failure, chronic liver disease, chronic corticosteroid use, or other immunocompromising condition. Wound factors include delay (more than 10 hours) to cleansing and repair, extensive devitalized tissue, heavy contamination or retained debris, bites, oral lacerations, foot wounds, open fractures, or injury to poorly perfused tissue (bone, joint, tendon).3,28,33 Tetanus is caused by Clostridium tetani, an organism found in soil and the excrement of humans and animals. The often fatal disease can be prevented by immunization, but 40% of Americans age 60 years or older lack seropositivity.31 Tetanus immunization status must be evaluated for all patients with traumatic wounds, and a booster dose of toxoid and/or immune globulin administered if the patient is at risk for infection (Table 22-5). The formulation of tetanus toxoid booster depends on the age of the patient and vaccination history (Table 22-6).10,27 Dressings serve a few limited purposes: protect the wound from the elements and contamination, absorb fluid from the wound and thereby protect surrounding skin, and provide an environment conducive to healing. Generally these goals can be achieved by dry gauze secured with a bit of tape. Gauze dressings should be changed once daily or more frequently as needed when soiled. For wounds left open to heal by secondary intention, episodic dressing changes are required to provide gradual debridement
Complications
History of Immunization (Doses of Adsorbed Tetanus Toxoid Previously Received)
Cellulitis is diagnosed by the presence of blanching erythema around and spreading away from the edges of a wound and may demonstrate proximal streaking along lymphovascular channels. It is important to distinguish this from the hyperemia that commonly surrounds the edges of a healing wound. Erythema associated with normal wound healing is not as bright red as is cellulitis, has less dramatic blanching with pressure, is symmetric around the edges of the wound, and extends not more than a centimeter from the wound edges. If erythema is not limited by these characteristics, or it progresses in size, wound infection is present. The treatment for cellulitis is a systemic antibiotic. The chosen antibiotic (first-generation cephalosporin or antistaphylococcal penicillin) should cover typical skin flora but also take into consideration any particular exposures (e.g., open water injury, animal bite, soil contamination) that may be associated with the trauma and dictate coverage of different microbes.6 Cellulitis without abscess does not require suture removal. If cellulitis persists or progresses after 36 hours of the above treatments, the antibiotic spectrum should be broadened and the wound reevaluated to ensure that there is not an underlying abscess. Abscess is a suppurative soft tissue infection. Pus is a mixture of dead organisms, leukocytes, and debris contained within a deep tissue space. An abscess will continue to expand, causing progressive pain, surrounding cellulitis, and potential systemic illness until drained (Figure 22-11, online). Antibiotics may stunt the growth or spread of associated cellulitis, but abscesses require drainage. This is accomplished by removing any sutures, staples, or tape keeping the wound closed. The abscess cavity is then copiously irrigated, and a soft probe is used to ensure that any loculated collections are properly drained. An excellent probe is a cotton-tipped swab dipped in antiseptic ointment to prevent deposition of cotton threads. Necrotizing soft tissue infections are true emergencies and require surgical intervention. These can take the form of superficial infections or deep fasciitis. The superficial variety can be easily recognized by the foul-smelling gray (“dirty dishwater”) drainage, but necrotizing fasciitis can develop surreptitiously because skin findings are often subtle and mistaken for simple cellulitis. The signs of deep infection include pain on passive motion, woody induration, and rapid spread.20 Antibiotics may stall the pace of progression, but these conditions are uniformly fatal if not addressed by a general surgeon. The definitive treatment is wide incision and drainage along with fluid resuscitation and intensive supportive care. This typically results in large, disfiguring wounds. Compartment syndrome results from elevated pressures within a contained compartment; as pressure rises, it exceeds venous pressure, then eventually arterial pressure, resulting in tissue ischemia. In the wilderness setting, this is most likely to occur from blunt trauma, particularly with crush injury or a closed fracture. The classic evidence of increased compartment pressures are pulselessness, pallor, pain on passive motion, poikilothermia, and paresthesia.47 Pain on passive motion is the most sensitive and earliest sign to develop, but all are relatively late signs of compartment syndrome. Immediate surgical evaluation is needed because the definitive intervention is incision and release of the involved compartment. If signs of compartment syndrome develop from a penetrating injury, it suggests that there was an occult vascular injury and an expanding hematoma is trapped beneath the closure. The closure should be opened, blood/hematoma evacuated, and a fresh attempt made to control bleeding. If compartment syndrome is not addressed, irreversible tissue necrosis begins by 6 hours. Persistent bleeding is a common concern of wilderness medical providers. Typically this indicates a missed injury or inadequate direct pressure. If a wound continues to bleed through a dressing, the bandage should be removed to allow direct inspection. Consider that a discrete vascular injury may have been missed, and an exposed vein or artery requires direct pressure or ligation.24 If a prolonged period of direct pressure does not stop hemorrhage, one may need to use hemostatic adjuncts or tourniquet application as discussed earlier.
Unknown/less than series of three doses Three or more Last within 5 yr Last within 10 yr Last over 10 yr
Clean and Minor Wound †,‡,§
All Other Wounds*
Toxoid
Toxoid and TIG‡,§,॥
No prophylaxis No prophylaxis Toxoid
No prophylaxis Toxoid Toxoid and TIG‡,§,॥
TIG, Tetanus immune globulin. *Such as contaminated with dirt, soil, saliva, or feces. Includes punctures, avulsions, missile injuries, crush, burns, and frostbite. † Tetanus toxoid formulation depends on the age of the patient (see Table 22-6). ‡ No toxoid should be administered to infants younger than 6 weeks of age. § Patients with acquired immunodeficiency syndrome (AIDS) should receive TIG regardless of immunization history. ॥ TIG 250 units intramuscularly (for both adults and children). Toxoid should not be administered at the same site.
and prevent desiccation. The simplest and most traditional approach is to apply gauze moistened with water, normal saline, or lactated Ringer’s solution directly onto the wound and covered by a layer of dry gauze. These dressings should be changed 3 times daily as the outer dry gauze wicks fluid away from the wound surface. In the absence of infection, this process can be simplified by use of hydrogels that do not evaporate as quickly as do crystalloid solutions. Tegagel and Curafil are two of the most widely used hydrogels available in an amorphous form (gel in a squeezable tube). This is a more effective formulation for a wilderness provider (as opposed to prepackaged individual gauze and hydrogel dressings). If hydrogels are used, moist-todry gauze dressings can be changed just once a day. The last few years have witnessed a proliferation of wound care products intended to accelerate healing and increase simplicity of care. One of the most notable and applicable to wilderness care is Mepilex. This is a silicone foam dressing designed to wick exudates away from wounds while keeping them hydrated to allow healing. This versatile adjunct self-adheres to the skin surrounding the wound and can be left in place for up to 5 consecutive days to manage open or weeping wounds. The foam should be trimmed to cover the wound and overlap onto surrounding skin by about 2 cm (0.8 inch). It should be stored in dry conditions at a temperature under 35° C (95° F); sunlight will discolor the material but not alter its function. Antiseptic ointment is produced in a variety of formulations by many manufacturers. These greasy or gelatinous materials contain povidone-iodine, bacitracin, polymyxin B, or a combination of topical antimicrobials; no substantive evidence exists for the superiority of one formulation over another. However, one must be sure that the patient is not allergic to any of the agents in the ointment. Antiseptic ointments are useful topical agents for injured areas that do not penetrate the skin but are predisposed to desiccation (e.g., superficial abrasions or burns). The viscosity of these ointments make them particularly effective in areas that are difficult to dress and are in constant motion (such as the face or hands). TABLE 22-6 Recommended Tetanus Toxoid Types Age
Tetanus Toxoid Formulation
<6 wk >6 wk and <7 yr 7-10 yr 11-64 yr
No toxoid DTaP Td Td if previously received Tdap or if pregnant Tdap if never received Tdap Td
65 yr or older
DTaP, Pediatric diphtheria and tetanus toxoids and acellular pertussis; Td, tetanus and diphtheria toxoids; Tdap, tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis.
