AUERBACH’S

WILDERNESS
MEDICINE
AUERBACH’S
WILDERNESS
MEDICINESEVENTH EDITION

EDITOR
PAUL S. AUERBACH
MD, MS, FACEP, MFAWM, FAAEM
Redlich Family Professor
Department of Emergency Medicine
Stanford University School of Medicine
Stanford, California

ASSOCIATE EDITORS
TRACY A. CUSHING, MD, MPH
Associate Professor
Department of Emergency Medicine
University of Colorado School of Medicine
Aurora, Colorado
N. STUART HARRIS, MD, MFA, FRCP (Edin)
Associate Professor of Emergency Medicine
Harvard Medical School
Chief, Division of Wilderness Medicine
Department of Emergency Medicine
Massachusetts General Hospital
Boston, Massachusetts
1600 John F. Kennedy Blvd.
Ste. 1800
Philadelphia, PA 19103-2899

AUERBACH’S WILDERNESS MEDICINE, SEVENTH EDITION ISBN: 978-0-323-35942-9

Copyright © 2017 by Elsevier, Inc. All rights reserved.

Chapter 12 is in the public domain.
Chapter 25 Copyright © 2017 Grant S. Lipman, Brian J. Krabak.
Chapter 70 Copyright © 2017 Charles Gideon Hawley, Michael Jacobs.
Chapter 5, Mary Ann Cooper retains rights for images.
Chapter 5, Ronald L. Holle retains rights for images.
Chapter 36, David Warrell retains rights for images.
Previous editions copyrighted 2012, 2007, 2001, 1995 by Mosby, an imprint of Elsevier, Inc.

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 products
liability, negligence or otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.

International Standard Book Number: 978-0-323-35942-9

Executive Content Strategist: Kate Dimock

Content Development Manager: Lucia Gunzel
Publishing Services Manager: Patricia Tannian
Senior Project Manager: John Casey
Designer: Brian Salisbury

Printed in United States of America

Last digit is the print number:  9  8  7  6  5  4  3  2  1

 Contributors

Javier A. Adachi, MD, FACP, FIDSA Brian S.S. Auerbach, JD, MA, BE
Associate Professor Associate
Division of Internal Medicine Pepper Hamilton LLP
Department of Infectious Diseases, Infection Control and Philadelphia, Pennsylvania
Employee Health
Adjunct Professor Paul S. Auerbach, MD, MS, FACEP, MFAWM, FAAEM
Section of Infectious Diseases Redlich Family Professor
Department of Medicine Department of Emergency Medicine
Baylor College of Medicine Stanford University School of Medicine
Adjunct Professor Stanford, California;
Center for Infectious Diseases Adjunct Professor
The University of Texas Health Science Center at Houston Department of Military and Emergency Medicine
School of Public Health F. Edward Hébert School of Medicine
Houston, Texas Uniformed Services University of the Health Sciences
Bethesda, Maryland
Norberto Navarrete Aldana, MD
Emergency Physician Howard D. Backer, MD, MPH, FACEP, FAWM
Burns Intensive Care Unit Director
Hospital Simón Bolivar California Emergency Medical Services Authority
Bogotá, Colombia Sacramento, California

Martin E. Alexander, PhD, RPF Aaron L. Baggish, MD

Adjunct Professor Assistant Professor
Wildland Fire Science and Management Cardiology Division
Department of Renewable Resources Department of Medicine
Alberta School of Forest Science and Management Associate Director
University of Alberta Cardiovascular Performance Center
Senior Fire Behavior Research Officer (Retired) Massachusetts General Hospital
Canadian Forest Service, Northern Forestry Centre Boston, Massachusetts
Edmonton, Alberta, Canada
Buddha Basnyat, MD, MSc, FACP, FRCP (Edin)
Susan Anderson, MD Director
Clinical Associate Professor Oxford University Clinical Research Unit–Nepal
Division of Infectious Disease and Geographic Medicine Medical Director
Center for Innovation and Global Health Nepal International Clinic and Himalayan Rescue Association
Stanford, California; Kathmandu, Nepal
Director of Travel Medicine
Palo Alto Medical Foundation Pete Bettinger, PhD
Palo Alto, California Professor
School of Forestry and Natural Resources
Christopher J. Andrews, BE, MBBS, MEngSc, University of Georgia
PhD, JD, EDIC, GDLP, DipCSc, ACCAM Athens, Georgia
Senior Lecturer, Medicine
University of Queensland Paul D. Biddinger, MD
Brisbane, Queensland, Australia Vice Chairman for Emergency Preparedness
Department of Emergency Medicine
E. Wayne Askew, PhD Massachusetts General Hospital
Professor Emeritus Director
Department of Nutrition and Integrative Physiology Emergency Preparedness Research, Evaluation and Practice
University of Utah Program
Salt Lake City, Utah Harvard T.H. Chan School of Public Health
Boston, Massachusetts
Dale Atkins, BA
President, American Avalanche Association Greta J. Binford, PhD
Vice President, Avalanche Rescue Commission Associate Professor
International Commission for Alpine Rescue, North America Department of Biology
Training and Education Manager, RECCO, AB Lewis & Clark College
Boulder, Colorado Portland, Oregon

v
 Rebecca S. Blue, MD, MPH George H. Burgess, MSc
CONTRI BUTORS
Assistant Professor Director
Department of Preventive Medicine and Community Health Florida Program for Shark Research
University of Texas Medical Branch at Galveston Curator
Galveston, Texas International Shark Attack File
Florida Museum of Natural History
Ryan Blumenthal, MBChB (Pret), MMed (Forens) FC University of Florida
Path (SA), Dip Med (SA), PhD (Wits) Gainesville, Florida
Senior Specialist
Department of Forensic Medicine Sean P. Bush, MD, FACEP
University of Pretoria Professor
Pretoria, Gauteng, South Africa Department of Emergency Medicine
Brody School of Medicine
Jolie Bookspan, PhD East Carolina University
Philadelphia, Pennsylvania Greenville, North Carolina

Ralph S. Bovard, MD, MPH, FACSM Frank K. Butler Jr, MD

Director Chairman, Committee on Tactical Combat Casualty Care
Occupational and Environmental Medicine Residency Director, Prehospital Trauma Care
Program Joint Trauma System
Midwest Center for Occupational Health and Safety San Antonio, Texas;
HealthPartners Medical Group Adjunct Professor
St. Paul, Minnesota Department of Military and Emergency Medicine
F. Edward Hébert School of Medicine
Warren D. Bowman Jr, MD Uniformed Services University of the Health Sciences
Clinical Associate Professor Emeritus Bethesda, Maryland
Department of Internal Medicine
University of Washington School of Medicine Dale J. Butterwick, MSc, CAT(C)
Seattle, Washington Associate Professor Emeritus
Faculty of Kinesiology
Leslie V. Boyer, MD University of Calgary
Associate Professor Calgary, Alberta, Canada
Department of Pathology
Director Christopher R. Byron, DVM, MS, DACVS
Venom Immunochemistry, Pharmacology, and Emergency Associate Professor of Large Animal Surgery
Response Institute Large Animal Clinical Sciences
University of Arizona Virginia-Maryland College of Veterinary Medicine
Tucson, Arizona Blacksburg, Virginia

Michael B. Brady, MA Michael D. Cardwell, MS

Department of Geography Adjunct Faculty
Rutgers University Department of Biological Sciences
Piscataway, New Jersey California State University
Sacramento, California
Mark A. Brandenburg, MD
Medical Director Steven C. Carleton, MD, PhD
Bristow Medical Center Professor and W. Brian Gibler Chair of Emergency Medicine
Bristow, Pennsylvania Education
Department of Emergency Medicine
Beau A. Briese, MD University of Cincinnati College of Medicine
Director Cincinnati, Ohio
International Emergency Medicine
Department of Emergency Medicine Christopher R. Carpenter, MD, MSc, FACEP,
Houston Methodist Hospital FAAEM, AGSF
Houston, Texas Associate Professor
Division of Emergency Medicine
Millicent M. Briese, MA Department of Medicine
Chief Executive Officer Washington University in St. Louis School of Medicine
Emergen International LLC St. Louis, Missouri;
Houston, Texas President, Academy for Geriatric Emergency Medicine
Chicago, Illinois
Calvin A. Brown III, MD
Department of Emergency Medicine Scott P. Carroll, PhD
Brigham and Women’s Hospital Research Associate
Assistant Professor of Emergency Medicine Department of Entomology and Nematology
Harvard Medical School University of California, Davis
Boston, Massachusetts Davis, California

Colin M. Bucks, MD John W. Castellani, PhD

Clinical Assistant Professor Research Physiologist
Department of Emergency Medicine Thermal and Mountain Medicine Division
Stanford University School of Medicine US Army Research Institute of Environmental Medicine
Stanford, California Natick, Massachusetts

vi
Michael J. Caudell, MD, FACEP, FAWM, DiMM Mary Ann Cooper, MD

CONTRI BUTORS
Professor Professor Emerita
Department of Emergency Medicine and Hospitalist Services University of Illinois at Chicago
Medical Director Chicago, Illinois;
Wilderness and Survival Medicine Founding Director
Medical College of Georgia at Augusta University African Centres for Lightning and Electromagnetics
Augusta, Georgia; Kampala, Uganda
President
Appalachian Center for Wilderness Medicine Kevin Coppock, MSc
Morganton, North Carolina Head of Mission—Myanmar
Médecins Sans Frontières (Doctors Without Borders)
Steven Chalfin, MD, FACS
Professor Larry I. Crawshaw, PhD
Department of Ophthalmology Professor Emeritus
University of Texas Health Science Center at San Antonio Biology Department
San Antonio, Texas Portland State University
Professor Emeritus
Nisha Charkoudian, PhD Department of Behavioral Neuroscience
Research Physiologist Oregon Health & Science University
Thermal and Mountain Medicine Division Portland, Oregon
US Army Research Institute of Environmental Medicine
Natick, Massachusetts Gregory A. Cummins, DO, MS
Adjunct Instructor
Samuel N. Cheuvront, PhD, RD Division of Primary Care
Research Physiologist Department of Internal Medicine
Thermal and Mountain Medicine Kansas City University of Medicine and Biosciences
US Army Research Institute of Environmental Medicine Kansas City, Missouri
Natick, Massachusetts
Tracy A. Cushing, MD, MPH
Richard F. Clark, MD Associate Professor
Professor of Clinical Medicine Department of Emergency Medicine
Division of Medical Toxicology University of Colorado School of Medicine
Department of Emergency Medicine Aurora, Colorado
University of California, San Diego
San Diego, California Jon Dallimore, MBBS, MSc
Specialty Doctor
Kenneth S. Cohen, MA Emergency Department
Traditional Healer Bristol Royal Infirmary
Sacred Earth Circle Bristol, United Kingdom;
Nederland, Colorado Co-Director, International Diploma in Expedition and
Wilderness Medicine
Richard W. Cole, MD, MPH, FACEP Royal College of Physicians and Surgeons of Glasgow
Assistant Professor Glasgow, United Kingdom;
Division of Aerospace Medicine General Practitioner
Department of Preventive Medicine and Community Health Vauxhall Practice
University of Texas Medical Branch at Galveston Chepstow, United Kingdom
Galveston, Texas;
Clinical Instructor Shawn D’Andrea, MD, MPH
Ultrasound Division Instructor of Emergency Medicine
Department of Emergency Medicine Harvard Medical School
The University of Texas Health Science Center at Houston Boston, Massachusetts;
Houston, Texas Chief
Emergency Medicine
Benjamin B. Constance, MD, FACEP, FAWM Tsehootsooi Medical Center
Clinical Instructor Fort Defiance, Arizona
Department of Family Medicine
University of Washington School of Medicine Daniel F. Danzl, MD
Chief and Medical Director Professor and Chair
Tacoma Emergency Care Physicians Department of Emergency Medicine
Tacoma General Hospital University of Louisville
Tacoma, Washington Louisville, Kentucky

Daniel G. Conway, DO, FACEP Kathleen M. Davis, BS, MS

Medical Corps Superintendent (Retired)
United States Army Medical Department Montezuma Castle and Tuzigoot National Monument
Department of Emergency Medicine National Park Service, Department of the Interior
Fort Belvoir, Virginia Camp Verde, Arizona

Donald C. Cooper, PhD, MBA Kevin Davison, ND, LAc

President and Chief Executive Officer Director
National Rescue Consultants, Inc. Maui Regenerative Medicine
Cuyahoga Falls, Ohio Haiku, Hawaii

vii
 Chad P. Dawson, MPS, PhD Thomas Eglin, MD
CONTRI BUTORS
Professor Emeritus Assistant Professor of Family Medicine
Department of Forest and Natural Resources Management Regional Assistant Dean
State University of New York College of Environmental Science Pacific Northwest University of Health Sciences
and Forestry Attending Physician
Syracuse, New York Emergency Department
Yakima Valley Memorial Hospital
George R. Deeb, DDS, MD, FAWM Yakima, Washington
Associate Professor
Division of Oral and Maxillofacial Surgery Timothy B. Erickson, MD, FACEP, FACMT, FAACT
Department of Surgery Professor
Virginia Commonwealth University Division of Toxicology
Richmond, Virginia Department of Emergency Medicine
Director, UIC Center for Global Health
Janice A. Degan, RN, MS University of Illinois College of Medicine at Chicago
Assistant Director of Research Chicago, Illinois
Venom Immunochemistry, Pharmacology, and Emergency
Response Institute Thomas Evans, PhD
Arizona Health Sciences Center Chief Executive Officer
University of Arizona SAR3
Tucson, Arizona Mountain View, California

Thomas G. DeLoughery, MD, MACP, FAWM Andrew J. Eyre, MD

Professor Clinical Fellow
Division of Hematology and Medical Oncology Harvard Medical School
Departments of Medicine, Pathology, and Pediatrics Attending Physician
Knight Cancer Institute Department of Emergency Medicine
Oregon Health & Science University Brigham and Women’s Hospital
Portland, Oregon Boston, Massachusetts

Arlene E. Dent, MD, PhD Joanne Feldman, MD, MS, UHM

Assistant Professor Assistant Clinical Professor
Division of Pediatric Infectious Diseases and Rheumatology Department of Emergency Medicine
Department of Pediatrics University of California, Los Angeles
Case Western Reserve University Los Angeles, California
Cleveland, Ohio
D. Nelun Fernando, PhD
Alexandra E. DiTullio, MD Hydrologist
Attending Physician Surface Water Resources
Department of Emergency Medicine Water Science and Conservation
The Queen’s Medical Center Texas Water Development Board
Honolulu, Hawaii Austin, Texas

Katherine R. Dobbs, MD Paul G. Firth, MD

Instructor Assistant Professor
Division of Pediatric Infectious Diseases Harvard University
Department of Pediatrics Pediatric Anesthesiologist
Case Western Reserve University Department of Anesthesia, Critical Care, and Pain Medicine
Cleveland, Ohio Massachusetts General Hospital
Boston, Massachusetts
Eric L. Douglas, BA, EMT, DMT
Staff Instructor, Instructor Development Course Mark S. Fradin, MD
Emeritus Medic First Aid Master Trainer Clinical Associate Professor
Professional Association of Diving Instructors Department of Dermatology
Pinch, West Virginia University of North Carolina School of Medicine
Private Practice, Chapel Hill Dermatology, P.A.
Jennifer Dow, MD Chapel Hill, North Carolina
Medical Director
National Park Service—Alaska Region Bryan L. Frank, MD, FAAMA, FAAPM, FAAARM
Director President
Emergency Department Global Mission Partners, Inc.
Alaska Regional Hospital Yukon, Oklahoma
Anchorage, Alaska
Esther E. Freeman, MD, PhD, FAAD
Herbert L. DuPont, MD, MACP Assistant Professor
Mary W. Kelsey Distinguished Chair in Medical Sciences Department of Dermatology
Director, Center for Infectious Diseases Massachusetts General Hospital
School of Public Health and McGovern Medical School Harvard Medical School
The University of Texas Health Science Center at Houston Boston, Massachusetts
Clinical Professor
Department of Medicine
Baylor College of Medicine
Houston, Texas

viii
Luanne Freer, MD Donald L. Grebner, PhD

CONTRI BUTORS
Medical Director Professor
Medcor at Yellowstone Department of Forestry
Yellowstone National Park Mississippi State University
Yellowstone, Wyoming; Starksville, Mississippi
Founder and Director
Everest ER Colin K. Grissom, MD
Himalayan Rescue Association Professor
Mt Everest, Nepal Department of Internal Medicine
University of Utah School of Medicine
Tom Garrison, PhD Salt Lake City, Utah;
Professor Emeritus Associate Medical Director
Marine Science Department Shock Trauma Intensive Care Unit
Orange Coast College Intermountain Medical Center
Costa Mesa, California; Murray, Utah
Adjunct Professor of Higher Education
Rossier School of Education Peter H. Hackett, MD
University of Southern California Director, Institute for Altitude Medicine
Los Angeles, California Telluride, Colorado;
Clinical Professor
Alan Gianotti, MD, MS Department of Emergency Medicine
Department of Emergency Medicine University of Colorado Denver School of Medicine
Mills-Peninsula Medical Center Aurora, Colorado
Burlingame, California;
Volunteer Physician Charles Handford, MBChB (Hons), MRCS
Himalayan Rescue Association Nepal General Duties Medical Officer
Kathmandu, Nepal Royal Army Medical Corps
British Army
Robert V. Gibbons, MD, MPH
Task Area Manager N. Stuart Harris, MD, MFA, FRCP (Edin)
Battlefield Pain Management Associate Professor of Emergency Medicine
United States Army Institute of Surgical Research Harvard Medical School
Joint Base San Antonio Chief, Division of Wilderness Medicine
Fort Sam Houston, Texas Department of Emergency Medicine
Massachusetts General Hospital
Gordon G. Giesbrecht, PhD, FAsMA Boston, Massachusetts
Professor
Faculty of Kinesiology and Recreation Management; Seth C. Hawkins, MD, EMD
Department of Anesthesia Assistant Professor
Director, Laboratory for Exercise and Environmental Medicine Department of Emergency Medicine
Health, Leisure and Human Performance Research Institute Wake Forest University
University of Manitoba Winston-Salem, North Carolina
Winnipeg, Manitoba, Canada
Charles G. Hawley, BS
Alina Goldenberg, MD, MAS Chairman
Department of Dermatology Safety at Sea Committee
University of California, San Diego United States Sailing Association
San Diego, California Portsmouth, Rhode Island

Craig Goolsby, MD David M. Heimbach, MD, FACS

Associate Professor Professor Emeritus
Department of Military and Emergency Medicine Department of Surgery
F. Edward Hébert School of Medicine University of Washington
Uniformed Services University of the Health Sciences Seattle, Washington
Bethesda, Maryland;
Director, Hybrid Simulation Lab Carlton E. Heine, MD, PhD, FACEP, FAWM
Val G. Hemming Simulation Center Clinical Associate Professor
Silver Spring, Maryland; Elson S. Floyd College of Medicine
Attending Emergency Physician Washington State University
Howard County General Hospital Spokane, Washington
Columbia, Maryland
Lawrence E. Heiskell, MD, FACEP, FAAFP
Kimberlie A. Graeme, MD, FACMT Emergency Physician
Clinical Associate Professor Founder and Director
Department of Emergency Medicine International School of Tactical Medicine
University of Arizona College of Medicine Rancho Mirage, California
Medical Toxicologist
Department of Medical Toxicology John C. Hendee, PhD
Banner—University Medical Center Phoenix Professor Emeritus
Phoenix, Arizona Department of Conservation Social Sciences
College of Natural Resources
University of Idaho
Moscow, Idaho

ix
 Andrew A. Herring, MD Kirsten N. Johnson, MD, MPH
CONTRI BUTORS
Director Assistant Professor
Pain and Addiction Treatment Division of Emergency Medicine
Department of Emergency Medicine Department of Family Medicine
Highland Hospital McGill University
Oakland, California CEO, Humanitarian U
Montréal, Québec, Canada
Ronald L. Holle, MS
Meteorologist Hemal K. Kanzaria, MD, MS
Holle Meteorology and Photography Assistant Professor
Oro Valley, Arizona Department of Emergency Medicine
University of California, San Francisco
John R. Hovey, BS San Francisco, California
Senior Instructor
Wilderness Medicine Institute Misha R. Kassel, MD
National Outdoor Leadership School Department of Emergency Medicine
Lander, Wyoming Pali Momi Medical Center
Aiea, Hawaii
Martin R. Huecker, MD
Assistant Professor and Research Director Stephanie Kayden, MD, MPH, CEDE
Department of Emergency Medicine Assistant Professor
University of Louisville Harvard Medical School
Louisville, Kentucky Chief
Division of International Emergency Medicine and
Christopher H. E. Imray, MB BS, DiMM, MSc, PhD, Humanitarian Programs
FRCS, FRCP, FRGS Department of Emergency Medicine
Professor Brigham and Women’s Hospital
Department of Vascular Surgery Boston, Massachusetts
University Hospital Coventry and Warwickshire NHS Trust
Warwick Medical School and Coventry University Katherine M. Kemen, MBA
Coventry, United Kingdom Program Manager
Emergency Preparedness
Hillary R. Irons, MD, PhD Partners HealthCare
Assistant Professor Boston, Massachusetts
Department of Emergency Medicine
University of Massachusetts Medical School Robert W. Kenefick, PhD
UMass Memorial Medical Center Research Physiologist
Worcester, Massachusetts Thermal and Mountain Medicine Division
US Army Research Institute of Environmental Medicine
Kenneth V. Iserson, MD, MBA Natick, Massachusetts
Professor Emeritus
Department of Emergency Medicine Michael L. Kent, MD
University of Arizona Commander
Tucson, Arizona Medical Corps, United States Navy
Assistant Professor
Michael E. Jacobs, MD, MFAWM Department of Anesthesiology
Martha’s Vineyard, Massachusetts F. Edward Hébert School of Medicine
Uniformed Services University of the Health Sciences
Ramin Jamshidi, MD, FACS Staff Anesthesiologist
Assistant Professor Bethesda, Maryland
Department of Surgery
Department of Child Health Minjee Kim, MD
University of Arizona College of Medicine Assistant Professor
Medical Director of Pediatric Trauma Division of Neurocritical Care
Surgical Director of Pediatric Intensive Care Ken and Ruth Davee Department of Neurology
Maricopa Medical Center Northwestern University Feinberg School of Medicine
Phoenix, Arizona Chicago, Illinois

Joshua M. Jauregui, MD Alexa B. Kimball, MD, MPH

Acting Assistant Professor Professor
Division of Emergency Medicine Department of Dermatology
University of Washington School of Medicine Harvard Medical School
Seattle, Washington Boston, Massachusetts

James M. Jeffers, BA, LLB, LLM, MPhil, PhD W. Taylor Kimberly, MD, PhD
Senior Lecturer in Human Geography Assistant Professor of Neurology
College of Liberal Arts Harvard Medical School
Bath Spa University Division of Neurocritical Care and Emergency Neurology
Bath, United Kingdom Department of Neurology
Massachusetts General Hospital
Amber M.H. Johnson, DO, DMD Boston, Massachusetts
Department of Oral and Maxillofacial Surgery
Virginia Commonwealth University
Richmond, Virginia

x
Sean M. Kivlehan, MD, MPH Charlotte A. Lanteri, PhD

CONTRI BUTORS
Clinical Instructor Deputy Director, Microbiology Section
Department of Emergency Medicine Department of Pathology and Area Laboratory Services
Brigham and Women’s Hospital Brooke Army Medical Center
Harvard Medical School San Antonio, Texas
Boston, Massachusetts
Gordon L. Larsen, MD, FACEP, FAWM
Judith R. Klein, MD Department of Emergency Medicine
Assistant Clinical Professor Intermountain Health Care (IHC)
Department of Emergency Medicine Dixie Regional Medical Center
University of California, San Francisco St. George, Utah;
San Francisco General Hospital Medical Advisor
San Francisco, California Zion National Park
Washington County, Utah
Karyn Koller, MD, MPH
Associate Professor Justin S. Lawley, PhD
Department of Emergency Medicine Instructor
Oklahoma University Institute for Exercise and Environmental Medicine
Tulsa, Oklahoma Texas Health Presbyterian Hospital
University of Texas Southwestern Medical Center
Brian J. Krabak, MD, MBA, FACSM Dallas, Texas
Clinical Professor
Department of Rehabilitation Medicine David J. Ledrick, MD, MEd
Department of Orthopedics and Sports Medicine Associate Residency Director
University of Washington School of Medicine Department of Emergency Medicine
Seattle, Washington Mercy Health—St. Vincent Medical Center
Toledo, Ohio
Andrew C. Krakowski, MD
Chief Medical Officer Jay Lemery, MD
DermOne, LLC Associate Professor
West Conshohocken, Pennsylvania Department of Emergency Medicine
University of Colorado School of Medicine
Michael J. Krzyzaniak, MD Aurora, Colorado;
Trauma, Critical Care, and Emergency Surgery Fellow and Visiting Scientist
Department of Surgery François-Xavier Bagnoud Center for Health and Human Rights
Naval Medical Center San Diego Harvard T.H. Chan School of Public Health
San Diego, California Boston, Massachusetts

Peter Kummerfeldt, AD Lisa R. Leon, PhD, FAPS

Former Owner, OutdoorSafe Inc. Research Physiologist
Former Survival Training Director Thermal Mountain Medicine Division
United States Air Force Academy US Army Research Institute of Environmental Medicine
Colorado Springs, Colorado Natick, Massachusetts

Mark R. Lafave, PhD, CAT(C) Benjamin D. Levine, MD, FACC, FAHA, FACSM
Professor and Athletic Therapy Program Coordinator Professor
Department of Health and Physical Education Division of Cardiology
Mount Royal University Department of Internal Medicine
Calgary, Alberta, Canada Distinguished Professor of Exercise Sciences
University of Texas Southwestern Medical Center
Ashley R. Laird, MD Director, Institute for Exercise and Environmental Medicine
Emergency Medicine Texas Health Presbyterian Hospital
Asante Rogue Regional Medical Center Dallas, Texas
Medford, Oregon
Matthew R. Lewin, MD, PhD
Bruce Lampard, MD, FRCP, MIA Director
Lecturer Center for Exploration and Travel Health
Division of Emergency Medicine California Academy of Sciences
Department of Medicine San Francisco, California
University of Toronto Faculty of Medicine
Toronto, Ontario, Canada James R. Liffrig, MD, MPH, FAAFP
Medical Director, FirstHealth Convenient Care
Michael A. Lang, BSc, DPhil FirstHealth of the Carolinas Physicians Group
Assistant Adjunct Professor Pinehurst, North Carolina
Department of Emergency Medicine
Co-Director, San Diego Center of Excellence in Diving Robin W. Lindsay, MD
University of California, San Diego Assistant Professor
San Diego, California Division of Facial Plastics and Reconstructive Surgery
Massachusetts Eye and Ear Infirmary
Carolyn S. Langer, MD, JD, MPH Department of Otolaryngology
Associate Professor Harvard Medical School
Department of Family Medicine and Community Health Boston, Massachusetts
University of Massachusetts Medical School
Worcester, Massachusetts

xi
 Grant S. Lipman, MD, FACEP, FAWM
CONTRI BUTORS
Clinical Associate Professor
Department of Emergency Medicine
Stanford University School of Medicine
Stanford, California
Armando Márquez Jr, MD
Assistant Clinical Professor
Department of Emergency Medicine
University of Illinois College of Medicine at Chicago
Chicago, Illinois

Michael S. Lipnick, MD Thomas H. Marshburn, MD

Assistant Professor Astronaut
Department of Anesthesia and Perioperative Care National Aeronautics and Space Administration
University of California, San Francisco Lyndon B. Johnson Space Center
Dive Medical Officer Houston, Texas
California Academy of Sciences
San Francisco, California Denise M. Martinez, MS, RD
Greenland, New Hampshire
Joanne Liu, MD, IMHL
International President Nicholas P. Mason, PhD, MB ChB
Médecins Sans Frontières (Doctors Without Borders) Consultant
Geneva, Switzerland Critical Care Medicine
Royal Gwent Hospital
Andrew M. Luks, MD Newport, United Kingdom
Associate Professor
Division of Pulmonary and Critical Care Medicine Michael J. Matteucci, MD
Department of Medicine Assistant Professor
University of Washington School of Medicine Department of Military and Emergency Medicine
Seattle, Washington F. Edward Hébert School of Medicine
Uniformed Services University of the Health Sciences
Binh T. Ly, MD Bethesda, Maryland;
Professor Emergency Medicine Department
Department of Emergency Medicine Naval Medical Center San Diego
University of California, San Diego San Diego, California
San Diego, California
Vicki Mazzorana, MD, FACEP, FAAEM, FAWM
Darryl J. Macias, MD Associate Professor
Professor Emergency Medicine
Department of Emergency Medicine Touro University Nevada College of Osteopathic Medicine
Medical Director Las Vegas, Nevada
International Mountain Medicine Center
University of New Mexico Loui H. McCurley
Albuquerque, New Mexico Chief Executive Officer
Pigeon Mountain Industries, Inc.
Martin J. MacInnis, PhD Lafayette, Georgia;
Postdoctoral Fellow Technical Rescue Specialist
Exercise Metabolism Research Group Alpine Rescue Team
Department of Kinesiology Evergreen, Colorado
McMaster University
Hamilton, Ontario, Canada Henderson D. McGinnis, MD
Associate Professor
Monika Brodmann Maeder, MD, MME Department of Emergency Medicine
Senior Consultant Wake Forest School of Medicine
Department of Emergency Medicine Winston-Salem, North Carolina
Bern University Hospital
Bern, Switzerland; Marilyn McHarg, O.Ont., MSc(A)
Senior Researcher Private Consultant
Institute of Mountain Emergency Medicine Dundas, Ontario, Canada
European Academy of Bozen/Bolzano
Bolzano, South Tyrol, Italy Scott E. McIntosh, MD, MPH, FAWM, DiMM
Associate Professor
Edgar Maeyens Jr, MD Division of Emergency Medicine
Private Practice Department of Surgery
Dermatology University of Utah School of Medicine
Coos Bay, Oregon Salt Lake City, Utah

David S. Markenson, MD, MBA, FAAP, FACEP, Carolyn Sierra Meyer, MD

FCCM, FACHE Associate Physician
Chief Medical Officer Emergency Medicine
Sky Ridge Medical Center Kaiser West Los Angeles Medical Center
Lone Tree, Colorado; Los Angeles, California
National Chair
American Red Cross Scientific Advisory Council
Washington, DC

xii
Richard S. Miller, MD Ken Nguyen, PhD

CONTRI BUTORS
Professor of Surgery Chief, Bacteriology Laboratory
Chief, Division of Trauma and Surgical Critical Care Microbiology Section
Section of Surgical Sciences Department of Pathology and Laboratory Services
Vanderbilt University Medical Center Brooke Army Medical Center
Nashville, Tennessee San Antonio, Texas;
Company Commander
Michael G. Millin, MD, MPH, FACEP Troop Command, Brooke Army Medical Center
Associate Professor Joint Base San Antonio
Division of Special Operations Fort Sam Houston, Texas
Department of Emergency Medicine
Johns Hopkins University School of Medicine Vicki E. Noble, MD
Baltimore, Maryland; Associate Professor
Medical Director Harvard Medical School
Maryland Search and Rescue Director, Division of Emergency Ultrasound
State of Maryland Department of Emergency Medicine
Massachusetts General Hospital
Alicia B. Minns, MD Boston, Massachusetts
Assistant Clinical Professor
Division of Medical Toxicology Robert L. Norris, MD, FACEP, FAAEM
Department of Emergency Medicine Professor Emeritus
Fellowship Director Department of Emergency Medicine
Medical Toxicology Fellowship Stanford University School of Medicine
University of California, San Diego Stanford, California
San Diego, California
Timothy C. Nunez, MD, FACS
John Mioduszewski, PhD Associate Professor
Center for Climatic Research Division of Trauma and Surgical Critical Care
University of Wisconsin—Madison Section of Surgical Sciences
Madison, Wisconsin Vanderbilt University Medical Center
Tennessee Valley Veterans Administration Medical Center
James K. Mitchell, PhD Nashville, Tennessee
Professor Emeritus
Department of Geography Karen K. O’Brien, MD
Rutgers University American Lake Division
Piscataway, New Jersey Veterans Administration Puget Sound Healthcare System
Tacoma, Washington
James Moore, BSc (Hons) Emergency Care
Director, Travel Health Consultancy Francis G. O’Connor, MD, MPH
Exeter, Devon, United Kingdom; Professor and Chair
Co-Director, International Diploma in Expedition and Department of Military and Emergency Medicine
Wilderness Medicine F. Edward Hébert School of Medicine
Royal College of Physicians and Surgeons of Glasgow Uniformed Services University of the Health Sciences
Glasgow, United Kingdom Bethesda, Maryland

Roger B. Mortimer, MD, FAAFP Terry O’Connor, MD

Clinical Professor Emergency Physician
Department of Family and Community Medicine St Luke’s Wood River Medical Center
University of California, San Francisco Ketchum, Idaho
San Francisco, California;
Western Region Coordinator Lisa K. Oddy, MPH
National Cave Rescue Commission Humanitarian U
Huntsville, Alabama Montréal, Québec, Canada

Michael J. Mosier, MD, FACS, FCCM Bohdan T. Olesnicky, MD

Associate Professor CEO and President
Department of Surgery SWAT Fuel, Inc.
Division of Trauma, Surgical Critical Care, and Burns Indian Wells, California
Loyola University Medical Center
Maywood, Illinois Edward J. Otten, MD, FACMT, FAWM
Professor
Alice F. Murray, MB ChB Departments of Emergency Medicine and Pediatrics
Instructor Director, Division of Toxicology
Department of Emergency Medicine Department of Emergency Medicine
Boston Medical Center University of Cincinnati
Boston, Massachusetts Cincinnati, Ohio

Robert W. Mutch
Consultant
Fire Management Applications
Missoula, Montana

xiii
 Parveen K. Parmar, MD, MPH Sheila B. Reed, MS
CONTRI BUTORS
Associate Professor Consultant
Director Disaster Risk Reduction and Development
Division of International Emergency Medicine Middleton, Wisconsin
Department of Emergency Medicine
Keck School of Medicine Martin Rhodes, MBChB, DiMM
University of Southern California Medical Director
Los Angeles, California Antarctic Logistics & Expeditions LLC
Salt Lake City, Utah
Sheral S. Patel, MD, FAAP, FASTMH
U.S. Food and Drug Administration Gates Richards, MEd, WEMT-I, FAWM
Silver Spring, Maryland Special Programs Manager
Wilderness Medicine Institute
Ryan D. Paterson, MD, DiMM, DTM&H National Outdoor Leadership School
Assistant Adjoint Professor Lander, Wyoming
Section of Wilderness and Environmental Medicine
Department of Emergency Medicine Robert C. Roach, PhD
University of Colorado School of Medicine Associate Professor
Aurora, Colorado Director
Altitude Research Center
Suchismita Paul, MD Department of Emergency Medicine
Department of Dermatology & Cutaneous Surgery University of Colorado School of Medicine
University of Miami Miller School of Medicine Aurora, Colorado
Miami, Florida
George W. Rodway, PhD, APRN
Lara L. Phillips, MD Associate Clinical Professor
Clinical Assistant Professor Betty Irene Moore School of Nursing
Director University of California, Davis
Wilderness Medicine Sacramento, California
Department of Emergency Medicine
Thomas Jefferson University Hospital Nancy V. Rodway, MD, MPH
Philadelphia, Pennsylvania Medical Director
Lake County General Health District
Justin T. Pitman, MD Painesville, Ohio
Attending Physician
Department of Emergency Medicine Brent E. Ruoff, MD
Mt. Auburn Hospital Associate Professor and Chief
Cambridge, Massachusetts; Division of Emergency Medicine
Instructor of Emergency Medicine Washington University in St. Louis School of Medicine
Harvard Medical School St. Louis, Missouri
Boston, Massachusetts
Renee N. Salas, MD, MPH
Robert H. Quinn, MD Division of Wilderness Medicine
Professor and John J. Hinchey MD and Kathryn Hinchey Chair Department of Emergency Medicine
Department of Orthopaedic Surgery Massachusetts General Hospital
The University of Texas Health Science Center at San Antonio Clinical Instructor
San Antonio, Texas Department of Emergency Medicine
Harvard Medical School
Martin I. Radwin, MD Boston, Massachusetts
Chief of Gastrointestinal Endoscopy
Jordan Valley Medical Center Richard S. Salkowe, DPM, PhD, FACFAS, FAWM
Salt Lake City, Utah Medical/Training Officer
Florida Region 4 State Medical Response Team
S. Christopher Ralphs, MS, DVM, DACVS Master Instructor–Leidos
Staff Surgeon Federal Emergency Management Agency Center for Domestic
Small Animal Surgery Preparedness
Ocean State Veterinary Specialists Research Associate
East Greenwich, Rhode Island School of Public Affairs
University of South Florida
Wayne D. Ranney, MS Tampa, Florida
Adjunct Professor (Retired)
Department of Geology Tod Schimelpfenig, WEMT-I, FAWM
Yavapai College Curriculum Director
Prescott, Arizona; Wilderness Medicine Institute
President National Outdoor Leadership School
Grand Canyon Historical Society Lander, Wyoming
Flagstaff, Arizona
Andrew C. Schmidt, DO, MPH
Mark A. Read, PhD, BSc Assistant Professor
Manager Department of Emergency Medicine
Operations Support University of Florida–Jacksonville
Great Barrier Reef Marine Park Authority Jacksonville, Florida
Townsville, Queensland, Australia

xiv
Sandra M. Schneider, MD, FACEP Tatum S. Simonson, PhD

CONTRI BUTORS
Professor of Emergency Medicine Assistant Professor
Hofstra Northwell School of Medicine Division of Physiology
Hempstead, New York; Department of Medicine
Attending Physician University of California, San Diego
John Peter Smith Hospital La Jolla, California
Fort Worth, Texas
Eunice M. Singletary, MD, FACEP
Robert B. Schoene, MD Associate Professor
Clinical Professor Department of Emergency Medicine
Division of Pulmonary and Critical Care Medicine University of Virginia
Department of Medicine Charlottesville, Virginia
University of Washington School of Medicine
Seattle, Washington; William “Will” R. Smith, MD, FAWM
Sound Physicians President and Medical Director
The Intensivist Group Wilderness and Emergency Medical Consulting, LLC
St. Mary’s Medical Center Jackson, Wyoming;
San Francisco, California Medical Director
National Park Service
John Semple, MD, MSc, FRCSC, FACS Washington, DC
Head, Division of Plastic Surgery
Women’s College Hospital Hans Christian Sørenson, MD, IMM
Professor The Hospital, Tasiilaq
Department of Surgery Tasiilaq, East Greenland
University of Toronto
Toronto, Ontario, Canada Susanne J. Spano, MD
Director
Justin Sempsrott, MD, FAAEM Wilderness Medicine Education
Executive Director University of California, San Francisco Fresno
Lifeguards Without Borders Fresno, California;
Jacksonville Beach, Florida Assistant Clinical Professor
Department of Emergency Medicine
Jamie R. Shandro, MD, MPH University of California, San Francisco
Associate Professor San Francisco, California
Division of Emergency Medicine
Department of Medicine Matthew C. Spitzer, MD, DTMH
University of Washington School of Medicine Past President, Board of Directors
Seattle, Washington Médecins Sans Frontières (Doctors Without Borders)—USA
Assistant Clinical Professor of Medicine
David Shaye, MD Center for Family and Community Medicine
Instructor College of Physicians and Surgeons
Division of Facial Plastic and Reconstructive Surgery Columbia University
Massachusetts Eye and Ear Infirmary New York, New York
Department of Otolaryngology
Harvard Medical School Brian Stafford, MD, MPH
Boston, Massachusetts Founder and Lead Guide
Wilderness Is Medicine
Susan B. Sheehy, PhD, RN, FAEN, FAAN Ojai, California
Associate Professor
Daniel K. Inouye Graduate School of Nursing Alan M. Steinman, MD, MPH
Uniformed Services University of the Health Sciences Rear Admiral (Retired)
Bethesda, Maryland United States Public Health Service
Director of Health and Safety
Robert L. Sheridan, MD, FAAP, FACS United States Coast Guard
Burn Service Medical Director Olympia, Washington
Boston Shriners Hospital for Children
Division of Burns Giacomo Strapazzon, MD, PhD
Massachusetts General Hospital Vice Head
Professor of Surgery Institute of Mountain Emergency Medicine
Harvard Medical School European Academy of Bozen/Bolzano
Boston, Massachusetts International Commission for Mountain Emergency Medicine
Bolzano, South Tyrol, Italy
Charles S. Shimanski, BA
Air Rescue Commission Jeffrey R. Suchard, MD, FACEP, FACMT
International Commission for Alpine Rescue (ICAR) Professor
Kloten, Switzerland; Departments of Emergency Medicine and Pharmacology
Education Director University of California, Irvine School of Medicine
Mountain Rescue Association Irvine, California
San Diego, California

