Wilderness Medicine: Expert Consult Premium Edition, 6th Edition

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

xvii

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.

47

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

49

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.)

53

PART 1  MOUNTAIN MEDICINE

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

CHAPTER 2  AVALANCHES

100

PART 1  MOUNTAIN MEDICINE

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.

61

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

12 4

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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PART 1  MOUNTAIN MEDICINE

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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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.)

86

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.

CHAPTER 3  Lightning Injuries

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

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7.7

pH

PART 2  COLD AND HEAT

BOX 5-3  Signs of Hypothermia

7.4 7.1

ter

l wa

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6.8 0 40 37

30

20

10

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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

145

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

147

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.

149

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.

151

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.)

153

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

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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),

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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).

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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

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30

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

171

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

CHAPTER 7  Nonfreezing Cold-Induced Injuries

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