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CHAPTER 22 Wound Management
TABLE 22-5 Postinjury Tetanus Prophylaxis
TABLE 22-7 Wound Care First-Aid Kit
Personal protection
Instruments
Wound preparation
Closure materials
Dressings
Medications
Core Items
Optional Items
Gloves (nonlatex) Eye shield Mask Headlamp Needle driver (15.2 cm [6 inches]) Scissors (iris tip) Toothed forceps (Adson type) Nontoothed forceps (DeBakey type) 60-mL syringe 18-guage needle or blunt cannula 21-guage needle Water filtration system Povidone-iodine swab packets 2-0 nylon (cutting needle) 4-0 nylon (cutting needle) 3-0 Vicryl (tapered needle) Skin stapler Dermabond skin glue vials Adhesive strips (1.3 cm [0.5 inch]) Gauze (10 × 10 cm [4 × 4 inches]) Porous paper tape (1.3 cm [0.5 inch]) Gauze roll (11.4 cm × 3.7 m [4.5 inches × 4 yards]) Flexible, reusable splint 0.25% bupivacaine (10-mL vials) Antiseptic ointment (30 g [1 oz]) Cephalexin (500 mg) Ciprofloxacin (500 mg)
Sterile gloves (nonlatex, nonpowdered) Surgical cap
Many wounds can be managed in a backcountry environment without interrupting the activities. However, some injuries mandate evacuation. These include open fractures, compartment syndrome, persistent bleeding, tourniquet use, progressive loss of sensation or motor function, progressive infection, and fullthickness burns that are circumferential or involve more than 5% of body surface area. Many wilderness-acquired wounds that do not necessitate evacuation still require formal medical evaluation upon return to civilization.35 These include any persistent detriment in motor function or sensation, ongoing drainage from the wound, persistent open wound, burns over the face or genitals, and burns over joints.
Hemostats (curved)
Splash shield Chlorhexidine surgical scrub brush
5-0 nylon (cutting needle) 6-0 nylon (cutting needle) 4-0 Vicryl (tapered needle) Mastisol (15 mL) Elastic roll (7.6 cm × 4.6 m [3 inches × 5 yards]) Mepilex (10 × 20.3 cm [4 × 8 inches]) Surgicel Nu-Knit (2.5 × 8.9 cm [1 inch × 3.5 inches]) QuikClot (10 × 10 cm [4 × 4 inches]) Silver sulfadiazine 1% cream (50 g [1.8 oz]) 5% lidocaine jelly (35 g [1.2 oz])
Wound Care Kit Many adjuncts are available to facilitate wilderness wound care, but a kit with core supplies will suffice in the majority of circumstances. Table 22-7 lists suggested components of such a kit.
REFERENCES Complete references used in this text are available online at www.expertconsult.com.
CHAPTER 23
Improvised Medicine in the Wilderness KENNETH V. ISERSON AND HOWARD J. DONNER
At the heart of wilderness medicine is improvisation, a cre ative amalgam of formal medical science and commonsense problem solving. Medical emergencies can arise at any time in wilderness settings; clinicians in these environments often encounter situations requiring their interventions with little or no medical equipment at hand. Even when they have supplies, as they might if they are the designated providers for a wilderness group or part of a search and rescue team, clinicians venturing into a wilderness environment will soon discover that some improvisation may still be nece ssary. When improvising medical equipment, consider whether it (1) will accomplish the purpose for which it is intended, 442
(2) is practical, or (3) may worsen the situation.23 Improvisa tion encompasses many variations, is governed by few abso lute rights and wrongs, and is limited more often by imagination than by personnel or equipment. As Louis Pasteur reportedly said, “Chance favors the prepared mind.” This chapter is in no way exhaustive but suggests the types of improvisations that may be possible in wilderness or remote settings. Of note is that all these methods have been tested, with many appearing in peer-reviewed literature. Although some of the improvisations, such as transportation methods, border on first aid, they are an integral part of the complexities of remote medical care.
For online-only figures, please go to www.expertconsult.com
HEIGHT To measure an ambulatory patient’s height, use marks in 0.5-cm (or 0.5-inch) increments on any rigid, vertical surface, such as a wall or the side of a doorway. For infants and bedridden patients, put similar marks along the sides of stretchers or beds. Height approximations can be made with marks 0.25 m (or one foot) apart. To estimate a sitting adult’s height, measure the distance (in centimeters) from midsternum to the extended middle finger. Patient’s height = [ 0.73 × (2 × half arm span )] + 43 cm. 79 Alternatively, doubling the longest measurement from mid sternum to the tip of the patient’s third finger produces a very accurate height estimate.45
WEIGHT
FIGURE 23-2 Blood pressure cuff on forearm.
A relatively accurate way to obtain an adult patient’s weight is to use weight estimates by experienced health care workers. Esti mates by paramedics, for example, have been shown to correlate well with the patients’ actual weights in adult cardiac arrest victims.49 Weight estimates of children can be more difficult. Parents can estimate their child’s weight (ages 1- to 11-years-old) within 10% of the measured weight only 78% of the time. This is better, however, than what is estimated by the Broselow tape, which is within 10% of the measured weight only 61% of the time and is less accurate as children get older. In less-developed coun tries, the Broselow tape underestimates children’s weights.4,8,35,48 All other forms of guessing a child’s weight, including the Argall, the Advanced Pediatric Life Support, and the Best Guess methods, perform poorly.43 If the parents are not around, use the following formula: (2 × age in years ) + 8 = weight in kilograms.
PULSES IN INFANTS The typical method of deciding whether an infant has a pulse requires providers to palpate the pulse. This means knowing where and how to locate it, even if it is barely (or not) palpable. Palpating an infant’s pulse, especially when the child is critically ill and a decision must be made immediately about whether to begin resuscitation, can be very difficult. However, determining infant cardiac activity is quickly and easily done by simply placing one’s ear against the infant’s chest wall and listening for heart sounds (Figure 23-1).38
RADIAL PULSE AND TRAUMA PROGNOSIS Tachycardia is a much more reliable sign of hypovolemia than is blood pressure (BP). In trauma patients who are 18 to 50 years old without a head injury, a weak radial pulse indicates a
FIGURE 23-1 Direct precordial auscultation.
markedly increased mortality (29%) compared with only 3% of patients with a normal pulse, as well as a high likelihood that the victim will require intubation and intensive care unit admis sion. Patients with no radial pulse are usually moribund.51
BLOOD PRESSURE Research has shown that the “ability to obtain a blood pressure measurement in an austere environment is often limited by time constraints, equipment availability, and noisy conditions.”51 Blood Pressure Without a Cuff Pulse characteristics are an unreliable sign—and “should be used only as a last resort.”51 Originally, the advanced trauma life support (ATLS) course taught that systolic blood pressure can be estimated from whether radial (>80 mm Hg), femoral (70 to 80 mm Hg), or carotid (60 to 70 mm Hg) pulses are pal pable. This tends to overestimate the patient’s blood pressure. Although the radial pulse always disappears before the femoral, which always disappears before the carotid, most patients’ actual BP is lower than that predicted by these guidelines. But that, by itself, is useful information in a crisis.15 Although an exact BP measurement cannot be obtained, patients with cool extremities compared with those of other patients have hypoperfusion. This can be localized to one extremity, but if it is located in multiple extremities—especially in both an arm and a leg—checking palpable temperature is an effective diagnostic technique. These patients have lower cardiac indexes, lower pH, lower bicarbonate levels, lower mixed venous oxygen saturation, and higher lactate levels.42 A cold or dusky sole of a neonate’s foot can indicate one or all of the following: hypothermia, hypoxemia, or hypotension.14 Blood Pressure Without a Stethoscope Because it may be hard to auscultate BP when transporting patients by air or in a noisy ambulance, palpate the systolic pres sure. If done carefully, this method is as accurate as using a stethoscope. Alternatively, use a pulse oximeter by obtaining a good waveform on a finger, inflating the sphygmomanometer until the waveform disappears, and then slowly deflating the cuff until the waveform reappears. The cuff measurement that reap pears is the systolic pressure.50 Wrist and Calf Blood Pressure Measurements To be accurate, a BP cuff must be the correct size for the arm. It should cover two-thirds of the length of the upper arm. A BP cuff that is too small causes an abnormally high BP reading; one that is too large results in an abnormally low reading. If you do not have a cuff that fits the arm correctly, move it to a location where it fits properly. Place a BP cuff on the patient’s forearm (Figure 23-2) or ankle (Figure 23-3) to obtain better access during patient transport (1) with very obese patients on whom the standard adult cuff is too small, (2) for adults when only a child’s-size cuff is available, (3) to avoid periodically occluding an arteriovenous fistula (e.g., 443
CHAPTER 23 Improvised Medicine in the Wilderness
Vital Signs
PART 4 INJURIES AND MEDICAL INTERVENTIONS
FIGURE 23-3 Blood pressure cuff on calf above ankle.
TABLE 23-1 Clinical Measurements Using Body
Parts*
Approximate Length 1.3 cm (0.5 inch) 2.5 cm (1 inch)
3.8 cm (1.5 inch)
Measurement Site(s) Finger width: greatest width of the distal phalanx of the small finger Phalanx: length of the middle phalanx of the small finger (Figure 23-4) Thumb: width of thumb at the interphalangeal joint (Figure 23-5) Span: when opening the hand and spreading the fingers widely, from the tip of the thumb to the tip of the index finger (Figure 23-6) Grasp: the greatest diameter of the circle formed with the thumb and index finger (Figure 23-7)
*Some of these measurements were suggested by White J, editor: Handbook of Indians of Canada, published as an appendix to the Tenth Report of the Geographic Board of Canada, Ottawa, 1913, pp 280-281. http:// faculty.marianopolis.edu/c.belanger/quebechistory/encyclopedia/ MeansofMeasurementbyIndians.htm. Adapted from Iserson KV: Improvised Medicine: Professional Treatment with Scarce Resources. McGraw-Hill (in press).