Joshua D. Shofner, MD
Dermatology Associates of Winchester
Winchester, Massachusetts

xv
 Julie A. Switzer, MD Sydney J. Vail, MD, FACS
CONTRI BUTORS
Assistant Professor Associate Professor
Department of Orthopaedic Surgery Department of Surgery
University of Minnesota University of Arizona College of Medicine—Phoenix
Minneapolis, Minnesota Chief, Division of Trauma and Surgical Critical Care
Director, Tactical Medicine Program
Noushafarin Taleghani, MD, PhD, FAAEM Vice Chairman
Clinical Associate Professor Department of Surgery
Department of Emergency Medicine Maricopa Medical Center
Stanford University School of Medicine Phoenix, Arizona
Stanford, California
Karen B. Van Hoesen, MD
John Tanner, MD Clinical Professor
Department of Emergency Medicine Department of Emergency Medicine
Yakima Valley Memorial Hospital Co-Director, San Diego Center of Excellence in Diving
Yakima, Washington University of California, San Diego
San Diego, California
Shana L. Tarter, WEMT-I, FAWM
Assistant Director Michael VanRooyen, MD, MPH
Wilderness Medicine Institute Associate Professor of Emergency Medicine
National Outdoor Leadership School Harvard Medical School
Lander, Wyoming Chairman
Department of Emergency Medicine
Owen D. Thomas, BMedSc (Phys), MBChB (Hons), Director
DTM&H Division of International Health and Humanitarian Programs
Birmingham Medical Research Expeditionary Society Brigham and Women’s Hospital
Birmingham, United Kingdom Boston, Massachusetts

Stephen H. Thomas, MD, MPH Raghu Venugopal, MD, MPH, FRCPC

Chairman Assistant Professor
Emergency Department Division of Emergency Medicine
Hamad General Hospital and Hamad Medical Corporation Department of Medicine
Department of Medicine University of Toronto
Weill Cornell Medical College in Qatar Toronto, Ontario, Canada
Doha, Qatar
Julian Villar, MD, MPH
Todd W. Thomsen, MD Chief Fellow
Instructor in Medicine Division of Critical Care Medicine
Department of Emergency Medicine Department of Medicine
Harvard Medical School Stanford University School of Medicine
Boston, Massachusetts; Stanford, California
Attending Physician
Department of Emergency Medicine Brandee L. Waite, MD
Mount Auburn Hospital Associate Professor
Cambridge, Massachusetts Associate Director Sports Medicine Fellowship
Department of Physical Medicine and Rehabilitation
Robert I. Tilling, PhD University of California, Davis School of Medicine
Volcanologist Emeritus Sacramento, California
US Geological Survey
Menlo Park, California John B. Walden, MD, DTMH
Professor
David A. Townes, MD, MPH, DTM&H Department of Family and Community Health
Associate Professor Director, International Health
Division of Emergency Medicine Joan C. Edwards School of Medicine
Department of Medicine Marshall University
Adjunct Associate Professor Huntington, West Virginia
Department of Global Health
University of Washington School of Medicine David A. Warrell, MA, DM, DSc, FRCP, FRCPE, FZS,
Seattle, Washington FRGS, FMedSci
International Director
Stephen J. Traub, MD, FACEP, FACMT Royal College of Physicians
Associate Professor and Chair London, United Kingdom;
Department of Emergency Medicine Emeritus Professor of Tropical Medicine
Mayo Clinic Arizona Nuffield Department of Clinical Medicine
Phoenix, Arizona University of Oxford
Oxford, United Kingdom

Ashley Kochanek Weisman, MD

Harvard Affiliated Emergency Medicine Residency
Brigham and Women’s Hospital
Massachusetts General Hospital
Boston, Massachusetts

xvi
Timothy J. Wiegand, MD, FACMT, FAACT, FASAM Megann Young, MD, FACEP

CONTRI BUTORS
Associate Clinical Professor Director
Departments of Emergency Medicine and Public Health Wilderness Medicine Fellowship
Sciences University of California, San Francisco Fresno
Director of Toxicology Fresno, California;
University of Rochester Medical Center Assistant Clinical Professor
Rochester, New York Department of Emergency Medicine
University of California, San Francisco
Stacie L. Wing-Gaia, PhD, RD, CSSD San Francisco, California
Associate Professor
Department of Nutrition and Integrative Physiology Ken Zafren, MD, FAAEM, FACEP, FAWM
University of Utah Clinical Professor
Salt Lake City, Utah Department of Emergency Medicine
Stanford University Medical Center
Sarah A. Wolfe, MD Stanford, California;
Assistant Professor Vice President
Department of Dermatology International Commission for Mountain Emergency Medicine
Duke University School of Medicine Associate Medical Director
Durham, North Carolina Himalayan Rescue Association
Kathmandu, Nepal

xvii
 Foreword
Before partaking of an urban existence, men, women, and chil-
dren lived in austerity in the wilderness. So, the human race is
not encountering wilderness medicine for the very first time.
Before the advent of such wonders as antisepsis, randomized
clinical trials, and emphasis on evidence, and therefore through-
out most of the history of human existence and eventually, civi-
lization, the practice of medicine was largely improvised and
based on anecdotes and dogma, rather than evolving science.
Given that humans had to make do with little or nothing before
they had access to tests, drugs, and devices, the history of wilder-
ness medicine might be considered to largely be the history of
medicine itself. Advances in medicine have in general paralleled
other sciences, with periodic insights into its essences, but there
remain geographies and circumstances where wilderness medi-
cine is uniquely essential.
We are in the midst of a scientific revolution, but recognize
that optimal urban science is not necessarily applicable in austere
environments. So, as we intentionally place ourselves in wild
places isolated from cities and machines, wilderness medicine
comes full circle and needs to remain different in certain ways
from big city medicine. From this perspective, one might identify
many potential starting points for our 21st century iteration of
wilderness medicine. However, thoughtful reflection identifies
two prominent threads. First, today’s wilderness medicine “began”
when urban, high-resource medicine became too sophisticated
to practice in austere environments—when improvisation was
required to replace more sophisticated methodology that was not
available. Second, and very significant from a definition stand-
point, wilderness medicine gained true identity when men and
women began in earnest to explore environments that stressed
normal human physiology to the point that unique pathophysiol-
ogy was discovered. This phenomenon notably occurred with
human endeavors at high altitude (mountaineering and aviation),
under the ocean surface (diving), at extremes of temperature
(cold and heat), and at the limits of endurance posed by natural
disasters or forays into the ultimate frontier of space travel.
The history of wilderness medicine could be a textbook unto
itself. The following paragraphs attempt to provide key examples
of how the evolution of modern medicine simultaneously drew
from and shaped the specialty.
Military medicine provides many examples of this interaction.
For much of history, the greatest threats to soldiers were not
battlefield combatants, but weather and infectious diseases.
During the American Revolutionary War, 6,200 American soldiers
were killed in action, while 10,000 died of disease. Typhus,
smallpox, dysentery, diarrhea, and pneumonia were prevalent.
The War of 1812 generated 2,200 American combat deaths and
nearly 13,000 deaths from noncombat causes. Napoleon invaded
Russia in 1812 with 680,000 soldiers, and retreated back to France
five months later with 27,000. Most of the remainder had suc-
cumbed to hypothermia, frostbite, and typhus. It wasn’t until
World War II that the number of soldiers killed in combat out-
numbered those who died from other causes, many of them
environmental.
“Medicine Under Sail,” Zachary Friedenberg’s history on the
subject,1 chronicles an oft-overlooked perspective of the early
history of medicine. In the same vein, Homer made reference in
book 4 of the Iliad to a medical naval incident in the Trojan
War.2 When Menelaus was wounded by a Trojan bowman, the
fleet surgeon, Machaon (son of Aesculapius, god of medicine),
was called to treat the wound:
Without delay he drew
the arrow from the fairly fitted belt.
The barbs were bent in drawing.
Then he loosed the plate—the armorer’s work—and
carefully
O’er looked the wound where fell the bitter shaft.
Cleansed it from blood, and sprinkled over it
with skill the soothing balsam of yore which
the friendly Chiron to his father gave.
Thomas Woodall (1569-1643) perhaps deserves the title “Father
of Marine Medicine” because he was ahead of his time with
observations of scurvy and views on the treatment of wounds,
fractures, and amputations.1 His extensive practical experience,
astute observations, and cautious judgment persuaded him that
the theories of oracles, such as Galen, often offered little in the
way of useful medical knowledge. As stated in his 1655 book
The Surgeon’s Mate, Woodall divided wounds into three catego-
ries: (1) puncture wounds and lacerations, (2) gunshot wounds,
and (3) bone fractures.3 His treatment recommendations have a
modern ring: “…remove unnatural things forced into the wound…
which should be done with the least pain to the patient and
avoiding arteries, nerves, and veins.” The “unnatural things” to
which he referred might include wood splinters from spars and
masts, fragments from cannon fire, and other foreign objects
embedded into people during commerce and conflict. Anesthesia
was nonexistent in this era. In the case of removal being too
difficult or painful, Woodall recommended “tarry if you may,
while nature helps.” His suggestions to ligate specific vessels that
contributed to excessive bleeding and to place dressings soaked
in wine over wounds were significant departures from the usual
treatment of the day, which was wound cauterization with hot
oil or a red-hot searing iron.
When limb wounds were severe, Woodall was not in a rush
to amputate. This approach ran counter to the prevailing custom
and for several hundred years afterward. Woodall reasoned that
the need for amputation should be dictated by specific criteria:
one-half or more of the limb should have been dismembered or
irreparably damaged; a chronic suppurating wound be present;
the patient’s life be imminently in danger; or the remaining
portion of the limb be unserviceable. His concepts were far more
conservative and reasonable than those of military surgeons who
practiced for the next two centuries, such as during the American
Civil War, where immediate amputation of any limb with a
gunshot wound was the customary practice. Woodall’s conserva-
tive principles from three centuries past seem reasonable for
modern physicians providing care for trauma patients in harsh
or remote environments.
It was Admiral Horatio Nelson, a senior nonmedical officer in
the British Royal Navy, who near the turn of the nineteenth
century brought about a revolution in medicine, particularly in
disease control, practiced on the high seas. Nelson’s well-
documented personal medical history provides a window into
certain typical maladies and injuries for the ocean-going warrior
or explorer of his era. As a midshipman, he sustained partial
xix
 paralysis from an illness contracted at age 17, was stricken with
FOREWORD
malaria in the West Indies, contracted yellow fever in Nicaragua,
suffered a laceration of his back and lost sight in his left eye
during battles near Corsica, endured an abdominal wound during
a military encounter at Cape St. Vincent, and had his right arm
amputated below the shoulder after a severe injury from grape-
shot during battle in the Canary Islands. His luck ran out in 1805
at Trafalgar, where a French sharpshooter’s bullet delivered a
fatal blow.
Largely as a result of Admiral Nelson’s impressive understand-
ing of the challenges of providing effective shipboard medical
care, medical reforms in his and other navies became a reality.
Much emphasis was directed at proper diet as it relates to disease
prevention, a unique perspective at that time that is increasingly
popular today. The success of this strategy is obvious from the
historical record; the proportion of men sent sick to hospital from
ships between the last decade of the 18th century and the first
decade of the 19th century fell from a high of 38.4% (in 1793)
to a low of 6.4% (in 1806).4
After the end of the American Civil War, the U.S. Army fought
with many Native American tribes in the western states and ter-
ritories. Military medical personnel and civilian practitioners
became adept at extracting arrows and other primitive penetrat-
ing weapons. Instruments devised as early as 500 BC (such as
the belulcum) for removing arrows became invaluable during the
1870s. These tools could dilate the point of entrance and widen
the channel containing the arrow, to allow the head of the arrow
to be grasped. North American Indian arrows were typically fired
with great speed and force, and if not stopped by bone, could
easily pass through a horse or bison. Not surprisingly, mortality
from arrow wounds was high, with one 1871 report suggesting
a fatality rate of approximately 30%.
The ensuing maturation of military medicine marked a turning
point back to appreciation of wilderness medicine, or perhaps
more appropriately, austere medicine. This occurred when the
military began to move medicine to the front lines. Re-emergence
of tourniquets applied in the field to extremities to control bleed-
ing are illustrative. In the past two decades, bringing medicine
to the point of action led to creation of tactical combat casualty
care (TCCC)5 and formation of the Special Operations Medical
Association (SOMA), including collaboration with the Wilderness
Medical Society (WMS). Soldiers with life-threatening injuries that
previously would have been fatal are now stabilized on or near
the battlefield before being evacuated to definitive trauma centers
in their home countries.
Parallel to the contributions of military medicine were those
of intrepid explorers. Many of the early “practitioners” of wilder-
ness medicine were adventurers who accepted additional respon-
sibilities. Although not a physician, Captain William Clark had
sufficient medical knowledge to serve as the expedition doctor
on the heralded Lewis and Clark expedition.6 In the early days
of exploration, expedition doctors were integral members of a
dedicated team with expertise related to the logistics of the
mission. The current expeditionary practice of retaining expert
medical guests is a relatively recent phenomenon.
Infection from nonsterile surgical procedures and penetrating
missiles was but one major challenge of this bygone era. Early
explorers also had to contend with infectious diseases that could
easily be passed between persons and that had the potential to
bring any journey to a sudden halt. Throughout much of the
course of its explorations, the Lewis and Clark expedition
encountered indigenous tribes. These tribes had not been
exposed to European-based diseases for many centuries, so were
neither educationally nor immunologically capable of effective
self-defense. The Americans learned of many settlements (espe-
cially along the Missouri River) that had been decimated by
devastating epidemics of smallpox following contact with persons
of European background. The concept of vaccination was gather-
ing proponents at this time, and President Thomas Jefferson sent
a sample of cowpox on the expedition with Lewis in hope that
he could attempt to vaccinate the “natives.”7 Other infectious
maladies of regular concern to Lewis and Clark included omni-
present venereal diseases, such as syphilis. Prior to 1800, mercury,
already used as therapy for many infections and diseases, had
xx
become the treatment of choice for syphilis. It was typically taken
orally or used as a topical ointment in very liberal doses. Cures
were few and far between, and the patient often succumbed to
mercury poisoning before the syphilis entered its secondary or
tertiary phase. During this era, cinchona for malaria was one of
only a handful of medications that had the ability to produce an
intended result. Thus, early physicians “were like hunters going
into the field and shooting blanks.”8
As exploration of the last great terrestrial and oceanic “blanks
on the map” evolved into ever more sophisticated ventures in the
19th and early 20th centuries, wilderness medical care further
evolved. “Physician/naturalists,” trained physicians who could
multitask as field biologists, began to accompany long, arduous
explorations to the ends of the earth. While their medical training
was certainly superior to that of William Clark and they could be
considered more competent healers, these physicians still needed
to be extremely skilled outdoorsmen to participate in these
demanding adventures. To appreciate the extent of the sacrifices
sometimes made by these physician-explorers, one need only
recall the Englishman Edward Wilson—physician, polar explorer,
natural historian, painter, and ornithologist. Wilson accompanied
two of Robert Scott’s exploratory Antarctic voyages in the early
years of the 20th century, tragically perishing with his companions
in March 1912 on the Antarctic plateau during the British team’s
return sledge journey from the South Pole. Edward Atkinson,
research parasitologist and senior expedition surgeon for Scott’s
final, ill-fated 1910-1913 Terra Nova expedition, was part of the
shore party that did not accompany Scott, Wilson, and their three
companions during the final push to the Pole. By March 1912,
Scott’s party was clearly overdue and fear mounted that they had
perished. That month, Atkinson, as senior officer in command of
13 men facing 4 months of darkness and intense cold, led a futile
effort to locate Scott. In October of 1912, with the sun at last
shedding some light and heat on the bleak Antarctic landscape,
Atkinson once again set out with a search party. On November
12, they discovered the dead explorers within Scott’s tent, which
was partially buried in snow. Atkinson was first to enter the tent,
where he read the diary entries of the polar party’s final days of
privation and suffering.9
During the 20th century, exploration of the limits of the
human body and those of the earth’s physical domain altered
the manner in which people viewed the world and their place
in it. While the pursuits of physical exploration and medicine
may seem unlikely siblings, they deeply informed each other.
Dr. Charles Houston, who served as an inspiration to many
current wilderness medicine researchers and clinicians, embod-
ied the modern adventurer-physician.10 An accomplished moun-
taineer and Harvard-trained physician, Houston led two attempts
to summit K2, included the ill-fated attempt in 1953 that claimed
the life of one team member and nearly wiped out the entire
team. While a naval flight surgeon during World War II, Houston
conceived, and ultimately was one of the physician/scientists in
charge of, Operation Everest in 1946. This study, sponsored by
the U.S. Navy, was intended to benefit the aviation community
by shedding light on human adaptation to and tolerance of
extreme altitudes. Such research efforts were particularly timely
because they occurred at a time when airplanes became capable
of flying higher than humans could tolerate without support,
such as from pressurized suits or cabins. Houston’s high-altitude
chamber research led to the first successful simulated “ascent” to
the barometric pressure equivalent of the summit of Mt Everest,
proving it could perhaps be reached in real life without supple-
mental oxygen. His research team’s findings led to great advances
in understanding the challenges of altitude and etiology of high-
altitude illnesses. Houston later became a founding member of
the WMS, and in doing so, drew attention to its mission and
potential.
Houston’s achievements were part of a blossoming of science
exemplified by the discoveries of other legendary figures in alti-
tude research and mountain medicine, including Drs. Herb Hult-
gren, John West, Robert Schoene, and Peter Hackett. While
serving as a member of the American Medical Research Expedi-
tion to Everest in 1981, Hackett accomplished a successful summit
of Mt Everest, climbing alone to the top from high camp, falling
while traversing the Hillary step, and thereby fortunately uncov-
ering a fixed rope that enabled him to self-rescue and live to tell
the tale. He too became one of the founding members
of the WMS. During this modern era, brave and high-spirited
physician high-altitude adventurers Drs. Oswald Oelz, Charles
Clarke, and Bruno Dürrer were pioneering by exploring, discov-
ering, and innovating. There were and will be so many brilliant
men and women who combine adventure with medicine.
One could write equally about the oceans that cover most of
our planet, and about forests, rivers, canyonlands, or polar caps.
There will hopefully always be mountains to climb, woods to
wander, deserts to cross, and lagoons to explore. Each has its
wilderness medicine history, from antiquity to modern times.
There are lost people to find, victims of mishaps to rescue, and
ever the need to make do with very little at the worst possible
moments. We know more now about how to direct doctors, and
how to facilitate location, stabilization, and transport of victims
from remote and geographically challenging locales. Wilderness
first responders are equipped with knowledge and training that
allow for more advanced intervention that occurs with shorter
transport times.11 Search and rescue team training has become
sophisticated and intense, in large measure because the wilder-
ness medicine community has set the bar higher.
The logical evolution (and practical admixture) of wilderness
medicine and wilderness search and rescue can be clearly seen
in today’s international Diploma in Mountain Medicine (DiMM).
A cooperative idea initially developed in Europe in the late 1990s
by the International Commission for Alpine Rescue, International
Climbing and Mountaineering Federation, and International
Society of Mountain Medicine, the extensive and comprehensive
DiMM curriculum blends rigorous didactic and practical educa-
tion in wilderness medicine with technical mountain rescue and
self-sufficiency in the backcountry. Many mountain medicine
organizations worldwide now offer the standard (or specialty
module) DiMM curriculum, in the process bridging many nations
and cultures.
The final linchpin in the modern enactment of wilderness
medicine as a distinct entity is the selfless act of delivering
medical care to the farthest reaches of the globe. Less fortunate
people benefit from the emotionally taxing and sometimes coura-
geous efforts of many wilderness medicine–trained volunteers
who deliver medical support that ranges from immunizations
during peaceful times to surgeries in the aftermath of natural
disasters. Wilderness medicine breeds an ethos of service. Medical
teams populated by wilderness medicine providers depart at a
moment’s notice to assist in humanitarian relief and disaster
FOREWORD
response. After many lessons learned from earlier treat-and-leave
approaches, providers and organizations have embarked upon
much more sustainable approaches to health care delivery,
including vital education and training.
The modern history of wilderness medicine spawned the
founding and maturation of important scientific societies dedi-
cated to the discipline or one of its subspecialties. The WMS was
formed in 1982; the International Society of Mountain Medicine
in 1985; and the International Society of Travel Medicine in 1991.
Phenomenal individuals who contributed to modern wilderness
medicine have become too numerous to count. Modern wilder-
ness medicine was conceptualized and organized by a dedicated
and ambitious group of prime movers, and has become an enor-
mous, growing community, reflected in part by the contributors
to this textbook, some of whom have been involved in wilder-
ness medicine for many decades. We admire the pioneers of the
past, and have every confidence in the ability of today’s leaders
and innovators to carry us with great enthusiasm into the future.
Robert H. Quinn, MD
George W. Rodway, PhD
REFERENCES
1. Friedenberg ZB. Medicine Under Sail. Annapolis, MD: Naval Institute
Press; 2002.
2. Homer. The Iliad and the Odyssey. London: John Ogilby; 1660.
3. Woodall T. The Surgeon’s Mate. London: John League; 1655.
4. Allison RS. Sea Diseases: The Story of a Great Natural Experiment
in Preventive Medicine in the Royal Navy. London: John Bale Medical
Publications; 1943.
5. Butler FK, Hagmann J, Butler G. Tactical combat casualty care in
special operations. Mil Med 1996;161(Suppl. 1):1–16.
6. Larsell O. Excerpts from: Medical aspects of the Lewis and Clark
expedition (1804-1806). Wilderness Environ Med 2003;14:265–71.
7. Chuinard EP. Only One Man Died: The Medical Aspects of the Lewis
and Clark Expedition. Fairfield, WA: Ye Galleon Press; 1999.
8. Paton BC. Adventuring with Boldness: The Triumph of the Explorers.
Golden, CO: Fulcrum Publishing; 2006.
9. Campbell WC. Edward Leicester Atkinson: Physician, parasitologist,
and adventurer. J Hist Med Allied Sci 1991;46:219–40.
10. McDonald B. Brotherhood of the Rope: the Biography of Charles
Houston. Seattle, WA: The Mountaineers; 2007.
11. Backer HD. Editorial: what is wilderness medicine? Wilderness
Environ Med 1995;6:3–10.
xxi
 Preface
As the specialty of wilderness medicine matures, obligations
grow. Education is the objective of this textbook and certainly
essential, but to advance the field in all aspects, leadership and
inspiration are required. In this seventh edition of Wilderness
Medicine, the contributors are many of these leaders, and their
writing and creativity are outstanding. Authors who are practitio-
ners and researchers with an inestimable amount of experience
share their knowledge and wisdom, and seek not only to teach,
but to inspire those who will follow them. They have superbly
pointed out not only what we already know, but also what we
need to discover and learn, thereby directing a path toward
observation, service, and experimentation, each of which is inte-
gral to the unique influence of wilderness medicine.
The breadth and depth of content of wilderness medicine
have grown to the extent that two volumes of Wilderness Medi-
cine are now required. The authors, assistant editors, and I are
grateful to the publisher for using innovative techniques to create
a comprehensive book with outstanding visual appeal, so that
the blend of academia and art is at once logical and stimulating.
In this edition, I am enormously grateful to the remarkable team
at Elsevier, including Kate Dimock, Lucia Gunzel, Lauren Boyle,
and Linda Belfus. My publishing family always sets the bar high
and patiently helps me leap. My global academic family embraces
this exciting specialty, and my biological family graciously allows
me the time to pursue this endeavor.
Acquisition of new knowledge is exciting and challenging for
academicians, practitioners, and students. Wilderness medicine
draws not only from the timeless medical specialties of surgery,
internal medicine, obstetrics and gynecology, pediatrics, and
psychiatry, but from anywhere that medical science reaches out
to improve the health and safety of patients. New chapters and
deeper discussions within revised chapters introduce the reader
to the trends that are most likely to become influential as we
approach the next five years. Evidence-based medicine, genom-
ics and personalization, and the imperative to translate all of this
into how we live our lives and practice our craft in the field and
hospital are new features of this edition. Other notable changes
from the previous edition are a chapter on medical wilderness
adventure races and expanded discussion of high-altitude medi-
cine, improvisation, technical rescue, and wilderness medicine
education, to name a few. We are proud to continue emphasis
on how we approach the health of planet Earth. Wilderness
conservation and preservation will remain in part the purview of
wilderness medicine as we await a more concerted effort by the
entire house of medicine to fulfill its obligation to play a leader-
ship role in efforts to maintain the desired environment to support
life on our planet.
The efforts of people and organizations engaged in all aspects
of wilderness medicine are growing and increasingly collabora-
tive. Wilderness medicine is firmly embedded in the activities of
the military, and vice versa. As a responder to the 2015 earth-
quake disaster in Nepal, I witnessed once again that my remark-
able colleagues in the wilderness medicine community are
regularly at the front lines when calamity strikes. Whether it is
an Ebola outbreak in West Africa, a typhoon in the Philippines,
or a wildfire in Washington State, this book’s contributors enthu-
siastically volunteer to serve. What I have learned since the last
edition is that anywhere the ability to practice medicine in an
austere setting is the task at hand, wilderness medicine knowl-
edge and experience are essential.
In medical schools across the United States, and now in many
other countries, wilderness medicine courses are taught and
usually among the most popular electives. Wilderness experi-
ences are used by undergraduate universities and medical schools
to introduce students to one another early in their careers and
facilitate collaborations. Competitive wilderness adventures in the
cloaks of competitions and races are the backbone of reality
entertainment. They all require medical planning and support.
Wilderness recreation outpaces all other forms of time away from
the urban work existence. Respite and renewal are inextricably
linked to the wilderness. And when we seek to reach beyond
ourselves, where do we go first to explore? The wilderness, of
course.
At a time when humans are generally considered more of a
burden to than saviors of the environment, we will more often
be in the wilderness, learning its ways and hopefully not
encroaching upon it. To impress upon others the need to pre-
serve it, we will understand its offerings and document its beauty.
To eliminate health care disparities, we will find a way to interact
with indigenous people in a way that can preserve their sur-
roundings and bring healing in the midst of horrific infectious
diseases, violent conflicts, and post-disaster social and economic
chaos. To fuel our existence, we will go beyond clear-cutting
forests, pillaging oceans, and extracting fossil fuels that might
never be replaced. If wilderness medicine helps make us aware
that there is a wilderness and that without a concerted effort it
will disappear, then that is a precious accomplishment by a noble
specialty.
Judging by the quality of research, number of important pub-
lications, and attendance at educational gatherings, such as the
combined sessions of the Wilderness Medical Society and Inter-
national Society for Mountain Medicine, wilderness medicine is
here to stay. For that, we are in great debt to those who came
before us, who preached and practiced wilderness medicine long
before anyone contemplated coalescing a specialty. One such
visionary is Dr. Bruce Paton, whose artwork graces this Preface.
We all have mentors and partners, and I have certainly had mine.
Notable among them are Herb Hultgren and Charlie Houston in
high-altitude medicine, Jeff Davis and Bruce Halstead in dive
medicine, Warren Bowman in prehospital care, Bob Mutch in
wildland fire management, Donald Trunkey in trauma care,
Bruce Dixon in clinical diagnosis, Murray Fowler in veterinary
medicine, Sherman Minton in envenomation, Bruno Dürrer in
rescue, Steve French in bear behavior and attack, Cam Bangs
and Alan Steinman in hypothermia, Joe Serra and Ed Geehr in
humanism, Wongchu Sherpa in spirituality, and Ken Kizer in
determination.
The spark has become a flame. I regularly see young people
beam when they realize that medicine can be so enjoyable. There
are hardcore science and service in wilderness medicine, but we
are still “out there,” away from electronic medical records, cost
containment, and endless political debates about universal health
care. We are in the field, responding because we are responsive,
sticking our necks out to accept the adventure and risk, and then
xxiii
 put something back. There is heroism in medicine, and wilder-
PREFACE
ness medicine has its fair share, delightfully unsung. It is brave
to document the wisdom of an indigenous healer, courageous
to teach mountain safety to sherpas, and selfless to assist layper-
sons to fill the gaps in health care that cannot be provided during
a humanitarian crisis. The settings in which we practice may
sometimes be uncontrolled, but it is the domain of wilderness
medicine experts to bring best practices to the unique bedsides
posed on the side of a mountain, in a cave during a lightning
storm, or on the beach of a faraway atoll. Wilderness medicine
takes everything we have learned and then adds to it the spice
of life. How much fun is that? Seven editions now, and I can’t
wait for the eighth.
Paul S. Auerbach

Aiming High
Bruce Paton

xxiv
 Video Contents
Video 2-1 Periodic Breathing
Video 8-1 Ocean Ranger Disaster
Video 8-2 Marine Electric Disaster
Video 8-3 The Cold, Hard Facts of Winter
Road Safety
Video 8-4A Cold Water Immersion and Drowning, Part 1
Video 8-4B Cold Water Immersion and Drowning, Part 2
Video 8-4C Cold Water Immersion and Drowning, Part 3
Video 8-5A Hypothermia
Video 8-5B Hypothermia: Shivering
Video 8-5C Hypothermia and Alcohol
Video 8-5D Hypothermia: Mild vs. Severe
Video 8-5E Hypothermia and CPR
Video 8-5F Hypothermia Treatment
Video 8-5G Hypothermia: Rewarming
Video 8-6A Cold Water Boot Camp: Life Jackets
Video 8-6B Cold Water Boot Camp: 1-10-1 Principle
Video 8-6C Cold Water Boot Camp: Surviving
Cold Water
Video 8-6D Cold Water Boot Camp: The First
60 Seconds
Video 8-7 Cold Water Boating
Video 8-8 Transport Canada: Boating Safety
Video 40-1 WHO: Malaria Key Facts
Video 40-2 Malaria Life Cycle, Part 1: Human Host
Video 40-3 Malaria Life Cycle, Part 2: Mosquito Host
Video 40-4 Malaria Life Cycle, Animation
Video 40-5 African Child with Severe Malaria
Video 40-6 CDC: Blood Specimen Processing
Video 40-7 BinaxNOW Malaria, the First Rapid
Diagnostic Test Approved by the FDA
for Use in the United States
Video 44-1 Neuromuscular Hyperactivity in Children
with Scorpion Envenomation
Video 49-1A Tooth Splinting Instruments
Video 49-1B Tooth Splinting Procedure
Video 49-2A Recementing a Crown: Armamentarium
Video 49-2B Recementing a Crown: Procedure
Video 49-3A Replacing a Lost Filling: Armamentarium
Video 49-3B Replacing a Lost Filling: Procedure
Video 83-1 Ushahidi Haiti
Video 126-1 Flight Deck Camera View of the
STS-135 Crew
Video 126-2 Astronaut Karen Nyberg Demonstrates Use
of U.S. Treadmill
Video 126-3 Astronaut Mike Hopkins Demonstrates
Two Exercises Astronauts Can
Perform Using the Advanced Resistive
Exercise Device
Video 126-4 Montage of Experienced Astronauts
Moving About Aboard the International
Space Station
Video 126-5 Astronaut Trains for a Spacewalk in the
Neutral Buoyancy Laboratory
Video 126-6 Use of Water as an Acoustic Medium
for Ultrasound Imaging in Space
xxix
 PHOTO CREDITS

Front and Back Cover, Spine, Part 17 Part 8

Copyright 2016 Elizabeth Carmel Copyright iStockphoto.com/osmanpek

Parts 1 to 5, 9, 12, 14, 16 Part 10

Courtesy Paul S. Auerbach Copyright 2016 Norbert Wu

Part 6 Part 11
Copyright iStockphoto.com/meikesen Copyright iStockphoto.com/Rumo

Parts 7, 15 Part 13
Copyright 2016 Mathias Schar Copyright iStockphoto.com/koldunova

xxxi
PART 1

Mountain
Medicine
 CHAPTER 1 
High-Altitude Physiology
ROBERT C. ROACH, JUSTIN S. LAWLEY, AND PETER H. HACKETT
More than 40 million tourists visit recreation areas above 2400
meters (m), or 7874 feet, in the American West each year. Hun-
dreds of thousands visit central and south Asia, Africa, and South
America, many traveling to altitudes above 4000 m (13,123 feet).
In addition, millions of persons 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 persons live above 2500 m (8202 feet) in Colo-
rado alone. Increasingly, physicians and other health care provid-
ers are confronted with questions of prevention and treatment
of high-altitude medical problems, as well as the effects of alti-
tude on pre existing medical conditions. Despite advances in
high-altitude medicine, significant morbidity and mortality persist.
Clearly, better education of the population at risk and those
advising them is essential.
High-altitude medicine and physiology are discussed in the
first three chapters of this textbook. In this chapter the reader is
introduced to the basic physiology of high-altitude exposure.
Chapter 2 describes the pathophysiology, recognition, manage-
ment, and prevention of altitude illnesses and other clinical issues
likely to be encountered in both “lowlanders” and high-altitude
residents. Chapter 3 focuses on patients with preexisting medical
problems who travel to high altitudes (Box 1-1).
DEFINITIONS
HIGH ALTITUDE
(1500 to 3500 meters [4921 to 11,483 feet])
The onset of physiologic effects of diminished partial pressure
of inspired oxygen (PIO2) includes decreased exercise perfor-
mance and increased ventilation (lower arterial carbon dioxide
partial pressure [PaCO2]). Minor impairment exists in arterial
oxygen transport (arterial oxygen saturation [SaO2] at least 90%),
but arterial oxygen partial pressure (PaO2) is significantly dimin-
ished. 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 of altitudes (see Chapter 2).
VERY HIGH ALTITUDE
(3500 to 5500 meters [11,483 to 18,045 feet])
Maximal SaO2 falls below 90% as PaO2 falls below 50 mm Hg
(Figure 1-1 and Table 1-1). Extreme hypoxemia may occur during
exercise, sleep, and high-altitude pulmonary edema (HAPE) or
other acute lung conditions. Severe altitude illness occurs most
frequently in this range of altitudes.
EXTREME ALTITUDE
(higher than 5500 meters [18,045 feet])
Marked hypoxemia, hypocapnia, and alkalosis characterize
extreme altitude. Progressive deterioration of physiologic func-
tion eventually outstrips acclimatization. As a result, no perma-
nent human habitation is above 5500 m (18,045 feet). A period
of acclimatization is necessary when ascending to extreme alti-
tude; abrupt ascent without supplemental oxygen for other than
brief exposures invites severe altitude illness.
2
THE ENVIRONMENT OF
HIGH ALTITUDE
Barometric pressure (PB) falls with increasing altitude in a loga-
rithmic manner (Table 1-2). Therefore, the partial pressure of
oxygen (PO2, 21% of PB) also decreases, resulting in the primary
insult of high-altitude: hypoxia. At approximately 5800 m (19,029
feet), PB is one-half that at sea level, and on the summit of Mt
Everest (8848 m [29,029 feet]), PIO2 is approximately 28% that at
sea level (see Figure 1-1 and Table 1-1).
The relationship of PB to altitude changes with distance from
the equator. Thus, in addition to extreme cold, polar regions
afford greater hypoxia at any given altitude. West90 calculated
that PB on the summit of Mt Everest (27 degrees north latitude
[N]) would be about 222 mm Hg instead of 253 mm Hg if Mt
Everest were located at the latitude of Denali (62 degrees N).
Such a difference, he claims, would be sufficient to render impos-
sible 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 low-
pressure trough can reduce pressure 10 mm Hg in one night on
Denali, making climbers awaken “physiologically higher” by
200 m (656 feet). The degree of hypoxia is thus directly related
to PB, not solely to geographic altitude.90
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 HAPE.59,93
Ultraviolet (UV) 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 Denali.
Heat problems, primarily heat exhaustion, are often unrecog-
nized 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 hy-
poxia 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, com-
bined with increased water loss through the lungs from increased
respiration and through the skin, typically results in dehydration
that may be debilitating. Thus, the high-altitude environment
imposes multiple stresses, some of which may contribute to, or
may 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 con-
sciousness in a few minutes and death shortly thereafter, climbers
can ascend Mt Everest over a period of weeks without supple-
mental 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 physiol-
ogy determine whether the body successfully acclimatizes or is
 CHAPTER 1  High-Altitude Physiology
BOX 1-1  Glossary of Physiologic Terms* SaO2
160 100

Partial pressure oxygen (mm Hg)

PB Barometric pressure
PO2 Partial pressure of oxygen 140
90
PIO2 Inspired PO2 (0.21 × [PB − 47 mm Hg])
120 PIO2
(47 mm Hg = vapor pressure of H2O at 37° C
[98.6° F]) 80

SaO2 (%)
PAO2 PO2 in alveolus 100
PACO2 PCO2 in alveolus
PaO2 PO2 in arterial blood 80 70
PaCO2 PCO2 in arterial blood PaO2
SaO2 Arterial oxygen saturation (HbO2 ÷ total Hb × 100) 60
RQ Respiratory quotient (CO2 produced ÷ O2 60
consumed) 40
Alveolar gas PAO2 = PIO2 − (PACO2/RQ)
20 50
equation
0 2000 4000 6000 8000 10,000
*Pressures are expressed as millimeters of mercury (1 mm Hg = 1 torr).
Altitude (m)

overwhelmed. Importantly, acclimatization is the only known
means to improve physical and cognitive performance at high
altitude.
The recent revolution in our understanding of the molecular
mechanisms of human responses to hypoxia has focused on
hypoxia-inducible factor (HIF). This transcription factor modu-
lates the expression of hundreds of genes, including those in-
volved in apoptosis, angiogenesis, metabolism, cell proliferation,
and permeability processes.20,27,67,69,88 In chronic hypoxia, HIF
activation by hypoxia has the positive effect of elevating oxygen
delivery by boosting hemoglobin mass. However, HIF also plays
a role in carotid body sensitivity to hypoxia, which in turn largely
determines the ventilatory response to hypoxia.55,56,70 As a master
regulator of the hypoxia response in humans, HIF has beneficial
and harmful effects at different stages during human exposure
to hypoxia and in different cells in the body.36,47 Figure 1-2 pro-
vides an overview of some of the hundreds of processes by
which the response to hypoxia is modulated by HIF.
Individuals vary in their ability to acclimatize, 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
fail to acclimatize even with gradual exposure over weeks. The
tendency to acclimatize well or to become ill is consistent on
FIGURE 1-1  Increasing altitude results in decreasing inspired oxygen
partial pressure (PIO2), arterial PO2 (PaO2), and arterial oxygen satura-
tion (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.)
repeated exposure if rate of ascent and altitude gained are
similar, supporting the role of important genetic factors and an
individual’s predisposition. Successful initial acclimatization pro-
tects 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 HAPE,
on reascent. The improved ability to do physical work at high
altitude, however, persists for up to 3 weeks.43,77 Persons who
live at high altitude during growth and development appear to
realize the maximum benefit of acclimatization changes; for

TABLE 1-1  Arterial Blood Gases and Altitude*

Altitude
Population Meters Feet PB (mm Hg) PaO2 (mm Hg) SaO2 (%) PaCO2 (mm Hg)

Altitude residents 16461 5400 630 73.0 (65.0-83.0) 95.1 (93.0-97.0) 35.6 (30.7-41.8)
Acute exposure 28102 9219 543 60.0 (47.4-73.6) 91.0 (86.6-95.2) 33.9 (31.3-36.5)
36602 12,008 489 47.6 (42.2-53.0) 84.5 (80.5-89.0) 29.5 (23.5-34.3)
47002 15,420 429 44.6 (36.4-47.5) 78.0 (70.8-85.0) 27.1 (22.9-34.0)
53402 17,520 401 43.1 (37.6-50.4) 76.2 (65.4-81.6) 25.7 (21.7-29.7)
61402 20,144 356 35.0 (26.9-40.1) 65.6 (55.5-73.0) 22.0 (19.2-24.8)
Subacute exposure 65003 21,325 346 41.1 ± 3.3 75.2 ±6 20 ± 2.8
70003 22,966 324
80003 26,247 284 36.6 ± 2.2 67.8 ± 5 12.5 ± 1.1
84004 27,559 272 24.6 ± 5.3 54 13.3
88483 29,029 253 30.3 ± 2.1 58 ± 4.5 11.2 ± 1.7
88485 29,029 253 30.6 ± 1.4 11.9 ± 1.4
1
Data from Loeppky JA, Caprihan A, Luft UC: VA/Q inequality during clinical hypoxemia and its alterations. In: Shiraki K, Yousef MK, editors. Man in stressful
environments, Springfield, Ill, 1987, Thomas; pp 199-232.
2
Data from McFarland RA, Dill DB: A comparative study of the effects of reduced oxygen pressure on man during acclimatization, J Aviat Med 9:18-44, 1938.
3
Data for chronic exposure during Operation Everest II from Sutton JR, Reeves JT, Wagner PD, et al: Operation Everest II: Oxygen transport during exercise at
extreme simulated altitude, J Appl Physiol 64:1309-1321, 1988.
4
Data from near the summit of Mt Everest from Grocott MP, Martin DS, Levett DZ, et al: Arterial blood gases and oxygen content in climbers on Mount Everest,
N Engl J Med 360:140-149, 2009.
5
Data from the simulated summit of Mt Everest from Richalet JP, Robach P, Jarrot S, et al: Operation Everest III (COMEX ‘97): Effects of prolonged and progressive
hypoxia on humans during a simulated ascent to 8,848 m in a hypobaric chamber, Adv Exp Med Biol 474:297-317, 1999.
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 (standard deviation), where available. All values are for people age 20 to 40 years who were acclimatizing well.