FIGURE 23-5 Thumb (2.54 cm [1 inch]).
MEASURING LENGTH, AREA, AND VOLUME A way to most accurately estimate the sizes of wounds is to measure them against the clinician’s own body parts. Table 23-1 gives approximate lengths and areas for upper extremity body parts to use with measurements corresponding most closely with adult white men. Because body sizes vary greatly, especially between men and women, practitioners should measure these sites on their own bodies before using them to measure patient lesions. Standard measurements, in centimeters or in inches, can be made on personal medical equipment, such as the metal ear pieces of a stethoscope (Figure 23-8), a reflex hammer handle, penlights, and scissors.
dialysis patients) or intravenous (IV) line, (4) or to avoid com pressing an area with traumatic injuries. BP cuffs at these sites produce the same or nearly the same mean and diastolic pressure readings, but the systolic pressures vary. Use the mean BP with a forearm or calf BP cuff. (Calculate this by multiplying the diastolic pressure by 2 and adding the systolic pressure. Then divide the result by 3. Alternatively, take one-third of the difference between the systolic and the diastolic pressures, and add this number to the diastolic pressure.)40
Volume Measurement Volume measurements are used to determine the outputs of urine, blood, and other secretions, and to measure fluids and medications. To obtain an accurate volume measurement, use kitchen measuring devices or food containers that have their volume indicated on the label. Generally, they only need to be cleaned of food or whatever else they previously contained. Sterilize the measuring container only if the specimen also has to go to the laboratory or will be used to measure injectable medications. Measuring containers for items that will be taken orally need to be “potable clean,” meaning that one could safely drink from them.
FIGURE 23-4 Phalanx (2.54 cm [1 inch]).
FIGURE 23-6 Span (15.24 cm [6 inches]).
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Rubber tubing
Funnel
FIGURE 23-9 Improvised stethoscope.
Precordial Stethoscope
Ear to Patient If no other option is available, use the method that was common before Laennec invented the stethoscope: put one ear directly against the chest, heart, or abdomen. The sound quality will not be as good as through a stethoscope, but one can get a general idea of cardiac rhythm, abnormal chest sounds, and bowel sounds. Putting one’s ear on an infant’s chest is the fastest and most accurate method for assessing the presence of cardiac activity.
5
Improvised Standard Stethoscopes Laennec-type stethoscopes can easily be fashioned by using rolled paper or, even better, a hollow wooden tube, such as bamboo. The cardboard tube from toilet paper or paper towels also works well. When one end is placed on a patient’s chest and the clinician’s ear is at the other end, one can hear the heartbeat clearly. This, of course, depends on ambient noise and the patient’s body habitus. Use any hollow tube, including short lengths of garden hose, ivory or wood tubes, and metal pipes, as a monaural stethoscope. A simple way to construct a slightly more sophisticated stetho scope is to attach a funnel to two pieces of tubing as shown in Figure 23-9. The juncture of IV tubing works well as a T-tube connector. Put the tube ends directly in your ears, or fashion earpieces as described in Stethoscope Earpiece, later.
20
STETHOSCOPES
15
Improvised Diagnostic Equipment/ Supplies
10
FIGURE 23-7 Grasp (3.81 cm [1.5 inches]).
One very useful monitor during patient transport or procedural sedation is a precordial stethoscope. Taped to the patient’s chest, a precordial stethoscope provides the clinician with continuous assessment of the patient’s audible heart rate and rhythm and breath sounds. Only one earpiece is normally used so that the caregiver can also monitor everything around him or her. In adults, place the stethoscope over the midsternum, in the supra sternal notch, in the perilaryngeal area, or in the axilla. In infants, place the stethoscope to the left chest so that both the heartbeat and breath sounds can be heard. Several improvised methods will produce a workable precordial stethoscope. The quickest way to make a precordial stethoscope is to attach a piece of rubber tubing (that goes in the clinician’s ear) to the top of a screw-top plastic bottle that has a narrow, tapered opening, such as a ketchup/mayonnaise dispenser. Alternatively, cut off the tapered end of a rubber bulb suction syringe or stethoscope head, if one is available.16,77 A slightly more complex method is to make a precordial stethoscope from a 20-mL syringe, a 3-way stopcock, IV tubing, and an earpiece (Figure 23-10). Cut the 20-mL syringe 2.5 cm
A
B
C
D FIGURE 23-8 Stethoscope marked to measure lengths.
E FIGURE 23-10 Improvised precordial stethoscope.
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CHAPTER 23 Improvised Medicine in the Wilderness
T-tube
PART 4 INJURIES AND MEDICAL INTERVENTIONS
(1 inch) from the infusion end (see Figure 23-10, A). Then, smooth the edges with a file, and place adhesive tape around the cut end of the syringe. Remove the plunger’s rubber sealer (see Figure 23-10, B), cut a large hole in its center (see Figure 23-10, C), and insert the rubber piece into the small piece cut off the syringe barrel (see Figure 23-10, D). After connecting this to a three-way stopcock, connect the stopcock to IV tubing (or other tubing) and then to an earpiece (see Figure 23-10, E).32 Esophageal Stethoscope Another way to simultaneously monitor respirations and cardiac rhythm in austere situations and during transport is to use an esophageal stethoscope. Make an esophageal stethoscope from a rubber glove, a nasogastric (NG) tube, suture, and a regular stethoscope. Cut a finger off of the glove, and tie the finger over the end of the NG tube (Figure 23-11). Remove the bell from the stethoscope. Pass the NG tube approximately halfway down the esophagus, and connect the proximal end to the end of the stethoscope. The NG tube can also be passed through the nose.17
A
Hearing Aid When necessary, substitute a stethoscope for a patient’s hearing aid during an examination. Put the earpieces in the patient’s ears and talk into the diaphragm. Unfortunately, this only works, as do hearing aids, for patients with specific types of hearing loss. Stethoscope Earpiece To replace a stethoscope earpiece, use the nipple from a baby bottle or pacifier, or the rubber bulb from a medicine or an eye dropper (Figure 23-12). Make the normal pinhole opening in the nipple slightly larger, and tie the nipple in place on the stetho scope. Cut the nipple so that only the distal 1 to 2 cm (0.4 to 0.8 inch) of the rubber piece is used.40
B FIGURE 23-12 Earpieces for a stethoscope.
Improvised Treatment Equipment/Supplies GOWNS, GLOVES, MASKS, BOOTIES, AND GOGGLES Standard Precautions In an austere environment the basic protective gear used for standard or universal precautions often must be made rather than purchased. Gowns A plastic garbage bag with head and arm holes cut out is the simplest waterproof gown, and can be enhanced with arm pieces cut from another bag and stapled or taped in place. Although not waterproof, a sheet cut like a poncho will also work. Fold a flat sheet so that one-third is doubled over to form the arms. In the center of the folded edge, cut out a hole large enough for the head to pass through. The sleeve is fashioned by cutting slits on both sides of the sheet, midway down the folded section. The slits should extend to the approximate sites of the axillae (Figures 23-13 and 23-14). Once the patient dons the gown, the arms can be secured with safety pins, staples, or tape (Figure 23-15). The large pieces are wrapped around the back under the arms, and the flap on the back makes a tie for the gown. (Depending on the person’s girth, the tie may also need to be pinned.)55,40
A
B FIGURE 23-11 Making an esophageal stethoscope.
446
Caps and Masks Masks are useful to protect both the examiner and patients against particulate matter, virulent organisms, and nauseating smells (tincture of benzoin on one’s mask covers up most bad smells). Caps protect patients’ wounds from the examiner’s hair. The most basic masks are towels or a cloth held to the mouth and nose, either with one’s hand or tied in place. Make an improvised surgical mask and cap from a piece of cloth about 46 × 31 cm (18 × 12 inches). Cut a 10-cm (4-inch) narrow oval to fit over the eyes, about 12.5 cm (5 inches) from one end. The cloth should allow a person to breathe through it
B FIGURE 23-16 Improvised cap-mask.
Eye Protection Put tape around the edges of standard eyeglasses to help to protect the eyes from splattered blood and fluids. An alternative is to wear ski or woodworking goggles—separately or over eyeglasses. FIGURE 23-13 Improvised surgical/patient gown, Step 1.