3
 TABLE 1-2  Altitude Conversion: Barometric Pressure,*
response begins at altitudes as low as 1500 m (4921 feet) (PIO2
= 124.3 mm Hg; see Table 1-2) and within the first few minutes
Estimated Partial Pressure of Inspired Oxygen,† and to hours of high-altitude exposure. The carotid body, sensing a
the Equivalent Oxygen Fraction at Sea Level‡ decrease in PaO2, through a HIF-mediated process, signals the
central respiratory center in the medulla to increase ventila-
Meters Feet PB PIO2 FIO2 at SL tion.3,51,57 This carotid body function, the hypoxic ventilatory
response (HVR), is genetically determined89 but is influenced by
Sea level Sea level 759.6 149.1 0.209 a number of extrinsic factors. Respiratory depressants such as
1000 3281 678.7 132.2 0.185 alcohol and soporific drugs, as well as fragmented sleep, depress
1219 4000 661.8 128.7 0.180 HVR. Agents that increase general metabolism, such as caffeine
1500 4921 640.8 124.3 0.174 and coca, as well as specific respiratory stimulants, such as pro-
1524 5000 639.0 123.9 0.174 gesterone37 and almitrine,25 increase HVR. Acetazolamide, a respi-
1829 6000 616.7 119.2 0.167 ratory stimulant, acts on the central respiratory center rather than
2000 6562 604.5 116.7 0.164 on the carotid body. Physical conditioning apparently has no
2134 7000 595.1 114.7 0.161 effect on HVR. Numerous studies have shown that a good ven-
2438 8000 574.1 110.3 0.155 tilatory response enhances acclimatization and performance,77
2500 8202 569.9 109.4 0.154 and that a very low HVR may contribute to illness61 (see Acute
2743 9000 553.7 106.0 0.149 Mountain Sickness and High-Altitude Pulmonary Edema in
3000 9843 536.9 102.5 0.144 Chapter 2).
3048 10,000 533.8 101.9 0.143 As ventilation increases, hypocapnia produces alkalosis,
3353 11,000 514.5 97.9 0.137
which acts as a braking mechanism on the central respiratory
center and limits a further increase in ventilation. To compensate
3500 11,483 505.4 95.9 0.135
for the alkalosis, within 24 to 48 hours of ascent, the kidneys
3658 12,000 495.8 93.9 0.132
excrete bicarbonate, decreasing the pH toward normal; ventila-
3962 13,000 477.6 90.1 0.126 tion increases as the braking effect of the alkalosis is removed.
4000 13,123 475.4 89.7 0.126 Ventilation continues to increase slowly, reaching a maximum
4267 14,000 460.0 86.4 0.121
MOUNTAIN MEDICINE

only after 4 to 7 days at the same altitude (see Figure 1-3). The
4500 14,764 446.9 83.7 0.117 plasma bicarbonate concentration continues to drop and ventila-
4572 15,000 442.9 82.9 0.116 tion continues to increase with each successive increase in alti-
4877 16,000 426.3 79.4 0.111 tude. Persons with lower oxygen saturation at altitude have
5000 16,404 419.7 78.0 0.109 higher serum bicarbonate values. Whether the kidneys might be
5182 17,000 410.2 76.0 0.107 limiting acclimatization or whether this reflects poor respiratory
5486 18,000 394.6 72.8 0.102 drive is not clear.16 This process is greatly facilitated by acetazol-
5500 18,045 393.9 72.6 0.102 amide (see Acetazolamide Prophylaxis in Chapter 2).
5791 19,000 379.5 69.6 0.098 The paramount importance of hyperventilation is readily
6000 19,685 369.4 67.5 0.095 apparent from the following calculation: the alveolar PO2 on the
6096 20,000 364.9 66.5 0.093 summit of Mt Everest (approximately 33 mm Hg) would be
6401 21,000 350.7 63.6 0.089 reached at only 5000 m (16,404 feet) if alveolar PCO2 stayed at
PART 1

6500 21,325 346.2 62.6 0.088 40 mm Hg, limiting an ascent without supplemental oxygen to
6706 22,000 337.0 60.7 0.085 near this altitude. Table 1-1 lists the measured arterial blood gas
7000 22,966 324.2 58.0 0.081
values resulting from acclimatization to various altitudes.
7010 23,000 323.8 57.9 0.081
7315 24,000 310.9 55.2 0.077 CIRCULATION
7500 24,606 303.4 53.7 0.075
The circulatory pump is the next step in the transfer of oxygen,
7620 25,000 298.6 52.6 0.074 moving oxygenated blood from the lungs to the tissues.
7925 26,000 286.6 50.1 0.070
8000 26,247 283.7 49.5 0.069 Systemic Circulation
8230 27,000 275.0 47.7 0.067 Increased sympathetic activity on ascent causes an initial mild
8500 27,887 265.1 45.6 0.064 increase in blood pressure, moderate increases in heart rate and
8534 28,000 263.8 45.4 0.064 cardiac output, and increase in venous tone. Stroke volume is
8839 29,000 253.0 43.1 0.060 low because of decreased plasma volume, which drops as much
8848 29,029 252.7 43.1 0.060 as 12% over the first 24 hours95 as a result of the bicarbonate
9000 29,528 247.5 42.0 0.059 diuresis, a fluid shift from the intravascular space, and suppres-
9144 30,000 242.6 40.9 0.057 sion of aldosterone.7 Resting heart rate returns to near sea level
9500 31,168 230.9 38.5 0.054 values with acclimatization, except at extremely high altitude.
10,000 32,808 215.2 35.2 0.049 Maximal heart rate follows the decline in maximal oxygen uptake
with increasing altitude. As the limits of hypoxic acclimatization
FIO2, fraction of inspired oxygen; PB, barometric pressure; PIO2, partial pressure are approached, maximal and resting heart rates converge.
of inspired oxygen; SL, sea level. During Operation Everest II (OEII), cardiac function was appro-
*PB is approximated by Exponent (6.6328 − {0.1112 × altitude − [0.00149 ×
altitude2]}), where altitude is terrestrial altitude in meters/1000 or kilometers (km).
priate for the level of work performed, and cardiac output was
†PIO2 is calculated as PB − 47 × fraction of O2 in inspired air, where 47 is water not a limiting factor for performance.58,76 Interestingly, myocardial
vapor pressure at body temperature. ischemia at high altitude has not been reported in healthy
‡The equivalent FIO2 at sea level for a given altitude is calculated as persons, despite extreme hypoxemia. This is partly because of
PIO2 ÷ (760 − 47). Substituting ambient PB for 760 in the equation allows reduction in myocardial oxygen demand from reduced maximal
similar calculations for FIO2 at different altitudes.
heart rate and cardiac output. Pulmonary capillary wedge pres-
sure is low, and catheter studies have shown no evidence of left
example, their exercise performance matches that of persons at ventricular dysfunction or abnormal filling pressures in humans
sea level.8,50 at rest.24,29 On echocardiography, the left ventricle is smaller than
normal because of decreased stroke volume, whereas the right
ventricle may become enlarged.76 The abrupt increase in pulmo-
VENTILATION nary artery pressure can cause a change in left ventricular dia-
By reducing alveolar carbon dioxide, increased ventilation raises stolic function, but because of compensatory increased atrial
alveolar oxygen, improving oxygen delivery (Figure 1-3). This contraction, no overt diastolic dysfunction results.2 In trained

4
 FIGURE 1-2  Regulation of oxygen sensing by hypoxia-inducible factor

CHAPTER 1  High-Altitude Physiology

Cell proliferation Transcriptional
(HIF). HIF is produced constitutively, but in normoxia the α subunit is
Cyclin G2 regulation
degraded by the proteasome in an oxygen-dependent manner.
IGF2 DEC1
Hypoxic conditions prevent hydroxylation of the α subunit, enabling
IGF-BP1 DEC2
the active HIF transcription complex to form at the hypoxia-response
IGF-BP2 ETS-1 element (HRE) associated with HIF-regulated genes. A range of 
IGF-BP3 NUR77 cell functions are regulated by the target genes, as indicated. ADM,
WAF1 adrenomedullin; AMF, autocrine motility factor; CATHD, cathepsin 
TGF-α pH regulation D; EG-VEGF, endocrine gland–derived vascular endothelial growth
TGF-β3 Carbonic anhydrase 9 factor; ENG, endoglin; ENO1, enolase 1; EPO, erythropoietin; ET1,
endothelin-1; FN1, fibronectin 1; GAPDH, glyceraldehyde-3-phosphate- 
Cell survival Regulation of dehydrogenase; GLUT1, glucose transporter (1, 3); HK1, hexokinase 1;
ADM HIF-1 activity HK2, hexokinase 2; IGF2, insulin-like growth factor 2; IGF-BP, IGF-
EPO p35srj binding protein (1, 2, 3); KRT, keratin (14, 18, 19); LDHA, lactate
IGF2 dehydrogenase A; LEP, leptin; LRP1, LDL receptor–related protein 1;
IGF-BP1 Epithelial homeostasis MDR1, multidrug resistance gene 1; MMP2, matrix metalloproteinase
IGF-BP2 Intestinal trefoil factor 2; NOS2, nitric oxide synthase 2; PFKBF3, 6-phosphofructo-2-kinase/
IGF-BP3 fructose-2,6-biphosphatase-3; PFKL, phosphofructokinase L; PGK 1,
NOS2 phosphoglycerate kinase 1; PAI1, plasminogen-activator inhibitor 1;
Drug resistance
TGF-α PKM, pyruvate kinase M; TGF-β3, transforming growth factor-β3; TPI,
MDR1
VEGF triosephosphate isomerase; VEGF, vascular endothelial growth factor;
UPAR, urokinase plasminogen activator receptor; VIM, vimentin. (Mod-
Nucleotide metabolism ified from Semenza G: Targeting HIF-1 for cancer therapy, Nat Rev
Apoptosis Adenylate kinase 3
NIP3 Cancer 3[10]:721-732, 2003.)
Ecto-5′-nucleotidase
NIX
RTP801 Iron metabolism
Ceruloplasmin
Motility Transferrin
AMF/GPI Transferrin receptor
c-MET demonstrated that even with a mean PAP of 60 mm Hg, cardiac
LRP1 HIF-1
Glucose metabolism output remained appropriate, and right atrial pressure did not
TGF-α rise above sea level values. Thus, right ventricular function was
HK1
HK2 intact despite extreme hypoxemia and pulmonary hypertension
Cytoskeletal structure AMF/GPI in these well-acclimatized individuals.
KRT14 ENO1 Administration of oxygen does not completely restore PAP to
KRT18 GLUT1 sea level values,45 likely because of vascular remodeling with
KRT19 GAPDH medial hypertrophy. (See Stenmark and associates71,72 for excel-
VIM LDHA lent recent reviews of molecular and cellular mechanisms of the
PFKBF3 pulmonary vascular response to hypoxia, including remodeling.)
Cell adhesion PFKL PVR returns to normal within a few weeks after descent to low
MIC2 PGK1 altitude.
PKM
Erythropoiesis TPI Cerebral Circulation
EPO Cerebral oxygen delivery, the product of arterial oxygen content
Extracellular-matrix and cerebral blood flow (CBF), depends on the net balance
Angiogenesis metabolism between hypoxic vasodilation and hypocapnia-induced vasocon-
EG-VEGF CATHD striction. Despite hypocapnia, CBF increases when PaO2 is less
ENG Collagen type V (α1) than 60 mm Hg (altitude >2800 m [9186 feet]). In a classic study,
LEP FN1 CBF increased 24% on abrupt ascent to 3810 m (12,500 feet) and
LRP1 MMP2 returned to normal over 3 to 5 days.68 These findings have been
TGF-β3 PAI1 confirmed by positron emission tomography (PET) and brain
VEGF Prolyl-4-hydroxylase α (I) magnetic resonance imaging (MRI) studies showing both eleva-
UPAR
tions in CBF in hypoxia in humans and striking heterogeneity of
Vascular tone the CBF, with CBF rising up to 33% in the hypothalamus and
α1B-adrenergic receptor Energy metabolism
20% in the thalamus, and with other areas showing no significant
ADM LEP
change.9,54 Cerebral autoregulation, the process by which cerebral
ET1
Haem oxygenase-1 Amino-acid metabolism
perfusion is maintained as blood pressure varies, is impaired in
NOS2 Transglutaminase 2 hypoxia. Interestingly, this occurs with acute ascent,31,41,81,84 after
successful acclimatization,79,82 and in natives to high altitude.31
The uniform “impairment” in all humans who become hypoxic
raises questions about the importance of cerebral autoregulation,
specifically as it pertains to altitude illness (see Chapter 2 for
athletes doing an ultramarathon, the strenuous exercise at high advanced discussion on AMS and cerebral autoregulation).
altitude did not result in left ventricular damage; however, Overall, global cerebral metabolism seems well maintained with
wheezing, reversible pulmonary hypertension, and right ventricu- moderate hypoxia.1,17,49
lar dysfunction occurred in one-third of those completing the
race and resolved within 24 hours. BLOOD
Pulmonary Circulation Hematopoietic Responses to Altitude
On ascent to high altitude, a prompt but variable increase in Ever since the observation in 1890 by Viault85 that hemoglobin
pulmonary vascular resistance (PVR) from hypoxic pulmonary concentration was higher than normal in animals living in the
vasoconstriction increases pulmonary artery pressure (PAP). Mild Andes, scientists have regarded the hematopoietic response to
pulmonary hypertension is greatly augmented by exercise, with increasing altitude as an important component of the acclimatiza-
PAP reaching near-systemic values,24 especially in persons with tion process. On the other hand, hemoglobin values apparently
a prior history of HAPE.6,19 During OEII, Groves and colleagues24 have no relationship to susceptibility to high-altitude illness.

5
 (AMREE), hematocrit was reduced by hemodilution from 58%
14 ±1.3% to 50.5% ±1.5% at 5400 m (17,717 feet) with increased
cerebral functioning and no decrement in maximal oxygen

VE (L/min, BTPS)
uptake.65
12
Oxyhemoglobin Dissociation Curve
The oxygen dissociation curve (ODC) plays a crucial role in
10
oxygen transport. The sigmoidal shape of the curve allows SaO2
to be well maintained up to 3000 m (9843 feet), despite signifi-
·

8
cant decreases in PaO2 (see Figure 1-1). Above 3000 m, small
changes in PaO2 cause large changes in SaO2 (Figure 1-5). Because
40 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
PACO2 (mm Hg)

35 well preserved. At high altitude, small changes in PaO2 lead to

lower oxygen uptake that can have a large effect on systemic

30

50 Men
25
Women (+Fe)
100 48

Hematocrit (%)
46
SaO2 (%)
MOUNTAIN MEDICINE

Women (−Fe)
90
44

42
80
Sea level
0 1 2 3 4 5 40
Denver 1 20 40 60
Days at 4300 m Days at 4300 m
FIGURE 1-3  Change in minute ventilation ( V E), alveolar (end-tidal) FIGURE 1-4  Hematocrit changes on ascent to altitude in men and in
carbon dioxide partial pressure (PACO2), and arterial oxygen saturation women with (+Fe) and without (−Fe) supplemental iron. (Modified from
PART 1

(SaO2) during 5 days’ acclimatization to 4300 m (14,108 feet). BTPS, Hannon JP, Klain GJ, Sudman DM, Sullivan FJ: Nutritional aspects of
Body temperature pressure saturated. (Modified from Huang SY, Alex- high-altitude exposure in women, Am J Clin Nutr 29:604-613, 1976.)
ander JK, Grover RF, et al: Hypocapnia and sustained hypoxia blunt
ventilation on arrival at high altitude, J Appl Physiol 56:602-606, 1984.)

100 ~ No change
In response to hypoxemia, erythropoietin is secreted by the
kidneys and stimulates bone marrow production of red blood
cells (RBCs).66 The hormone is detectable within 2 hours of ~10% decrease
ascent, nucleated immature RBCs can be found on a peripheral 80
blood smear within days, and new RBCs are in circulation within
4 to 5 days. Over weeks to months, RBC mass increases in pro-
portion to the degree of hypoxemia. Iron supplementation can
be important; women who take supplemental iron at high alti- 60
SaO2 (%)

tude approach the hematocrit values of men at altitude26 (Figure

1-4). The field of erythropoietin and iron metabolism has
exploded in recent years, with discovery of two new iron-
regulating hormones, hepcidin23 and erythroferrone,10,22,34,38 and 40
a novel, soluble erythropoietin receptor with function directly
linked to performance at high altitude.86 How all these new find-
ings are integrated and their responses during acclimatization to B A
hypoxia remain to be determined. 20
The increase in hemoglobin seen 1 to 2 days after ascent is
caused by hemoconcentration secondary to decreased plasma
volume, rather than by a true increase in RBC mass. This results
in a higher hemoglobin concentration at the cost of decreased 0
blood volume, a trade-off that might impair exercise perfor- 0 20 40 60 80 100 120
mance. Longer-term acclimatization leads to an increase in PaO2 (mm Hg)
plasma volume as well as in RBC mass, thereby increasing total
blood volume. Overshoot of the hematopoietic response causes FIGURE 1-5  Oxygen-hemoglobin dissociation curve showing effect of
excessive polycythemia, which may impair oxygen transport 10–mm Hg decrement in arterial partial pressure of oxygen (PaO2) on
because of increased blood viscosity. Although the “ideal” hema- arterial oxygen saturation (SaO2) at sea level (A) and near 4400 m
tocrit at high altitude is not established, phlebotomy is often (14,436 feet) (B). Note the much larger drop in SaO2 at high altitude.
recommended when hematocrit values exceed 60% to 65%. (Modified from Severinghaus JW: Blood gas calculator, J Appl Physiol
During the American Medical Research Expedition to Mt Everest 21:1108-1116, 1966.)

6
hypoxemia, and thus on clinical status, while SaO2 may appear

CHAPTER 1  High-Altitude Physiology

180
relatively unchanged.
In 1936, Ansel Keys and colleagues35 demonstrated an in vitro Endurance time
right shift in position of the ODC at high altitude, favoring release ·
160 VO2max
of oxygen from blood to tissues. This change, caused by increased
2,3-diphosphoglycerate, is proportional to the severity of hypox-

Sea level performance (%)

emia. In vivo, however, the alkalosis at moderate altitude offsets 140
this, and no net change occurs. In contrast, the marked alkalosis
of extreme hyperventilation, as measured on the summit and 120
simulated summit of Mt Everest (PaCO2 = 8 to 10 mm Hg; pH
>7.5), shifts the ODC to the left, facilitating oxygen-hemoglobin
binding in the lung, which raises SaO2 and is advantageous.64 100
Persons with a very left-shifted ODC caused by an abnormal
hemoglobin (Andrew-Minneapolis), when taken to moderate 80
(3100 m [10,171 feet]) altitude, had less tachycardia and dyspnea
and remarkably no decrease in exercise performance.28 High-
altitude–adapted animals also have a left-shifted ODC. 60

TISSUE CHANGES
The next link in the oxygen transport chain is tissue oxygen
transfer, which depends on capillary perfusion, diffusion dis-
tance, and driving pressure of oxygen from the capillary to the
cell. Banchero5 has shown that capillary density in dog skeletal
muscle doubles in 3 weeks at PB of 435 mm Hg. A recent study
in humans noted no change in capillary density or in gene
expression thought to enhance muscle vascularity.42 Ou and
Tenney53 revealed a 40% increase in mitochondrial number but
no change in mitochondrial size, whereas Oelz and colleagues52
showed that high-altitude climbers had normal mitochondrial
density. A significant decrease in muscle size is often noted after
high-altitude expeditions because of net energy deficit, 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.42,44
EXERCISE
Maximal oxygen consumption drops dramatically on ascent to
high altitude.21,62 Maximal oxygen uptake ( VO  2 max) falls from
sea level value by approximately 10% for each 1000 m (3281
feet) of altitude gained above 1500 m (4921 feet). Persons with
the highest VO  2 max values at sea level have the largest decre-
ment in VO 2 max at high altitude, but overall performance at high
 2 max.52,60,91 In
altitude is not consistently related to sea level VO
fact, many of the world’s elite mountaineers, in contrast to other
endurance athletes, have quite average VO  2 max values.52 Accli-
matization at moderate altitudes enhances submaximal endur-
ance time but does not enhance VO  2 max (Figure 1-6).21 Two
groups recently confirmed that acclimatization leads to improve-
40
0 2 4 6 8 10 12
Days at altitude
FIGURE 1-6  On ascent to altitude, maximal oxygen consumption
 2max ) decreases and remains suppressed. In contrast, endurance
( VO
time (minutes to exhaustion at 75% of altitude-specific VO  2max)
increases with acclimatization. (Modified from Maher JT, Jones LG,
Hartley LH: Effects of high-altitude exposure on submaximal endur-
ance capacity of men, J Appl Physiol 37:895-898, 1974.)
 2 max.11 However, mechanisms to explain impaired gas
loss in VO
exchange and lower blood flow remain elusive. Wagner87 pro-
poses that the pressure gradient for diffusion of oxygen from
capillaries to the working muscle cells may be inadequate. Others
propose that increased cerebral hypoxia from exercise-induced
desaturation is the limiting factor.15,30,78,80 Mountaineers, for
example, become lightheaded and their vision dims when they
move too quickly at extreme altitude (Figure 1-7).92
40
Alveolar
Arterial
30
PO2 (torr)

ment in submaximal work capacity using field tests,39,77 and 20

Subudhi and associates77 showed that adaptation to submaximal Mixed
work performance persists for up to 3 weeks after descent to venous
Assumed critical PO2
low altitude. This occurs despite a marked drop in hemoglobin
concentration, suggesting that other factors are involved. Loss of consciousness
Oxygen transport during exercise at high altitude becomes
increasingly dependent on the ventilatory pump. The marked rise 10 ·
VO2max
in ventilation produces a sensation of breathlessness, even at low Man on summit
work levels. The following quotation is from a high-altitude PB 253 torr
mountaineer:48 DMO2 100 mL/min/torr
After every few steps, we huddle over our ice axes, mouths
agape, struggling for sufficient breath to keep our muscles 0
going. I have the feeling I am about to burst apart. As we
0 200 400 600 800 1000 1200
get higher, it becomes necessary to lie down to recover
our breath. Oxygen uptake (mL O2/min)
In contrast to the increase in ventilation with exercise, at FIGURE 1-7  Calculated changes in the oxygen partial pressure (PO2) of
increasing altitudes in OEII, cardiac function and cardiac output alveolar gas and arterial and mixed venous blood as oxygen uptake is
were maintained at or near sea level values for a given oxygen increased for a climber on the summit of Mt Everest. Unconsciousness
consumption (workload).58 Recent work attributed the altitude- develops at a mixed venous PO2 of 15 mm Hg. PB, Barometric pressure;
induced drop to the lower PIO2, impairment of pulmonary  2max , maximal oxygen consump-
DMO , muscle-diffusing capacity; VO
2

gas exchange, and reduction of maximal cardiac output and tion (intake). (Modified from West J: Human physiology at extreme
peak leg blood flow, each explaining about one-third of the altitudes on Mount Everest, Science 223[4638]:784-788, 1984.)

7
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 >3 minutes) at altitudes above
2000 m (6562 feet), acclimatization for 10 to 20 days is necessary
to maximize performance.18 For events occurring above 4000 m
(13,123 feet), acclimatization at an intermediate altitude is recom-
mended. Highly anaerobic events at intermediate altitudes require
only arrival at the time of the event, although AMS may become
a problem.
The benefits of training at high altitude for subsequent per-
formance at or near sea level depend on choosing the training
altitude that maximizes the benefits and minimizes the inevitable
“detraining” when VO  2 max is limited (altitude >1500 to 2000 m
[4921 to 6562 feet]). Therefore, 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.33,83 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.4 The “live high–train low” approach pioneered by
Levine and Stray-Gundersen40,74 has been adopted by many
endurance athletes. The optimal dose for specific sports is still
being determined,12,13,94 but overall, endurance athletes believe
and science supports a small but significant improvement in sea
level performance after participating in a live high–train low
training camp.75 The benefit appears to result from enhanced
erythropoietin production and increased RBC mass, which
requires adequate iron stores and thus usually iron supplementa-
tion.46,63,73 Some individuals do not respond to the live high–train
low approach, perhaps related to genetic polymorphisms and
inability to increase erythropoietin levels sufficiently to increase
RBC mass and thus increase oxygen-carrying capacity.12,14,32
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 CHAPTER 2 
High-Altitude Medicine and
Pathophysiology
PETER H. HACKETT, ANDREW M. LUKS, JUSTIN S. LAWLEY, AND ROBERT C. ROACH
Increasingly, physicians and other health care providers are con-
fronted with questions of prevention and treatment of high-
altitude medical problems (Box 2-1). Despite advances in
high-altitude medicine, significant morbidity and mortality persist
(Table 2-1). Clearly, better education of the population at risk
and those advising them is essential. Given the number of
persons impacted, altitude illness should be considered a public
health problem. In this chapter, we review recognition, patho-
physiology, and management of medical problems for high-
altitude visitors and residents.
HIGH-ALTITUDE SYNDROMES
High-altitude syndromes are attributed directly to hypobaric
hypoxia. Clinically, these syndromes overlap. Rapidity of hypoxia
exposure is crucial in determining the syndrome. 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 acute mountain sickness (AMS) or no
illness at all. An example of overlap is the vague line between
acute hypoxia of more than 1-hour duration and AMS, as reflected
in the classic experiments of Bert.47 For neurologic syndromes,
the spectrum of illness encompasses high-altitude headache,
AMS, and high-altitude cerebral edema (HACE) (Table 2-2). The
pulmonary problems range from pulmonary hypertension to
interstitial and alveolar edema (HAPE). These problems all occur
within the first few days of ascent to a higher altitude and have
many common features, and patients respond to descent or
oxygen, thus reflecting some commonality of pathogenesis.
Longer-term problems of altitude exposure include high-altitude
deterioration in sojourners and chronic mountain sickness, pul-
monary hypertension, and right-sided heart failure in high-altitude
residents.
8
ACUTE CEREBRAL HYPOXIA
Acute, profound hypoxemia, although of greatest interest in avia-
tion medicine, may also occur when ascent is too rapid or
hypoxia abruptly worsens. Carbon monoxide (CO) poisoning,
pulmonary edema, sudden overexertion, sleep apnea, or a failed
oxygen delivery device may rapidly impair blood and tissue
oxygenation. Unacclimatized persons become unconscious from
acute hypoxia at arterial oxygen saturation (SaO2) of 40% to
60%, arterial oxygen partial pressure (PaO2) of less than about
30 mm Hg, or mixed venous PO2 of 15 mm Hg. The effects of
acute severe hypoxia are best described by Tissandier, the sole
survivor of the flight of the balloon Zenith in 1875, who gave a
graphic description of the effects of their overly rapid ascent to
very high elevation:
But soon I was keeping absolutely motionless, without
suspecting that perhaps I had already lost use of my move-
ments. 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 con-
trary. 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
 in oxygen. Both will die after having presented the same

CHAPTER 2  High-Altitude Medicine and Pathophysiology

BOX 2-1  Medical Problems of High Altitude
Lowlanders on Ascent to Altitude
Acute hypoxia
High-altitude headache
Acute mountain sickness
High-altitude cerebral edema
Focal neurologic conditions
High-altitude pulmonary edema
Symptomatic pulmonary hypertension
High-altitude deterioration
Organic brain syndrome (extreme altitude)
Peripheral edema
High-altitude retinal hemorrhage
Impaired sleep
Nocturnal periodic breathing
High-altitude pharyngitis, bronchitis, and cough
Ultraviolet keratitis (snowblindness)
Exacerbation of preexisting medical conditions
Lifetime or Long-Term Residents of Altitude
Chronic mountain sickness (chronic mountain polycythemia)
Symptomatic high-altitude pulmonary hypertension with or without
right-sided heart failure
Problems of pregnancy: preeclampsia, hypertension, and
low-birth-weight infants
Reentry high-altitude pulmonary edema
out “We are at 8,000 meters.” But my tongue was para-
lyzed. Suddenly I closed my eyes and fell inert, completely
losing consciousness.47
The ascent to over 8000 m (26,247 feet) took 3 hours, and
the descent less than 1 hour. When the balloon landed, Tis-
sandier’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 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
symptoms.47
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 alti-
tudes, very quickly also … the normal proportion of
oxygen reappears in the blood. There is an unfailing con-
nection here.47
Bert was also able to prevent and immediately resolve symp-
toms by breathing oxygen. Modern studies of acute hypoxic
exposure use the measurement of “time of useful consciousness,”
that is, the time until a person can no longer take corrective
measures, such as putting on an oxygen mask. For a sea level
resident with exposure to 8500 m (27,887 feet), that time is 60
seconds during moderate activity and 90 seconds at rest.
Acute hypoxemia can be quickly reversed by immediate
administration of oxygen, rapid pressurization or descent, or cor-
rection of an underlying cause, such as relief of apnea, repair of
an oxygen delivery device, or cessation of overexertion. Hyper-
ventilation increases alveolar oxygen pressure (PAO2) and 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 patho-
physiology and treatment of HAH have been reported. Ravenhill,
writing in 1913, first described the headache of AMS, which is
the same as HAH:
It is a curious fact that symptoms of puna do not usually
evince themselves at once. The majority of newcomers
have expressed themselves as being quite well on first
arrival. As a rule, towards the evening the patient begins
to feel rather slack and disinclined for exertion. He goes
to bed, but has a restless and troubled night, and wakes
up the next morning with a severe frontal headache.
There may be vomiting, frequently there is a sense of

TABLE 2-1  Incidence of Altitude Illness in Various Groups

Number Sleeping Maximum Average Percent with

at Risk Altitude Altitude Rate of Percent HAPE and/or
Study Group per Year (m [ft]) Reached (m [ft]) Ascent* with AMS HACE Reference

Western state visitors 30 million ~2000 (6562) 3500 (11,483) 1-2 18-20 0.01 178
~2500 (8202) 22
~≥3000 (9843) 27-42
Mt Everest trekkers 37,000† 3000-5200 5500 (18,045) 1-2 (fly in) 47 1.6 155
(9843-17,060) 10-13 (walk in) 23 0.05
30-50 310
Denali climbers 1200 3000-5300 6194 (20,322) 3-7 30 2-3 148
(9843-17,388)
Mt Rainier climbers 10,000 3000 (9843) 4392 (14,409) 1-2 67 — 238
Mt Rosa, Swiss Alps ‡ 2850 (9350) 2850 (9350) 1-2 7 — 270
4559 (14,957) 4559 (14,957) 2-3 27 5 99, 270, 390
Indian soldiers Unknown 3000-5500 5500 (18,045) 1-2 ‡ 2.3-15.5 409, 410
(9843-18,045)
Aconcagua climbers 4200 3300-5800 6962 (22,841) 2-8 39 (LLS >4) 2.2 332
(10,827-19,029)

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.
†Data for 2014, extracted from Sagarmatha National Park entry station, Jorsale Nepal, on March 26, 2015.
‡Reliable estimate unavailable.