Booties Make waterproof booties from a large plastic bag. Cut it open so that it lays flat. From that piece, for a standard-sized foot, cut out a portion that is as long as the distance from the foot to the knee and as wide as three lengths of the foot. Make them larger if longer booties are needed, such as in a bloody procedure or when caring for a victim of trauma. Secure them on the foot (not too tight) with duct tape. Clear plastic bags can also work. Cut open as many as needed and tape them to cover the shoes. When using either type of plastic bootie, but especially those made from clear plastic bags, use tape on the bottom to prevent slipping.40
DRESSINGS AND BANDAGES FIGURE 23-14 Improvised surgical/patient gown, Step 2.
as easily as is done through a normal surgical mask. Attach a long piece of tape, extending over the edges of the material, at both sides of the slit. Also attach a long piece of tape to the bottom of the short end. Adjust the slit over the eyes, flip the long piece of material over the head for a cap, and then tie both pieces of the tape behind the neck (Figure 26-16). Cover your head with a long cloth or towel (Figure 23-17) and pin or tape it to the nape of your neck to make a simple cap.56,40
Dressings go directly on wounds and can be adherent or non adherent, wet or dry, and absorbent or not. Dressings are often sterile. Bandages cover dressings, can hold them in place, and place pressure on the wound. Although most clean fabrics can be used as dressings or as bandages, do not use paper products because they disintegrate when wet and leave fibers in the wound. Dressings Most clean, closed wounds do not need a dressing. Wounds without dressings permit easier inspection for infection or dehis cence, eliminate a moist, possibly anaerobic, space over the wound, and make it much easier to keep the wound clean. Have the patient clean the wound with soap and water. Dressing Material. If a dressing is being used to help absorb serosanguineous drainage, to keep the wound moist after small
FIGURE 23-15 Improvised surgical/patient gown, completed.
FIGURE 23-17 Improvised cap.
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A
PART 4 INJURIES AND MEDICAL INTERVENTIONS
plastic closures, or to keep air off an open wound to lessen pain, any absorbent material may be used. A menstrual pad works well to absorb exudates, and more absorbent cotton fabrics can also be useful. If nothing else is available, use moss, especially sphag num (peat) moss, a traditional absorbent dressing. Make nonad herent dressings from sheer synthetic materials, such as parachute cloth or nylon stockings. Use any clean piece of plastic sheeting, such as a plastic bag, to fashion an occlusive dressing for openchest wounds. Using clean, rather than sterile, dressings will rarely affect the incidence of infection. Bandages Bandages hold dressings in place. If there is a dressing, there is no need for a bandage. The most expedient bandages are torn from expendable pieces of cloth—often clothing. If no cloth bandage is available, use duct tape to secure a dressing after first shaving the area to help the dressing adhere and reduce pain on removal. Poke holes in the tape (especially thick adhesives, such as duct tape) to reduce moisture and allow fluids and sweat to escape. Clean the skin with soap and water or alcohol to remove oils. To make an adhesive dressing, cover a small square of dressing with a piece of tape. If you need to see the wound but still want it covered, make a transparent bandage from clear plastic wrap (e.g., Saran Wrap) or a piece of clear plastic bag with its edges affixed to the skin with tape or cyanoacrylate glue.40 A pressure bandage over dressings, used when there is sig nificant seepage or concern about hematoma development, is most easily constructed from an elastic bandage, a bungee cord (use only over fabric stiff enough to distribute the cord’s force), or the elastic from a piece of clothing or equipment.
SYRINGES, NEEDLES, AND INTRAVENOUS EQUIPMENT Venipuncture Tourniquet A rubber glove (sterile or unsterile, but “stretchy”) works well as a venous tourniquet when starting IV lines or drawing blood. Even better, cut the wrist portion off of a surgical glove and slip it over the arm (or an infant’s head).60 Needles When necessary, use needles for injection as IV needles. Note, however, that they may be more difficult to thread into a vein, because injection needles tend to puncture the vessel wall rather than slide in as does the plastic-coated needle on a catheter. Take care when securing an injection needle, using an arm board or generous bandaging so that the needle does not perforate the vessel. Saline Locks To quickly make a saline lock, slip the rubber end of the plunger from a 2- or 3-mL disposable syringe over the end of an IV catheter (Figure 23-18). This also works on a straight needle if it needs to be used as an IV catheter. Simply fill the catheter with saline (or heparin) as would normally be done.40
FIGURE 23-18 Improvised saline lock.
the end of the suture appears, hold it in place and break off the hub by repeatedly bending it (Figure 23-19). Then pull the suture through the needle so that only a small amount remains within the needle. Finally, crimp the “hub” end of the needle to fix the suture in place.31 Do this either at the patient’s bedside or prepare several in advance, wrapping the sutures around a piece of cardboard and autoclaving them en masse.75 Newer safety needles may make this process difficult.
SCALPELS When necessary use any clean, preferably sterile, sharp object to perform surgical procedures. Nearly any piece of metal can be sharpened sufficiently to serve as a scalpel. Honing the entire length of a blade to surgical sharpness takes special metal, tools, and expertise. One option is to start with a straight razor or a cutting knife and sharpen it as well as possible before steriliz ing it. Make a scalpel from a common multi-blade disposable razor by first carefully separating a blade from its plastic holder. Use pliers or a similar tool to bend one end; the blades pop out (Figure 23-20, online). Then put a few drops of cyanoacrylate glue on both the blade and the utensil/holder; the blade can be affixed along the metal blade of a butter knife, the handle of a spoon, or similar items that can be easily held and manipulated during a procedure. The blade should extend over the side of the handle
Intravenous Tubing One way to adjust IV flow rates is to wrap a small piece of mal leable metal (e.g., heavy aluminum foil) around the tubing. Tighten it to the tubing to achieve the desired flow rate. Pressure for Intravenous Fluids/Blood Bags Apply external pressure to IV bags so that, especially when patients must be transported, the pressurized IV bag can simply lie on or next to the patient. Ways to increase the IV or blood bags’ external pressure include inflating a blood pressure cuff around them, and wrapping them with an elastic bandage, a belt (“stretchy” if possible), nylon stockings, a rope, or similar materi als. The IV bag can also be placed under an adult patient; body pressure keeps the IV flowing. Suture Needles To make a “swaged” suture needle from a hypodermic needle, first pass the suture through the needle from the sharp end. When 448
FIGURE 23-19 Improvised swaged suture.
When trying to guide health care professionals in their reuse of single-use devices, many major governing bodies cannot agree on their recommendations. The United States, however, has a consistent policy among several agencies. According to the U.S. government’s report, equipment and supplies “will be rationed and used in ways consistent with achieving the ultimate goal of saving the most lives (e.g., disposable supplies may be reused).”34 Other federal agencies concur, noting that whether medical equipment should be reused depends on the type of equipment and the disinfection method used. 47,12,46
A
B FIGURE 23-21 Improvised skin hooks.
and be parallel to the other side for better control of the scalpel. Wait about 10 minutes for the cyanoacrylate glue to dry.
SKIN HOOKS The best way to handle wound tissue with the least amount of trauma is to use skin hooks. To improvise a skin hook, grasp the tip of a small-gauge needle with a utility tool and bend it into a U-shaped curve (Figure 23-21). Then attach it to a 1- to 10-cc syringe, which serves as a handle. Alternatively, unbend a safety pin so that the two “limbs” on each side of the spring form a straight line. Then bend the sharp end into a U-shape. Sterilize them before use.24
RETRACTORS Self-retaining retractors make procedures easier when working alone or with inexperienced assistants. To make these retractors, bend stiff metal rods into the form shown in Figure 23-22. Use 3-mm rods for minor surgery and heavier rods for major wounds.37 If made from lighter material, such as paper clips, they can be used on more delicate tissues.
TWEEZERS Fashion tweezers to remove foreign bodies or for surgical proce dures from pieces of thin metal strips, such as the metal straps that secure boxes for shipping. If folded with a slight bulge in the end they are less likely to break at the fold after repeated use (Figure 23-23). Use a file to make as fine of an end as you need.
Cleaning and Reusing Medical Supplies and Equipment Much modern medical equipment is labeled as “disposable.” When resources are scarce, this is a luxury that cannot be sus tained. On the other hand, is it safe to reuse this equipment? Caregivers do not want to put patients at risk by introducing infections from previously used equipment or by using malfunc tioning equipment.
FIGURE 23-22 Lightweight self-retaining retractor.
RISK STRATIFICATION The infection risk that medical equipment poses to patients differs and can be stratified according to the equipment’s use, as follows:67 • High-risk items (sterilization required) that come into close contact with breaks in the skin or mucous membranes or are introduced into a normally sterile body area. These include surgical instruments, needles, and urinary or other catheters. • Intermediate-risk items (disinfection required) that come into close contact with mucous membranes or are items contaminated with particularly virulent or readily transmis sible organisms. Examples are respiratory equipment (including laryngoscope blades), endotracheal and trache ostomy tubes, and oropharyngeal and nasal airways. • Low-risk items (cleaning required) that only come into contact with normal, intact skin. These include stetho scopes, stretchers and wheelchairs, other physical examination equipment, and electrocardiography and elec troencephalography leads.