9
 TABLE 2-2  Clinical Characteristics of Neurologic High-Altitude Illnesses
Clinical Classification
HAH Mild AMS
Symptoms Headache only Headache plus one more
symptom (nausea/vomiting,
fatigue/lassitude, dizziness,
or difficulty sleeping)
Symptoms of mild severity
LL-AMS score* 1-3, headache only 2-4
Physical signs None None
Findings None None
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.
*Lake Louise self-reported score. (From Roach RC, Bärtsch P, Oelz O, Hackett PH: The Lake Louise acute mountain sickness scoring system. In Sutton JR, Houston CS,
Coates G, editors: Hypoxia and molecular medicine, Burlington, Vt, 1993, Queen City Press, pp 272-274.)
MOUNTAIN MEDICINE
oppression in the chest, but there is rarely any respiratory
distress or alteration in the normal rate of breathing so
long as the patient is at rest. The patient may feel slightly
giddy on rising from bed, and any attempt at exertion
increases the headache, which is nearly always confined
to the frontal region.344
Drawing a distinction between HAH and AMS is rather
PART 1
artificial because they overlap. Headache is generally the first
unpleasant—and sometimes the only—symptom resulting from
high-altitude exposure.178 Headache without other symptoms is
called HAH, and if associated with other typical symptoms, it is
called AMS. Therefore, investigations on HAH are also to some
extent studies of AMS. Headache lends itself to investigation
better than some other symptoms because headache scores have
been well validated.199 One could argue that the headache itself
causes other symptoms, such as anorexia, nausea, lassitude, and
insomnia, as often seen in migraine or tension headaches, and
that mild AMS is essentially caused by headache.
Researchers have attempted to characterize the clinical fea-
tures and incidence of headache at altitude. In one study, 50 of
60 trekkers (83%) in Nepal up to 5100 m (16,732 feet) devel-
oped at least one headache when over 3000 m (9843 feet).406
Older persons were less susceptible; women and those with
headaches in daily life had more severe headaches, but no more
headaches than did others. Of those with headache, 52% did not
have AMS by the Lake Louise criteria. Although the clinical fea-
tures were widely variable, in general the headaches were mild
to severe in intensity, frontal (41%) or frontal-temporal (23%),
bilateral (81%), dull (53%) or pulsatile (32%), exacerbated by
exertion or movement (81%), often occurred at night, had onset
in the first 24 hours at a new altitude, and resolved within the
next 24 hours. The headaches were considered to have some
features of increased intracranial pressure. Persons with history
of migraine did not have a higher incidence of headache. In
contrast, another investigator found a history of migraine associ-
ated with a higher incidence of headache at altitude.62 Various
medications alleviated the headaches, especially mild ones, in
70% of cases. Based on these investigations, the International
Headache Society has defined HAH as headache developing
after ascent to altitude above 2500 m (8202 feet) and resolving
within 24 hours of descent and having at least two of the
following characteristics: (1) bilateral, (2) mild or moderate
intensity, and (3) aggravated by exertion, movement, straining,
10
Moderate to Severe AMS HACE
Headache plus one or more ±Headache
symptoms (nausea/vomiting, Worsening of symptoms seen
fatigue/lassitude, dizziness, in moderate to severe AMS
or difficulty sleeping)
Symptoms of moderate to
severe intensity
5-15 —
None Ataxia
Altered mental status
Papilledema; concurrent HAPE
common
Antidiuresis Positive chest radiograph if
Slight desaturation HAPE present,
Widened A-a gradient Elevated ICP
White matter edema in some White matter edema (CT, MRI)
(CT, MRI)
coughing, or bending.443 This may not be useful for diagnosis,
however, because headaches from a variety of causes fulfill
these criteria.
Pathophysiology
Sanchez del Rio and Moskowitz381 have provided a useful mul-
tifactorial concept of the pathogenesis of HAH, based on current
understanding of headaches in general. They suggest that the
trigeminovascular system is activated at altitude by both mechani-
cal and chemical stimuli (vasodilation, nitric oxide, and other
noxious agents), and that the threshold for pain is likely altered
at high altitude (Figure 2-1). If AMS and especially HACE ensue,
altered intracranial dynamics may also play a role, through
compression or distention of pain-sensitive structures (see AMS
Pathophysiology, below). Oxygen is often immediately (within
10 minutes) effective for HAH in persons with and without
AMS, which indicates a rapidly reversible mechanism of the
headache, most likely related to cerebral vasodilation with in-
creased cerebral blood flow and cerebral blood volume.21,159 More
investigation should lead to a better understanding of the patho-
physiology of these often debilitating headaches, as well as new
treatments.
Prevention and Treatment
In general, HAH can be prevented by nonsteroidal antiinflamma-
tory drugs (NSAIDs),325 acetaminophen,170 and the drugs typically
used for prophylaxis of AMS, acetazolamide and dexamethasone
(Table 2-3). Some agents appear more effective than others, with
ibuprofen and aspirin apparently superior to naproxen.57,60,63
Sumatriptan, a serotonin type 1 (5-HT1) receptor agonist, was
reported to be effective for HAH prevention and treatment in
some studies61,198 but not in others.23 Flunarizine, a specific
calcium antagonist used for treatment of migraine, was not effec-
tive for HAH in one study.38 The response to different agents
might reflect multiple components of HAH pathophysiology or
merely the nonspecific nature of many analgesics.
ACUTE MOUNTAIN SICKNESS
Epidemiology and Risk Factors
Although the syndrome of AMS has been recognized for centu-
ries, modern rapid transportation and proliferation of participants
in mountain sports have increased the number of persons affected
and therefore public awareness (see Table 2-1). Incidence and
 CHAPTER 2  High-Altitude Medicine and Pathophysiology
Hypothalamus Autonomic
Brainstem response
Lower threshold
for pain

Trigeminovascular CNS High-altitude

Hypoxia
system activation processing headache

eNOS
upregulation ↑ NO

FIGURE 2-1  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.)

severity of AMS depend on rate of ascent and altitude attained
(especially sleeping altitude), duration of altitude exposure, level
of exertion, recent altitude exposure, and inherent physiologic
(genetic) susceptibility.49,156,364,390 For example, AMS is more
common on Mt Rainier because of rapid ascents, whereas high-
altitude pulmonary or cerebral edema is uncommon because of
short duration (<36 hours) of exposure on the mountain. Persons
with demonstrated susceptibility to AMS had twice the incidence
of AMS compared with nonsusceptible persons, independent of
rate of ascent.390 The basis for inherent susceptibility is still
unknown.
Acclimatization induced by recent altitude exposure can be
protective; 4 nights 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 and was as effective as slow
ascent390 (Figure 2-2). Repeated overnight normobaric hypoxia
exposures before ascent may also have a preventive effect.90,130
Depending on the duration of stay at high altitude, the pro-
tective effects of acclimatization persist after descent to low
altitude. AMS did not develop in persons who acclimatized to
4300 m (14,108 feet) for 16 days, returned to low altitude for 8
days, and then were reexposed to high altitude in a hypobaric
chamber.265 In addition, ventilation, SaO2, and exercise perfor-
mance at altitude were maintained for at least 7 days after accli-
matization,41,265,311 with some enhanced physical performance
retained for several weeks.53,54,122,226,227 Epidemiologic studies
suggest that protection from AMS may persist for months after
acclimatization for 2 or more weeks.390,486 Retention of aug-
mented hypoxic ventilatory response (HVR) might explain these
results;255,359 however, studies showed that HVR returned to pre-
ascent values 7 days after descent.311 Recently, the AltitudeOmics
project confirmed many of these findings, with retention of
acclimatization for protection from AMS and improvement in
exercise performance lasting for up to 3 weeks after 16 days
of acclimatization.112,120,141,360,377,426-428 It was proposed that altered
gene expression was maintained after acclimatization through
DNA methylation and hypoxia-sensitive microRNAs (so-called
hypoxamirs),234,257 and that these processes may account for at
least part of the memory of acclimatization.109
Compared with persons living at a lower altitude, residents at
900 m (2953 feet) or above had less AMS (8% vs. 27%) when
ascending to between 2000 and 3000 m (6562 and 9843 feet) in
Colorado.178 Age may have an influence on incidence,156 with
persons older than 50 years somewhat less vulnerable.363,406 In a
large study in Colorado, persons older than 60 years had one-half
the incidence of AMS as those under 60, whereas a study of 827
mountaineers in Europe showed no influence of age on suscep-
tibility.390 Different populations and physical activity may explain
differing results. No study has ever shown older people to be
more susceptible. The evidence regarding risk of AMS in children

TABLE 2-3  Recommended Dosages for Medications Used in the Prevention and Treatment of Altitude Illness

Medication Indication Route Dosage

Acetazolamide AMS, HACE prevention Oral 125 mg bid

Pediatric dose: 2.5 mg/kg/dose q12h, max 125 mg
AMS treatment Oral 250 mg bid
Pediatric dose: 2.5 mg/kg/dose q12h, max 250 mg
Dexamethasone AMS, HACE prevention Oral 2-4 mg q6h or 4 mg q12h (see text)
Pediatrics: should not be used for prophylaxis
AMS, HACE treatment Oral, IV, IM AMS: 4 mg q6h
HACE: 8 mg once then 4 mg q6h
Pediatric dose: 0.15 mg/kg/dose q6h up to 4 mg
Nifedipine HAPE treatment Oral 30 mg SR version q12h
HAPE prevention Oral 30 mg SR version q12h
Tadalafil HAPE prevention Oral 10 mg bid
Sildenafil HAPE prevention Oral 50 mg q8h
Salmeterol HAPE prevention Inhaled 125 mcg bid*

Modified from Luks AM, McIntosh SE, Grissom CK, et al: Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness:
2014 update, Wilderness Environ Med 25:S4-S14, 2014.
AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema; IM, intramuscular; IV, intravenous; SR, sustained-release;
bid, twice daily; q, every; h, hours; mcg, micrograms.
*Should not be used as monotherapy and should only be used in conjunction with oral medications.

11
 70%
Nonsusceptible
60% Susceptible
50%
Prevalence of AMS
40%
30%
20%
10%
0%
Ascent >3 days Either ascent Ascent <4 days
and preexposure >3 days or and preexposure
≥5 days preexposure <5 days
≥5 days
Rate of ascent and preexposure
FIGURE 2-2  Prevalence of acute mountain sickness (AMS) and 95%
MOUNTAIN MEDICINE
confidence intervals in nonsusceptible (blue bars) and susceptible (red
bars) mountaineers in relation to the state of acclimatization defined
as slow ascent (>3 days), fast ascent (≤3 days), preexposed (≥5 days
above 3000 m [9843 feet] in preceding 2 months), and not preexposed
(≤4 days above 3000 m in preceding 2 months). (Modified from
Schneider M, Bernasch D, Weymann J, et al: Acute mountain sickness:
Influence of susceptibility, preexposure, and ascent rate, Med Sci
Sports Exerc 34:1886-1891, 2002.)
is mixed. Children from 3 months to puberty studied in Colorado
PART 1
had the same incidence as did young adults,444,494 whereas a small
study of tourists in Chile found lower oxygen saturation (SpO2)
and higher AMS in those age 6 to 48 months at 4440 m (14,567
feet).304 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%, respec-
tively.480 Kriemler and colleagues229 found a lower prevalence of
AMS in children than in adolescents and adults on the first day
at 3500 m (11,483 feet). The subjective nature of symptom report-
ing is problematic, especially in children, and must be taken into
account when interpreting these studies.416
Women apparently have the same incidence390 or slightly
greater incidence156,178,455 of AMS but may be less susceptible
to pulmonary edema.85,415 Most studies show no relationship
between physical fitness and susceptibility to AMS. However,
obesity seems to increase the risk of developing AMS.178,355 The
relationship of tobacco smoking to AMS is unclear. A recent study
demonstrated that smoking was a risk factor for AMS in workers
at a mine at 4000 m (13,123 feet), with an odds ratio of 1.9 for
every 10 cigarettes smoked per day.456 Although one study
reported smoking as a risk factor for AMS in trekkers,283 most
studies in trekkers and tourists have found no such relation-
ship,178,210,355 and some have reported apparent reduction in AMS
in persons who smoked.414,484,495 There is no good evidence that
the use of oral contraceptives increases risk for AMS.210,322
In summary, the most important variables related to AMS
susceptibly are genetic predisposition, altitude of residence, alti-
tude reached, rate of ascent, and prior recent altitude exposure.
It remains difficult to move beyond these established risk
factors and accurately predict which individuals are susceptible
to severe AMS, HACE, and high-altitude pulmonary edema
(HAPE). Canoui-Poitrine66 and Richalet353 and colleagues have
proposed a prediction tool that takes into account a variety of
clinical and physiologic factors, including ventilatory and gas
exchange responses during hypoxic exercise. This model, based
on a large derivation cohort and subsequently validated in a
12
similarly large cohort, seems to perform well. However, the
requirement for conducting an exercise test in hypoxic conditions
limits its wide applicability, particularly in travel clinics and
primary care clinics, where many high-altitude travelers obtain
consultation before their trip.
Diagnosis
Diagnosis of AMS is based on setting, symptoms, and exclusion
of other illnesses. The setting is generally rapid ascent of unac-
climatized persons to 2500 m (8202 feet) or higher from altitudes
below 1000 m (3281 feet), although AMS has been reported at
altitude as low as 2000 m (6562 feet).301 For persons recently
acclimatized, AMS can occur from abrupt ascent to a higher
altitude, overexertion, use of respiratory depressants, and perhaps
onset of infectious illness.310
The cardinal symptom of early AMS is headache, followed in
incidence by fatigue, dizziness, and anorexia.156,178,410 The head-
ache is usually throbbing, bitemporal, typically worse during the
night and on awakening, and made worse by the Valsalva maneu-
ver or stooping over (see High-Altitude Headache, earlier).
Decreased appetite and nausea are common. These initial symp-
toms are highly nonspecific and similar to those seen in other
situations, such as alcohol hangover and dehydration. Frequent
awakening may fragment sleep, and periodic breathing often
produces a feeling of suffocation. Although difficulty with sleep
is almost universal at high altitude, also affecting persons without
AMS, these symptoms may be exaggerated during AMS. Affected
persons usually complain of a deep inner chill, unlike mere
exposure to cold temperature, accompanied by facial pallor.
Other symptoms may include vomiting, especially in children,
and irritability. Lassitude can be disabling, with the patient too
apathetic to contribute to basic needs. Although pulmonary symp-
toms such as cough and dyspnea on exertion are quite common
at high altitude, these are not features of AMS. Worsening respira-
tory symptoms or dyspnea at rest should prompt further evalu-
ation, with the primary concern being HAPE rather than AMS.
Specific physical findings are lacking in mild AMS. A higher
heart rate has been noted in persons with AMS,29,322 but Singh
and associates410 noted bradycardia (heart rate <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,270 but this has also been observed in
persons without AMS.153 Slightly increased body temperature with
AMS may be present but is not diagnostic.267 Peripheral oxygen
saturation measured by pulse oximetry (SpO2) correlated poorly
with presence of AMS during rapid ascent322,363,369 but was related
to AMS during trekking.34,225 Although these studies suggest that
pulse oximetry is of limited utility in diagnosing AMS, others
suggest it may be useful for predicting who will develop AMS
with further ascent.206,361 It seems clear that higher-than-average
SpO2 is associated with wellness and lack of AMS.
Funduscopy reveals venous tortuosity and dilation; retinal
hemorrhages may or may not be present and are neither diag-
nostic nor specific for AMS. Although more common in AMS than
in non-AMS individuals at 4243 m (13,921 feet),153 a study exam-
ining retinal hemorrhages in climbers on Muztagh Ata suggests
these are not a harbinger of impending severe altitude illness.18
Absence of the normal altitude diuresis, evidenced by lack of
increased urine output accompanied by retention of fluid, is an
early finding in AMS, although not always present.30,155,253,410,433
Neurologic signs, including altered mental status and ataxia, are
not a feature of AMS and, when present, should raise concern
for HACE (see later).
Because there are no characteristic physical examination find-
ings, the severity of AMS is classified solely on the basis of
symptoms (see Table 2-2).
Differential Diagnosis
Given the nonspecific nature of the symptoms, AMS is frequently
confused with other conditions (Box 2-2). AMS is most often
misdiagnosed as a viral flulike illness, hangover, exhaustion,
dehydration, or medication or drug effect. Unlike infectious
illness, uncomplicated AMS is not associated with fever and
myalgia. Hangover is excluded by history, whereas dehydration

BOX 2-2  Differential Diagnosis of High-Altitude
Illnesses
Acute mountain Dehydration, exhaustion, alcohol hangover,
sickness and hypothermia, carbon monoxide poisoning,
high-altitude migraine, hyponatremia, hypoglycemia,
cerebral diabetic ketoacidosis, central nervous system
edema infection, transient ischemic attack, ruptured
cerebral arteriovenous malformation or
aneurysm, stroke, seizures, brain tumors,
ingestion of toxins or drugs, acute psychosis
High-altitude Asthma exacerbation, acute bronchitis,
pulmonary pneumonia, mucus plugging,
edema hyperventilation syndrome, pulmonary
embolism, heart failure, myocardial
infarction, pneumothorax
can be distinguished from AMS by response to fluid administra-
tion. AMS is not improved by fluid administration alone; contrary
to conventional wisdom, body hydration does not influence AMS
susceptibility.12,68 Migraine may be difficult to distinguish from
AMS but may be distinguished by observing the response to
oxygen administration or descent. Hyponatremia, caused by
volume depletion or more likely excessive free water intake, can
mimic AMS and in severe cases HACE,417 but it is difficult to
diagnose in the field without access to laboratory studies. Sei-
zures are much more common in hyponatremia than in HACE.
CO toxicity should always be considered for persons cooking in
poorly ventilated tents or snow shelters.
Pathophysiology
The basic cause of HAH and AMS is hypoxemia (Figure 2-3).
However, symptoms are somewhat worse with hypobaric hypoxia
than with normobaric hypoxia, implying hypobaria plays a minor
role, most likely through its effect on fluid retention.197,212,253,254,365
Because of a time lag in onset of symptoms after ascent and lack
of complete reversal of all symptoms with oxygen, AMS is
thought to be secondary to the body’s responses to modest
hypoxia. Even though an altitude of 2500 to 2700 m (8202 to
8858 feet) presents only a minor decrement in arterial oxygen
transport (SaO2 still >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 hypoven-
tilation,282,302 impaired gas exchange (interstitial edema),144,238 fluid
retention and redistribution,30,253,254,433 and increased sympathetic
drive.26,29 Physiologic and pathologic processes, including report-
ing of symptoms, occur concurrently and in a hypoxic dose-
dependent manner; thus, epiphenomena are common. and
discriminating physiology from pathophysiology is difficult.
Mechanisms of Acute Mountain Sickness.  For decades,
clinicians have postulated that AMS is a mild form of cerebral
edema. Although this appears true for severe AMS,124,166,184,230,248,281,410
it now seems unlikely that mild to moderate AMS, or high-altitude
headache alone, is due to brain edema.195,204,241,306,397 In most
studies, brain volume increases slightly in most persons ascend-
ing rapidly to moderate altitude,15,103,240,274,306 but without a clear
link to HAH or AMS. Available data portray a clear picture of
increased brain volume immediately on exposure to altitude,
increasing over the first 10 hours, and remaining elevated through
32 hours. Spatial compensation occurs, made evident by decreased
cerebrospinal fluid (CSF) volume. Thus, total intracranial volume
remains normal, although with interindividual variability.240 The
link between increasing brain volume and susceptibility to AMS
may be explained by the tight-fit hypothesis.
The Tight-Fit Hypothesis.  Intracranial compliance is a
measure of the brain’s ability to buffer changes in volume without
significant increases in pressure. However, as brain volume
increases, intracranial compliance is reduced.243 When spatial
compensatory mechanisms are exhausted, intracranial pressure
(ICP) rises. Spatial compensation is largely determined by CSF
dynamics, particularly compliance of the spinal sac, CSF outflow
resistance, and pressure gradients across the arachnoid villi. Rate
and magnitude of volume expansion are mostly determined by
CHAPTER 2  High-Altitude Medicine and Pathophysiology
altitude gain, ascent rate, cerebrovascular reactivity to hypoxia
and carbon dioxide, and susceptibility to develop vasogenic brain
edema (Figure 2-3).
Ross375 hypothesized 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. Displacement of CSF
through the foramen magnum into the spinal canal is the first
compensatory response to increased brain volume, followed by
increased CSF absorption and decreased CSF formation. In light
of our present understanding of increased brain volume on
ascent to altitude, this hypothesis is still very attractive. Prelimi-
nary data that showed a relationship between preascent ventricu-
lar size or brain volume/cranial vault ratios and susceptibility to
AMS support this hypothesis.150,204,475,496 Moreover, robust evi-
dence suggests that intracranial compliance is altered,228,240,489 and
that although ICP might not be elevated at rest, it rises abruptly
with isometric maneuvers such as lifting a pack, with Valsalva
maneuver, or even with turning the head, which slightly elevates
sagittal venous pressure.171,475 Pressure waves may be observed
spontaneously450 or after hypotensive stimuli because of further
transient increases in intracranial blood volume caused by auto-
regulation.357 Intracranial compliance and the tight-fit hypothesis
in HAH and AMS deserve further study.
Intracranial Pressure.  In individuals with moderate to
severe AMS and HACE, ICP is elevated.184,230,281,410,472 Therefore, it
is certain that exposure to a hypoxic environment can lead to
increases in ICP, either because intracranial volume exceeds
craniospinal compensatory capacity or because sagittal sinus
pressure becomes elevated, or both. It is currently unknown
whether altered CSF dynamics and elevated ICP can explain
susceptibility to mild forms of mountain sickness (Figure 2-3).
In one report, a neurosurgeon measured ICP changes from a
self-implanted ICP-monitoring bolt in himself and in two others.475
ICP increased slightly (~5 mm Hg) in two of the three at rest,
but the single participant with AMS showed a dramatic increase
in ICP even on minimal exertion. This study is consistent with
recent indirect assessment of elevated ICP in AMS patients based
on optic nerve sheath diameter116,429 and magnetic resonance
imaging (MRI).240 A study that measured opening lumbar pressure
revealed significant elevations in AMS patients compared with
controls or after AMS resolved.410 In contrast, one recent study
of normobaric hypoxia reported no elevation of ICP in AMS
patients when measured indirectly by repeat lumbar puncture
after 16 hours of the hypoxia.204 This result should not be pre-
sumed to be contradictory, but in fact may support the major
role of spatial compensation in normalizing ICP during prolonged
periods of hypoxia.
Hypoxia can cause intracranial venous hypertension,240,471,473,474
but the impact on HAH and AMS is uncertain. Wilson and col-
leagues473 observed modest correlation between cerebral venous
sinus blood flow in normoxia and HAH, implying an anatomic
venous outflow predisposition to altitude illness. However,
despite quantitative analysis of venous sinus morphology, this
observation has not been replicated.240 Further research is needed
to delineate the possible role of cerebral venous hypertension in
the pathology of high-altitude illness.
In contrast to the steady-state condition, ICP is subject to
normal and pathologic fluctuations. The best example and analog
of AMS may be patients with idiopathic intracranial hypertension
without papilledema. In these patients, steady-state ICP remains
normal for prolonged periods, but pathologic pressure waves are
observed, especially during sleep. Headache is the primary com-
plaint in these patients.
Treatment
Management of AMS is based on severity of illness at presenta-
tion, 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 2-3 and Table 2-3). Proceeding
to a higher sleeping altitude in the presence of symptoms is
contraindicated. The person must be carefully monitored for
progression of illness. If symptoms worsen despite 24 hours of
13
 Blood pressure Hypoxia
Vessel deformation
Trigeminal vascular activation Arterial and venous dilatation

Cerebral blood volume

Sagittal sinus
pressure
Psag
Pain

Transverse sinus
ICP stenosis

Acute Mountain Sickness

• Headache
• Fatigue Spatial compensation
• Dizziness
• Nausea/vomiting
Normalized steady-state ICP

Acclimatization
Transient increases in ICP Overexpression of
• Reduced cerebral blood flow and volume
(exercise, Valsalva, sleep apnea, hypertension and corticotropin releasing factor
MOUNTAIN MEDICINE

• Normalized intracranial CSF dynamics

• Desensitization of pain pathways hypotension)

Blood pressure Enhanced glymphatic

oscillations Arterial/venous pulsatilty water influx via
water channel aquaporin-4
(2)
Inflammation
VEGF Disruption of the
Cytokines blood-brain barrier
ROS
PART 1

(1)

Uncompensated elevation in brain volume

ICP
High-altitude cerebral edema
• Ataxic gait
• Altered consciousness
FIGURE 2-3  Pathophysiology of cerebral forms of altitude illness. Hypoxemia initially causes an increase in
arterial and venous blood volume and acute rise in intracranial pressure (ICP). Over time, translocation of
cerebrospinal fluid (CSF) into the spinal canal and increased CSF absorption (spatial compensation) returns
mean ICP to normal levels. However, if transverse sinus stenosis and elevated sagittal sinus pressure (Psag)
are present, ICP remains elevated (ICP must be higher than Psag to maintain CSF absorption through arach-
noid villi). Irrespective of the steady-state ICP, intracranial compliance is reduced, and large transient fluctua-
tions in ICP will occur (1) during transient increases in Psag (i.e., during Valsalva maneuver), (2) with increases
in blood pressure, and (3) with small increases in intracranial volume after hypotensive stimuli because of
autoregulation. Four hemodynamic mechanisms are proposed to independently or in combination cause
vessel deformation and activation of the trigeminal vascular system, leading to headache and symptoms of
acute mountain sickness (AMS). Hypoxic release of chemical mediators may also directly sensitize or activate
trigeminal vascular fibers (see Figure 2-1). The fact that several factors could potentially cause headache and
symptoms of AMS may explain the preponderance of headache and variability in symptom intensity with
rapid ascent to very high altitude. Although dependent on ascent rate and altitude gain, persons resistant
to AMS may exhibit an advantageous physiologic response at any stage in this schema (i.e., greater ventila-
tory drive and PaO2 at any given altitude, lower cerebrovascular reactivity to hypoxia, greater spatial com-
pensatory capacity, or a low nociceptive threshold for trigeminal activation or pain processing). Increased
leakiness of endothelial tight junctions from circulating inflammatory mediators, in concert with blood
pressure–dependent opening of the blood-brain barrier, may lead to fluid flux into the cerebral parenchyma
from the vascular space (1). Alternatively, increased brain water may originate from the CSF via the newly
discovered glymphatic (paraarterial pathway) system (2). Overexpression of corticotropin-releasing factor
and increased arterial pulse pressure may contribute to fluid influx through the glial-bound water channel
aquaporin-4 and explain the early accumulation of intracellular water seen on MRI. In contrast to opening of
the blood-brain barrier, alterations in interstitial osmotic potential would “pull” more fluid into the brain,
leading to brain edema and diagnosis of high-altitude cerebral edema (HACE). Brain edema may occur in
many individuals who ascend rapidly and sleep at very high altitude. Brain edema would lead to further
enlargement of brain volume and ICP. Persons with poor spatial compensatory capacity will experience ataxic
14 gait, altered consciousness, and ultimately death. Dashed lines indicate new theoretical processes with
limited available data. ROS, Reactive oxygen species; VEGF, vascular endothelial growth factor.
 Singh and colleagues410 successfully used furosemide (80 mg

CHAPTER 2  High-Altitude Medicine and Pathophysiology

BOX 2-3  Field Treatment of High-Altitude Conditions
twice daily for 2 days) to treat 446 soldiers with all degrees of
High-Altitude Headache and Mild Acute Mountain Sickness AMS; furosemide induced brisk diuresis, relieved pulmonary
Stop ascent, rest, and acclimatize at same altitude. congestion, and improved headache and other neurologic symp-
Symptomatic treatment as necessary with analgesics and toms.410 It has not since been studied for treatment and is not
antiemetics considered part of standard protocols at this time.262 Spironolac-
Consider acetazolamide, 125 to 250 mg bid, to speed tone, hydrochlorothiazide, and other diuretics have not yet been
acclimatization. evaluated for treatment (see Prevention).262
or Descend 500 m (1640 ft) or more The steroid betamethasone was initially reported by Singh and
Moderate to Severe Acute Mountain Sickness associates410 to improve symptoms of soldiers with severe AMS.
Low-flow oxygen, if available
Subsequent studies have found dexamethasone to be effective
Acetazolamide, 250 mg bid, or dexamethasone, 4 mg PO, IM, or for treatment of all degrees of AMS.121,164,214 Hackett and col-
IV q6h, or both leagues164 used 4 mg orally or intramuscularly (IM) every 6 hours,
Hyperbaric therapy and Ferrazinni and associates121 gave 8 mg initially, followed by
or Immediate descent 4 mg every 6 hours. Both studies reported marked improvement
within 12 hours, which was the first postdrug assessment, but
High-Altitude Cerebral Edema
clinical experience suggests improvement of AMS within 4 hours.
Immediate descent or evacuation
There were no significant side effects. Symptoms returned slightly
Oxygen, 2 to 4 L/min; titrate to SpO2 >90%
Dexamethasone, 8 mg PO, IM, or IV, then 4 mg q6h when dexamethasone was discontinued after 24 hours.164 Other
Hyperbaric therapy steroids at equivalent dosage are likely effective.
Clinicians debate whether the use of dexamethasone should
High-Altitude Pulmonary Edema also mandate descent and whether it is safe to continue ascent
Minimize exertion and keep warm. after treatment with dexamethasone or while taking the medica-
Immediate descent or hyperbaric therapy tion. In reality, people do continue ascent, and problems seem
Oxygen, 4 to 6 L/min until improving, then 2 to 4 L/min; titrate to
to be few. In our opinion, dexamethasone use should be limited
SpO2 >90%
If above measures unavailable, use one of the following:
to less than 72 hours to minimize side effects. This generally is
Nifedipine, 30-mg extended-release tablet q12h sufficient time to descend, or better acclimatize, with or without
Sildenafil, 50 mg q8h acetazolamide. The exact mechanism of action of dexamethasone
Tadalafil, 10 mg q12h is unknown; it does not affect SaO2, fluid balance, or periodic
Consider inhaled β-agonist as adjunct. breathing.248 The drug blocks the action of vascular endothelial
growth factor (VEGF),391 diminishes the interaction of endothe-
Nocturnal Periodic Breathing
lium and leukocytes (thus reducing inflammation),140 and may
Acetazolamide, 62.5 to 125 mg at bedtime as needed also reduce cerebral blood flow.203 Dexamethasone seems not to
IM, Intramuscularly; IV, intravenously; PO, orally; SpO2, oxygen saturation as improve acclimatization, because some symptoms recur when
measured by pulse oximetry; bid, twice daily; q, every; h, hours. the drug is withdrawn. Therefore, an argument could be made
for using dexamethasone to relieve symptoms and using acet-
azolamide to speed acclimatization.46
acclimatization or treatment, descent is indicated. Individuals
with AMS should also descend if they begin to develop any Prevention
neurologic finding suggestive of HACE, respiratory symptoms, or Optimal prevention strategy is based on assessment of risk asso-
hypoxemia suggestive of HAPE. ciated with the planned ascent profile (Table 2-4).262 Graded
Mild AMS can be treated by halting ascent and waiting for ascent with slow increases in sleeping elevation is the surest and
acclimatization to improve, which can take from 12 hours to 4 safest method of prevention, although particularly susceptible
days. Acetazolamide (250 mg twice a day orally, or as a single individuals may still become ill. Current recommendations are to
dose) speeds acclimatization and thus terminates the illness if avoid abrupt ascent from low altitude to sleeping altitudes greater
given early.144,272 Symptomatic therapy includes analgesics such
as aspirin (500 or 650 mg), acetaminophen (650 to 1000 mg
every 6 hours), ibuprofen (600 mg every 8 hours),57 or other
NSAIDs for headache. Ondansetron (4-mg oral disintegrating
tablet every 4 hours as necessary) is useful for nausea and vomit-
ing. Persons with AMS should avoid alcohol and other respiratory
depressants because of possible exaggerated hypoventilation and
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. Supplemental
oxygen is particularly effective (and supply is conserved) if given
at low flow (0.5 to 1 L/min by mask or cannula), particularly
during the night (e.g., sleep). Hyperbaric chambers are effective
and do not require supplemental oxygen but generally are not
necessary in most cases of AMS and instead are typically reserved
for patients with severe AMS, HACE, or HAPE. Lightweight
(<7 kg) fabric pressure bags inflated by manual pumps can be
used to simulate descent and treat AMS (Figure 2-4). Chamber
inflation of 2 psi is approximately equivalent to a drop in altitude
of 1600 m (5249 feet); the exact equivalent depends on initial
altitude.208,362 A few hours of pressurization result in symptomatic
improvement and can be an effective temporizing measure while
awaiting descent or the benefit of medical therapy.208,309,326,366,440
Long-term (≥12 hours) use of these portable devices is necessary
to resolve AMS completely. FIGURE 2-4  Fabric hyperbaric (pressure) bag being used on Denali for
Acetazolamide is now typically and successfully used to treat treatment of severe altitude illness; 2 psi of pressure is equivalent to
AMS, although data supporting a role in treatment are minimal.144,272 a drop of approximately 1600 m (5249 feet) in altitude.

15
 TABLE 2-4  Risk Categories for Acute Mountain Sickness
Risk
Category* Description†
Low Individuals with no prior history of altitude illness
and ascending to <2800 m (9186 ft)
Individuals taking >2 days to arrive at 2500-3000 m
(8202-9843 ft) with subsequent increases in
sleeping elevation <500 m (1640 ft)/day and an
extra day for acclimatization every 1000 m (3281 ft)
Moderate Individuals with prior history of AMS and ascending
to 2500-2800 m (8202-9186 ft) in 1 day
No history of AMS and ascending to >2800 m
(9186 ft) in 1 day
All individuals ascending >500 m (1640 ft)/day
(increase in sleeping elevation) at altitudes above
3000 m (9843 ft) but with an extra day for
acclimatization every 1000 m (3281 ft)
High History of AMS and ascending to >2800 m (3281 ft)
in 1 day
All individuals with a prior history of HAPE or HACE
All individuals ascending to >3500 m (11,483 ft) in
1 day
All individuals ascending >500 m (1640 ft)/day
MOUNTAIN MEDICINE
(increase in sleeping elevation) above >3000 m
(9843 ft) 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 Practice Guidelines for the Prevention and Treatment of Acute Altitude
Illness: 2014 update, Wilderness Environ Med 25:S4-S14, 2014.
AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE,
high-altitude pulmonary edema.
*The risk categories described above pertain to unacclimatized individuals.
†Altitudes listed in the table refer to the altitude at which the person sleeps.
Ascent is assumed to start from elevations below 1200 m (3937 feet).
PART 1
than 2800 m (9186 feet) in 1 day, to spend at least 2 nights at
2500 to 3000 m (8202 to 9843 feet) before going higher, not to
advance sleeping altitude more than 500 m (1640 feet) per day,
and to take an extra night for acclimatization every 1000 m if
continuing ascent.49,262
A study on Aconcagua reinforced the idea that individual
susceptibility is a key factor, and that persons who are resistant
to AMS can proceed much more quickly on the mountain
safely.332 Day trips to higher altitude, with a return to lower alti-
tude for sleep, aid acclimatization. Alcohol and sedative-hypnotics
are best avoided the first 2 nights at high altitude. Whether a diet
high in carbohydrates reduces AMS symptoms is controver-
sial.82,169,437 Heavy exertion early in altitude exposure contributes
to altitude illness,364 whereas limited exercise seems to aid accli-
matization. Because altitude exposure in the previous weeks is
protective, a faster rate of ascent may be possible in individuals
who use a program of preacclimatization to high altitude,
although the optimal preacclimatization regimen has not been
determined.130,312,352,390,486
Acetazolamide Prophylaxis.  Acetazolamide is the drug of
choice for AMS prophylaxis. A carbonic anhydrase inhibitor,
acetazolamide slows hydration of carbon dioxide (CO2). The
effects are protean, involving particularly red blood cells, brain,
lungs, and kidneys. By inhibiting renal carbonic anhydrase, acet-
azolamide reduces reabsorption of bicarbonate and sodium and
thus causes bicarbonate diuresis and metabolic acidosis, beginning
within 1 hour after ingestion and having full effect at 8 hours.434,439
This rapidly enhances ventilatory acclimatization, thereby improv-
ing oxygenation. Importantly, by decreasing periodic breathing,
the drug maintains oxygenation during sleep and prevents periods
of extreme hypoxemia.160,431,436,439 Because of its diuretic action,
acetazolamide counteracts the fluid retention of AMS. It also
diminishes nocturnal antidiuretic hormone (ADH) secretion77 and
decreases CSF production and volume and possibly CSF pressure.
16
Acetazolamide impacts brain aquaporin channels, possibly pre-
venting water transport into the brain.400,441 Which of these effects
is most important in preventing AMS is unclear, but most experts
attribute acetazolamide’s benefit to respiratory stimulation and
increased alveolar and arterial oxygenation. Numerous studies
together indicate that acetazolamide is approximately 75% effec-
tive in preventing AMS in persons rapidly transported to altitudes
of 3000 to 4500 m (9843 to 14,764 feet).113
Acetazolamide prophylaxis should be considered for persons
with moderate to severe risk of acute altitude illness, as indicated
in Tables 2-3 and 2-4. The ideal dose of acetazolamide for pre-
vention is debated. Many studies have shown that 250 mg two
or three times a day was effective, as well as a 500-mg sustained-
action capsule every 24 hours.74,134,143,156,238,348,477 To reduce the side
effects, especially paresthesia, clinicians have more recently been
using smaller doses (125 mg twice daily),290 and a number of
studies now support this.32,67,453,258 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 begin 24 hours before ascent.
For individuals ascending to and remaining at the same elevation
for a period of time, the medication can be stopped after 2 days
at that elevation, although the duration might be extended if the
individual ascended to that elevation at a very fast rate. For
individuals climbing to a peak elevation and then descending
quickly (e.g., climbing Mt Kilimanjaro), the medication is contin-
ued until descent is initiated. 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 discon-
tinued. Although the danger of altitude illness passes after a few
days of acclimatization, a single dose of acetazolamide at night
may still be useful to promote more effective sleep.
Acetazolamide has side effects, most notably peripheral par-
esthesia and polyuria, and less often nausea, drowsiness, impo-
tence, and myopia. Because it inhibits the instant hydration of
CO2 on the tongue, acetazolamide allows CO2 to be tasted and
can ruin the flavor of carbonated beverages, including beer. The
issue of sulfonamide allergy and acetazolamide was recently
reviewed.215 As a nonantibiotic sulfonamide drug, acetazolamide
is usually tolerated well by persons with a history of sulfa antibi-
otic allergy; approximately 10% may have an allergic reaction.423
In persons without a history of allergy to sulfa antibiotic, the
incidence of hypersensitivity reaction to a sulfonamide nonanti-
biotic was 1.6%.423 The same analysis concluded that persons who
are penicillin allergic are actually more likely to react to drugs
such as acetazolamide than are those who are sulfa allergic.
Nonetheless, it is wise to be cautious in persons with a history of
allergy, especially those with anaphylaxis to either sulfa or penicil-
lin or those planning travel into remote areas away from medical
resources. Although the usual allergic reaction is a rash starting
a few days after ingestion, anaphylaxis to acetazolamide does
rarely occur. Although not completely ruling out a future allergic
reaction, many experts recommend a trial of acetazolamide well
before the altitude sojourn, to determine if the drug is tolerated.
Dexamethasone Prophylaxis.  Dexamethasone effectively
prevents AMS. A dose of 2 mg every 6 hours or 4 mg every 12
hours was sufficient for sedentary individuals,203 but for exercis-
ing individuals at or above 4000 m (13,123 feet), this dosing was
insufficient,45,164,367 and 4 mg every 6 hours was necessary to
prevent AMS.368 The initial chamber study in 1984 was with sed-
entary persons.203 Dexamethasone reduced incidence of AMS
from 78% to 20%, comparable to previous studies with acetazol-
amide. Dexamethasone was not as effective in exercising indi-
viduals on Pike’s Peak,367 but subsequent work has shown
effectiveness comparable with acetazolamide.37,113,248,299,497 The
combination of acetazolamide and dexamethasone proved supe-
rior to dexamethasone alone.497 Because of potential serious side
effects and the rebound phenomenon, dexamethasone is best
reserved for treatment rather than prevention of AMS, or it can
be used for prophylaxis when necessary in persons intolerant of
or allergic to acetazolamide. Because of the risk of adrenal sup-
pression and other complications, dexamethasone should not be
used for prophylaxis for more than 7 days. A recent case report
of severe complications in a Mt Everest climber who used
dexamethasone for altitude illness prevention for 29 days sup-
ports this recommendation.425 If use longer than 7 days is
unavoidable, the medication should not be stopped abruptly and
the dose slowly tapered over time.
Other Preventive Agents.  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,135,303,371 whereas two studies were nega-
tive.74,134 These conflicting results can possibly be explained by
differences in dosing, duration of pretreatment, and varying rates
of ascent, but most likely are caused by differences in prepara-
tions of ginkgo.242,452 Ginkgo biloba is a complicated plant extract
whose active ingredient in terms of preventing AMS is unknown.
Even in “standardized” preparations (24% flavonoids and 6%
terpene ginkolides), the amounts of specific elements can vary
considerably. Until the active ingredient is discovered and stan-
dardized, results with ginkgo will continue to be mixed. Acetazol-
amide remains the superior agent and should be used rather than
ginkgo when pharmacologic AMS prophylaxis is warranted.262
Recent studies suggest ibuprofen may have a role in AMS
prevention,325 but it has not been shown to be superior to acet-
azolamide and has not been adopted in recent expert guidelines
on AMS prevention.262 In addition, ibuprofen has not been shown
to improve nocturnal periodic breathing or nocturnal SaO2. Spi-
ronolactone,200,237 naproxen, salicylic acid, calcium channel block-
ers, antacids, leukotriene receptor antagonists, sumatriptan, and
medroxyprogesterone acetate have also been studied and are
ineffective for AMS prevention. Despite being frequently recom-
mended for travelers in South America for AMS prophylaxis, coca
leaves, coca tea, and other coca-derived products have not been
studied in a systematic manner, and it remains unclear if they
provide any benefit. Bailey and Davies14 tested an antioxidant
“cocktail” for prevention of AMS. They reasoned that free radical–
mediated damage to the blood-brain barrier might play a role in
the pathophysiology. They preloaded nine individuals with daily
L-ascorbic acid, DL-α-tocopherol acetate, and α-lipoic acid, and
nine with placebo for 3 weeks, and then during a 10-day trek to
the Mt Everest base camp. Those taking antioxidants had a
slightly lower AMS score, higher SaO2, and better appetite.14
Another study failed to confirm any benefit of antioxidant therapy
for preventing AMS.16 (See Bärtsch and associates20 for a detailed
discussion of the antioxidant hypothesis.)
HIGH-ALTITUDE CEREBRAL EDEMA
An uncommon but deadly condition, HACE usually occurs in
persons with AMS or HAPE. Although HACE occurs most often
above 3000 m (9843 feet), it has been reported at altitudes as
low as 2100 m (6890 feet).96 Reliable estimates of incidence range
from 0.5% to 1% in unselected high-altitude visitors,28,156 and
incidence was 3.4% in trekkers who had developed AMS.156
However, HACE incidence in persons with AMS likely is lower
now than in this 1976 study because awareness and treatment
of AMS have greatly improved. 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 HAPE131,175,189 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 patients with a primary diagnosis
of HACE also had HAPE. Pure cerebral edema, without pulmo-
nary edema, appears to be uncommon at lower altitudes, but it
accounted for 54 of 66 HACE cases in Tibet.485 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.190
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. A more complete discussion is available in a prior
review158 and case series.485
Clinical Presentation
High-altitude cerebral edema causes encephalopathy, whereas
AMS does not. The hallmarks of HACE are ataxic gait, severe
lassitude, and altered consciousness, including confusion,
CHAPTER 2  High-Altitude Medicine and Pathophysiology
impaired mentation, drowsiness, stupor, and coma. Headache,
nausea, and vomiting occur frequently but are not always
present. Hallucinations, cranial nerve palsy, hemiparesis, hemi-
plegia, seizures, and focal neurologic signs have also been
reported.98,167,184,410,485 However, focal neurologic deficits should
not readily be attributed to HACE; if they are present without
altered mental status, or persist after treatment with oxygen or
descent, they should prompt concern for stroke or other issues
(discussed later). Seizures are distinctly uncommon. Retinal hem-
orrhages are common but not diagnostic. Progression from mild
AMS to unconsciousness may be as rapid as 12 hours but usually
requires 1 to 3 days; HACE can develop more quickly in persons
with HAPE. Arterial blood gas (ABG) determination or pulse
oximetry often reveals exaggerated hypoxemia. Clinical examina-
tion and chest radiography may reveal pulmonary edema. Labo-
ratory studies and lumbar puncture are useful only to rule out
other conditions. Computed tomography (CT) may show com-
pression of sulci and flattening of gyri, as well as 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.166,479,485 Initial diagnosis in the field
must be made based on clinical assessment alone, but the MRI
findings may be present for days after evacuation or recovery
and thus can be useful if the diagnosis was previously unclear.
In fact, hemosiderin deposits in the corpus callosum may be
present on MRI for years after HACE.396
Case Study 2-1 illustrates a typical clinical course of HACE in
conjunction with HAPE.
Case Study 2-1  HIGH-ALTITUDE CEREBRAL EDEMA:
CLINICAL PRESENTATION
H.E. was a 26-year-old German lumberjack with extensive
mountaineering experience. Climbing Denali, 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 coordi-
nation. 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
and slightly cyanotic, and was noted to have Cheyne-Stokes
respirations. After 10 minutes of high-flow oxygen, H.E. began
to regain consciousness, although he was completely disori-
ented 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 and was able to
move his extremities but unable to stand. Respiratory rate was
60 breaths/min and heart rate 112 beats/min. Papilledema and
a few rales were present. SaO2 was 54% on room air (normal,
85% to 90%). On a nonrebreather mask with 14 L/min oxygen,
SaO2 increased to 88% and respiratory rate decreased to 40
breaths/min. Dexamethasone (8 mg) was administered IM 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 heart-
ily. He was evacuated by air to Anchorage (sea level) at 12 PM.
On admission to the hospital at 3:30 PM, about 36 hours
after regaining consciousness, H.E. was somewhat confused
and mildly ataxic. ABG studies on room air showed PO2 of
58 mm Hg, pH of 7.5, and PCO2 of 27 mm Hg. Bilateral pulmo-
nary infiltrates were present on the chest radiograph. Brain
MRI revealed white matter edema, primarily of the corpus cal-
losum (Figures 2-5 and 2-6). On discharge the next morning,
H.E. was oriented, bright, and cheerful and had very minor
ataxia and clear lung fields.
17