CLEANING Cleaning must be done so that equipment can be properly disin fected or sterilized. Cleaning removes visible dirt or secretions, including dust, soil, large numbers of microorganisms, and organic matter (e.g., blood, vomit) on which microorganisms grow.67 Immediately after use, clean equipment by washing it thoroughly with warm water without soap. Then brush it thoroughly with warm water and soap, rinse with water, and dry completely. Clean surgical instruments with a small brush, such as a soft toothbrush. Leave scissors and forceps open during drying.40
DISINFECTION Disinfection reduces the number of microorganisms to a level that is not harmful to health, although the process does not necessarily kill or remove all microorganisms or bacterial spores.67 The CDC recognizes three levels of disinfection: high, intermedi ate, and low.12 • High-level disinfection using a chemical germicide, includ ing bleach and ethyl alcohol, kills all organisms, except when there are high levels of bacterial spores. • Intermediate-level disinfection kills mycobacteria, most viruses, and bacteria with a chemical germicide registered as a “tuberculocide” by the U.S. Environmental Protection Agency. • Low-level disinfection kills some viruses and bacteria with a chemical germicide, such as soap. Boiling The best way to disinfect equipment in austere environments is to boil it (100° C [212° F] for 10 to 30 minutes at sea level) in clean water, with or without soap. The time starts when the water has come to a full boil. The temperature at which water boils decreases 449
CHAPTER 23 Improvised Medicine in the Wilderness
FIGURE 23-23 Surgical “pickups.”
PART 4 INJURIES AND MEDICAL INTERVENTIONS
at higher altitudes, so a longer boiling time will be required. In theory, the time should be increased by 5 minutes for each 300-m (1,000-foot) rise in altitude. For example, at 4000 m (approxi mately 12,000 feet) above sea level, water boils at 86° C (187° F), so boiling for 60 minutes or longer is required for disinfection. A way to increase the disinfectant effect of boiling is to use “double boiling.” Boil the instruments for 30 to 40 minutes. Let them cool, and then boil for another 30 to 40 minutes.36 This process kills all organisms except for certain bacterial spores. Alcohols Alcohols (e.g., methanol, ethanol, and isopropanol) have good activity against bacteria and viruses so long as the equipment first has been cleaned—or, at least, after all the visible surface dirt has been removed from the area to be disinfected. Use 70% or greater concentrations, and have the equipment in contact with the alcohol for 10 minutes or longer; the longer the contact time the better. To prepare a 70% ethanol solution, add 8 parts 90% ethanol to 2 parts water. To prepare a 70% isopropanol solution, add 7 parts standard isopropanol to 3 parts water.71 Povidone-Iodine Povidone-iodine (PVD-I; Betadine) may be used for disinfecting instruments. Although exact information about this is sketchy, studies seem to support its use. Use 1 part 10% povidone-iodine solution to 3 parts water for 15 minutes.71
DISINFECTING SPECIFIC ITEMS “Sterile” Dressings Clean and disinfect cloth for dressings by boiling it in water for 15 minutes or saturating it in alcohol. Syringes and Needles It is not possible to clean the interior of disposable syringes and needles well enough to use them safely on another patient. Although syringe reuse is a common practice throughout the world, it is so dangerous that it negates any good that medical treatment produces. Only when no other option exists should cleaning and reusing syringes be considered. If that is the case, the best option is one that the U.S. governmental agencies rec ommend for needles and syringes potentially contaminated with human immunodeficiency virus. That is, they should be thor oughly cleaned and then immersed in full-strength bleach (5.25% sodium hypochlorite).64 Single-Use Needle on Same Patient With proper precautions, single-use needles can be used multiple times on the same patient. For example, diabetics routinely reuse the same syringe for up to a week. They do this by keeping the needle clean, storing it in a clean container, and ensuring that no one else uses it.
FIGURE 23-24 Rescue/recovery position.
POSITIONING FOR SAFE AIRWAY Preventing aspiration may be all that is necessary in many patients to maintain an airway, especially in the presence of copious secretions or vomiting. Use the “rescue” or “recovery” position—with the patient on his or her side with face aimed down (Figure 23-24). If possible, elevate the patient’s feet so that he or she is in the head-down position.
OPENING THE AIRWAY Chin Lift/Jaw Thrust Elevating the chin is often the easiest method of maintaining an open airway (Figure 23-25). For many patients with diminished consciousness, this is often all that is needed to keep the airway patent. If a cervical spine injury is suspected, the alternative is to push the jaw forward from the mandibular angles. Head Turn When cervical spine injury is not a concern, turning the patient’s head to one side is a simple but rarely used procedure to open an airway. In patients with significant amounts of redundant tissue in the pharynx and hypopharynx this procedure usually improves airflow. Positioning the Tongue If a suspected cervical spine injury prevents head repositioning or the patient’s tongue still blocks the airway after positioning the head, grasp the tongue with gauze and pull it forward. If this opens the airway (it usually does), put a heavy (approximately 2-0) suture vertically through the tip of the tongue in the midline (Figure 23-26), or use a wire fishing line (or similar material), or safety pin (Figure 23-27). This placement avoids significant bleeding. Initially, have someone hold the suture; if needed longterm, pass it through the skin of the lower lip and tie it. Do not use a clamp or forceps that “may in the excitement of the
Surgical Instruments Use alcohol or, if the equipment does not contain plastic or polymers, acetone to chemically sterilize sharp or delicate instru ments. Following this soak, rinse them in hot, sterile water and let them dry.66 Surgical instruments without a fine tolerance or sharp edges, such as mosquito clamps, towel clips, and large needle holders, may be disinfected in boiling water.66 If you do not mind that sharp instruments will lose their edge, metal can be sterilized by holding it over a flame or, even better, by placing the instrument in a pot with a small amount of isopropyl alcohol (enough to create a small pool on the bottom of the pot). Ignite the alcohol, and allow it to burn out, which takes about 5 to 10 minutes. The alcohol burns without leaving significant carbon residue. These techniques may be used when sterilization is really needed or when available resources or time do not allow for disinfection by boiling or soaking in alcohol.40
Improvised Airway Management Because establishing or maintaining a patient’s airway is the most fundamental lifesaving skill, clinicians must be able to do this despite limited or unusual equipment. 450
FIGURE 23-25 Chin lift.
When placing a nasal airway, lubricate it well, and pass it along the floor of the nose (straight back, not cephalad).40
MOUTH-TO-MOUTH RESCUE BREATHING BARRIER A glove can be modified and used as a barrier shield for perform ing rescue breathing. Cut the middle finger of the glove at its halfway point and insert it into the victim’s mouth. Stretch the glove across the victim’s mouth and nose, and blow into the glove as if inflating a balloon. After each breath, remove the part of the glove covering the nose to allow the victim to exhale. The slit creates a one-way valve, preventing backflow of the victim’s saliva (Figure 23-29).
FIGURE 23-26 Suture used to hold the tongue out.
moment be so firmly applied as to nip a piece out of the tongue.”25 Physicians, surgeons, and anesthetists have used these methods since at least the 19th century without complication.40 Nasal Airways One of the most useful pieces of airway equipment, a nasal airway, or “trumpet,” is easy to improvise. Put a safety pin through the end of any soft piece of rubber tubing (e.g., Foley catheter, uncuffed endotracheal tube, radiator hose, solar shower hose, siphon tubing, or inflation hose from a kayak flotation bag or sport pouch) that is the appropriate size for the patient’s nose (Figure 23-28). In adults, the tube’s length beyond the safety pin equals the length from their nares to the meatus of their ears (11 to 13 cm [4.5 to 5 inches]).10 This “Goldman’s airway” can be made to fit any nose. Consider using nasal airways bilaterally.
Surgical Airway (Cricothyrotomy) Cricothyrotomy—the establishment of an opening in the crico thyroid membrane—is indicated to relieve life-threatening upper airway obstruction when a victim cannot be ventilated effectively from the mouth or nose and endotracheal intubation is not fea sible. This may occur in a victim with severe laryngeal edema or with trauma to the face and upper larynx. Cricothyrotomy may also be useful when a person’s upper airway is obstructed by a foreign body that cannot be extracted by abdominal thrusts or direct laryngoscopy. To perform a cricothyrotomy, cut a hole in the thin cricothy roid membrane and place an endotracheal tube or, in austere circumstances, a suitable hollow object into the trachea to allow ventilation (Box 23-1). Locate the cricothyroid membrane by palpating the victim’s neck, beginning at the top. The first and largest prominence felt is the thyroid cartilage (“Adam’s apple”); the second prominence (below the thyroid cartilage) is the cricoid cartilage. The small space between these two, noted by a depression, is the cricothyroid membrane (Figure 23-30). With the victim lying on his or her back, cleanse the neck around the cricothyroid membrane with an antiseptic if one is readily avail able. Put on protective gloves. Make a vertical 2.5-cm (1-inch) incision with a knife through the skin over the membrane (go a little bit above and below the membrane) while using the fingers of your other hand to pry the skin edges apart. Anticipate bleed ing from the wound. After the skin is incised and spread, punc ture the exposed membrane by stabbing it with a knife or other sharp, penetrating object (Figure 23-31, A). Stabilize the larynx between the fingers of one hand and insert the improvised cri cothyrotomy tube through the membrane with the other hand (Figure 23-31, B). Secure the object in place with tape. BOX 23-1 Improvised Cricothyrotomy Tubes
FIGURE 23-27 Safety pin holding the tongue out.
Intravenous (IV) administration set drip chamber: Cut the plastic drip chamber of a macro drip (15 drops/mL) IV administration set at its halfway point with a knife or scissors. Remove the end protector from the piercing spike and insert the spike through the cricothyroid membrane. The plastic drip chamber is nearly the same size as a 15-mm endotracheal tube adapter and fits snugly in the valve fitting of a bag-valve device (Figure 23-32). Syringe barrel: Cut the barrel of a 2- or 3-mL syringe with the plunger removed at a 45-degree angle at its midpoint to create an improvised cricothyroid airway device. The proximal flange of the syringe barrel helps secure the device to the neck and prevents it from being aspirated (Figure 23-33). Any small hollow object: Examples include a small flashlight or penlight casing, some pen casings, or small hollow tube. The key question is whether sufficient air can pass through the tube for effective ventilation.
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FIGURE 23-28 Goldman’s nasopharyngeal airway.
PART 4 INJURIES AND MEDICAL INTERVENTIONS
FIGURE 23-29 An improvised cardiopulmonary resuscitation (CPR) barrier is created using a latex or nitrile glove.
Adam’s apple (thyroid cartilage) Adam’s apple
Cricothyroid membrane
Cricothyroid membrane
A
FIGURE 23-30 The cricothyroid membrane is found in the depression between the Adam’s apple (thyroid cartilage) and the cricoid cartilage.
Complications associated with this procedure include hemor rhage at the insertion site, subcutaneous or mediastinal emphy sema resulting from faulty placement of the tube into the subcutaneous tissues rather than into the trachea, and perforation through the posterior wall of the trachea with placement of the tube into the esophagus.
Improvised Wound Management The same principles that govern wound management in the emergency department apply in the wilderness setting. The main problem faced in the wilderness is access to adequate supplies. In deciding whether to close a wound or pack it open, take into account the mechanism of injury, degree of contamination, patient’s age, site of the wound, and ability to effectively clean the wound. 452
B FIGURE 23-31 Cricothyrotomy. A, Locate the cricothyroid membrane and make a vertical 1-inch incision through the skin. B, Insert the pointed end of an improvised cricothyrotomy tube through the membrane.
WOUND IRRIGATION The primary determinants of infection are bacterial counts and amount of devitalized tissue remaining in the wound.21 Ridding a wound of bacteria and other particulate matter requires more than soaking and gentle washing with a disinfectant.44 Irrigating the wound with a forceful stream is the most effective method
Wound Irrigation
A
B
1. Fill a sandwich or garbage bag with disinfected water. 2. Disinfect the water with iodine tablets, iodine solution, or povidone-iodine, or by boiling it. 3. Normal saline can be made by adding 9 g (2 teaspoons) of table salt per liter of water. 4. Seal the bag. 5. Puncture the bottom of the bag with an 18-gauge needle, safety pin, fork prong, or knife tip. 6. Squeeze the top of the bag forcefully while holding it just above the wound and directing the stream into it. 7. Use caution to ensure that none of the irrigation fluid splashes into your eyes.
of reducing bacterial counts and removing debris and contami nants.68 The cleansing capacity of the stream depends on the hydraulic pressure under which the fluid is delivered.20 Irrigation is best accomplished by attaching an 18- or 19-gauge catheter to a 35-mL syringe, or a 22-gauge needle to a 12-mL syringe. This creates hydraulic pressure in the range of 0.49 to 0.56 kg/cm2 and 0.91 kg/cm2 (7 to 8 psi and 13 psi), respectively.63 The solu tion is directed into the wound from a distance of 1 to 2 inches (2.5 to 5 cm) at an angle perpendicular to the wound surface. The amount of irrigation fluid varies with the size and contamina tion of the wound but should average no less than 250 mL.20 Remember: “The solution to pollution is dilution.” Tap water (and presumably boiled/cooled water) has been found to be as effective as sterile saline for irrigating wounds. In one study, the infection rate was significantly lower after irriga tion with tap water, and no infections resulted from the bacteria cultured from the tap water.3 Improvised wound irrigation requires only a container that can be punctured to hold the water, such as a sandwich or garbage bag, and a safety pin or 18-gauge needle (Box 23-2).
WOUND CLOSURE
C FIGURE 23-32 Improvised cricothyrotomy tube. A, Cut the plastic drip chamber at its halfway point. B, Insert the spike from the drip chamber through the cricothyroid membrane. C, A bag-valve device will fit over the chamber for ventilation.
Before a wound is closed, remove all foreign material and grossly devitalized tissue. Debridement can be accomplished using scis sors, a knife, or any sharp object, and wounds can be closed with sutures, staples, tape, pins, or glue. Although suturing is still the most widely used technique, stapling and gluing are ideal methods for closing wounds in the wilderness.
ADHESIVES Cyanoacrylate adhesive is the improviser’s best tool. Duct tape is a close second. One can always use sutures to hold vital equip ment in place. This includes putting a suture through the anteriorinferior part of the nasal septum and using the ends to tie NG tubes. A heavy suture or orthopedic/dental wire can be tied around an anterior tooth and then used to secure an endotracheal tube. Another method of securely fixing tapes and leads is to use tincture of benzoin. Absent that, the same effect can be achieved by saturating alcohol gauze with povidone-iodine. As the alcohol evaporates, the remaining residue is similar to that from tincture of benzoin. This method is convenient and readily applied without using extra 4 × 4’s.61 Alternatives to tape (for IV lines, equipment, bandaging) include cellophane tape, duct tape, electrician’s or other very sticky tape, and sutures.
WOUND GLUES
FIGURE 23-33 An improvised cricothyroid airway device can be created by cutting the barrel of a syringe at a 45-degree angle at its midway point.
Tissue glue is ideal for backcountry use because it precludes the need for topical anesthesia, is easy to use, reduces the risk for needlestick injury, and takes up much less room than a conven tional suture kit. When applied to the skin surface, tissue glue provides strong tissue support and peels off in 4 to 5 days 453
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BOX 23-2 Recommended Technique for
PART 4 INJURIES AND MEDICAL INTERVENTIONS
BOX 23-3 Technique for Gluing Lacerations
Staples
1. Irrigate the wound with copious amounts of disinfected water. 2. Control any bleeding with direct pressure. Place a gauze pad moistened with oxymetazoline (Afrin) nasal spray into the wound to help control bleeding. 3. Once hemostasis is obtained, approximate the wound edges using fingers or forceps. 4. Paint the tissue glue over the apposed wound edges using a very light brushing motion of the applicator tip. Avoid excess pressure of the applicator on the tissue because this could separate the skin edges, forcing glue into the wound. Apply multiple thin layers (at least three), allowing the glue to dry between each application (about 2 minutes). 5. Glue can be removed from non-tissue surfaces with acetone, or loosened from skin with petroleum jelly.
Although staples are a great way to quickly close wounds, they cannot be improvised. The best suggestion, if you know that you will be in an austere medical situation, is to carry a staple gun and the staples with you. They are lightweight and relatively inexpensive.