FIGURE 2-5  Magnetic resonance image of a patient with high-altitude
cerebral edema. Increased T2 signal in splenium of corpus callosum
(arrow) indicates edema. (Reprinted from Hackett PH, Yarnell PR, Hill
MOUNTAIN MEDICINE
Pathophysiology
The pathophysiology of HACE is a progression of the same
mechanism noted for advanced AMS (see AMS Pathophysiology,
earlier, and Figure 2-3) and appears to be mixed vasogenic and
cytotoxic edema. In cases similar to this, lumbar punctures have
revealed elevated CSF pressure (often >300 mm H2O),184,472 evi-
dence of cerebral edema on CT and MRI,166,224 and gross cerebral
edema on autopsy.98,99 Small petechial hemorrhages were also
consistently found on autopsy, and venous sinus thromboses
were occasionally seen.98,99 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, gray
matter (presumably cytotoxic) edema also develops, culminating
in brain herniation and death. As Klatzo223 has noted, as vaso-
genic 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 ischemic, leading to
intracellular (cytotoxic) edema. Increased ICP produces many of
its effects by decreasing cerebral blood flow, and brain tissue
also becomes ischemic on this basis.287 Focal neurologic signs
caused by brainstem distortion and by extraaxial compression,
such as third and sixth cranial nerve palsies, may develop,372
making cerebral edema difficult to differentiate from primary
cerebrovascular events. The most common clinical presentation
of HACE is a change in consciousness associated with ataxia,

R, et al: High-altitude cerebral edema evaluated with magnetic reso- without focal signs.485,491
nance imaging: Clinical correlation and pathophysiology, JAMA 280:
1920-1925, 1998.)

1 2 3
PART 1

4 5 6

FIGURE 2-6  Magnetic resonance imaging (MRI) scans of patient with high-altitude cerebral edema (HACE).
A fluid-attenuated inversion recovery (FLAIR) image (1) shows edema 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 is the characteristic
MR 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 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 28:1635-1642, 2008.)

18
Treatment and Prevention
Given the sporadic nature and generally remote locations at
which this disorder occurs, it is not surprising that there are no
controlled trials on treatment of HACE. All experts agree that
successful treatment is vastly enhanced by early recognition. At
the first sign of ataxia or change in consciousness, descent should
be started, dexamethasone (4 to 8 mg IV, IM, or PO 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 2-3). Oxygen can be titrated to maintain SaO2 at greater
than 90% if oximetry is available. Comatose patients require
additional airway management and bladder drainage. Hyper­
ventilation has historically been mentioned as a tool for address-
ing intracranial hypertension but should be avoided because
excessive hyperventilation and respiratory alkalosis can worsen
cerebral perfusion and result in disastrous cerebral ischemia.
Managing this issue in the field without access to end-tidal CO2
monitoring or ABG measurement can be challenging and dan­
gerous. Loop diuretics such as furosemide (40 to 80 mg) or
bumetanide (1 to 2 mg) may reduce brain hydration and have
been used successfully,97,410 but maintenance of adequate intra-
vascular volume and cerebral perfusion pressure is critical.
Hypertonic solutions of saline, mannitol, or oral glycerol have
been suggested but are rarely used in the field and have not
been studied in a controlled manner for this purpose. Hypertonic
saline has an advantage over mannitol in that it will not cause
intravascular volume depletion. Controlled studies are lacking,
but empirically the response to corticosteroids and oxygen seems
excellent if these are given early in the course of the illness but
is disappointing if these are not started until the patient is
unconscious.
Coma may persist for days, even after evacuation to low alti-
tude. Other causes of coma must be considered and ruled out
by appropriate evaluation.184 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.165 Two patients of the 44 in the series by
Dickinson98 remained in coma for 3 weeks.98 Sequelae lasting
weeks are common;166,184 longer-term follow-up has been limited,
but presumed permanent impairment has been reported.158,184 In
the Chinese series of 66 patients, HACE was diagnosed early,
and descent was uniformly successful. Ataxia resolved in all but
one patient within 7 days, and only one patient had long-term
sequelae (clonic convulsions affecting the left hand).485
The nonpharmacologic approach to prevention of HACE is
the same as for the other forms of acute altitude illness, and the
same pharmacologic measures used for AMS prevention are
believed to be effective for HACE prevention.
FOCAL NEUROLOGIC CONDITIONS
WITHOUT ACUTE MOUNTAIN SICKNESS
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.36 Cortical blindness is one such condition. Hackett and
colleagues162 reported six cases of transient blindness in climbers
or trekkers with intact pupillary reflexes, which indicated that
the condition was caused by a cortical process. Treatment with
breathing either CO2 (a potent cerebral vasodilator) or oxygen
resulted in prompt relief, suggesting that the blindness was
caused by inadequate regional circulation or oxygenation.
Descent provided relief more slowly. Other conditions that could
be attributed to spasm or “TIA” have included transient hemiple-
gia or hemiparesis, transient global amnesia, unilateral paresthe-
sias, aphasia, and scotoma.31,36,51,69,250,478,500 The true mechanism of
these focal findings is unknown and may be multifactorial.
Young, healthy high-altitude sojourners are unlikely to have TIA
syndrome from cerebrovascular disease. The focal findings more
likely represent hypoxic/ischemic events resulting from a com-
bination of low SaO2 and low regional perfusion.
Other neurologic complications at high altitude include globus
CHAPTER 2  High-Altitude Medicine and Pathophysiology
pallidum lesions, which were considered complications of AMS
or HACE and reported to lead to Parkinson’s disease.201,424,432,451
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 CO poisoning, and can also be damaged by ischemia.
CEREBROVASCULAR ACCIDENT (STROKE)
The occurrence of cerebrovascular accident (CVA, stroke) in a
young, fit person at high altitude is uncommon and tragic. A
number of case reports have described climbers with resultant
permanent dysfunction.76,183,413 Indian soldiers at extreme alti-
tude have a high incidence of stroke.202 Cerebral venous
thrombosis manifests more insidiously, and diagnosis is often
delayed.149,207,379,413,447,500 Factors contributing to stroke may include
polycythemia, dehydration, increased ICP if AMS/HACE is pres-
ent, increased cerebral venous pressure, cerebrovascular spasm,
and familial thrombophilia.33 Stroke may be confused with
HACE. Neurologic symptoms, especially focal abnormalities
without AMS or HAPE that persist despite treatment with oxy-
gen, corticosteroids, and descent, suggest a cerebrovascular
event and mandate careful evaluation with a complete neuro-
logic workup (see Case Study 2-2).
Treatment of stroke is supportive. Oxygen and corticosteroids
may be worthwhile to treat any AMS or HACE component. Imme-
diate evacuation to a hospital is indicated; thrombolytics should
be withheld until neuroimaging is available to rule out cerebral
hemorrhage. Persons with TIA at high altitude should probably
start 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
Studies have documented cognitive dysfunction on ascent to
altitudes greater than 5500 m (18,045 feet) in some individuals,
in the absence of altitude illness and correctable with supple-
mental oxygen administration. Because acute central nervous
system (CNS) dysfunction in this setting must be related to neu-
ronal oxygenation, it is the tissue PO2 that likely affects function.
Given the marked variation in arterial and tissue oxygenation
among individuals on ascent to altitude, the threshold altitude
and appearance and magnitude of such cognitive changes are
likely to be quite variable.
Although cerebral oxygen consumption is constant, there are
well-documented but mild cognitive changes at high altitude.
This phenomenon may be related to specific neurotransmitters.
For example, tryptophan hydroxylase in the serotonin synthesis
Case Study 2-2  CEREBROVASCULAR ACCIDENT
(STROKE): 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 feet]), 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 persisted. The hematocrit value on the mountain
was greater than 70%, high enough for increased viscosity and
microcirculatory sludging to contribute to ischemia and infarc-
tion. No familial thrombophilia was detected.
19
 pathway has a high requirement for oxygen (Michaelis constant
[Km] = 37 mm Hg).81,137 Tyrosine hydroxylase in the dopamine
pathway is also oxygen sensitive. It has been suggested that
decrease in acetylcholine activity during hypoxia might explain
lassitude.137 One study showed that increased dietary tyrosine
reduced mood changes and symptoms of environmental stress
in persons at simulated altitude.17 Further work with neurotrans-
mitter agonists and antagonists will help shed light on their role
in cognitive dysfunction at altitude and could lead to new phar-
macologic 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 sud-
denly 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 “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 suf-
focative catarrh accompanied by acute edema of the
lungs. … I have gone into the particulars of this sorrowful
MOUNTAIN MEDICINE
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.308
On an expedition to K2 (Karakorum Range, Pakistan) in 1902,
Alistair Crowley86 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 alti-
tude,196,252 but it was not until Hultgren and Spickard193 and
Houston182 offered their observations that the English-speaking
world became aware of HAPE (see Rennie349 for a review). Hult-
PART 1
gren and colleagues194 then published hemodynamic measure-
ments 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. Further information is available in several reviews
on this topic.27,89,259,266,384,388,392,422,435
Individual susceptibility, rate of ascent, altitude reached,
degree of cold,346 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
Denali (6194 m [20,322 feet]) and up to 6% of mountaineers in
the Alps ascending rapidly to 4559 m (14,957 feet).24 Hultgren
and associates192 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) (see Singh and Roy411 and Table 2-1). Wu
and colleagues485 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 above 7000 m (22,966 feet) without
illness.19,25, HAPE appears to be less common in women.84,189,415
Whether all persons are capable of developing HAPE (with a
very rapid ascent to a sufficiently high altitude and with heavy
exercise) is arguable.27 Some studies suggest that many persons
contract subclinical extravascular lung water,85 whereas other
studies contradict this.92 Even well-acclimatized individuals with
a sudden push to a higher altitude can succumb to HAPE.85 A
population of HAPE-susceptible persons with unique physiologic
characteristics has been described (see Susceptibility to High-
Altitude Pulmonary Edema, later). These individuals represent
the small percentage of people who develop HAPE when others
in the same circumstances do not. HAPE in children is addition-
ally associated with antecedent viral infections, trisomy 21,106 and
20
Case Study 2-3  HIGH-ALTITUDE PULMONARY
EDEMA: CLINICAL PRESENTATION
D.L., a 34-year-old man, was in excellent physical condition and
had been on numerous high-altitude backpacking trips, occa-
sionally suffering mild symptoms of AMS. He drove from sea
level to the trailhead and hiked to a sleeping altitude of 3050 m
(10,007 feet) 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 dry cough. He com-
plained 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 suf-
fered coughing spasms and headache. On the fourth morning,
D.L. was too exhausted and weak to exit his sleeping bag. His
companions noted that he was breathless, cyanotic, and ataxic
but had clear mental status. A few hours later he was trans-
ported by helicopter to a hospital at 1200 m (3937 feet). On
admission he was cyanotic, oral temperature was 37.8° C
(100° F), blood pressure 130/76 mm Hg, heart rate 96 beats/
min, and respiratory rate 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. ABG determinations on room air revealed
PO2 24 mm Hg, PCO2 28 mm Hg, and pH 7.45. Chest radio-
graph showed extensive bilateral patchy infiltrates (see Figure
2-7C). 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 ABG 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.
underlying congenital cardiovascular malformations, such as uni-
lateral absence of the pulmonary artery.87
Clinical Presentation
Case Study 2-3 illustrates typical aspects of HAPE. Patients are
frequently young, fit males who ascend rapidly from sea level
and may not have previously developed HAPE, even with
repeated altitude exposures; the particular ascent may have been
faster than any the patient had previously undertaken. HAPE
usually occurs within the first 2 to 4 days of ascent to higher
altitudes (>2500 m [8202 feet]), most often on the second night.147
Decreased exercise performance and increased recovery time
from exercise are the earliest indications of HAPE. The patient
shows fatigue, weakness, and dyspnea on exertion, especially
when walking uphill; the person often ascribes these nonspecific
symptoms to various other causes. Signs of AMS are present in
about 50% of cases.189 A persistent dry cough develops. Nail beds
and lips become cyanotic. Dyspnea at rest is the key clinical sign
of HAPE, and tachycardia and tachypnea develop. The condition
typically worsens at night. Increasing respiratory distress alerts
the patient and travel partners to 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.458 Orthopnea is uncommon (7%). Pink or
blood-tinged, frothy sputum is a very late finding. Hemoptysis
was present in 6% of patients in one series.192 Severe hypoxemia
may produce hypoxic encephalopathy or cerebral edema, with
mental changes, ataxia, decreased level of consciousness, and
coma. Hultgren and colleagues192 reported an incidence of HACE
of 14% in persons with HAPE at ski resorts.
On admission to the hospital, the patient does not generally
appear as ill as expected based on ABG and radiographic
findings. Elevated temperature up to 38.5° C (101.3° F) is common.
Tachycardia correlates with respiratory rate and severity of illness.
Rales194 may be unilateral or bilateral and usually originate from
the right middle lobe. Concomitant respiratory infection is some-
times present.
Pulmonary edema may also manifest with predominantly neu-
rologic manifestations caused by hypoxic encephalopathy and
minimal pulmonary symptoms and findings, most likely in
persons with blunted ventilatory responses to hypoxemia. Cere-
bral edema, especially with coma, may obscure the diagnosis of
HAPE.157 Chest radiography and pulse oximetry can be used to
confirm the diagnosis. In fact, absence of hypoxemia in a patient
with respiratory complaints at high altitude should prompt con-
sideration of diagnoses other than HAPE, because previous series
have shown these patients have marked hypoxemia compared
to normal individuals at a given elevation. Differential diagnosis
includes pneumonia, bronchitis, mucus plugging, pulmonary
embolism or infarct, heart failure, acute myocardial infarction,
and sometimes asthma (see Box 2-2). Complications include
infection, cerebral edema, pulmonary embolism or thrombosis,
and such injuries as frostbite or deep vein thrombosis (DVT)
secondary to incapacitation.190,19,157
Hemodynamics
Hemodynamic measurements by catheter show elevated pulmo-
nary artery pressure (PAP) and pulmonary vascular resistance,
low to normal pulmonary artery wedge pressure, and low to
normal cardiac output and systemic arterial blood pressure.191,271,330
Echocardiography demonstrates high PAP, tricuspid regurgita-
tion, normal left ventricular systolic function, somewhat abnormal
diastolic function,7 and variable right-sided heart findings of
increased atrial and ventricular size.161,323
The electrocardiogram (ECG) usually reveals sinus tachycar-
dia. 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.189,19 Atrial flutter has been reported, but not
ventricular arrhythmias.
Laboratory Studies
Kobayashi and colleagues224 reported clinical laboratory values
in 27 patients with HAPE that showed mild elevations of hema-
tocrit and hemoglobin, probably caused by intravascular volume
depletion and plasma leakage into the lungs. Elevation of periph-
eral white blood cell count is common but is rarely above
14,000 cells/mL. Serum concentration of creatine phosphokinase
(CPK) is increased, mostly from muscle damage, although in two
patients, CPK isoenzymes showed brain fraction levels of 1% of
total, which may have indicated brain damage.224 Gao and associ-
ates132 found that NT-ProBNP (brain natriuretic peptide) levels
were moderately elevated in patients with HAPE,132 and that
levels resolved on treatment, suggesting NT-ProBNP as a poten-
tial useful HAPE biomarker.
Arterial blood gases consistently reveal respiratory alkalosis
and marked hypoxemia, more severe than expected for the
patient’s clinical condition. Because respiratory or primary meta-
bolic acidosis has not been reported, ABG studies are unneces-
sary if noninvasive pulse oximetry is available to measure arterial
oxygenation. At 4200 m (13,780 feet) on Denali, 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 patients at 4300 m (14,108 feet) ranged from 40% to 70%,
with a mean of 56% ±8%.395 At 2928 m (9606 feet), mean SaO2
was 74%.192 Arterial acid-base values may be misleading in
patients taking acetazolamide, because this drug produces sig-
nificant metabolic acidosis.
Radiographic Findings
The radiographic findings in HAPE have been described in origi-
nal reports194,275,460,461 (Figure 2-7). 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 B lines. The pulmonary arteries
increase in diameter.461 Infiltrates are frequently described as
fluffy and patchy, with areas of aeration between infiltrates and
CHAPTER 2  High-Altitude Medicine and Pathophysiology
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 auscultated
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, a condition
known to predispose to HAPE.152,356
Clearing of infiltrates is generally rapid once treatment is initi-
ated. Depending on severity, complete clearing may take from 1
day 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 diag-
nosis of HAPE.
An ultrasound technique known as “comet-tail” scoring, previ-
ously 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 and consistent with inter-
stitial and alveolar edema. Eleven patients at 4240 m (13,911 feet)
with a clinical diagnosis of HAPE underwent chest ultrasound
examinations using this technique.117 Seven patients with no
evidence of HAPE or other altitude illness served as controls.
HAPE patients had much higher comet-tail scores and lower SpO2
than did controls, 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.
Another study has reported use of a satellite telemedical con-
nection with a remote expert to guide thoracic ultrasound exami-
nations at Advanced Base Camp on Mt Everest; high-quality
images were obtained that verified increases in lung water.324
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
PAP.337 As technology improves and cost decreases, use of ultra-
sound in the wilderness setting may increase. 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.13,99,314,410,411,472 Of those whose cranium was opened,
more than one-half had cerebral edema. All lungs showed exten-
sive 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 mem-
branes was characteristic. All lungs had areas of inflammation
with neutrophil accumulation. The diagnosis of bronchopneumo-
nia 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 capillary and arteriolar thrombi and alveolar fibrin
deposits, as well as microvascular and gross pulmonary hemor-
rhage and infarcts. 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,393 who found
a 100-fold increase in lavage fluid protein levels in patients
with HAPE compared with well controls and AMS patients.395
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.151 In addition, the lavage fluid contained
vasoactive eicosanoids and complement proteins, indicative of
endothelium-leukocyte interactions. Research using repeated
bronchoalveolar lavage as HAPE was developing found that
21
 A B
MOUNTAIN MEDICINE

Congenital Absence of Right Pulmonary Artery

Ventilation scan
PART 1

Perfusion scan

C D
FIGURE 2-7  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 (see
Case Study 2-3). D, Ventilation and perfusion scans in a person with congenital absence of right pulmonary
artery after recovery from HAPE.

inflammation was absent early, suggesting that inflammation is a
response to the alveolar damage, rather than an initiating event.438
Mechanisms of High-Altitude Pulmonary Edema
An acceptable explanation for HAPE must take into account three
well-established facts: excessive pulmonary hypertension, high-
protein 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
caused by uneven hypoxic vasoconstriction (Figure 2-8).
Role of Pulmonary Hypertension.  Excessive PAP is the
sine qua non of HAPE; HAPE has not 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 and preserve gas exchange. For
example, when local areas of the lungs are poorly ventilated
because of infection or atelectasis, the HPVR 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 pulmonary arterioles in all areas of the
lung constrict, causing a restricted vascular bed and increase in
PAP, which is of little if any value for ventilation-perfusion

22

Altitude hypoxia
HVR, sleep, and exercise
↓ PAO2
↑ Sympathetic
activity
Uneven HPV
Exercise
PHTN Pulmonary and
peripheral venous
constriction
Overperfusion
↑ Pulmonary
blood volume
↑ Pcap
Capillary
stress failure
↓ Alveolar Na and
Capillary leak H2O clearance
High-altitude
pulmonary edema
FIGURE 2-8  Proposed pathophysiology of high-altitude pulmonary
edema. HPV, Hypoxic pulmonary vasoconstriction; HVR, hypoxic ven-
tilatory response; PAO2, alveolar partial pressure of oxygen; Pcap,
capillary pressure; PHTN, pulmonary hypertension.
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
later).91,146 The relationship between the PAP increase and edema
formation was well demonstrated by Swenson and colleagues,438
who performed bronchoalveolar lavage on HAPE-susceptible and
normal individuals following rapid ascent to 4559 m (14,957
feet). They demonstrated that individuals with the greatest rise
in PAP had the most red blood cells and protein in their bron-
choalveolar lavage fluid. 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.
Overperfusion and Capillary Leak.  To explain how pul-
monary hypertension might lead to edema, Hultgren suggested
that in persons who develop HAPE, hypoxic pulmonary vaso-
constriction is uneven, and the delicate microcirculation in an
unconstricted (relatively dilated) area is subjected to high pres-
sure and flow, leading to leakage (edema).439
The unevenness of HPVR could be caused by anatomic char-
acteristics, such as distribution of muscularized arterioles, or to
functional factors, such as loss of HPVR in severely hypoxic
regions.186 Uneven perfusion is suggested clinically by the typical
patchy radiographic appearance and is supported by lung CT
and MRI during acute hypoxia showing uneven perfusion in
persons with a history of HAPE.93,179,459 Persons born without a
right pulmonary artery are highly susceptible to HAPE (see Figure
2-7D),152 supporting the concept of overperfusion of a restricted
vascular bed as a cause of edema, since the entire cardiac output
flows into one lung. Other causes of overperfusion of the pul-
CHAPTER 2  High-Altitude Medicine and Pathophysiology
monary 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,
may also play a role in HAPE.263 We have in several cases
observed onset of HAPE after large salt intake. Some studies have
also suggested a role for pulmonary venous constriction, which
would contribute to increased capillary hydrostatic pressure.271,161
The end result of overperfusion and increased capillary pres-
sure271 is distention, increased filtration of fluid, and even rupture
of the aveolocapillary membrane, called “stress failure,”467,468 with
subsequent leakage of cells and proteins.
Alveolar Fluid Balance.  Fluid filtration into the interstitial
and alveolar space, reabsorption back across the epithelial mem-
brane, 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 alti-
tude.85,142,337,462 Despite this, frank alveolar flooding is uncommon.
This may well be caused by differences in hydrostatic pressure
in persons resistant and susceptible to HAPE. However, persons
who develop HAPE appear also to have impaired ability to clear
alveolar fluid. On a constitutive (genetic) basis, HAPE patients
have lower activity of the epithelial sodium channel and therefore
reduced ability to transport sodium across the epithelium back
into the interstitial space.273,383,385 (The sodium gradient across
the epithelium determines movement of water from alveoli.) In
addition, epithelial sodium transport is diminished by hypoxia,
so that persons with already-impaired function become more
impaired at altitude. How large a role this mechanism plays in
HAPE is uncertain180 (Figure 2-8).
Control of Ventilation.  As in AMS, persons with HAPE
had a lower hypoxic ventilatory response (HVR) than did persons
who acclimatized well,163,279 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 have lower PAO2 and
presumably develop greater pulmonary hypertension. Possibly
more important, low HVR may permit episodes of extreme
hypoxemia during sleep.147,163 In addition, a low HVR may allow
further ventilatory depression through CNS suppression (hypoxic
ventilatory depression). Such persons, when given oxygen, show
a “paradoxical” increase in ventilation.163 Despite correlation of
HAPE with low HVR, pretravel identification of patients with
blunted HVR has not been able to predict subsequent develop-
ment of HAPE.91
Susceptibility to High-Altitude Pulmonary Edema
During testing at sea level, persons susceptible to HAPE (HAPE-
s) show abnormal rise of PAP and pulmonary vascular resistance
(PVR) during hypoxic challenge at rest and exercise, and even
during exercise in normoxia, suggesting overreactivity of the
pulmonary circulation to both hypoxia and exercise.91,111,146,209
Part of this reactivity may be related to greater alveolar hypox-
emia secondary to lower HVR,163,176,280 but other factors have
been uncovered. Microneurographic recordings from the pero-
neal nerve during hypoxia established a direct link in HAPE-s
between the rise in PAP and greater sympathetic activation,105
indicating that sympathetic overactivation might contribute to
HAPE. Smaller and less distensible lungs have been noted in
HAPE-s patients, which might limit the ability to accommodate
increased flow by vascular recruitment and thus result in higher
PVR.111,176,418 Another characteristic of HAPE-s is abnormal endo-
thelial function, evidenced by reduced nitric oxide (NO) synthe-
sis during hypoxia44,64,389 and during HAPE104 and higher levels
of endothelin, a potent pulmonary vasoconstrictor.43,386,419 The
importance of reduced NO is reinforced by studies showing
improvement in pulmonary hemodynamics when either NO or
23
 Nitric oxide—overview
Hypoxia eNOS NO c-GMP
PDE-5 inhibitor
L-arginine
Vascular Degradation
muscle by PDE-5
relaxation
FIGURE 2-9  Nitric oxide pathway and action of phosphodiesterase-5
(PDE-5) inhibitors. In the presence of an inhibitor, cyclic guanosine
monophosphate (c-GMP), the second messenger of nitric oxide (NO),
is not degraded, and vasodilation is therefore enhanced. eNOS, Endo-
thelial nitric oxide synthase.
a phosphodiesterase-5 (PDE-5) inhibitor was given to HAPE
patients9,136,269,389 (Figure 2-9). As mentioned previously, HAPE-s
patients are also characterized by impairment of respiratory
transepithelial sodium and water transport, making it more dif-
ficult to reabsorb alveolar fluid.273,383,385
Patent foramen ovale (PFO) is more common among HAPE-
susceptible than among HAPE-resistant adult mountaineers.6
Since the initial report of Levine and co-workers,247 the associa-
MOUNTAIN MEDICINE
tion of PFO and HAPE has been confirmed, but cause and effect
have not been established. Allemann and associates6 performed
a case-control study of 16 HAPE-susceptible participants and 19
mountaineers resistant to HAPE. Presence of PFO was deter-
mined by transesophageal echocardiography (TEE) and esti-
mated PAP by Doppler echocardiography at low altitude (550 m
[1804 feet]) and high altitude (4559 m [14,957 feet]).6 The fre-
quency of PFO was more than four times higher in HAPE-
susceptible than in HAPE-resistant participants, both at low
altitude (56% vs. 11%) and high altitude (69% vs. 16%). At high
altitude, SaO2 before the onset of pulmonary edema was signifi-
cantly lower in HAPE-susceptible participants than in the control
PART 1
group (73% vs. 83%). Also, in the HAPE-susceptible group, par-
ticipants with a large PFO had more severe arterial hypoxemia
(SaO2 65% vs. 77%) than did those with smaller or no PFO. The
authors speculated that at high altitude, a large PFO may con-
tribute to exaggerated arterial hypoxemia and facilitate HAPE.6
Others pointed out, however, that the greater hypoxemia may
have been caused by subclinical pulmonary edema,119 or that
PFO was a marker of a reactive pulmonary vascular bed.88
HAPE-s patients are known to have exaggerated PAP response
to exercise at sea level, which could maintain an open shunt.
Because occurrence of PFO is so common in the general popula-
tion, more compelling evidence is required before suggesting that
PFO is a predisposing factor to HAPE. We do not recommend
that those with PFO should consider closure of the defect before
significant altitude exposure, or as a result of an episode of
HAPE.71
Genetics of High-Altitude Pulmonary Edema
Although many characteristics of HAPE-susceptible persons are
apparently genetically determined, actual genetic studies are
conflicting and difficult to interpret.* The genes associated with
HAPE include those in the renin-angiotensin-aldosterone system
pathway,94,340,420 NO pathway,1,2,101 and hypoxia-inducible factor
(HIF) pathway.39,59 Some studies showed that polymorphisms of
nitric oxide synthase (NOS3),1,2,101 angiotensin-converting enzyme
(ACE),94,420,341 heat shock protein (HSP) 70,339 pulmonary surfac-
tant proteins A1 and A2,387 and aquaporin-5403 were associated
with HAPE incidence and susceptibility, but much work remains
to find specific genetic factors causing HAPE.264 Further investiga-
tions using whole-genome scanning and studies of gene expres-
sion, gene methylation, and microRNA expression in HAPE-s,
*References 1, 2, 94, 100, 101, 168, 181, 235, 256, 300, 307, 340, 339, 376,
412, 421, 446, 463, 466, 499.
24
and in patients during HAPE and on recovery, will lead to a
much clearer understanding of the genomic contributions to
HAPE.293-295,402,464,490
Treatment
Treatment choices for HAPE depend on severity of illness and
logistics. As with all high-altitude illnesses, early recognition
vastly improves the likelihood of successful outcome (see Box
2-3). In the wilderness setting away from medical resources,
persons with HAPE need to be urgently evacuated to lower
altitude. However, because of augmented pulmonary hyperten-
sion and greater hypoxemia with exercise, exertion must be
minimized. Because cold stress elevates PAP, the patient should
be kept warm.70 Early HAPE responds rapidly to descent of only
500 to 1000 m (1640 to 3281 feet), and the patient may be able
to reascend slowly 2 or 3 days later. When descent is not feasible
because of weather or other logistical factors, ill individuals can
be treated with oxygen or with hyperbaric therapy using an
inflatable pressure bag.362 If mobilized in these circumstances,
rescue groups should make delivery of oxygen to the patient, by
airdrop if necessary, the highest priority. In high-altitude loca-
tions with oxygen supplies, such as ski resorts, bed rest with
supplemental oxygen may suffice, but severe HAPE may require
high-flow oxygen (4 L/min) for more than 24 hours.
Oxygen immediately increases arterial oxygenation and
reduces PAP, heart rate, respiratory rate, and symptoms. 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.394 The same airway
pressure changes can be accomplished with pursed-lip breathing,
but this intervention is difficult for an individual to sustain for
long periods, particularly when ill. An unusual case report sug-
gested that a climber may have saved his partner’s life by using
postural drainage to expel airway fluid.50
Drugs are of limited necessity in HAPE because oxygen and
descent are so effective.261 Medications that reduce pulmonary
blood volume, PAP, and PVR are physiologically rational to use
when oxygen is not available or descent delayed. Singh and
associates410 reported good results with furosemide (80 mg
every 12 hours), and greater diuresis and clinical improvement
occurred when 15 mg of parenteral morphine was given with
the first dose of furosemide. Their use, however, has been
eclipsed by recent results with vasodilators. Caution is also war-
ranted with diuretic use because HAPE is a capillary-leak phe-
nomenon, and many affected individuals have intravascular
volume depletion at presentation. The calcium channel blocker
nifedipine (30-mg sustained-release tablet every 12 to 24 hours)
was effective in reducing PVR and PAP during HAPE and slightly
improved arterial oxygenation.25 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 hypovo-
lemia from diuretics. Clinical improvement is much better,
however, with oxygen and descent than with any medication.
Inhaled NO, a potent pulmonary vasodilator, improves hemody-
namics in HAPE but is rarely available, and in any event, NO is
usually given with oxygen. The PDE-5 inhibitors, which increase
cyclic guanosine monophosphate (c-GMP) to produce pulmo-
nary vasodilation during hypoxia (Figure 2-9),136,350,351 have
shown value for prevention of HAPE268 but have not yet been
studied for treatment. Whether these agents will prove to be
more effective than nifedipine for treatment is unknown. A
theoretical advantage is that the PDE-5 inhibitors produce less
systemic vasodilation. Nifedipine, and perhaps other vasodila-
tors, might be useful adjunctive therapy but is not a substitute
for definitive treatment (see Box 2-3 and Table 2-3). β-adrenergic
agonists154,262 may also have an adjunctive role but should not be
considered for monotherapy.262
After evacuation of the patient to a lower altitude, hospital-
ization may be warranted for severe cases; home oxygen is also
a reasonable approach. Treatment consists of bed rest and
oxygen sufficient to maintain SaO2 greater than 90%; medications
are rarely necessary after descent, and rapid recovery is the

FIGURE 2-10  Chest radiograph of severe high-altitude pulmonary
edema (HAPE) in a 4-year-old girl with a small, previously unrecognized
patent ductus arteriosus that predisposed her to HAPE.
rule.502 In a series of 110 patients with HAPE from the Indian
Army, Deshwal and colleagues95 found no benefit of adding
nifedipine when patients were treated with descent and oxygen.
Antibiotics are only indicated when there is a high suspicion for
infection. Occasionally, pulmonary artery catheterization or
Doppler echocardiography is necessary to differentiate cardio-
genic from high-altitude pulmonary edema. Endotracheal intuba-
tion and mechanical ventilation are rarely needed. A HAPE
patient demonstrating unusual susceptibility, such as onset of
HAPE despite adequate acclimatization or onset below 2500 m
(8200 feet), might require further investigation, such as echocar-
diography, to rule out an intracardiac shunt or preexisting pul-
monary hypertension, or chest radiography to evaluate for
unilateral absence of a pulmonary artery. In children, undiag-
nosed congenital heart disease is worth considering87 (Figure
2-10). Hospitalization until ABG values are completely normal is
not warranted; all persons returning from high altitude are at
least partially acclimatized to hypoxemia, and hypocapnic alka-
losis persists for days after descent. Distinct clinical improve-
ment, radiographic improvement over 24 to 48 hours, and PaO2
of 60 mm Hg or SaO2 greater than 90% are adequate criteria for
discontinuation of oxygen therapy.
Patients are advised to resume normal activities gradually and
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 con-
traindication to subsequent high-altitude exposure, but education
to ensure proper preventive measures and recognition of early
symptoms are critical.
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 respiratory
depressants.262 Exertion may contribute to onset of HAPE, espe-
cially 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. Menon289
clearly showed that sedentary men taken abruptly to higher
altitude were just as likely to develop HAPE. Considerable clinical
experience suggests that acetazolamide prevents HAPE in persons
with a history of recurrent episodes. A growing body of both
animal and human research demonstrate that acetazolamide
blocks hypoxic pulmonary hypertension42,177,213,333,405,442 and pro-
vides support for this practice, although acetazolamide has never
formally been studied for HAPE prevention. Nifedipine (20-mg
slow-release tablet every 8 hours) prevented HAPE in persons
CHAPTER 2  High-Altitude Medicine and Pathophysiology
with a history of repeated episodes.25 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 pul-
monary hypertension and therefore will prevent HAPE.268 Tadala-
fil (10 mg every 12 hours) prevented HAPE with rapid ascent in
HAPE-susceptible individuals. The optimal dose has not been
established.266 Regimens for sildenafil have varied from a single
dose of 50 or 100 mg just before exposure for acute studies136,350
to 40 mg three times daily for 2 to 6 days at altitude,351,331 and
for tadalafil, 10 mg every 12 hours was effective.125,268 Rather
surprisingly, dexamethasone was also effective in preventing
HAPE in susceptible individuals. Maggiorini266gave 8 mg of dexa-
methasone 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 explains this observed effect is unknown.27 As
these studies demonstrate, any agent that blocks hypoxic pulmo-
nary hypertension will block onset of HAPE, reinforcing the
concept of pulmonary hypertension as the sine qua non of HAPE.
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 after
a sojourn to low altitude.107 Clinicians have suggested that the
incidence of HAPE on reascent of altitude residents may be
higher than that during initial ascent by flatlanders,29,188 but data
on true incidence are difficult to obtain. Children and adolescents
are more susceptible than adults. The phenomenon has been
observed most often in Peru, where high-altitude residents can
return from sea level to high altitude quite rapidly. Hultgren187
found HAPE prevalence in Peruvian natives of 6.4 per 100 expo-
sures in persons 1 to 20 years old and 0.4 per 100 exposures in
persons older than 21. Cases have also been reported throughout
Colorado,399 but reports are conspicuously rare from Nepal and
Tibet,482 perhaps because Himalayan highlanders are better
adapted or because very rapid return back to high altitude was
not readily available until recently.487 Wu482 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.482 Severinghaus401 postulated that increased
muscularization of pulmonary arterioles that develops with
chronic high-altitude exposure generates inordinately high PAP
on reascent, causing edema. Whether uneven pulmonary vaso-
constriction is present has not been investigated. Changes in fluid
balance with descent and reascent might also play a role.481 The
optimal prevention strategy for reentry HAPE is not known, but
clinical experience suggests acetazolamide has benefit in this
regard.
Chronic Mountain Sickness.  In 1928, Carlos Monge296
described a syndrome in Andean high-altitude natives that was
characterized by headaches, insomnia, lethargy, plethoric appear-
ance, and polycythemia greater than expected for the altitude.
Known variously as Monge’s disease, chronic mountain polycy-
themia, or chronic mountain sickness (CMS), the condition has
now been recognized in all high-altitude areas of the world.
Lowlanders who relocate to high altitude as well as native resi-
dents are susceptible.231,297,328 Chinese investigators reported that
13% of lowland Chinese males and 1.6% of females who had
relocated to Tibet developed excessive polycythemia (hemoglo-
bin level >20 g/dL).488 The incidence in Leadville, Colorado, is
also high in men older than 40 years and is distinctly low in
women.233 Increased hematopoiesis is apparently related to
greater hypoxic stress, which may be caused by a number of
conditions, such as lung disease, sleep apnea syndromes, and
idiopathic hypoventilation. A diagnosis of “pure” chronic moun-
tain polycythemia excludes lung disease and is characterized by
relative alveolar hypoventilation, excessive nocturnal hypoxemia,
and respiratory insensitivity to hypoxia.246,297 Some studies suggest
that even for the degree of hypoxemia, the red blood cell mass
is excessive, implying excessive amounts or overactivity of eryth-
ropoietin.476 International guidelines propose a hemoglobin value
25
 greater than 21 g/dL for males and 19 g/dL for females as essen-
tial for the diagnosis of CMS, as well as residence above 2500 m
(8202 feet) and absence of lung disease.246 The reader is referred
to reviews for in-depth information.298,345,347,483 In addition, an
international consensus group has defined and scored CMS.245
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
subjective improvement, although without significant objective
changes.476 The respiratory stimulants medroxyprogesterone
acetate (20 to 60 mg/day)232 and acetazolamide (250 or 500 mg/
day)354 have also been shown to reduce hematocrit value by
improving oxygenation. Acetazolamide (250 mg) increased noc-
turnal SaO2 by 5%, decreased mean nocturnal heart rate by 11%,
the number of apnea/hypopnea episodes during sleep by 74%,
and hematocrit by 7%.354 The fact that these responses likely
occur as a result of increased ventilation after acetazolamide
administration358 emphasizes the contribution of hypoventilation
and nocturnal desaturation to CMS.329 Another approach was
based on the knowledge that ACE inhibitors blunt hypoxia-
mediated erythropoietin release. Plata and associates334 showed
that 5 mg/day of enalapril for 2 years reduced hemoglobin con-
centration, packed cell volume, proteinuria, and need for phle-
botomy.334 Pulmonary hypertension and right-sided heart failure
may also occur in persons with CMS.
MOUNTAIN MEDICINE
Symptomatic High-Altitude Pulmonary Hypertension.  at altitude, including symptoms of AMS unique to infants.320
Children living at high altitude may be at risk for symptomatic
high-altitude pulmonary hypertension (SHAPH)321,329 This clinical
entity has also been described in adults.5 SHAPH has been iden-
tified in South America, North America, and Asia, with a pre­
dilection in populations not genetically adapted to altitude.
Former names for SHAPH have included “pediatric high-altitude
heart disease” and “subacute infantile mountain sickness.” The
underlying pathophysiology is pulmonary hypertension result-
ing in hypertrophy and dilation of the right ventricle, with even-
tual right-sided heart failure. Clinically, these children have poor
growth, fatigue, irritability, dyspnea, and cyanosis or pallor. On
PART 1
physical examination, as the illness advances, hepatomegaly
and leg edema signal right-sided heart failure. ABGs and pulse
oximetry reveal exaggerated hypoxemia. Chest radiography
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 of SHAPH 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 inhibi-
tors.246 A similar phenomenon has been also been described in
adults after weeks to years of high-altitude residence5,8 and may
respond to treatment with PDE-5 inhibitors.4
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.319 In populations better
adapted to high altitude over many generations, neonatal transi-
tion has not been as well scrutinized, but there does appear to
be some morbidity. High-altitude residence does not clearly
impact eventual stature, but growth and development are
slowed.321,470 In low-income countries, 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.87
Although several studies have shown that lowland children
traveling to high altitude are just as likely336 or less likely than
26
adults to develop AMS,229 no data indicate that children are more
susceptible to altitude illness. Studying this issue is difficult,
however, because diagnosis can be more difficult in preverbal
children.493 Despite this somewhat reassuring fact, very conserva-
tive recommendations are made regarding taking children to high
altitude; it should be clarified that these opinions are not based
on science.35,335 Durmowicz and colleagues107 showed that chil-
dren with HAPE had a high frequency of concomitant respiratory
infections. Children with Down syndrome, past repair of con-
genital shunts, following chemotherapy, and with other problems
are more susceptible to HAPE.107 Acetazolamide can be used for
prevention and treatment of AMS/HACE in children (5 mg/kg/
day in divided doses) (see Table 2-3),108 while dexamethasone
should be reserved for treatment only and not used for preven-
tion. Pollard and associates336 provide an excellent consensus
document on children at altitude,336 and excellent reviews are
available.108,321,493 Healthy term newborns of 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.320 Infants with viral infections, neonatal intensive care unit
stay, transient oxygen treatment, Down syndrome, or any pul-
monary condition or cardiac defect should be carefully evaluated
by a physician regarding altitude exposure (see Figure 2-10). For
all infants going to altitude, pulse oximetry monitoring should
be considered. Parents need to be aware of potential problems
OTHER MEDICAL CONCERNS
AT HIGH ALTITUDE
CARBON MONOXIDE POISONING
Carbon monoxide poisoning is a danger at high altitude, where
field shelters are designed to be small and windproof. Cooking
inside poorly ventilated tents and snow shelters during storms is
a particular hazard.126,216,244,373,445,449 The effects of CO and high-
altitude hypoxia are additive. A reduction in oxyhemoglobin
caused by CO increases hypoxic stress, rendering a person at a
“physiologically higher” altitude, which may precipitate AMS.
Because of preexisting hypoxemia, smaller amounts of carboxy-
hemoglobin produce symptoms of CO poisoning. These two
problems may coexist. Immediate removal of the victim from the
CO source and provision of supplemental oxygen, if available,
constitute the treatment of choice. Portable hyperbaric therapy
might also be useful.
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.217 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 sup-
plemental oxygen, death can occur within 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.123
Loss of body weight is a prominent feature during expeditions
to extreme high altitude. Pugh338 reported 14 to 20 kg (30.9 to
44 lb) of body weight loss in climbers on the 1953 British Mt
Everest Expedition. Almost 30 years later, with improvement in
food and cooking techniques, climbers on the American Medical
Research Expedition to Mt Everest (AMREE) still lost an average
of 6 kg (13.2 lb).55 This was caused in part by 49% decrease in
fat absorption and 24% decrease in carbohydrate absorption.
During Operation Everest II (OEII), in which the “climbers” were
allowed to eat foods of their choosing ad libitum, they still had
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).374,185 At
4300 m (14,108 feet), weight loss was attenuated by adjusting
caloric intake to match caloric expenditure.65 In fact, recent work
supports hypoxic exposure as a treatment for obesity.249,315,342,404
Thus, significant weight loss with prolonged exposure to high
altitude may be overcome with adequate caloric intake, but
decreased appetite is a problem.448,211 At very high altitudes, an
increase in caloric intake may not be sufficient to counteract
completely the severe anorexia and weight loss, because other
mechanisms may come into play.
Regarding extreme altitude, Ryn378 reported an incidence of
acute organic brain syndrome in 35% of climbers going above
7000 m (22,966 feet), in association with high-altitude deteriora-
tion. 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 altitude316,317 but is not observed in mountaineers at
higher altitudes; it is a problem of acute induction to altitude.305
The mechanism is an unstable cardiovascular control system, and
it is considered a form of neurohumoral (or neurocardiogenic)
syncope.128 An unstable state of cerebral autoregulation may also
play a role.498 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.36
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).178 The effect of alcohol on altitude tolerance and acclima-
tization might therefore be of considerable relevance. Roeggla
and co-workers370 measured ABGs 1 hour after ingestion of 50 g
of alcohol (equivalent to 1 L of beer, five mixed drinks, or five
3-oz glasses of wine) at 171 m (561 feet) and again after 4 hours
at 3000 m (9843 feet). A placebo-controlled, double-blind paired
design was used. For the 10 participants, alcohol had no effect
on ventilation at the low altitude, but at high altitude it depressed
ventilation, as gauged 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 AMS or
whether repeated doses would have greater effect was not tested.
Nonetheless, 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,285 who was concerned
about the interaction in aviators, stated that “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.”285 McFarland’s original observations were
made on two individuals in the Andes in 1936. McFarland and
Forbes386 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).286 Most subsequent studies refuted the increased blood
alcohol concentration data except at altitudes over 5450 m
(17,881 feet). A series of chamber studies173,174 found blood
alcohol levels were similar at 392 and 3660 m (1286 and 12,008
feet), and there were no synergistic effects of alcohol and
altitude.
Lategola and colleagues239 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 altitude of
3810 m (12,500 feet), with blood alcohol level of 88 mg%.79
Performance was not affected by hypoxia, only by alcohol, and
older persons were more affected. When more demanding tasks
CHAPTER 2  High-Altitude Medicine and Pathophysiology
were tested, a blood alcohol level of 91 mg% affected perfor-
mance, as did an altitude of 3660 m (12,008 feet) during night
sessions when the participants were sleep-deprived, but there
was no significant altitude-alcohol interaction.78 In the one study
in which investigators were able to discern some altitude effect,
there was a simple additive interaction of altitude (hypoxic gas
breathing) and alcohol.80 The authors concluded that perfor-
mance decrements caused by alcohol may be increased by alti-
tudes of 3660 m if subjects are negatively affected by that altitude
without alcohol. All 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. Alcohol affected auditory
evoked potentials the same as in Denver; that is, no influence
of altitude was detectable.127
In summary, limited data on ABGs at altitude after moderate
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 (12,008 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
unknown.
THROMBOSIS: COAGULATION AND
PLATELET CHANGES
Autopsy findings in deaths caused by altitude illness of wide-
spread thrombi in the brain and lungs, as well as the impression
that thrombosis is greater at altitude,202 have led to many inves-
tigations of the clotting mechanism at high altitude (for a review,
see Grover and Bärtsch145). Although changes in platelets and
coagulation have been observed in rabbits, mice, rats, calves,
and humans on ascent to high altitude,172 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 moun-
tains, and higher in chambers, have generally not found changes
in coagulation and fibrinolysis.145 Also, a recent field study using
thromboelastography in healthy volunteers ascending to Everest
Base Camp showed that coagulation may actually be slowed at
high altitude.276 Although the increased incidence of thrombosis
in soldiers and others at extreme altitude can be attributed to
dehydration, polycythemia, and forced inactivity,56,454 some evi-
dence indicates enhanced fibrin formation with stay of a few
weeks above 5000 m (16,404 feet).370 In addition, unexplained
thrombosis is reported at moderate altitude of 4000 to 5000 m72,118
and at extreme altitude.10,218
As for thrombosis in HAPE, Singh and colleagues408 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 vas-
cular disease in soldiers who had recently arrived at extreme
altitude.407 A series of experiments by Bärtsch and colleagues,22
however, carefully examined this issue in well individuals and
in those with AMS and HAPE.145 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 patho-
physiologic factor, and likely caused by inflammation from struc-
tural 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,10,33,52,205,218,313 although cause and effect cannot be estab-
lished with certainty. Schreijer and colleagues398 demonstrated
increased thrombin-antithrombin complex formation during 8
hours of hypobaric hypoxia on an airplane in patients with factor
V Leiden mutation, but neither this nor other studies have shown
that this is associated with increased risk of thromboembolism at
27
 high altitude. See Chapter 3 for more detailed discussion regard-
ing these patients and those with previous venous thromboem-
bolism problems.
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.153 Although not a serious clinical
problem, edema can be bothersome. When seen in conjunction
with dyspnea or neurologic symptoms and signs, presence of
peripheral edema should prompt evaluation 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 results in diuresis and resolu-
tion of peripheral edema. The mechanism is presumably similar
to fluid retention in AMS but may also merely be caused by
exercise.291
IMMUNOSUPPRESSION
Mountaineers have observed that infections are common at high
altitude, slow to resolve, and often resistant to antibiotics.310 On
the AMREE in 1981, serious skin and soft tissue infections devel-
MOUNTAIN MEDICINE
oped. “Nearly every accidental wound, no matter how small,
suppurated for a period of time and subsequently healed
slowly.”382 A suppurative hand wound and septic olecranon bur-
sitis 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 high-altitude 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.288 In contrast, B cells and active
PART 1
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
adrenocorticotropic hormone, cortisone, and β-endorphins, all of
which modulate the immune response.292,115 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 high alti-
tude should be anticipated in situations where infection could
be a complication, such as trauma, burns, and surgical and inva-
sive procedures.
SLEEP AT HIGH ALTITUDE
Disturbed sleep is common at high altitude for a variety of
reasons, which have been described in detail.3,58,260,457,465,469 Almost
all sojourners 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.220 The subjective complaints of poor sleep are dispro-
portionate to the small reduction (if any) in total sleep time and
appear to result from 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.11 The mechanisms of this change in
sleep architecture and fragmentation are poorly understood.
Periodic breathing appears to play only a minor role in altering
sleep architecture at high altitude.380 The arousals have been
28
linked to periodic breathing in some studies but not in others.
Other factors might include change in circadian rhythm and
perhaps body temperature.83 Obesity may explain susceptibility
to both deranged sleep and sleep-disordered breathing in some
individuals.133 Studies of infants and children492 and athletes in
simulated-altitude devices used for training have also revealed
deranged sleep quality in these groups.221,222,327 Although a fre-
quent complaint in high-altitude visitors, deranged sleep 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 Sick-
ness, earlier).
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 (Video 2-1). Unlike in obstructive sleep apnea, where
respiratory efforts are made but airflow does not occur because
of upper airway obstruction, the apnea of periodic breathing is
central in origin, not associated with snoring, and occurs with
absence of rib cage movement.
The phenomenon is caused by abnormal feedback control in
CNS respiratory centers.73,219 Hypoxemia leads to increased
peripheral chemoreceptor output and a subsequent increase in
minute ventilation. If the ventilatory response is large enough,
PaCO2 falls below the apnea threshold in the central chemorecep-
tors, and apnea ensues. The decrease in SaO2 and increase in
PaCO2 that occur during the apneic period eventually trigger an
increase in ventilation and termination of apnea. If this corrective
response is excessive, the PaCO2 again falls below the apnea
threshold in the central chemoreceptor, leading to another
episode of apnea. A key feature of this process is that the
response to the disturbance, in this case the increase in ventila-
tion with hypoxemia and increasing PaCO2, is excessive. This fits
with the observation that persons with high hypoxic ventilatory
response have more periodic breathing,48 with mild oscillations
in SaO2,236 whereas persons with low hypoxic ventilatory response
have more regular breathing overall but may have periods of
apnea with extreme hypoxemia distinct from periodic breath-
ing.160 As acclimatization progresses, periodic breathing lessens
but does not disappear, especially above 5000 m (16,404 feet),
and sleep SaO2 increases.11,48,430
Periodic breathing has not been implicated in the etiology
of high-altitude illness, but nocturnal oxygen desaturation has
been implicated.48,129,114 Eichenberger and colleagues110 have also
reported greater periodic breathing in persons with HAPE, sec-
ondary to lower SaO2. As with fragmented sleep, intensity
of periodic breathing is quite variable. Total sleep time with
periodic breathing has been shown to vary between 1% and
90%501 and to increase with increasing altitude.48 Most studies
report no association between periodic breathing and AMS.48
This may relate to the fact that persons with periodic breathing
tend to have higher HVR and greater average ventilation and
oxygenation.465
Pharmaceutical Aids for Sleep
Acetazolamide (125 mg at bedtime) diminishes periodic breath-
ing and awakenings, improves oxygenation and sleep quality,
and is a safe agent to use as a sleeping aid with the added benefit
of diminishing symptoms of AMS (Figure 2-11). 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.260 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.102,139,318 Another
option is to use both acetazolamide and a benzodiazepine. Acet-
azolamide (500 mg slow release PO) given with temazepam
(10 mg PO) improved sleep and maintained SaO2, counteracting
a 20% decrease in SaO2 when temazepam was given alone.318 The
nonbenzodiazepine hypnotic zolpidem (Ambien), 10 mg, was
shown to improve sleep at 4000 m (13,123 feet) without adversely
affecting ventilation.40
 play a role. In the field, these problems usually appear without
Placebo
fever or chills, myalgia, lymphadenopathy, exudate, or other
signs of infection. The increase in ventilation, especially with
Respiratory pattern exercise, forces obligate mouth breathing at altitude, bypassing
the warming and moisturizing action of the nasal mucous mem-
100 branes and sinuses. Movement of large volumes of dry, cold air
80 across the pharyngeal mucosa can cause marked dehydration,
SaO2 (%)
60 irritation, and pain, similar to pharyngitis. Vasomotor rhinitis,
40 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
Acetazolamide expedition medical kit. Other countermeasures include forced
hydration, hard candies, lozenges, and steam inhalation.
High-altitude bronchitis can be disabling because of severe
Respiratory pattern coughing spasms. Cough fracture of one or more ribs is not
rare.251 Purulent sputum is common. Response to antibiotics is
100
poor; most patients resign themselves to taking medications such
80
SaO2 (%) as codeine and do not expect a cure until descent.343 Mean
60 sputum production was 6 teaspoons per day. All reported that
40 onset was after a period of excessive hyperventilation associated
with strenuous activity. Although an infectious etiology is pos-
FIGURE 2-11  Respiratory patterns and arterial oxygen saturation sible, experimental evidence suggests that respiratory heat loss
(SaO2) with placebo and acetazolamide in two sleep studies of a person results in purulent sputum and sufficient airway irritation to cause
at 4200 m (13,780 feet). Note pattern of hyperpnea followed by apnea persistent cough.284 This is supported by the beneficial effect of
during placebo treatment, which is changed with acetazolamide. steam inhalation and lack of response to antibiotics. Many climb-
ers 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
HIGH-ALTITUDE PHARYNGITIS, BRONCHITIS fluticasone and salmeterol or similar inhaled agents and report
success; studies of these medications are underway. Differential
AND COUGH diagnosis of persistent cough in these conditions can be
Sore throat, chronic cough, and bronchitis are almost universal difficult.138
in persons who spend more than 2 weeks at an extreme altitude
(>5500 m [18,045 feet).75,251,277,305 All 21 members of the 1981
AMREE experienced these problems.382 Only two of eight persons REFERENCES
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threshold, thus exacerbating high-altitude cough.278 Other factors
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485. Wu T, Ding S, Liu J, et al. Ataxia: An early indicator in high altitude
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486. Wu TY, Ding SQ, Liu JL, et al. Reduced incidence and severity of
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29.e9

CHAPTER 3 
High Altitude and Preexisting
Medical Conditions
ANDREW M. LUKS AND PETER H. HACKETT
Given the prevalence of diseases such as asthma, hypertension,
and diabetes mellitus in the general population, it is likely that
many high-altitude travelers have one or several underlying
medical conditions. Although the majority of these individuals
have mild, well-controlled conditions that should not create
issues during planned travel, ongoing improvements in medical
care and the growing ease of travel have increased the likelihood
that some high-altitude travelers have more moderate to severe
forms of underlying disease that may pose challenges in this
environment. Regardless of the severity of their underlying prob-
lems, patients may present to their primary care provider or a
travel medicine clinic prior to travel seeking advice about the
safety of their planned trip and how best to manage their disease
during the sojourn. When faced with these situations, providers
must ask the following two questions:
CHAPTER 3  High Altitude and Preexisting Medical Conditions
1. Will the underlying disease worsen at high altitude?
2. Will the underlying disease affect acclimatization to hypobaric
hypoxia and predispose the individual to an increased risk of
acute altitude illness?
In addition, clinicians working in high-altitude locations are
often faced with consequences of the interaction between alti-
tude hypoxia and common preexisting medical conditions of
travelers. This chapter provides information that can be used to
address these questions. After presenting a general framework
for evaluating the high-altitude traveler with underlying medical
conditions, we describe the available evidence regarding a wide
variety of diseases likely to be encountered in such clinical situ-
ations. Additional information is available in extensive reviews
on this topic,67,93 and further disease-specific studies are cited in
the appropriate sections below.
29
 A GENERAL FRAMEWORK
FOR EVALUATING TRAVELERS
WITH UNDERLYING
MEDICAL CONDITIONS
One of the challenges of evaluating individuals with underlying
medical conditions who are planning high-altitude travel is that
for many diseases, such as chronic obstructive pulmonary disease
(COPD) or hypertension, research on how these patients fare at
high altitude is limited, whereas for other diseases, there is practi-
cally no evidence to guide the pretravel assessment. In light of
this situation, providers can apply the following general approach
to determining whether the planned sojourn is safe, whether
further evaluation is necessary before the trip, and whether risk
mitigation strategies are indicated.
The initial assessment should be framed around four general
questions, as follows:
1. Is my patient at risk for severe hypoxemia or impaired tissue
oxygen delivery at high altitude? Certain categories of patients,
such as those with chronic lung diseases, heart failure, cya-
notic congenital heart disease, or sleep-disordered breathing,
can be expected to develop increased hypoxemia beyond that
experienced by normal individuals at a given altitude. This
exaggerated hypoxemia will have the same effect as being at
a higher altitude. Further information about the extent to
MOUNTAIN MEDICINE
which this will happen is provided in the discussion of each
specific disease. More severe hypoxemia is a concern because
it may lead to increased dyspnea and decreased exertional
tolerance and, in some studies, has been associated with
increased risk of developing acute altitude illness. In addition,
it may impact comorbid conditions. Patients with severe
anemia will not experience a change in arterial oxygen partial
pressure (PaO2) at rest compared with normal individuals, but
anemia patients will have problems with decreased oxygen-
carrying capacity, which can lead to worsening dyspnea and
poor exertional tolerance.
2. Can my patient mount the expected ventilatory responses to
PART 1
hypobaric hypoxia at high altitude? Arterial hypoxemia at high
altitude stimulates the peripheral chemoreceptors, leading to
an increase in minute ventilation, the primary role of which
is to defend alveolar oxygen tension (PAO2) against the effects
of decreased ambient PO2. Although the magnitude of this
response varies between individuals, most are able to mount
this response. Patients with disorders affecting respiratory
mechanics, such as very severe COPD, morbid obesity, or
various neuromuscular disorders, and individuals at risk for
impaired chemoreceptor responses may not be able to mount
the expected ventilatory response and thus may be at risk for
increased levels of hypoxemia.
3. Is my patient at risk because of the expected pulmonary
vascular responses to hypobaric hypoxia at high altitude?
Decreased PAO2 triggers hypoxic pulmonary vasoconstriction,
which in conjunction with the increase in cardiac output fol-
lowing ascent, causes increased pulmonary artery pressure
(PAP). The magnitude of this response varies between indi-
viduals and is well tolerated by most travelers but could
represent a problem for patients with underlying pulmonary
hypertension. This is because the further increase in PAP
may worsen right-sided heart function, leading to increased
dyspnea, impaired hemodynamics, and as described later,
development of high-altitude pulmonary edema (HAPE).
4. Will hypobaric hypoxia at high altitude worsen control of the
underlying medical condition(s)? Although data are lacking
with regard to many chronic diseases, more information has
become available in recent years regarding the effects of
hypobaric hypoxia on common medical problems such as
asthma, hypertension, and obstructive sleep apnea, which are
reviewed in detail later. Patients should be assessed in light
of the available information to evaluate the likelihood of
worsening disease control after ascent (see Chapter 2).
If reassuring answers are obtained with regard to all these
questions, the individual is likely safe to travel to high altitude
without further evaluation. Nonreassuring answers to these ques-
30
tions should prompt evaluation to clarify the risk further and to
assess and develop risk mitigation strategies for the sojourn,
including evacuation to lower altitude. Depending on the under-
lying disease process, tests that may be considered as part of
such an evaluation would include pulmonary function testing,
hypoxia altitude simulation testing,44 echocardiography, and car-
diopulmonary exercise testing. Canceling the planned travel is a
consideration if risk is deemed to be too high or if adequate risk
mitigation strategies are not feasible. Details of this evaluation
are provided in the discussions of specific diseases and lead to
another question:
5. At what altitude does risk increase for patients with underlying
medical problems? In general, important physiologic responses
to hypobaric hypoxia, such as the ventilatory response to
hypoxia and hypoxic pulmonary vasoconstriction, occur at
about 2000 m (6560 feet) when PaO2 falls below 70 mm Hg,9
whereas the risk of altitude illness is thought to increase when
individuals ascend above 2500 m (8200 feet). These are useful
thresholds for trip planning, but one should not assume that
all patients with underlying medical conditions are safe below
these altitudes. Patients with unilateral absence of pulmonary
arteries have developed HAPE at as low as 1500 m (4920
feet),130 which shows that certain patients may fare poorly at
elevations lower than these thresholds. In other cases, the
underlying medical condition may not be an issue until ascent
to elevations far above these levels. In the end, the altitude
at which risk for problems increases will be a function of the
particular disease and its severity.
MITIGATING RISK WITH PLANNED ASCENT
Although the appropriate risk mitigation strategy will vary among
travelers based on the underlying medical condition, all travelers
with underlying medical problems should adhere to several
general principles. First, the traveler must ensure that the underly-
ing medical problem is under good control at the time of the
planned trip. Patients with worsening control of heart failure or
asthma, for example, should not travel to high altitude, particu-
larly into remote areas. Second, the traveler should continue
regular medications and therapies during the trip and, in some
cases, such as diabetes or poorly controlled hypertension, should
consider more frequent monitoring of the disease, with adjust-
ment of medications according to a prespecified plan. Third,
patients at risk for disease exacerbations, such as those with
asthma, COPD, or cardiac arrhythmia, should travel with an
adequate supply of rescue medications and a plan for using these
therapies. Lastly, travelers should identify medical resources at
their planned destination and travel with a plan to access these
resources or descend in the event of severe problems. Arranging
suitable travel insurance, particularly with international travel,
will greatly facilitate any necessary evacuation. Further details
about risk mitigation in specific conditions are provided in the
following discussions.
SPECIFIC MEDICAL CONDITIONS AT
HIGH ALTITUDE
Having considered this general framework, we now discuss a
variety of medical conditions that might pose problems for
individuals traveling to high altitude. Table 3-1 lists specific
patient groups and potential conditions that warrant consider-
ation as well as the relative safety or risk associated with high
altitude.
RESPIRATORY DISEASES
Chronic Obstructive Pulmonary Disease
Minimal data are available regarding outcomes for patients with
COPD who travel to high altitude, and most of the available
information pertains to changes in oxygenation rather than
changes in airway function.95 Aside from a single study of COPD
patients at terrestrial high altitude,65 most information about the
effects of hypobaric hypoxia on these patients comes from the
 CHAPTER 3  High Altitude and Preexisting Medical Conditions
TABLE 3-1  High-Altitude Travel Risk Associated with Various Underlying Medical Conditions

Likely No Extra Risk Caution Required Ascent Contraindicated

Children and adolescents Infants <6 weeks old Sickle cell anemia
Elderly individuals Compensated heart failure Severe to very severe COPD
Sedentary individuals Morbid obesity Pulmonary hypertension (systolic PAP >60 mm Hg)
Mild obesity Cystic fibrosis (FEV1 30-50% predicted) Unstable angina
Well-controlled asthma Poorly controlled arrhythmia Decompensated heart failure
Diabetes mellitus Poorly controlled asthma High-risk pregnancy
CAD following revascularization Poorly controlled hypertension Cystic fibrosis (FEV1 <30% predicted)
Mild COPD Moderate COPD Recent myocardial infarction or stroke (<90 days)
Low-risk pregnancy Stable angina Untreated cerebrovascular aneurysms or arteriovenous
Mild-moderate obstructive Non-revascularized CAD malformations
sleep apnea Sickle cell trait Cerebral space-occupying lesions
Controlled hypertension Poorly controlled seizure disorder
Controlled seizure disorder Cirrhosis
Psychiatric disorders Mild pulmonary hypertension
Neoplastic diseases Radial keratotomy surgery
Severe obstructive sleep apnea

CAD, Coronary artery disease; COPD, chronic obstructive pulmonary disease; FEV1, forced expiratory volume in 1 second; PAP, pulmonary artery pressure.

literature on commercial flight. The data suggest that patients
with a forced expiratory volume in 1 second (FEV1) of 1.0 to 1.5
liters (L) manifest hypoxemia when exposed to the equivalent of
2340 m (8000 feet), with average PaO2 values approximately
50 mm Hg (Table 3-2). Mild degrees of exertion, such as walking
on flat ground or cycling on an ergometer at a low work rate,
lead to further decreases below these levels. These values are
significant; guidelines from the British Thoracic Society, American
Thoracic Society, and Aerospace Medical Association all suggest
supplemental oxygen should be employed in patients whose PO2
is expected to be in this range at elevations of approximately
2340 m (8000 feet). Recognizing that these thresholds lack sup-
porting data and are somewhat arbitrary, it is reasonable to ask
whether COPD patients need supplemental oxygen with travel
to similar altitudes in the mountains. How to apply such guide-
lines at higher elevations is unclear, however, because even
normal individuals will have PaO2 of approximately 50 mm Hg
with acute exposure to elevations greater than 4200 to 4500 m
(13,770 to 14,760 feet) and clearly do not require supplemental
oxygen in these circumstances.
Predicting which patients will develop clinically significant
hypoxemia at high altitude is challenging. A variety of prediction
rules are available that take into account sea level blood gases,
pulmonary function test results, and other variables,30,42,61,62 but

TABLE 3-2  Changes in Oxygenation in Lung Disease Patients Exposed to Hypoxia

PaO2 at PaO2 in
Sea Level Hypoxia PaO2 with Exertion in
Study Patient Population (N) Disease Severity Exposure (mm Hg) (mm Hg) Hypoxia (mm Hg)

Graham and COPD (8) FEV1 1.27 ±0.36 L 1920 m (6300 ft) 66 ±7 52 ±7 47 ±9 (treadmill walking)
Houston65 (1978) (terrestrial)
Christensen et al30 COPD (15) FEV1 0.98 ±0.4 L 2430 m (7970 ft) 88 ±9 53 ±7 44 ±6 (cycle at 20-30 W)
(2000) (simulated)
Akero et al4 (2005) COPD (18) FEV1 1.5 ±0.6 L 1830 m (6000 ft) 77 ±9 63 ±6 SpO2 87 ±4% (walking in
(commercial aisle)
flight)
Seccombe et al140 COPD (10) FEV1 1.2 ±0.4 L 2430 m (7970 ft) 77 ±577 ±5 45 ±4 39 ±3 (walk 50 m on flat
(2004) (simulated) ground)
Interstitial lung disease FEV1 1.8 ±0.6 L 2430 m (7970 ft) 82 ±7 50 ±7 40 ±5 (walk 50 m on flat
(15) (simulated) ground)
Christensen Restrictive disease TLC 3.2 ±1 L 2430 m (7970 ft) 76 ±12 47 ±8 37 ±7 (cycle at 20 W)
et al31 (2002) (TB, kyphoscoliosis, (simulated)
fibrosis) (17)
Mestry et al106 Restrictive disease Median FEV1 0.7 L 2430 m (7970 ft) 75 ±10 49 ±4 No data
(2009) (polio, kyphoscoliosis, (range, 0.3-1.0 L) (simulated)
neuromuscular
disease) (19)
Fischer et al52 Cystic fibrosis (36) Median FEV1 66% 2650 m (8690 ft) 74 (range, 52 (range, 47 (range, 33-69) (cycle
(2005) predicted (range, (terrestrial) 60-98) 40-79) at 30 W)
<26-107%)
Thews et al149 Cystic fibrosis (10) FEV1 2.1 ±0.3 L 3000 m (9840 ft) 75 ±4 46 ±1 No data
(2004) (simulated)

COPD, Chronic obstructive pulmonary disease; FEV1, forced expiratory volume in 1 second; SpO2, oxygen saturation as measured by pulse oximetry; TB, tuberculosis:
TLC, total lung capacity; W, watts.