without leaving evidence of its presence.63 It provides a faster and less painful method for closing lacerations than does suturing and has yielded similar cosmetic results in children with facial lacerations (Box 23-3).62 Tissue glue evokes a mild acute inflam matory reaction with no tissue necrosis.74 Availability Cyanoacrylate (e.g., superglue), which bonds surfaces almost instantly, is available in a wide variety of commercial brands for medical and nonmedical use. Although nonmedical cyanoacry late is not approved for medical use, it has been used to treat patients for decades without complications. Although carrying medical grade (expensive) cyanoacrylate may be feasible, nonmedical superglues effectively close wounds in a similar manner to medical tissue adhesives. Although they are not sterile, they are unlikely to negatively affect the patient. Two benefits of medical grade cyanoacrylate (2-octyl cyanoacry late) are that its bond is about four times stronger than those of nonmedical brands and its more viscous gel form is better con trolled when applied to wounds. Nonmedical cyanoacrylate is often used to treat superficial painful fissures of the fingertips (“polar hands”), which commonly occur in cold climates and at high elevations.40 Advantages/Disadvantages In austere circumstances, cyanoacrylate’s advantages are that (1) it is readily available, (2) it can be applied rapidly, (3) it requires little technical knowledge, (4) a small tube can be used for many patients, and (5) it can be used on many parts of the body (e.g., skin, intraoral, intraabdominal). Its primary disadvantages are more frequent wound dehiscence because of its lower tensile strength compared with sutures, and contamination of other body parts. Also, using petroleum-based ointments and salves, includ ing antiseptic ointments, on wounds closed with cyanoacrylate can weaken the polymerized film and cause wound dehiscence. One can lessen the incidence of dehiscence by (1) not using cyanoacrylate on wounds over areas under tension, such as joints, and (2) using it only when a 5-0 or smaller suture would be appropriate to close a wound.22 Other common glues can also be used for wound closure. These include wood glue, panel adhesive, hobby cement, and various native substances. Be aware, however, that these common glues may irritate the tissues, the incidence of dehiscence is higher, and they may contain toxins. Contamination of Other Areas If cyanoacrylate spreads onto the eyelids or lips during wound closure on the face, it can seal them shut for hours. Avoid this by positioning the patient so that any extra cement runs away from, rather than toward, the eyes or mouth. This may require the patient to turn his or her head away from the wound, lie on his or her side, sit up, or, if the wound is above the eye, lie in Trendelenburg’s position. If cyanoacrylate does stick to an unwanted area, use a petroleum-based product such as ophthal mic bacitracin, erythromycin ointment, or mineral oil to remove it. Or, simply wait (usually less than a day) and the lids will open without treatment. 454
BINDING/TAPING Skin tapes are useful for shallow, nongaping wounds and have several advantages over suturing, including reduced need for anesthesia, ease of application, decreased incidence of wound infection, and availability. Nearly any tape can be used to close a wound. There is no magical quality to medical tapes. Other than cleaning and debriding a wound, using tape requires no technical expertise and is fast, painless, and virtually cost-free. Duct tape or any adhesive tape can be used to close a wound. Cut it lengthwise into strips, and allow gaps during placement if it is necessary to have part of the wound visible (Box 23-4). Puncturing holes in the tape before application helps prevent exudate from building up under the tape. Tapes do not stick well on areas that are hairy (therefore shave, if necessary), wet, or prone to perspiring, or are under tension, such as joints. As with medical tape, use benzoin, cyanoacrylate, or another adhesive to help the strips stick. Alter natively, wrap a bandage around the closed wound or use addi tional tape. Many materials can be used as sutures. Nylon fishing line, for example, provides results comparable to commercial nylon suture,30 and is used routinely around the world. Others must be improvised from available materials. Natural Materials Hair Tying (With Glue) for Scalp Wound Closure. If a patient with a scalp laceration less than 10 cm (3.9 inches) long has hair over the area that is longer than 3 cm (1.2 inches), use the hair to close the wound. To do this, twist a few strands of hair together on each side of the laceration. Tie them and immediately place benzoin or a similar adhesive on the knot to hold it in place. Cut these knots out after the wound heals. Alternatively, pull several strands of hair across the laceration to the opposite sides and twist them around each other one time. Place a drop of cyanoacrylate at the juncture (Figure 23-34). These “sutures” do not have to be removed; the cyanoacrylate gradually wears off.40 Tell the patient not to wash his or her hair or put petroleum hair products near the wound for 48 hours.54,57 Chicken Egg Membrane. Use a fresh chicken egg membrane (the thin layer just inside the shell) to close wounds and reduce bleeding. The membrane contains types I, V, and X collagen; retains albumen; and prevents penetration of bacteria. It has been BOX 23-4 Wound-Taping Technique 1. Obtain hemostasis and dry the wound edges. 2. Apply benzoin or cyanoacrylate glue to the skin adjacent to the wound. Benzoin should be allowed to dry long enough for it to become tacky, but tape should be applied to the glue while the glue is still wet. 3. Tape should be cut to 6- to 13-mm (0.25- to 0.5-inch) widths, depending on the size of the laceration, and to a length that allows for 2 to 2.5 cm (0.75 to 1 inch) of overlap on each side of the wound. 4. Secure one-half of the tape to one side of the wound. Appose the opposite wound edge using a finger while the tape is secured to the other side. 5. Wound tapes should have gaps of 1.5 to 3 mm (0.06 to 0.12 inches) between them to allow for serous drainage. 6. Cross-stays of tape can be placed perpendicular over the tape ends to prevent them from peeling off. 7. Additional glue can be applied to the tape edges every 24 hours to reinforce adhesion.
High-level disinfection of most alternative suture materials is more practical in austere situations than is sterilization. Boil the material in water or soak it in alcohol (medicinal, drinking), hydrogen peroxide, bleach, surgical or regular soapy water, or lemon juice. Note that some of the substances used to disinfect the suture (e.g., alcohol, bleach, lemon juice) may be painful; use local anesthetic if possible. If sterilizing the suture material is desired, wrap it in foil and put it in or near the coals from a fire. How well this works without destroying the suture material varies depending on the type of material used.
Blister Management FIGURE 23-34 Wound closure with hair and cyanoacrylate.
used as a skin graft donor-site dressing and, in one patient, used to close a full-thickness lip laceration. It stopped the bleeding and, when removed after 3 days, produced a well-healed wound.81 Horsehair Sutures. Hairs from the tail of a horse can also serve as effective sutures. First wash the hairs with soap and water, followed by alcohol. Sterilize them before use in boiling water or steam. They are not as strong as silk, but they are able to resist all the tension which any suture ought to have.26 Silk and Cactus (Agave) Fibers. Threads of natural silk or linen/flax are excellent for sutures and ligatures. These may be soaked in sterile water before use or waxed for better flexibility.37 Similarly, to use fiber “threads” from agave plants, pull on the point of the agave plant with your teeth and the thread comes out. Other Non-Traditional Materials5 Dental Floss. Although dental floss is often cited as a good suture alternative, most dental floss is about the size of a 0 or 00 suture. This is far too big for most wounds. Additionally, floss is produced from many different fibers (e.g., silk, nylon, or Teflon), which may make it difficult to know how tissues will react.18 Cotton Thread. Cotton and linen threads, long used as the standard surgical suture, are good, non-irritating substitutes for standard suture materials. They should be disinfected in boiling water; any colored thread should be boiled long enough to extract as much of the dye as possible.27 In austere circumstances, a guideline for use is to use ordinary sewing cotton, No. 30, white, for the heavier work on the abdominal wall, and No. 40 or No. 50, black, for finer work on intestine or delicate tissues.59
A
B
To dress blisters without moleskin, use Molefoam, or improvise another commercial blister dressing by using a piece of duct tape. Duct tape’s smooth outer surface provides protection from fric tion, while its adhesive side adheres strongly to skin. Duct tape is ideal for preventing blisters when “hot spots” are present. Avoid applying duct tape directly to formed blister surfaces. Cover the blister with a nonadhesive dressing, such as a plastic sandwich bag, and use the duct tape or glue to hold it in place. Cut the corner of the sandwich bag and apply a lubricant between the two surfaces (Figure 23-35).
Ring Removal Rings should always be removed soon after injury to fingers and trauma to the hands because progressive swelling may cause rings to act as tourniquets. If a ring cannot be removed with soap or lubricating jelly, the string wrap technique can be used. Pass a 51-cm (20-inch) length of fine string, dental floss, umbilical tape, or thick suture between the ring and the finger. Pull the string so that most of it is on the distal side of the digit. Then wrap it around the swollen finger from proximal to distal, beginning next to the ring and continuing past the proximal interphalangeal joint. Place successive loops of the wrap close enough together to prevent any swollen skin from bulging between the strands. Remove the ring by unwinding the proximal end of the string and forcing the ring over the distal string. If the string is not long enough, the technique may require repeated wraps (Figure 23-36).
Trauma TENSION PNEUMOTHORAX In dyspneic patients, signs and symptoms that suggest a tension pneumothorax include distended neck veins, tracheal deviation away from the side of the pneumothorax, unilateral absent breath sounds, hyperresonant hemithorax to percussion, subcu taneous emphysema, cyanosis, and cardiovascular collapse. In the wilderness, treat these patients as if they have a tension
C
FIGURE 23-35 A to C, Blister dressing improvised with plastic sandwich bag.
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Disinfecting Rather than Sterilizing Alternative Suture Materials
Super Glue
PART 4 INJURIES AND MEDICAL INTERVENTIONS
Glove finger
A
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FIGURE 23-37 A, Finger of (or, even better, the entire) glove is attached to needle or catheter to create flutter valve. B, Flutter valve allows air to escape. C, Flutter valve collapses to prevent air entry.