31
 the rules are designed to predict the degree of hypoxemia during
short exposures to 2340 m (8000 feet), the maximum allowed
altitude in cabin aircraft. These rules have not been validated for
the wide range of elevations that patients may visit or the dura-
tion of exposure they are likely to experience during their
travels. An alternative approach is the hypoxia altitude simula-
tion test, in which oxygenation and other parameters are moni-
tored while a patient breathes a hypoxic gas mixture at rest.44
This test should more accurately reflect the degree of expected
hypoxemia than do the prediction rules, but it is limited by
its short duration relative to the duration of exposure to high
altitude, the inability to account for changes in ventilation that
will occur over long stays at high altitude, and difficulties admin-
istering hypoxic gas mixtures simulating the altitude the patient
will visit.
An important question that arises from the available literature
is whether supplemental oxygen is necessary to counteract the
expected hypoxemia, as the guidelines recommend. It is note-
worthy that in the majority of studies previously cited, most
patients had mild symptoms and experienced few, if any, adverse
events despite having hypoxemia disproportionate to that
expected for normal individuals at the same elevation. Given this
issue, as well as the logistical difficulties of traveling with supple-
mental oxygen, a more practical alternative would be to travel
with plans to monitor symptoms and oxygen saturation (SpO2)
on arrival using a portable pulse oximeter and a prescription for
MOUNTAIN MEDICINE
supplemental oxygen to use if difficulties arise.91 In North
America, for example, home oxygen companies accept prescrip-
tions from physicians in any state, and oxygen is easily obtained.
Patients already receiving supplemental oxygen should continue
therapy during their travels but need to increase the gas flow to
account for the drop in barometric pressure. A useful rule of
thumb is to increase the inspiratory flow rate by the ratio of
higher to lower barometric pressure. Portable oxygen concentra-
tors provide a convenient alternative to oxygen gas cylinders,
provided patients can recharge the batteries. However, these
devices may not deliver the same inspired oxygen concentration
at altitude as at sea level.
PART 1
Except for the hypoxemia issue, no information in the litera-
ture addresses the risk of acute altitude illness in COPD patients.
Use of acetazolamide for altitude illness prophylaxis in COPD
patients has not been studied. Caution is necessary when con-
sidering acetazolamide in patients with FEV1 of less than 25%
predicted, because it may lead to impaired carbon dioxide elimi-
nation and worsening hypercarbia.95,97 In patients whose COPD
is complicated by pulmonary hypertension, further increases in
PAP after ascent could theoretically increase the risk of HAPE or
right-sided heart dysfunction. As discussed later, this issue has
not been formally studied in this patient population. No evidence
suggests that patients with bullous emphysema are at increased
risk for pneumothorax or other forms of pulmonary barotrauma
after ascent, or that ascent to high altitude leads to deterioration
in markers of pulmonary function.95 Patients should continue
taking their baseline medications at high altitude and travel with
an adequate supply of rescue inhalers and prednisone in the
event of an exacerbation during their trip, particularly if visiting
an area remote from medical care.
Interstitial Lung Disease
Compared with COPD patients, fewer studies are available
regarding the risks of hypobaric hypoxia in patients with inter-
stitial lung disease (ILD), such as idiopathic pulmonary fibrosis
or sarcoidosis. Limited evidence from the literature on hypoxemia
during commercial flight demonstrates that patients with a variety
of ILDs and FEV1 of about 50% to 55% predicted develop signifi-
cant hypoxemia with exposure to 2430 m (8000 feet), which
worsens with exertion (Table 3-2).31,140 Prediction rules to assess
the risk of hypoxemia in ILD patients are available as for COPD
patients, but utility is limited by the same considerations noted
earlier, and the hypoxia altitude simulation test likely remains
the best tool for assessing risk. Similar principles on traveling
with a prescription for supplemental oxygen and monitoring
symptoms and pulse oximetry after arrival should likely be
applied in ILD patients as well.
32
Asthma
Doan and Luks45 recently reviewed the issue of asthma manage-
ment in the wilderness, particularly at high altitude. From a theo-
retical standpoint, multiple factors at high altitude could affect
airway function in asthmatic patients. On the one hand, lower
air density and decreased number of dust mites155 would be
expected to lead to better control. On the other hand, many
asthmatic patients experience worsening control when exercis-
ing, particularly in the cold, dry air typical of the high-altitude
environment. A high incidence of asthma and asthma-like symp-
toms has been documented in epidemiologic studies of cross-
country skiers; this activity is associated with high minute
ventilation in a cold environment.81 Other studies have docu-
mented a 50% incidence of exercise-induced bronchoconstriction
(EIB) in highly trained ski mountaineers in the Alps, even though
almost three-quarters of these individuals had never been diag-
nosed with EIB.47
Current evidence suggests that despite these concerns, the
majority of well-controlled asthmatic patients do well with expo-
sures to altitudes as high as 6000 m (19,685 feet). Several studies
have documented decreased bronchial hyperresponsiveness to
hypoosmolar aerosols and methacholine after travel to altitudes
of 4559 and 5050 m (14,950 and 16,560 feet)5,32 and no increase
in symptoms, need for medications, exacerbations, or risk of
acute mountain sickness (AMS) with ascent to elevations of 5895
to 6400 m (19,335 to 20,990 feet).74,147 Other studies have noted
small decreases in FEV1 or peak expiratory flow at high altitude,
but these were not associated with any changes in patient symp-
toms and likely were not clinically significant.89,105, In a survey
study of asthmatic patients seen in a travel clinic, almost 75% of
whom traveled to high altitude, 43% reported worsening asthma
control during their trip, and 37% experienced the “worst asthma
attack of my life.”60 This study, however, did not account for the
altitudes attained by these patients or the fact that many high-
altitude trips require transit through large cities such as Kath-
mandu or Bangkok or environments with very poor air quality.
Aside from concerns about asthma control, the available literature
has not reported an increased incidence of acute altitude illness
in asthmatic patients.74,147 Acetazolamide use also appears to be
safe in this patient population.107
In summary, patients with mild, well-controlled asthma can
travel to altitudes over 6000 m (19,685 feet). Individuals with
worsening control at the time of their planned trip or with per-
sistent, moderate to severe disease should avoid high-altitude
travel, particularly travel into remote areas with inadequate
access to medical care. All patients should continue their baseline
medication regimen and carry an adequate supply of rescue
inhalers and prednisone in the event control worsens before they
can access care. Patients with known EIB or cold-induced bron-
choconstriction can consider adding or increasing the intensity
of their controller therapy or taking preexercise short-acting
β-agonists or leukotriene receptor blockers. Further details on
asthma control in the wilderness are provided in Chapters 53 and
94, and several reviews on this topic are available.33,45
Cystic Fibrosis
Although data on the effect of high altitude on pulmonary func-
tion in cystic fibrosis (CF) patients are inconsistent,52,133,149, CF
patients experience more severe hypoxemia than normal indi-
viduals when exposed to altitudes of 2000 to 3000 m (6560 to
9840 feet), with the largest decrements seen in patients with
greater degrees of impaired pulmonary function52,133 (Table 3-2).
As with the studies in COPD patients previously noted, these
exaggerated levels of hypoxemia were not associated with
increased symptoms or an increased risk of AMS,52,133 although
the duration of exposure was short. There are reports of patients
with severe CF (FEV1 ~1 L) developing pulmonary hypertension
and cor pulmonale during ski trips to this environment.145 Predic-
tion rules are available to assess the likelihood of severe hypox-
emia at high altitude but are poor predictors of PaO2 at altitude
in CF patients and are limited by the same issues noted with
COPD.52,77,118, Given significant improvements in the quality of CF
care in the past decade, it is also unclear whether older data
and prediction rules still apply to the current population of CF
patients. There is no evidence that exposure to high altitude leads
to an increased incidence of CF exacerbations.
As with asthmatic patients, CF patients should only travel to
high altitude when their disease is under good control. High-
altitude travel should be avoided in patients with worsening
symptom control, recent exacerbations, or FEV1 of less than 30%
predicted. Given difficulties with the prediction rules for hypox-
emia, patients with FEV1 of 30% to 50% predicted should travel
to high altitude with a prescription for supplemental oxygen that
can be filled in the event symptom and pulse oximetry monitor-
ing raise concerns. All patients should continue their baseline
antibiotic and mucolytic regimens and scheduled airway clear-
ance strategies.
Pulmonary Hypertension
The decrease in PAO2 after ascent leads to hypoxic pulmonary
vasoconstriction, which in conjunction with the rise in cardiac
output leads to an increased PAP. Most individuals tolerate this
rise in pressure without difficulty, but patients with underlying
pulmonary hypertension or right-sided heart dysfunction may be
at risk for capillary stress failure (pulmonary edema) or worsen-
ing right-sided heart function. Multiple case reports and case
series, for example, have documented development of HAPE
after ascent in patients with pulmonary hypertension as a result
of both anatomic and nonanatomic factors.48,68,112,130,153 Other
reports have documented right-sided heart failure in patients with
morbid obesity and severe kyphoscoliosis, two problems associ-
ated with pulmonary hypertension, during commercial flight.115,151
The degree of baseline pulmonary hypertension necessary to
increase risk is not clear because these patients had a broad PAP
range. How high an individual needs to ascend to increase risk
is also unclear, although in several reports, HAPE developed with
ascent to altitudes between 1500 and 2000 m (4920 and 6560
feet), lower than the altitudes typically associated with HAPE.48,130
Despite the 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 60 mm Hg at baseline should prob-
ably avoid travel to sleeping altitudes above 2500 m (8200 feet).
However, if such travel is undertaken, supplemental oxygen
should be recommended. Patients with milder degrees of pul-
monary hypertension may travel to altitudes below 3000 m (9840
feet) but should consider prophylactic measures, including pul-
monary vasodilators or supplemental oxygen, if not already
receiving such therapy.90 Instituting these measures is relatively
straightforward when it is known beforehand that the patient has
pulmonary hypertension. The challenge arises in patients with
conditions known to predispose to pulmonary hypertension,
such as bronchopulmonary dysplasia, cirrhosis, collagen vascular
diseases (e.g., scleroderma), congenital heart disease, and recur-
rent venous thromboembolism. These patients may not be rec-
ognized as having pulmonary hypertension at the time of their
planned trip. Strong consideration should be given to screening
such patients for pulmonary hypertension with echocardiography
or undertaking a hypoxia altitude simulation test with concurrent
echocardiography to measure the PAP response to hypoxia.
Patients found to have pulmonary hypertension at rest in nor-
moxia or larger-than-expected PAP responses to hypoxia66,40
should be managed according to the measures previously
outlined.
Sleep-Disordered Breathing
Two issues warrant consideration for patients traveling to high
altitude with sleep-disordered breathing: (1) the effect of high
altitude on their apnea-hypopnea index (AHI) and (2) the effect
of recurrent apnea on nocturnal oxygen saturation (SO2). With
AHI, an earlier chamber study using a normobaric hypoxia model
demonstrated a decrease in the number of obstructive apnea
episodes from 25.5 per hour at 60 m (200 feet) to 0.5 per hour
at 2750 m (9020 feet) that was offset by a significant increase
in the number of central events (0.4/hr at 60 m [200 feet] vs.
78.8/hr at 2750 m [9020 feet]).29 A subsequent field study by
Nussbaumer-Ochsner and colleagues117 confirmed the marked
increase in central apnea at 2590 m (8495 feet) in patients with
moderate to severe obstructive sleep apnea (OSA) but showed
CHAPTER 3  High Altitude and Preexisting Medical Conditions
Apnea/Hypopnea Index, NREM Sleep
2590 m, night 2 **
2590 m, night 1 **
1860 m, night 1 *
1860 m, night 1 *
490 m
80 60 40 20 0 20 40 60 80
Obstructive events/h Central events/h
FIGURE 3-1  Changes in the number of obstructive and central apnea
and hypopnea events during non–rapid eye movement (NREM) sleep
at increasing elevations. The width of each bar represents the median
values; the horizontal lines denote the quartile ranges. With increasing
altitude, the number of obstructive apnea/hypopnea events remains
unchanged, but there is a significant increase in the number of central
events. (From Nussbaumer-Ochsner Y, Schuepfer N, Ulrich S, Bloch
KE: Exacerbation of sleep apnoea by frequent central events in patients
with the obstructive sleep apnoea syndrome at altitude: A randomised
trial, Thorax 65:429-435, 2010.)
no significant change in the number of obstructive events after
ascent (Figure 3-1). These results support a smaller study from
Colorado that demonstrated a decrease in the number of central
apnea episodes but persistence of obstructive events when
patients with untreated OSA traveled to lower elevations.123
Apnea events at sea level are frequently associated with fluc-
tuations in nocturnal SO2. Average nocturnal SO2 worsens follow-
ing ascent to high altitude. Nussbaumer-Ochsner and colleagues,117
for example, showed a statistically significant decrease in SO2
from 94% at 490 m (1607 feet) to 90% at 1860 m (6100 feet) and
86% on the first night at 2590 m (8495 feet). Burgess and associ-
ates29 reported a mean SO2 of 85% ±4% at 2750 m (9020 feet)
compared to 94% ±1% at 60 m (200 feet). Increases in AHI and
worsening hypoxemia may have implications for patients; the
field study also demonstrated impaired tracking performance
during simulated driving at 2590 m compared to 490 m.117 In
addition, the authors found increased systolic blood pressure,
likely related to the increased number of nocturnal arousals, and
increased cardiac arrhythmias related to increased sympathetic
stimulation from greater hypoxemia.
Because obstructive events may persist following ascent,
patients with OSA traveling to high altitude should strongly con-
sider traveling with their continuous positive airway pressure
(CPAP) machines when access to electrical power can be ensured.
Strong consideration should also be given to adding acetazol-
amide to CPAP therapy; this combination has been shown to
decrease the number of central apnea events and AHI and to
improve nocturnal oxygenation compared with autotitrating
CPAP alone.82 Even if logistical issues prevent continuation of
CPAP after ascent, acetazolamide is still effective at improving
oxygenation, AHI, and overall sleep quality and should be
strongly considered in patients with OSA.116
CARDIOVASCULAR CONDITIONS
Hypertension
Studies have generated mixed results regarding the effects of
hypobaric hypoxia on blood pressure (BP) in individuals with
known hypertension. Some studies demonstrate BP increases on
exposure to various altitudes,121,132,135,159 and others show small,
non–statistically significant changes.41,143 The majority of studies
have examined patients with mild to moderate disease at modest
elevations (<3500 m [11,483 feet]) and thus may not inform evalu-
ation of the full range of hypertensive patients who may travel
to high altitude. On average, the increases in systolic BP are
modest (<15 mm Hg) and appear to be exaggerated by exer-
cise.41,135 There is significant interindividual variability at rest, with
33
 some persons experiencing marked rises in BP compared to
others,132 but a priori identification of persons at risk for such
responses remains challenging. Several studies suggest that the
initial BP rise is followed by a decline over days to weeks.132,159
A more recent study in normotensive individuals, however, sug-
gested that BP may remain elevated for several weeks as indi-
viduals steadily proceed to higher elevations.122
Patients receiving antihypertensive therapy should continue
their medications while traveling at high altitude. Because BP
increases are generally mild and do not appear to be associated
with significant side effects, the majority of individuals should
not monitor their BP after ascent. Monitoring should be reserved
for those with very labile or difficult-to-control hypertension.
These patients should adjust their medications according to a
prearranged plan for systolic BP above 180 mm Hg or diastolic
BP above 120 mm Hg and symptoms such as chest pain, vision
changes, or headache, or for systolic BP above 220 mm Hg or
diastolic BP above 140 mm Hg in the absence of symptoms.92
Travelers who adjust their medications following ascent should
return to their normal regimen on descent, because BP is expected
to fall as the altitude-induced sympathetic stimulation wanes.
The appropriate medication for managing severe hypertension
remains unclear. Since the BP rise is likely related to increased
α-adrenergic activity, α-blockers would appear to be a good
choice, but no data support this practice. Data are also lacking
regarding calcium channel blockers, the use of which could
MOUNTAIN MEDICINE
provide the further benefit of prophylaxis against HAPE. A recent
field study suggested that angiotensin receptor blockade lowered
BP at 3400 m (11,150 feet), but this study was performed in
normotensive individuals. Whether the same response would be
seen in a hypertensive patient at high altitude, particularly one
with difficult-to-control disease, is unclear.122
Coronary Artery Disease
The primary concern in patients with underlying coronary artery
disease (CAD) is that myocardial oxygen demand may outstrip
oxygen supply in the setting of hypobaric hypoxia, particularly
with exertion, thereby leading to myocardial ischemia. This
PART 1
problem may be exacerbated because coronary vasodilation is
impaired in these patients, and paradoxical vasoconstriction may
even occur during exercise.64 Despite these theoretical concerns,
patients with stable CAD appear to tolerate exposure to moderate
altitudes without significant complications. Levine and associ-
ates,85 for example, demonstrated a decrease in the ischemia
threshold, denoted by the double product and treadmill work-
load necessary to produce 1 mm of ST-segment depression on
the electrocardiogram (ECG), on acute exposure to high altitude,
which resolved after several days at the same elevation. Despite
these changes in the ischemia threshold, no new wall motion
abnormalities were detected by echocardiography, and individu-
als did not manifest evidence of high-grade ectopy or arrhythmia.
Similarly, Erdmann and colleagues49 performed cardiopulmonary
exercise test (CPET) at 1000 m (3280 feet) and 2 days after ascent
to 2500 m (8200 feet) on 23 patients with myocardial infarction
or revascularization within the preceding 4 months and with low
ejection fraction (<45%), and noted the same double product and
systolic BP at peak exercise between testing sites, with no evi-
dence of ischemia or arrhythmia. DeVries and associates38 per-
formed CPET at 4200 m (13,776 feet) on eight patients with
single-vessel disease and preserved ejection fraction; they found
no changes in wall motion score indices of left ventricular func-
tion and no evidence of arrhythmia or other adverse events.
These data suggest that patients with stable, well-controlled
CAD tolerate exposure to and exertion at altitudes as high as
4000 m (13,120 feet). Given the changes in the ischemia thresh-
old noted by Levine and associates,85 it may be prudent to
decrease the level of physical activity in the first few days at
altitude, although the study by Erdmann and colleagues49 sug-
gests heavy exertion may be possible as soon as 2 days after
arrival at high elevation. Patients should not engage in de novo
exercise at high altitude if they are not already engaged in an
exercise program at lower elevation. Sleeping at moderate alti-
tude before any exercise at high altitude may also reduce the
risk of complications, including the risk of sudden cardiac death
34
80
70
SCD frequency (%)
60
50
40
30
20
<700 700–999 1000–1299 >1299
Sleeping altitude (m)
FIGURE 3-2  Frequency of sudden cardiac death (SCD) on the first day
of physical activity at moderate altitudes (2000 to 3000 m [6560 to
9840 feet]) stratified according to the sleeping altitude. The higher the
individual sleeps on the first night at altitude, the lower the frequency
of SCD. (From Lo MY, Daniels JD, Levine BD, Burtscher M: Sleeping
altitude and sudden cardiac death, Am Heart J 166:71-75, 2013.)
(Figure 3-2).87 Patients with unstable angina, ischemia at low
workloads (<80 W or 5 METs), or recent myocardial infarction
should delay high-altitude travel until they have undergone
revascularization. Patients with prior ventricular tachycardia or
fibrillation should also avoid travel unless stable on a recent
exercise test. Travel should be delayed for 4 months or longer
after revascularization procedures, because studies have exam-
ined and demonstrated the safety of exertion in hypobaric
hypoxia only at 4 to 18 months after such interventions. Symptom-
limited exercise tests can be used in these patients, as well as
those thought to be at risk for CAD, to gauge the safety of a
planned ascent. Patients should continue their medication
regimen throughout their planned trip. Further information on
these issues is available in several reviews.11,39
Heart Failure
Heart failure patients face several physiologic challenges at high
altitude, including increased PAP that may lead to right-sided
heart strain, increased sympathetic nervous system activity, and
increased systemic BP. Together with the decreased ventilatory
reserve and pulmonary compliance seen in some patients, these
issues theoretically increase the risk of decompensated disease
with high-altitude travel.12,129 Only a limited number of studies
have evaluated this risk in detail. Erdmann et al49 examined
patients with CAD and stable heart failure (ejection fraction
<45%) and noted no greater decrement in exercise performance
compared to controls. In contrast, Agostoni and associates2 per-
formed CPET at simulated altitudes up to 3000 m (9840 ft) in
heart failure patients with varying degrees of functional limitation
and noted larger decrements in maximum work rate compared
to healthy controls, with the greatest decrease seen in those who
were most limited at baseline. No tests had to be interrupted for
ischemia in either study. Schmid and colleagues137 performed
CPET with echocardiography in New York Heart Association
(NYHA) Class I and II patients (mean ejection fraction, 28.8%
±5.4%), and found that although peak oxygen consumption
declined at high altitude by 22%, no patient developed ischemia,
pulmonary edema, or echocardiographic evidence of left or right
ventricular dysfunction. One patient developed self-limited ven-
tricular tachycardia during maximal exercise.
These studies may seem reassuring, but the duration of expo-
sure to high altitude before performance of exercise testing was
short relative to the duration of time patients may spend at high
altitude. This concern is supported by anecdotal evidence from
physicians in resort areas who have noted a tendency toward
acute decompensation in heart failure patients within 24 hours
of arrival. The etiology for this is not clear but may relate to
alterations in sodium and fluid balance that can develop after
ascent.148 Development of AMS may pose a similar risk to heart
failure patients, because AMS is often associated with fluid reten-
tion, which in turn can cause volume overload, worsening
peripheral edema, and possibly pulmonary edema.
Patients with stable, well-compensated heart failure can travel
to moderate altitudes (<3000 m [9840 feet]), but travel should be
avoided in patients with NYHA Class III or IV disease, high-grade
ventricular arrhythmias, recent exacerbation or evidence of wors-
ening symptoms, or worse fluid balance before their planned
sojourn. Patients should not engage in exercise at high altitude
if they are not already active at sea level. They should continue
their baseline medications but should travel with a prearranged
plan to adjust their diuretics and antihypertensive regimens in
response to adverse changes in body weight or systemic BP.
Among the β-blockers used in heart failure patients, carvedilol
may be associated with blunted ventilatory responses, greater
hypoxemia, and a greater decrement in exercise capacity com-
pared to placebo and nebivolol at a simulated altitude of 2000 m
(6560 ft).3 The duration of exposure to hypoxia in this study was
short, however, and data are insufficient to recommend patients
change to alternative β-blockers for the purpose of high-altitude
travel. When used for altitude illness prophylaxis, acetazolamide
may have the added benefit of improving overall fluid balance
because of its diuretic effect. Beyond such medication concerns,
it is important to remember that many heart failure patients also
have implanted pacemakers and defibrillators. Although limited
evidence suggests that pacemaker ventricular stimulation thresh-
olds remain unchanged with short hypoxic exposures,156 a 4%
incidence of defibrillator discharges has been noted at altitudes
above 2000 m [6562 feet].79 Whether this latter finding is related
to changes in the device’s defibrillation threshold or to the
patient’s underlying condition remains unclear at this time.
Congenital Heart Disease
Many patients with congenital heart disease (CHD) are living
longer and are able to engage in a variety of activities as a result
of improvements in medical care, but the evidence base guiding
management of these patients at high altitude remains limited.
In perhaps the only study focused on CHD patients at high alti-
tude, Garcia and associates56 demonstrated that patients with a
history of the Fontan procedure for correction of tricuspid atresia
tolerated submaximal exercise at 3050 m (10,000 feet) despite
lacking a functional right ventricle. Case series and reports have
documented an increased risk of HAPE in patients with unilateral
agenesis of a pulmonary artery,68,130 and a single study suggests
that patent foramen ovale (PFO) may be associated with an
increased risk of HAPE;6 however, a causal link between PFO
and HAPE has not been definitively established. Because HAPE-
susceptible patients are known to have exaggerated pulmonary
vascular reactivity,40,66 the PFO may occur because of the large
PAP responses to hypoxia and exercise and thus may be a phe-
nomenon associated with HAPE rather than a link in the causal
pathway.
Aside from the limited evidence base, another challenge in
evaluating CHD patients before planned high-altitude travel is
the wide variety of congenital disorders and their associated
repairs, which makes assessment of anticipated changes in hemo-
dynamics and gas exchange at high altitude difficult. Neverthe-
less, two groups of patients warrant increased attention. As
previously noted, patients whose congenital defects are associ-
ated with pulmonary hypertension may be at increased risk for
HAPE or worsening right ventricular function, whereas patients
with cyanotic diseases will be at risk for marked hypoxemia,
particularly when engaged in any physical activity.96 Whether the
latter group can maintain adequate tissue oxygen delivery in the
face of severe hypoxemia will be a function of their underlying
cardiac function22 and whether they have secondary polycythe-
mia as a result of chronic hypoxemia.28 Greater hypoxemia
secondary to intracardiac or intrapulmonary shunting will likely
increase the risk of altitude illness.
These concerns can be evaluated before any planned trip
using echocardiography to determine PAP, hypoxia altitude simu-
lation testing to assess the likelihood of severe hypoxemia, or
CPET in normoxia or hypoxia to assess exercise tolerance and
risk of exercise-induced hypoxemia, while being aware of the
limitations of these tests as discussed earlier. High-altitude travel
CHAPTER 3  High Altitude and Preexisting Medical Conditions
should be avoided in patients with moderate to severe pulmo-
nary hypertension, low maximum exercise capacity ( V O2max
<20 mL/kg/min), or cyanotic disease and anemia and/or impaired
cardiac output.96 There is no evidence to support closing a PFO
before ascent to high altitude to prevent HAPE.
Arrhythmia
From a theoretical standpoint, increased sympathetic activity in
response to hypoxemia would be expected to increase the inci-
dence or severity of tachyarrhythmia at high altitude. Although
there is evidence of sinus tachycardia, atrial and ventricular
ectopy, and atrial flutter in healthy individuals traveling to high
altitude,85,158 little is known about the effects of hypobaric hypoxia
on persons with preexisting arrhythmias, such as atrial flutter or
other supraventricular tachycardias. In one of the few studies on
this issue, Wu and associates159 performed ECG and 24-hour
ambulatory monitoring on 42 individuals with preexisting arrhyth-
mias at 1 week and at 3 months after arrival at 4500 to 5050 m
(14,760 to 16,564 feet) and found only a single case of asymp-
tomatic Wolff-Parkinson-White syndrome. No participants expe-
rienced life-threatening arrhythmias or exacerbation of their
preexisting arrhythmia. Given the lack of documented problems,
it is likely safe for arrhythmia patients to continue to go to high
altitude, provided their arrhythmia is under adequate control at
the time of their sojourn. Patients should continue their medica-
tion regimen through the duration of their trip and should have
a plan in place in the event of an exacerbation.
HEMATOLOGIC DISEASES
Hypercoagulable States
Because of scant evidence, it is unclear whether hypobaric
hypoxia increases the risk of thromboembolic disease in indi-
viduals with a history of venous or arterial thromboembolism or
known coagulopathy. Many case reports document thromboem-
bolic events at high altitude in which the patient was known or
subsequently found to have evidence of coagulopathy, such as
protein C deficiency,26 antiphospholipid antibody syndrome,16
hyperhomocysteinemia,8 or S/C hemoglobinopathy,69 but little
information exists about the relative risk of thromboembolism at
high altitude in such patients compared to sea level. In one of
the few studies that provides some insight into this issue, Sch-
reijer and associates139 exposed healthy individuals to hypobaric
hypoxia equivalent to 1800 to 2100 m (5904 to 6888 feet) and
found that levels of thrombin-antithrombin complexes were
increased only in individuals with factor V Leiden mutation and
oral contraceptive use, suggesting that a preexisting coagulopa-
thy might affect the response to hypobaric hypoxia. Other studies
examining changes in markers of coagulation during hypoxic
exposure in normal individuals have also failed to yield consis-
tent evidence regarding bleeding times,13,46 fibrinolytic activ-
ity,14,103 platelet count and function,73,141 or thrombin formation.15,20
However, a recent study using thromboelastography actually
showed evidence of slowed coagulation at high altitude rather
than a hypercoagulable state.104
Given the evidence that risk of thrombosis is not increased
by hypobaric hypoxia high altitude, there is no indication for
individuals with underlying coagulopathy who are not already
taking anticoagulants to start warfarin or antiplatelet therapy
before high-altitude travel. Individuals receiving anticoagulation
therapy should continue their regimen at high altitude, and
patients taking warfarin should arrange to monitor prothrombin
time during or immediately after stays lasting over 2 weeks,
because some evidence suggests that these values may change
as a result of changes in elevation.154 No data are available regard-
ing the effects of hypobaric hypoxia on direct thrombin inhibi-
tors. Limiting activities in remote areas should be considered to
reduce the risk of trauma and severe hemorrhage. Regardless of
whether they use anticoagulation, patients with a history of
thromboembolism or coagulopathy should maintain hydration
and adequate mobility throughout their stay, because these
factors may affect the risk of thrombosis independent of the
effects of hypoxia.
35
 Hemoglobinopathy
Sickle cell anemia patients should avoid travel to high altitude
because hypoxia can trigger red blood cell sickling and vasooc-
clusive crises.53 Even travel to modest elevations may be associ-
ated with risk. Previous work has demonstrated a 20% incidence
of vasoocclusive and splenic crises in patients with sickle cell
anemia or hemoglobin S/C traveling above 2000 m (6560 feet)
or flying in pressurized aircraft.102 Beyond the risk of vasooc-
clusive crises, sickle cell anemia patients can develop pulmonary
hypertension as a consequence of long-standing disease,84 which
could predispose to HAPE or worsening right-sided heart func-
tion in hypobaric hypoxia. If high-altitude travel cannot be
avoided, patients should travel with supplemental oxygen. Unlike
patients with COPD or other lung diseases, who might travel
with a prescription for supplemental oxygen and use it only if
they have problems at high altitude, sickle cell anemia patients
should plan on having oxygen available immediately on arrival.
The risk of problems in patients with sickle cell trait has not
been specified, but several reports document the occurrence of
splenic crises in patients traveling between 1600 and 3660 m
(5250 and 12,005 feet).80,54,63,150 Such reports should probably not
preclude high-altitude travel in all sickle cell trait patients, but
development of left upper quadrant pain following ascent to high
altitude should prompt urgent medical evaluation and descent to
lower elevation.
Thalassemia has not been reported to cause problems at high
MOUNTAIN MEDICINE
altitude.
Anemia
Depending on its severity, anemia impairs oxygen delivery and
limits exercise tolerance at high altitude. No study has assessed
whether anemia increases the risk of high-altitude illness or has
defined specific hemoglobin thresholds that are safe for high-
altitude travel. Depending on the anticipated length of stay and
level of exertion at high altitude, blood transfusion can be con-
sidered before the planned trip, although the appropriate target
hemoglobin concentration after transfusion is unclear. Anemic
patients planning trips longer than 2 weeks should consider oral
PART 1
iron supplementation.
Polycythemia Vera
As with anemia, evidence is scant regarding polycythemia vera
(PV) patients at high altitude. From a theoretical standpoint,
higher hemoglobin concentrations would be expected to improve
oxygen delivery in the setting of hypoxemia. On the other hand,
individuals traveling at high altitude are at increased risk for
dehydration because of lower humidity and altitude-induced
diuresis. In PV patients, this could raise hemoglobin concentra-
tion further, thereby worsening blood viscosity, impairing cardiac
output and oxygen delivery, and increasing risk of thrombosis.146
The effect of hypobaric hypoxia on risk of gastroduodenal ero-
sions in PV patients is unknown.152 Given these uncertainties, PV
patients can travel to high altitude but should maintain adequate
hydration and mobility and should consider using low-dose
aspirin to reduce the risk of thrombotic events. Patients with a
history of gastroduodenal erosions should avoid aspirin, as well
as dexamethasone, because either medication might increase the
risk of upper gastrointestinal bleeding.
NEUROLOGIC DISORDERS
Headaches
A history of nonmigrainous headaches at lower elevation may
predispose to headaches at high altitude23 and has been associ-
ated with increased severity of headaches when they occur after
ascent.142 Hypoxia may trigger migraine headaches at high alti-
tude in patients with a known history of the disorder138 (or a
family history of migraine), and these headaches may be of
greater severity and associated with focal neurologic deficits.111
Anecdotal reports67 and systematic studies127 also suggest that a
history of migraines may also predispose to acute altitude illness
after ascent. An important issue for these patients is distinguish-
ing a migraine headache from headaches associated with AMS,
with the key distinguishing factors being whether the patient has
36
an aura and focal neurologic deficits—features typically lacking
in AMS-associated headaches—and the character of the headache
compared to the typical migraine at lower elevations. Headaches
that are different in character than typical migraines or that do
not respond to standard migraine headache treatment, such as
sumatriptan, should be treated as AMS. Response to oxygen
breathing can also be helpful, because altitude headaches typi-
cally improve in 10 to 15 minutes, whereas migraine headaches
do not.
Seizures
High altitude may rarely induce seizure in healthy persons and
sometimes unmask preexisting seizure disorders.98 Individuals
with known seizure disorders well controlled with medication
are not thought to be at increased risk for increased frequency
or severity of seizures after ascent. They can trek or do other
activities at high altitude but should avoid technical climbing or
roped travel on glaciated terrain because of the risks to the indi-
vidual or travel partners if a seizure occurs in either setting.
Individuals who use topiramate as part of their seizure regimen
should use dexamethasone rather than acetazolamide for AMS
prophylaxis at high altitude; topiramate has carbonic anhydrase
activity similar to that of acetazolamide, and concurrent use of
the medications for more than a few days can lead to severe
metabolic acidosis and nephrolithiasis.97 Persons with a past
history of more than one seizure who are not taking antiseizure
medications should be cautious on ascent to altitude and should
pay close attention to ensuring an adequately slow ascent rate.
Cerebrovascular Diseases
Minimal information exists about the risk of high-altitude travel
in patients with cerebrovascular disease. As with patients who
have recently had a myocardial infarction and revascularization,
it is prudent to delay high-altitude travel after a recent transient
ischemic attack or cerebrovascular accident (stroke) for at least
90 days.18 Patients taking warfarin, clopidogrel, or a direct throm-
bin inhibitor as part of primary or secondary stroke prevention
should be cautious with travel into remote areas, where trauma
and bleeding can have significant consequences if the individual
cannot access care in a timely manner. Patients with known,
unsecured intracranial aneurysm or arteriovenous malformation
should probably avoid high-altitude travel because of a theoreti-
cal risk of rupture from cerebral vasodilation and increased flow,
or if systemic BP increases significantly after ascent. If high-
altitude travel cannot be avoided, efforts should be made to limit
exertion during the sojourn.
DIABETES MELLITUS
There are multiple issues for diabetic patients traveling to high
altitude. It is important to note that the literature on short-term
exposure to high altitude is based largely on studies done in
well-controlled type 1 diabetic patients engaged in climbing
expeditions.1,76,110,124 Significantly less information is available
about patients with poorly controlled type 1 or with type 2 dia-
betes of any severity, so care must be used in extrapolating
available data to these individuals.
Acclimatization and Risk of Altitude Illness
Multiple studies from climbing expeditions suggest that the ven-
tilatory and hematologic responses to acute hypoxia, risk of acute
altitude illness, and summit success rates are similar in well-
controlled type 1 diabetic patients and healthy individuals. Pavan
and colleagues,125 for example, measured blood gases and hema-
tologic parameters in well-controlled type 1 diabetic patients at
3700 and 5800 m (12,135 and 19,025 feet) during an ascent of
Cho Oyu and noted no difference in PaO2, PaCO2, bicarbonate,
or hematocrit. Multiple studies have reported no difference in
the incidence of AMS or Lake Louise AMS scores between dia-
betic and nondiabetic climbers during ascents of Aconcagua
(6962 m [22,835 feet]), Cho Oyu (8201 m [26,890 feet]), or Kili-
manjaro (5895 m [19,335 feet]).76,110,124 In only one of the studies
did diabetic climbers fail to summit the mountain, but summit
success rates were low in the nondiabetic climbers as well,
making it difficult to attribute the lack of summit success to dia-
betes alone. In one of the few studies examining type 2 diabetic
patients, del Mol and associates36 reported low AMS scores in 13
patients with no history of diabetes-related complications during
a 12-day trek to the summit of Mt Toubkal (4167 m [13,665 feet])
in Morocco.
Insulin Requirements and Glycemic Control
Multiple factors impact glycemic control at high altitude, includ-
ing changes in diet, degree and duration of exercise, sympathetic
nervous system responses to hypoxia, and other forms of stress
when traveling in this environment. The majority of studies
on insulin requirements and glycemic control report increased
requirements during high-altitude travel,1,35,124 whereas a single
study has noted decreased insulin requirements.110 Interpretation
of these data is difficult, however, because ascent rates, levels of
exertion, altitudes attained, and dietary factors varied significantly
between studies. These studies also involved travel to extreme
elevations (>5800 m [19,025 feet]) and may not be relevant to
most high-altitude travelers or to situations where individuals are
not engaged in the physical exertion of expedition climbing.128
Given the uncertainties about what will happen with insulin
requirements in most individuals, travelers with diabetes should
plan on checking blood glucose levels more frequently than they
would at home and should be prepared to change insulin dosing
as necessary.
Glucometer Function
Monitoring glucose levels more closely at high altitude requires
accurate glucometers. Many earlier studies reported issues with
glucometer accuracy at high altitude,51,57,59,110,126 possibly because
older monitors were glucose oxidase–based systems. Some of the
more recent-generation devices operate on a glucose dehydro-
genase reaction, which is not oxygen dependent and theoretically
less susceptible to the effects of altitude. Thus far, however, it
remains unclear which system performs best. Oberg and associ-
ates,119 for example, found that the glucose dehydrogenase meters
performed better at simulated altitudes of 2500 and 4500 m (8200
and 14,780 feet), whereas Olateju and colleagues120 noted no
difference in performance at a simulated altitude of 2340 m (8000
feet). De Mol and associates37 noted no difference at simulated
altitude but found that at terrestrial high altitude, one of the tested
glucose dehydrogenase systems was most accurate. The measure-
ment errors are generally not clinically significant. When readings
fall near the low end of normal, however, small measurement
errors may have greater implications because travelers may fail
to recognize true hypoglycemia. For this reason, diabetic travelers
at high altitude should err on the side of caution and react more
readily to values near the low end of normal rather than using
the typical thresholds for intervention.
Insulin Pumps
Diabetic patients are increasingly using insulin pumps rather than
intermittent subcutaneous injections for blood glucose regulation.
A single study has examined function of these pumps in hypo-
baric hypoxia and found that bubbles formed and expanded
within the system during commercial flight and in a hypobaric
chamber, with the potential to cause excess insulin administration
on ascent.78,88 Therefore, diabetic travelers using insulin pumps
should monitor closely for bubble formation in the system and
should consider either decreasing the dose administered by the
pump or switching to intermittent subcutaneous infection for the
duration of the trip.
Retinal Disease
Retinal hemorrhage is a common complication of travel at moder-
ate to extreme altitudes in normal individuals.25 Two studies
specifically examined this issue in diabetic patients, who are at
increased risk for retinal disease. Using ophthalmoscopy, Moore
and colleagues110 found asymptomatic hemorrhage in 2 of 15
diabetic climbers during an ascent of Kilimanjaro; Leal and asso-
ciates83 used retinography and noted development of asymptom-
atic hemorrhage in one of seven climbers ascending a 7100-m
(23,290-foot) peak; the one climber had known diabetic retinopa-
thy. These incidence rates are comparable to those seen in the
CHAPTER 3  High Altitude and Preexisting Medical Conditions
general population climbing at moderate to extreme elevation,
so without control groups, these small studies do not establish
that diabetes increases the risk of retinal hemorrhage. Given this
ongoing uncertainty, there is no reason to restrict high-altitude
travel in patients with retinal disease except in cases of severe
diabetic retinopathy.100 Aspirin or other nonsteroidal antiinflam-
matory drugs (NSAIDs) do not appear to increase the risk of
retinal hemorrhage at low elevations, but this has not been
studied at high altitude. It may be prudent to rely on acetamino-
phen as the first-line agent to treat AMS symptoms in patients
with retinopathy.
OBESITY
One of the first studies to provide information on the risk of
high-altitude travel in obese individuals was that of Honigman
and colleagues,70 who reported a higher incidence of AMS among
obese members of a general tourist population traveling to alti-
tudes of 1920 to 2950 m (6300 to 9675 feet) in Colorado. Ge and
associates58 exposed obese and nonobese individuals to a simu-
lated altitude of 3660 m (12,005 feet) for 24 hours and noted a
higher incidence of AMS and lower nocturnal SO2 in the obese
participants (Figure 3-3). Together, these studies suggest a link
between obesity and AMS but do not clarify the causal mecha-
nism behind this link or the degree of obesity necessary to
increase risk. Whether the efficacy of acetazolamide for AMS
prophylaxis is similar between obese and nonobese individuals
is unclear, although no theoretical rationale exists to suggest
there should be a difference.
Morbidly obese individuals who develop the obesity hypoven-
tilation syndrome, a disorder marked by alterations in pulmonary
mechanics and ventilatory control, may be at risk for additional
problems beyond AMS at high altitude. These patients often have
pulmonary hypertension caused by chronic alveolar hypoxia, so
further rises in PAP after ascent could predispose to HAPE or
worsening right-sided heart function. Sleep-disordered breathing
is another common problem in these patients. Sleep quality and
subsequent daytime function may worsen as a result of increased
central apnea events and increased nocturnal hypoxemia. Given
these risks, morbidly obese individuals with pulmonary hyperten-
sion should avoid high-altitude travel. If travel cannot be avoided,
individuals should travel with supplemental oxygen or a prescrip-
tion that can be filled at high altitude based on symptoms or
pulse oximetry monitoring. Individuals using nocturnal CPAP or
100
Nonobese
95 Obese
90
SaO2, %
85
80
75
Sea level Daytime Sleep
FIGURE 3-3  Oxygen saturation (SaO2) in normal (blue boxes) and
obese individuals (BMI >30 kg/m2) (red boxes) while awake at sea level
and while awake and sleeping at simulated high altitude (3658 m
[12,000 feet]). The bottom of each box represents the lowest 25th
quartile of SO2 and the top of the box represents the 75th quartile. The
dashed line represents the median; the vertical lines show the largest
and smallest values for each group of patients under each condition.
(From Ge RL, Chase PJ, Witkowski S, et al: Obesity: Associations with
acute mountain sickness, Ann Intern Med 139:253-257, 2003.)
37
 noninvasive positive-pressure therapy should continue these
therapies at high altitude for the duration of electrical power
access.95
GASTROINTESTINAL DISEASES
Gastrointestinal Bleeding
Several studies have raised concern about the risk of gastrointes-
tinal (GI) bleeding at high altitude. Wu and colleagues159 studied
more than 13,000 workers between 3500 and 4900 m (11,480 and
16,070 feet) on the Qinghai-Tibet railroad and noted a 0.49%
incidence of hematemesis, melena, or hematochezia, and Liu86
reported an incidence of 0.8% among Chinese soldiers stationed
between 3700 and 5380 m (12,135 and 17,550 feet) over a 1-year
period. Saito134 documented GI bleeding in 5 of 52 Mt Everest
climbers. Fruehauf and associates55 performed upper endoscopy
on 26 asymptomatic individuals before and after ascent to 4559 m
(14,950 feet) and noted new gastric or duodenal erosions/ulcers,
hemorrhagic gastritis or duodenitis, and reflux esophagitis in 28%
and 61% of individuals on the second and fourth days at high
altitude, respectively. Although these studies do not definitively
establish that high-altitude travel increases the risk of GI bleed-
ing, they do suggest that individuals with a recent history of GI
bleeding or poorly controlled esophagitis, gastritis, or peptic
ulcer disease may be at risk for problems at high altitude. It
would be prudent for such individuals to avoid extended use of
MOUNTAIN MEDICINE
aspirin or NSAIDs for prevention of AMS or treatment of other
conditions at high altitude.
Cirrhosis
No studies have examined how patients with liver cirrhosis fare
at high altitude, but there are strong theoretical reasons to suspect
that two groups of cirrhotic patients may be at risk for problems:
those with portopulmonary hypertension and those with hepa-
topulmonary syndrome. As noted earlier, patients with portopul-
monary hypertension, a form of pulmonary arterial hypertension
seen in up to 16% of cirrhotic patients,21 may be at risk for HAPE
or worsening right-sided heart function when PAP increases
PART 1
after ascent. Patients with hepatopulmonary syndrome, a disorder
seen in up to 32% of cirrhotic patients136 and marked by hypox-
emia from the presence of pulmonary arteriolar vascular dilation,
are at risk for exaggerated hypoxemia. Patients with portopul-
monary hypertension should likely avoid high-altitude travel, or
if travel is unavoidable, should receive pulmonary vasodilator
therapy or travel with supplemental oxygen. Hepatopulmonary
syndrome patients should travel with plans to monitor pulse
oximetry after ascent and fill a prearranged prescription for
supplemental oxygen in the event of severe symptoms or hypox-
emia. For cirrhotic patients not known to have these disorders,
screening for their presence should be considered before any
high-altitude travel.
Cirrhotic patients should not use acetazolamide for AMS
prophylaxis or treatment because this may increase the risk
of hepatic encephalopathy.97 Although development of altered
mental status at high altitude should always raise concern for
HACE, a broader differential should be considered in cirrhotic
patients and include the possibility of hepatic encephalopathy
provoked by infection, GI bleeding, or medication nonadher-
ence. Cirrhotic patients with altered mental status should not
simply be given dexamethasone, but instead be evacuated
to a lower elevation or health facility to undergo thorough
evaluation.
OPHTHALMOLOGIC CONDITIONS
Refractive Error Surgery Patients
Of patients who had the older refractory surgery options, those
with radial keratotomy appear to fare the worst at altitude,
because hypobaric hypoxia can cause uneven corneal swelling,
hyperopic shifts, and impaired vision after more than 24 hours
at altitudes as low as 3000 m (9840 feet).100 Individuals with a
history of this procedure who travel to high altitude should travel
with glasses with increasing plus power to compensate for such
shifts. Corneal swelling can occur with photoreactive radial kera-
38
totomy, but the swelling is more uniform and does not lead to
refractive errors.99 Laser-assisted in situ keratomileusis (LASIK) is
now performed more often than either radial keratotomy proce-
dure. The available data suggest that high-altitude travel, even to
extreme elevations, is tolerated in these patients. Small myopic
shifts have been demonstrated in controlled studies113 and case
reports,24,157 but climbers have still been able to reach summit
objectives at extreme elevations. In a detailed report by Dimmig
and Tabin,43 six climbers ascended above 7900 m (25,910 feet)
after LASIK in both eyes, and four reached the summit. Five of
the six had no visual changes up to 8000 m (26,240 feet), while
two climbers reported blurred vision at 8200 and 8700 m (26,900
and 28,535 feet), which improved with descent. Further details
on this issue are available in a recent review.101
Glaucoma
The effect of high altitude on intraocular pressure (IOP) is
unclear, with studies reporting an increase, decrease, or no
change in this parameter during exposure to hypoxia.19,27,50 In
one of the better-controlled studies, Somner and colleagues144
examined 76 individuals and found statistically significant but
clinically insignificant increases in IOP after an exertion-free
ascent to 5200 m (17,050 feet), which resolved after 7 days at
that elevation. There is no evidence that hypobaric hypoxia
provokes acute narrow-angle glaucoma or worsens open-angle
glaucoma. Acetazolamide would be a useful means for pharma-
cologic prophylaxis against AMS in glaucoma patients, given its
ability to decrease intraocular fluid production through carbonic
anhydrase inhibition.100
PREGNANCY
Because pregnancy-associated hypertension, preeclampsia, and
small-for-gestational age infants are more common among high-
altitude residents,108,109 the issue arises of whether short-term
exposure to hypobaric hypoxia poses risks to pregnant lowland
residents during high-altitude travel. Data are sparse, but limited
evidence suggests moderate altitude exposure is likely safe.71,72
There is no evidence that short-term exposures increase the risk
for pregnancy-induced hypertension, spontaneous abortion,
placental abruption, or placenta previa.114 Artal and colleagues7
performed submaximal and maximal exercise tests on seven
sedentary women at 34 weeks’ gestation at sea level and after 2
to 4 days of acclimatization at 1830 m (6000 feet) and docu-
mented the expected decrease in maximal aerobic work, but no
difference from sea level in fetal heart rate responses or maternal
lactate, epinephrine, or norepinephrine concentration. In another
study of 12 pregnant women exercising after ascent to 2225 m
(7300 feet), Baumann and associates17 also found no evidence of
abnormal fetal heart rate responses. Additional studies have
demonstrated that the fetus tolerates acute hypoxia at high alti-
tude, provided that placental fetal circulation is normal.10,34,131
When viewed together, the limited literature suggests that
physical exertion during short-term exposure to altitudes up to
3000 m (9840 feet) is likely safe for women with normal, low-risk
pregnancy.71,75 High-altitude travel should be avoided, however,
in certain groups of patients, particularly after the 20th week of
pregnancy (Box 3-1).75 Before any high-altitude travel, pregnant
BOX 3-1  Contraindications to High-Altitude Travel
in Pregnancy
Anemia
Chronic hypertension
Impaired placental function
Intrauterine growth retardation
Maternal heart or lung disease
Preeclampsia
Pregnancy-induced hypertension
Smoking
Data from Jean D, Moore LG: Travel to high altitude during pregnancy:
Frequently asked questions and recommendations for clinicians, High Alt Med
Biol 13:73-81, 2012.
women should have a checkup, including ultrasound, to ensure