FIGURE 23-36 String technique for removing a ring from a swollen finger (see text).
pneumothorax—with rapid pleural decompression; it may save their lives. Possible complications of pleural decompression include infection; profound bleeding from puncture of the heart, lungs, or a major blood vessel; or laceration of the liver or spleen. Improvised Pleural Decompression Technique Swab the entire chest with povidone-iodine or another antiseptic. If sterile gloves are available, put them on after washing your hands. If local anesthesia is available, infiltrate the puncture site down to the rib and over its upper border. Insert a large-bore IV catheter, needle, or any pointed sharp object that is available into the chest just above the third rib in the mid-clavicular line (midway between the top of the shoulder and the nipple in a line with the nipple approximates this loca tion) (Box 23-5). If you hit the rib, move the needle or knife upward slightly until it passes over the top of the rib, thus avoid ing the intercostal blood vessels that course along the lower edge of every rib. The chest wall is 4 to 6 cm (1.6 to 2.4 inches) thick, depending on the individual’s muscularity and amount of fat present. A gush of air signals that one has entered the pleural space; do not push the penetrating object any further. Releasing the tension converts the tension pneumothorax into an open pneumothorax. BOX 23-5 Improvised Pleural Decompression Devices • Large-bore (12- or 14-gauge) intravenous catheter or needle • Endotracheal tube (instead of a chest tube) • Section of a tent pole • Hose from a hydration pouch
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Leave the needle or catheter in place (it often comes out of the pleural space with respiration, so continue monitoring it), and use a rubber glove to make a flutter valve (Figure 23-37). Use the entire glove and push a needle through one finger (best) or cut the finger from a rubber glove, making a tiny slit cut at the tip. Place this over the external opening to create a unidirec tional flutter valve that allows continuous egress of air from the pleural space. To create a one-way flutter valve, cut one finger portion of a latex glove off at the proximal end of the finger and insert the needle or catheter into the open end of the glove finger, through the tip as shown (see Figure 23-37, A). The cutout finger portion of the glove creates a unidirectional flutter valve that allows egress of air from the pleural space during expiration, but collapses to prevent air entry on inspiration (see Figure 23-37, B and C). Note that this is a tenuous device that can easily slip out of place. If symptoms redevelop, insert another one. Also note that although an endotracheal tube and other semi-rigid devices work well as makeshift chest tubes, Foley catheters only work well in infants; they collapse because of pressure from the chest wall in older children and adults.40
OPEN (“SUCKING”) CHEST WOUND Penetrating trauma to the chest can produce a chest wound that allows air to be sucked into the pleura on inspiration. Place a piece of plastic food wrap or aluminum foil or one side of a plastic sandwich bag on top of the wound, and tape it on three sides. The untaped fourth side serves as a relief valve to prevent formation of a tension pneumothorax.
DRAINAGE SYSTEM (BOTTLES/BAGS) The fundamental idea of a chest tube drainage system is for air to leave the thorax (chest) without any air being able to re-enter the chest via the system. An example of a two-bottle chest tube drainage system was constructed from an empty 1-L plastic sterile water bottle, a 1-L IV bag, two IV tubing sets, and a 24F chest tube.76 This system collects and measures fluid that drains out of the tube. To reproduce this system, empty a plastic sterile water bottle and put two holes in the bottle, one in the cap and one
FIGURE 23-38 Sterile water bottle, IV tubing, and IV bag can serve as a chest tube drain. (From Vinson ED: Improvised chest tube drain for decom pression of an acute tension pneumothorax, Mil Med 169:403, 2004.)
in the bottle’s neck, each of which allow just enough room for passage of the IV tubing (Figure 23-38). Cut the patient end (IV catheter attachment) off one (the “first”) IV tubing set and insert this cut end into the hole in the top of the empty saline bottle. The other end (IV bag-spike) should fit into the end of the 24F chest tube. Now take the other (the “second“) IV tubing set and cut off the spike end between the filter and the reservoir. Posi tion the fluid-filled IV bag with ports up and the saline bag down, and insert the cut-off spike from the second IV tubing set into one port in the IV bag. This is now the system’s air vent. Open the other port (cut or remove the rubber cap) and insert the cut end of the second IV tubing so that it is well beneath the level of the saline in the bag. The other end of the second IV line should then be placed through the hole in the neck of the empty saline bottle. Use duct tape, cyanoacrylate, or any other cement to seal the tubes in position. Keep the IV bag inverted to provide a water seal for the system. To dispose of any accumulated fluid, clamp the chest tube and unscrew the cap from the water bottle and empty it out. Then screw the cap back on and unclamp the chest tube.40
Orthopedic Injury—Improvised Treatment GENERAL GUIDELINES When working with improvised systems, if time allows, test them on a noninjured person (“work out the bugs”) before applying them to the patient, and continually reevaluate them while in use. Creativity is needed when searching for improvisational materials, although it helps to carry materials that lend themselves to improvisation, as described later. The victim’s gear can also provide needed items, such as foam pads and the straps and internal stays from backpacks. Especially in patients with dimin ished consciousness, be observant for pressure points and friction potential, because these devices are not ergonomically efficient. When in doubt, add extra padding.
SPINAL TRAUMA Because of its mobility, the cervical spine is the spinal column area most commonly injured in trauma. Any obvious or suspected cervical spine injury demands full spinal immobilization using both a rigid or semirigid cervical collar and long-board immobi lization. Historically dogma about cervical spine injuries has specified a “splint ‘em as they lie” approach. Transporting a victim who is not in anatomic position is arduous in the
Improvised Cervical Collars Cervical collars are always adjuncts to full spinal immobilization; they should rarely be used alone. The improvised cervical collar is used in conjunction with manual cervical spine stabilization followed by complete immobilization of the victim on a spine board. A properly applied and fitted collar is a primary defense against axial loading of the cervical spine, particularly in an evacuation that involves tilting the victim’s body uphill or down hill. Improvised cervical collars have had a bad reputation, and textbooks continue to depict them made from a simple cravat wrapped around the neck. This type of system is no more effec tive than are the soft cervical collars often used by urban plaintiffs trying to impress a jury (i.e., not effective at all). An improvised cervical collar works effectively only if it has the following features: • It is rigid or semi-rigid. • It fits properly (many improvised designs are too small). • It does not constrict or choke the victim. • It allows the victim’s mouth to remain open if vomiting occurs. Improvisational approaches to cervical collars are outlined below. Closed-Cell Foam System. The best closed-cell foam systems incorporate a full-size or three-quarter–length pad folded longi tudinally into thirds that is centered over the back of the victim’s neck and wrapped forward. The pad is crossed under the chin, contoured underneath opposite axillae, and secured. If the pad is not long enough, tape or tie on extensions. This system also works well with blankets, beach towels, or even a rolled plastic tarp. Avoid small flexible cervical collars that do not optimally extend the chin-to-chest distance. Padded Hip Belt. A padded hip belt or fanny pack removed from a large internal- or external-frame backpack can sometimes be modified to work perfectly. Wider is usually better. Take up excess circumference by overlapping the belt, and secure the excess material with duct tape (Figure 23-39).
Hip belt of inverted backpack Cervical stabilizer Fanny pack as cervical collar
FIGURE 23-39 Inverted pack used as spine board. The backpack waist belt can be seen encircling the head.
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CHAPTER 23 Improvised Medicine in the Wilderness
backcountry. It is uncomfortable for the victim, difficult for the rescuers, and increases the risk for further injury. In general, gentle axial traction back to anatomic position is indicated unless (1) return to anatomic position significantly increases pain or focal neurologic deficit or (2) movement of the head and neck results in any noticeable mechanical resistance.39 All cervical spine injuries (or suspected injuries) warrant full long-board immobilization. Movement of the pelvis and hips laterally is potentially more dangerous than anterior–posterior movement; therefore it is appropriate during extended transport to allow gentle flexion at the hip with immobilization in that position if the victim is more comfortable. Soft pads behind the knees and small of the back also add to the victim’s comfort during a long transport.9
PART 4 INJURIES AND MEDICAL INTERVENTIONS
A
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D
FIGURE 23-40 Padded aluminum splint cervical collar. A, Place a vertical bend in the malleable aluminum splint approximately 6 inches from one end to form a vertical pillar. Then, add bilateral flares to make the splint comfortable for the victim where it rests against the lower mandible. B, Place the anterior pillar securely beneath the victim’s chin and wrap the remaining length of the splint around the victim’s neck. C, Side view of cervical collar fashioned from a SAM Splint. Note the formation of lateral, and if possible, posterior pillars. D, Frontal view. The end is angled inferiorly to provide an adequate chin-to-chest distance. Note the formation of the anterior pillar.
Clothing. Bulky clothing, such as a fiber pile or fleece jacket, can be rolled and then wrapped around the victim’s neck to make a cervical collar. The extended sleeves can be used to secure the collar. Prewrapping a wide elasticized (Ace) wrap around the jacket compresses the material and makes it more rigid and supportive. Malleable Aluminum Splint. Well-padded aluminum splints (e.g., SAM Splint) can be molded into various configurations to splint extremity injuries. They are built from a thin co