CHAPTER 3  High Altitude and Preexisting Medical Conditions

TABLE 3-3  Safety of High-Altitude Medications During
their pregnancy is low risk. Those who travel to high altitude
should not exceed levels of exertion done at home, maintain Pregnancy and Lactation
adequate hydration, and avoid travel to remote areas. Care
Safety During Safety During
should be taken to avoid high-altitude illness, because severe
Medication Pregnancy* Breastfeeding
hypoxemia during HAPE could impair fetal oxygenation. While
pharmacologic options are available for prophylaxis and treat-
Acetazolamide Category C Not established
ment of altitude illness (Table 3-3), slow ascent should be the
Dexamethasone Category C Debate about safety
primary prevention strategy and descent the primary treatment
strategy. Nifedipine Category C Compatible
Tadalafil Category B Not established
Sildenafil Category B Not established
MEDICATION CONSIDERATIONS IN Salmeterol Category C Not established
HIGH-ALTITUDE TRAVELERS WITH Modified from Luks AM, Swenson ER: Medication and dosage considerations in
UNDERLYING MEDICAL PROBLEMS the prophylaxis and treatment of high-altitude illness, Chest 133:744-755, 2008.
*Pregnancy Category B: presumed safe based on studies in animals, but no
Recently updated expert guidelines provide recommendations data from humans.
for pharmacologic approaches to prevention and treatment of Pregnancy Category C: no human studies demonstrating harm, but animal
acute altitude illness.94 Dosing, efficacy, and safety of the medica- studies show evidence of teratogenicity.
tions used for these purposes have been established largely
on the basis of studies done in healthy individuals; little informa-
tion exists about their use in patients with chronic underlying REFERENCES
medical conditions. These issues have been reviewed in detail.97 Complete references used in this text are available
Table 3-4 summarizes some key considerations for common online at expertconsult.inkling.com.
medications.

TABLE 3-4  Dose Adjustments and Other Medication Considerations for High-Altitude Travelers with Underlying
Medical Conditions
Dose Adjustments
Medication Renal Insufficiency Hepatic Insufficiency Other Considerations

Acetazolamide Avoid use in patients with GFR Acetazolamide use is Avoid in patients taking chronically high
<10 mL/min, metabolic acidosis, contraindicated. doses of aspirin.
hypokalemia, hypercalcemia, Avoid in patients with ventilatory limitation
hyperphosphatemia, or (FEV1 <25% predicted).
recurrent nephrolithiasis. Use caution in patients with documented
severe sulfa allergy.
Limit concurrent use with topiramate and
ophthalmic carbonic anhydrase inhibitors
to 3-5 days.
Dexamethasone No contraindication and no dose No contraindication and no dose May increase blood glucose values in
adjustments necessary adjustments necessary diabetic patients
Avoid in patients at risk for peptic ulcer
disease or upper gastrointestinal bleeding.
Use caution in patients at risk for
strongyloidiasis.
Nifedipine No contraindication and no dose Best to avoid Use caution in patients taking medications
adjustments necessary If use is necessary, give at metabolized by CYP-450 3A4 and 1A2
reduced dose (10 mg twice pathways.
daily) Use caution during concurrent use with other
antihypertensive medications.
Salmeterol No contraindication and no dose Insufficient data Potential for adverse effects in patients with
adjustments necessary coronary artery disease prone to arrhythmia
Avoid concurrent use of β-blockers.
Avoid concurrent use of monoamine oxidase
inhibitors or tricyclic antidepressants.
Sildenafil Dose adjustments necessary if Dose reductions recommended Increased risk of GER
GFR <30 mL/min Starting dose: 25 mg three times Use caution in patients taking medications
daily metabolized by CYP-450 3A4 pathway.
Avoid use in patients with known Avoid concurrent use of nitrates or
esophageal or gastric varices. α-blockers.
Tadalafil Dose adjustments necessary if Child’s Class A and Class B: Increased risk of GER
GFR <50 mL/min maximum 10 mg daily Use caution in patients taking medications
If GFR 30-50 mL/min, use 5-mg Child’s Class C: do not use metabolized by CYP-450 3A4 pathway.
dose, maximum 10 mg in 48 hr tadalafil. Avoid concurrent use of nitrates or
If GFR <30 mL/min, no more than α-blockers.
5 mg

Modified from Luks AM, Swenson ER: Medication and dosage considerations in the prophylaxis and treatment of high-altitude illness, Chest 133:744-755, 2008.
CYP-450, Cytochrome P-450; FEV1, forced expiratory volume in 1 second; GER, gastroesophageal reflux; GFR, glomerular filtration rate.

39
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39.e3
 CHAPTER 4 
Avalanches
COLIN K. GRISSOM, MARTIN I. RADWIN, SCOTT E. MCINTOSH, AND DALE ATKINS
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 destruction
of property. In the 10 years from 2003 to 2013 in the United
States, each winter an estimated 350 persons were caught in
avalanches, 90 of whom were partly buried, 40 fully buried, 40
injured, and 28 killed.1 The median yearly direct losses to prop-
erty are estimated at $100,000, although this varies significantly
from year to year. Annual losses from 2003 to 2013 ranged from
a low of about $30,000 to a high of $6 million for destruction
caused by a 2008 avalanche that destroyed a portion of the high-
power transmission lines supplying Juneau, Alaska. This chapter
describes the properties of the mountain snowpack that contrib-
ute to avalanche formation and discusses avalanche safety tech-
niques, rescue, and the physiology and treatment of avalanche
victims.
PROPERTIES OF SNOW
SNOW CLIMATES
Snow cover varies on both the broad geographic scale (e.g.,
Antarctic snow differs from snow found in the Cascade Moun-
tains of North America, which is different from the snow in the
southern Rocky Mountains of the United States) and the microscale
(e.g., snow conditions may vary greatly from one side of a rock
or tree to the other). All snow crystals are made of water mol-
ecules, but local and regional environmental conditions control
the type and character of the snow found at a given location.
To better understand geographic differences that affect ava-
lanche initiation, it is helpful to consider some basic climate
conditions. The character of the snow and 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 a significant cause
of avalanches when it falls on deep fresh snow. Arctic air intru-
sions are uncommon but can occur each winter. In general, the
snowpack gains strength quickly with time in the maritime 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 may cause avalanche danger to persist for days, weeks, or
even months. Avalanches released from these old, persistent,
weak layers are a distinguishing trait of a continental climate. In
this climate, especially during the early months of winter, the
shallow snow cover loses strength with time. Continental ranges
include the Canadian Rocky Mountains, southern Rocky Moun-
tains, and Brooks Range.
In between the maritime and continental regions is a transi-
tional 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
maritime and continental snow climates (Table 4-1). Examples
40
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 con-
currently 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 may vary greatly in strength and
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 millime-
ters in thickness often reflect conditions between storms. Exam-
ples include a melt-freeze crust or sun crust formed during fair
weather and a hard wind crust 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 atmo-
sphere onto the cold snow surface during a clear night. These
crystals are fragile and weak; after they are buried by subsequent
snowfalls, they may be persistent and major contributors to ava-
lanche 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 suitable for
skiing, to heavy and dense, impossible to penetrate with a shovel,
and firm enough to make it difficult for skiing. Arrangement of
the ice skeleton (i.e., the lattice of ice crystals within the snow-
pack) and the changing density (i.e., the mass per unit volume,
typically represented as kilograms per cubic meter [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.
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 others (Figure 4-1).
For example, needle crystals pack more closely than stellate
crystals (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 5
to 10 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. Minor
variations in atmospheric conditions can have an important influ-
ence 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 because of the
 CHAPTER 4  Avalanches
TABLE 4-1  Characteristics of Maritime, Transitional
(Intermountain), and Continental Snow Climates on the
Basis of 15-Year Means

Total Air Snow New Snow

Precipitation Temperature Depth Density
Type (mm) in °C (°F) (cm) (kg/m3)
Maritime 1286 −1.3° (29.7°) 186 120 (12%)
Transitional 854 −4.7° (23.5°) 170 90 (9%)
Continental 550 −7.3° (18.9°) 113 70 (7%)
Data from Armstrong R, Armstrong B: Snow and avalanche climates of the
Western United States: A comparison of maritime, transitional, and continental
conditions. In Proceedings of the Davos Symposium. Davos, Switzerland, 1986,
Swiss Avalanche Institute.
effects of gravity, weather, and crystal metamorphosis (settle-
ment). Because increase in density often equals 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 composed of air pockets, and snow 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 warmer temperature speeds settlement.
At the same time, the complex and intricate shapes that char-
acterize 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
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 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 1 or 2 weeks. 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
can pack more closely together, thereby enhancing further settle-
ment and strength (Figure 4-2).
Metamorphic changes in new snow generally occur within
hours to a few days. However, the structure of a seasonal snow
cover changes over weeks to months through other processes.
Settlement, which may initially have been rapid, continues at a
F1 Plate F6 Capped
column
Densification and strengthening of snowpack
FIGURE 4-2  Settlement. As the crystal shapes become more rounded,
the crystals can pack more closely together, and the layer settles or
shrinks in thickness.
much slower rate. Other factors begin to exert dominant influ-
ences on metamorphism throughout the snowpack. These factors
include the difference in temperature measured upward or down-
ward 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 rela-
tively warm ground (Figure 4-3). The effect of temperature gra-
dients 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 is trapped within the snow cover. The greater
the amount of water vapor, the greater is the pressure; therefore
both a pressure gradient and a temperature gradient exist through
the snow cover. When a pressure difference exists, it 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 (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 sup-
ported in the pore spaces diminishes. Some vapor changes to
ice and is deposited on the surrounding ice grains. A similar
process occurs 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 4-4 shows how the texture of the snow layer changes
during this temperature-gradient process. Water molecules sub-
limate from the upper surfaces of a grain. The vapor moves
upward along the temperature (and vapor) gradient and is depos-
ited 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
TEMPERATURE GRADIENT
Temperature (°C)
0° Energy exchange
–5° –10°
with atmosphere
150
Snow height

100
(cm)

F2 Stellar F7 Irregular Temperature profile

crystal crystal 50

F3 Column F8 Graupel 0
Heat supply
from Earth
F4 Needle F9 Ice pellet

FIGURE 4-3  As the insulating property of snow separates the warm

F5 Spacial F0 Hail ground (0° C/32° F) from the cold air, temperature gradients develop
dentrite across the snow layer. This graph depicts an example of the diurnal
variation in temperature gradients in the upper snowpack (20-30 cm)
FIGURE 4-1  International classification of solid precipitation: shape of affected by atmospheric energy change. The orange line represents
crystals (left) and shorthand recording method (right). (From the Inter- daytime heating by incoming short-wave radiation; the red line depicts
national Association of Scientific Hydrology, with permission.) nighttime cooling by outgoing long-wave radiation.

41

KINETIC METAMORPHISM
Low temperature
Ice grain
Water Heat
flow
vapor
High temperature
Ice grain
FIGURE 4-4  In the temperature-gradient process, ice sublimates from
the top of one grain, moves upward as water vapor, and then is depos-
ited on the bottom surface of the grain above. If conditions allow this
process to continue long enough, all the original grains are lost as
recrystallization produces a layer of new crystals.
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
MOUNTAIN MEDICINE
sides and sharp angles (also known as faceted crystals or sugar
snow) and may eventually evolve into a large, striated, hollow-
cup form. Examples of these crystals are shown in Figure 4-5.
This process is called temperature-gradient metamorphism 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.
PART 1
A in a more homogeneous manner, rather than showing the pref-
B snow force water vapor molecules to form bonds and thus drives
FIGURE 4-5  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.)
42
KINETIC METAMORPHISM
In the presence of a strong temperature gradient (e.g., ≥1° C
[1.8° F] per 10 cm [4 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 tempera-
ture gradients on the order of 2° C (1.8° F) per centimeter or more
(20° C [18° F] per 10 cm [4 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
(4 to 12 inches) of the snowpack, which is often related to the
effects of alternating incoming solar radiation (short-wave radia-
tion) and outgoing radiational cooling (long-wave 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 below the surface,
which changes more slowly and 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 less than 1 m (3.3 feet) deep. The persistent
gradient and warm basal snow layer temperature can cause very
large and complex faceted grains to form as well-developed
depth hoar. These large, cup-shaped crystals, typically 4 to
10 mm (0.16 to 0.4 inch) in size, are characterized by straight
sides, sharp angles, and multiple layers of faceted faces. The
grains can be described as resembling etched crystal glass, and
their organized striations can make them sparkle.
The strong temperature gradients that drive kinetic metamor-
phism are aided by low-density new snow because the larger
pore spaces allow for easier migration of water vapor. Typical
faceted crystals or grains, previously referred to as temperature-
gradient snow, are commonly called squares. Depth hoar is
reserved for well-developed, cup-shaped, and large-faceted crys-
tals. 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 (4 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 deposited on a colder grain tends to cover the total grain
erential 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
4-6). Bond growth, which is called sintering, yields a cohesive
texture, 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; Figure 4-7 shows such bonded and intercon-
nected grains. Weak temperature gradients and high-density new
equilibrium metamorphism.
The previous discussion of kinetic and equilibrium metamor-
phism provides an overview 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
 relatively little is known about the processes that cause these

CHAPTER 4  Avalanches
EQUILIBRIUM METAMORPHISM avalanches.

SLAB AVALANCHE FORMATION

Sharp concave regions Necks form—sintering
FIGURE 4-6  Equitemperature grain growth. In the presence of weak
temperature gradients, bonds grow at the grain contacts.
place, one of these two processes 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, depend-
ing on the strength or weakness of the temperature gradient.
Both processes accelerate with warmer snow temperature
because more water vapor is involved.
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 forma-
tion of slab avalanches: the cohesive layer of snow and weak
layer beneath. If the snow cover is homogeneous from the
ground to the surface, slab avalanche danger is low, regardless
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 ava-
lanches, 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, informa-
tion is needed about the entire snowpack and not just its surface.
A hard wind slab at the surface may intuitively appear strong

AVALANCHE TYPES
There are two basic types of avalanche release. The first is a
point-release avalanche or a loose snow avalanche (Figure 4-8).
A loose snow avalanche involves cohesionless snow; it is initiated
at a point, and 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 ava-
lanches 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 4-9). 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 to a loose snow avalanche, a slab ava-
lanche 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 research-
ers. The majority of the information in this chapter deals with
dry slab avalanches or dry, loose snow avalanches. Because wet
snow avalanches have received scant research attention,

FIGURE 4-7  Bonded or sintered grains that result from equitempera-

ture metamorphism. Grain size, 0.5 to 1 mm (0.02 to 0.04 inch). (Cour- FIGURE 4-8  Loose snow avalanche or point-release avalanche. (Cour-
tesy Doug Driskell.) tesy US Department of Agriculture Forest Service.)

43
 tion about these properties, layer by layer, throughout the thick-
ness of the snow cover; however, even detailed knowledge of
these properties does not provide all the information 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
measure directly.
Mechanical deformation occurs within the snow cover just
before its failure and the start of a slab avalanche. Snow cover
tends to settle simply from its own weight. When this occurs on
level ground, the settlement is perpendicular to the ground, and
snow layer increases in density and gains in strength. The situ-
ation 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 and tends to pull the snow down the
slope. Downslope 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 struc-
tures 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.
MOUNTAIN MEDICINE

Snow deforms in a highly variable manner 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 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 compared with
more familiar materials.
With regard to avalanche formation, it is important to know
when snow acts primarily as an elastic material and when it
FIGURE 4-9  Slab avalanche. (From US Department of Agriculture responds more like a viscous substance. These conditions are
PART 1

Forest Service; Williams K, Armstrong B: The snowy torrents, Jackson,
Wyo, 1984, Teton Bookshop, with permission. Top, Courtesy Alexis
Kelner.)
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 com-
binations can contribute to slab avalanche formation, but again,
the prerequisite conditions are a cohesive layer over a weak layer
sitting on a bed surface. Figure 4-10 describes other combinations
that result in brittle or cohesive layers of snow on a weak layer.
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 informa-
shown in Figure 4-11. Laboratory experiments have shown that
conditions of warm temperatures and 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 sub-
stance 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 snow slab.
The slab avalanche provides the best example of elastic defor-
mation 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 4-12). The crown face is almost always

Moderate to heavily Deposited by Warm, dense

rimed crystals strong winds
SLAB SLAB SLAB
Lightly rimed Deposited by Cold, light
crystals light winds e
tra
te
tra
te t rat
bs bs bs
u u su
a ks a ks ea
k
We We W

FIGURE 4-10  Snow-layer combinations that often contribute to avalanche formation.

44

Force
Snow
Viscous deformation
Elastic fracture
FIGURE 4-11  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.
perpendicular to the bed surface, which is evidence that snow
has failed in a brittle manner.
A full understanding of the slab avalanche condition or stabil-
ity of the snow cover requires consideration of its mechanical
state. Snow is always deforming in a downslope manner, but
throughout most of the winter, the strength of the snow is suf-
ficient 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
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 4-13); this
means that the strength at that point immediately goes to zero.
This is analogous to what would happen if someone on a tug-
of-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 strength at the weakest point having now gone
to zero, nothing happens beyond perhaps a localized movement
or collapse in the snow, often heard as a “whumpf” sound. If
the surrounding snow is not capable of compensating, however,
the area of snow next to the initial weak point fails, then at
the next area, and so forth, until a propagating chain reaction
begins.
FIGURE 4-12  The consistent 90-degree angle between the crown face
and bed surface of the avalanche shows that slab avalanches result
from an elastic fracture. (Courtesy A. Judson.)
As the initial crack forms in the now unstable snow, the elastic
CHAPTER 4  Avalanches
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 pres-
sure are still being studied. Although any environmental measure-
ment presents its own set of problems, it is clear that opportunities
are extremely limited for making measurements inside a moving
avalanche.
Avalanche paths exist in a variety of sizes and shapes, but
they all have three distinct parts with respect to dynamics (Figure
4-14). 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 ava-
lanche proceeds to the track, where it remains essentially con-
stant 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 signifi-
cant amount of snow can be entrained into the avalanche from
the track. Small avalanches often stop in the track. Larger ava-
lanches 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 decelerate
slowly across a gradual slope, such as an alluvial fan. As a general
rule, the slope angle of starting zones is 30 to 45 degrees, track
is 20 to 30 degrees, and 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 like 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 highly turbulent dry
powder avalanches, velocities are typically in the range of 34 to
45 meters per second (m/s), or 75 to 100 miles per hour (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 terrain features. However, the higher-speed avalanche may
deviate from this path. Terrain features (e.g., side walls 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 4-15). 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 resul-
tant impact pressures can be significant. Smaller and medium-size
events with impact pressures of 1 to 15 kilopascals (kPa) have
the potential to heavily damage wood-frame structures. Extremely
large avalanches with impact pressures of more than 150 kPa
possess the force to uproot mature forests and even to destroy
structures 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,
45
 A
MOUNTAIN MEDICINE
PART 1

B C
FIGURE 4-13  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.)

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 contrib-
utes significantly to the total impact force. Presence of snow
crystals can increase 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 an 80-m/s
(180-mph) wind, which is well beyond the destructive capacity
of a hurricane.

46

Starting
zone
Track
Runout zone
FIGURE 4-14  Three parts of an avalanche path: the starting zone,
track, and runout zone. (Courtesy B. Armstrong.)
IDENTIFYING AVALANCHE TERRAIN
The essential ingredients of an avalanche—snow and a steep-
enough 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.
FIGURE 4-15  The large powder cloud associated with a fast-moving,
dry snow avalanche. (Courtesy R. Armstrong.)
SLOPE ANGLE
CHAPTER 4  Avalanches
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
and to rip it from its underpinnings. A slope of 45 degrees pro-
duces many more avalanches than does a slope of 30 degrees.
On even steeper slopes (>45 degrees), the force of gravity wins;
snow generally rolls or sloughs off, thus preventing 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 such as sand. These are rare, however, 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
Avalanches occur on slopes facing every point of the compass.
Steep slopes are equally likely to face in any direction. 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 orienta-
tion 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 receive much more sunshine and heating than
north slopes, which frequently leads to radically different snow
covers. North-facing 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-facing and south-facing slopes.
The effect of the prevailing west wind at middle 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 rede-
posit 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
effect of sun and wind is to cause more avalanches on north-
facing through east-facing slopes.
AVALANCHE TERRAIN PATHS
The frequency with which a path produces avalanches depends
on a number of factors, with slope steepness being a major one.
Again, the easiest way to create high stress is to increase the
slope angle; gravity works that much harder to stretch out the
snow and rip it from its underpinnings. A 45-degree slope pro-
duces many more avalanches than does a 30-degree slope;
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. Slopes
47
 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. Alterna-
tively, 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.,
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 full-
depth 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 lubri-
cates the ground surface.
VEGETATION
Vegetation has a mixed effect on avalanche releases. Bushes
provide anchoring support until they become totally covered. At
that point, bushes may provide weak points in the snow cover,
because air circulates around the bush and provides an ideal
MOUNTAIN MEDICINE
habitat for 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. 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
PART 1
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 snowpack change daily or even hourly. Pre-
cipitation, wind, temperature, snow depth, snow surface, weak
layers, and settlement are factors that determine whether an
avalanche will occur.
SNOWFALL
New snowfall is the event that leads to most avalanches. More
than 80% of 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 re-
leases 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 pose closure problems for highways and railways. Snows of
60 to 120 cm (2 to 4 feet) are much more dangerous, and snow-
falls 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 25 cm (10 inches) whipped by strong
winds may be serious; a fall of 60 cm (2 feet) of featherlight 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
48
is much more hazardous than the same amount of snow falling
over 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., within the last 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 a snow
surface several days or more old produces few or no avalanches.
Despite the apparent addition of weight caused by rain (2.5 cm
of rain is the equivalent in weight to 25 to 30 cm [10 to 12 inches]
of snow), rain tends to drain down through the older snow grains
and invariably freezes into an ice crust, which adds strength to
the snow cover. Later, the smooth crust could become a sliding
layer beneath new snowfall. Heavy rain (usually >2.5 cm) greatly
weakens the snow cover. It adds weight to the snowpack, but
adds no internal strength of its own (in the form of a skeleton
of ice, as new snow would create). Rain 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 eleva-
tions 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, denser 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,
also called “soft hail”) 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.
Because of its low density, the weak layer has a marginal ability
to withstand the weight of layers above, thereby making it sus-
ceptible 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.
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 much
greater rates than can snow falling from clouds. Wind drives
fallen snow into drifts and cornices from where avalanches begin.
Winds pick up snow from exposed windward slopes and drive
it onto adjacent leeward slopes, where it is deposited into shel-
tered 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. Snow
grains are subjected to harsh treatment in their travels; each col-
lision 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 no wind had blown.
TEMPERATURE
The role of temperature in snow metamorphism occurs over
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 tem-
perature is not always easy to interpret. Whereas a temperature
increase may contribute to stabilization of the snow cover in one
situation, it might at another time lead to avalanche activity.
In several situations, increased temperature clearly produces
increased avalanche potential. In general, these conditions
include (1) a rise in temperature during or immediately after a
storm and (2) a prolonged period of warm, fair weather, such
as occurs with spring conditions. In the first example, tempera-
ture at the beginning of a snowfall may be well below freezing,
but as the storm progresses, 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 ava-
lanche is provided within the new snow layers of the storm: a
cohesive slab resting on a weak layer. If the temperature contin-
ues to rise, the falling snow turns to rain. This situation is seen
in lower-elevation coastal mountain ranges. When this occurs,
avalanches are almost certain. As rain falls, additional weight is
added to the avalanche slope, but no additional strength is pro-
vided, as might be by a new layer of snow.
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.
In these first two examples, the complete snow cover gener-
ally 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
CHAPTER 4  Avalanches
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
almost 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 because of
the overburden of additional weight is a weak link. Of the snow-
pack 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 (conti-
nental 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 over-
lying 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 because of the spatial variability of
weaknesses on the slope. In addition, most field stability 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 the past couple of decades, study has focused on the fre-
quency 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. Several
mechanisms involved in the evolution of these layers may
49
 account for the majority of avalanches in this region, because
significant depth-hoar–related avalanches are less common.
Graupel (pellet-like heavily rimed crystals) can act as ball
bearings after being buried in the snowpack and can be respon-
sible for the layer 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 lubri-
cating that layer and destroying its shear strength. This phenom-
enon 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 day-
by-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.
SAFE TRAVEL IN AVALANCHE
TERRAIN
The first major decision 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 prob-
ably not challenge avalanches. For this group, education to
recognize and avoid avalanche terrain is sufficient. At the other
MOUNTAIN MEDICINE
extreme, mountaineering expeditions that have specific goals and
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 prepara-
tions, including education and carrying safety and rescue equip-
ment. 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
PART 1
avalanche areas. An inclinometer can be used to measure slope
angles. Some compasses are 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 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 4-16). Route finding in avalanche
country should avoid avalanches, 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 them
and at a distance from them. When taking a route above ava-
lanche 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 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 runout zones 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
50
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 travers-
ing 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 is closely
involved 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 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 use of a large mountaineer-
ing pack will make a person 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 avalanche victim hinder extremity motions and
only serve to drag the victim under. A person who is wearing a
rescue transceiver should always be certain that it is transmitting.
When crossing potential avalanche slopes, it is always better
to cross as high or low as possible and to avoid the middle. All
persons should traverse in the same track, spaced sufficiently
apart to expose only one person at a time. 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 higher up, 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 com-
monsense principles underlie 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., rock outcropping); they should not stop in the middle of
a slope or in the runout zone. The second, third, or even tenth
person traversing or traveling down a slope may trigger the
avalanche. Trouble should always be anticipated, and an escape
route (e.g., moving to the side, grabbing a tree) should be kept
in mind.
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 location of weak layers, and check-
ing for instability demonstrates how well layers are adhering to
one another. Several simple but meaningful tests can be per-
formed 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. Hard-
snow layers and ice lenses may resist penetration altogether, but
 CHAPTER 4  Avalanches
Poor
route

Poor
Good route
route

Good
route

A B

Gentle
slopes
te
d rou
G oo
Poor route

Steep
Poor slopes
route

Good route

C D
FIGURE 4-16  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 US Department of Agriculture Forest
Service: Avalanche handbook, Agricultural Handbook 489, Washington, DC, 1976, US Government Printing
Office, with permission. Courtesy Alexis Kelner.)

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. Although of limited value, the ski pole test
can provide useful information that must then be correlated with
other testing.
The simple but useful 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 there-
fore 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 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 maneu-
ver, but the momentum—even if an avalanche is initiated—
increases the chances of escaping from the starting zone to a
safe position. An experienced snowmobiler can perform a similar
test by riding across the test slope.
A much better way to observe directly 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)

51
 wide should be dug. With the shovel, the uphill wall is shaved
until it is smooth and vertical. The layers of snow can now 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 used to
locate weak layers (especially very thin layers). However, its
small sample size and subjective nature make it less reliable for
determining 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 freestanding. 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. A 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
MOUNTAIN MEDICINE

easy” and “easy” shears indicate unconditionally weak snow, Tapping

“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 30 30
compression required to cause shear failure. cm cm
k
The compression test (CT) is an effective way to find weak ea r
W ye
layers near the surface (~1 m [3.3 feet]), and works well in soft, la
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
PART 1

the shovel blade turned upside down and held on the top of the
column, successive taps are made on the shovel: 10 taps from
the wrist using the fingertips, 10 from the elbow using the fin-
gertips, 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. Interpretation of the stability of the weak layer
that is discovered is defined as “easy” (taps 1 through 10), “mod-
erate” (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 4-17).
Most tests, including the ST and the CT, assess fracture initia-
tion (i.e., additional force or stress needed to start fractures), but
do not assess fracture propagation (i.e., propensity for fractures
to spread through a weak layer in the snowpack). Without assess-
ing 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 the
fracture does not propagate across the weak layer. In an unstable
snowpack, a fracture may be easy or difficult to initiate. After it
has been initiated, however, the fracture can propagate across
the weak layer and result in an avalanche.
To better assess fracture initiation, propagation, and instabil-
ity, 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 the skier would put on the snow.
A snow pit is dug with a vertical uphill wall. 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 approximately 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 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
Snow pit
FIGURE 4-17  Photo and schematic of a shovel compression test.
(From The American Avalanche Association, with permission. Top,
Courtesy Doug Richmond.)
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 the person 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 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
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 somewhat
objective results that may help answer the bigger question of
whether the snowpack will fail under the weight of a person,
and that may help the mountain traveler with risk evaluation.
Limitations include the time required to isolate the block; inability
to test deep, weak layers; spatial variability of the results; and
the problem of relying on the RB as a one-step stability
evaluation.

52
 A more practical test 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. An excellent video tutorial can
be viewed on the Utah Avalanche Center website at https://
utahavalanchecenter.org/how-do-extended-column-test.
To prepare an ECT, a snow pit is dug with a vertical uphill
wall and a column isolated 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 use of the same successive tap technique
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. As with 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.
The propagation saw test, developed and tested in Canada
and Switzerland, has the advantage of being able to assess the
propensity of a preidentified persistent weak layer and slab
combination to propagate a fracture. Only a shovel and snow
saw are needed, and the test’s interpretation is relatively straight-
forward. A column of snow 30 cm (1 foot) wide by at least
100 cm (3.3 feet) uphill is isolated. After the persistent weak layer
is identified and marked, the blunt edge of the saw is directed
uphill through the weak layer until a fracture propagates. The
spot where the saw was located at the time of the propagation
is marked. Fracture propagation in a similar snowpack is consid-
ered “unlikely” if it requires sawing more than 50% of the weak
layer to initiate propagation, or if the fracture fails to reach the
end of the column. Propagation would be considered “likely” if
the fracture reaches the end of the column, or if it requires
sawing less than 50% of the weak layer to fracture. Unlike many
other stability tests, the propagation saw test allows assessment
of the slab propagation propensity in deep instabilities.
Interpreting stability from a single snow pit or stability test is
dangerous because of spatial variability. Snow cover is not homo-
geneous 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 ava-
lanche. It might then be assumed, incorrectly, that the snow in
a ski area 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 RB 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%.4 On paper,
being correct 80% to 90% of the time may sound encouraging.
In practice, however, the false-stable rate is still too high, because
the consequences of an error can be fatal. The false-stable rate
of 3% with the ETC is more encouraging, but researchers caution
that more studies are needed.39
AVALANCHE RESCUE EQUIPMENT
Shovel
The first piece of safety equipment that an individual entering
avalanche terrain should bring is a shovel, which can be used
to dig snow pits for stability evaluation, dig snow caves for
overnight shelter, and rescue a buried partner. A shovel is man-
datory for digging in avalanche debris because of the snow’s
high density. Such snow is extremely difficult to move with hands
CHAPTER 4  Avalanches
or 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 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 attach together quickly by
pulling a stiffening cable to construct a full-length probe. Some
ski poles with removable grips and baskets can be screwed
together to make an avalanche probe. Probes are used to search
for buried victims by spot probing in likely burial areas or to
confirm transceiver findings before shoveling (see Small-Team
Rescue [Companion Rescue], later).
Avalanche Rescue Transceiver
Avalanche rescue transceivers (beacons) are one of the best
personal rescue devices for quickly finding buried companions.
With practice and proper use, transceivers are a fast and effective
way to locate buried victims. Worldwide, these devices have
become standard gear for ski area patrollers involved in ava-
lanche work and for helicopter or other mechanized skiing
guides and clients. Transceivers are also frequently used by
highway departments and search and rescue organizations and
should be used by anyone traveling into avalanche terrain. Since
transceivers were first introduced in the United States in 1971,
they have been credited with saving multiple lives each winter.
Transceivers act as electromagnetic transmitters that emit a
signal on a standard frequency of 457 kHz. A buried victim’s unit
emits this repetitive signal in radial “flux lines,” which the rescu-
ers’ units receive and analyze when switched to “receive” mode.
The signal carries approximately 30 to 50 m (100 to 150 feet).
When audibly or visibly detected, the signal can guide searchers
specifically to the buried unit in less than 5 minutes.
Transceiver technology has evolved dramatically. Current
transceivers offer a significant technologic advantage over the
original analog devices. Two major categories of transceivers can
be found: (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 trans-
ceiver approaches the sending unit, and (2) digital, which uses
a computer chip to microprocess the receiving analog signal in
order to display a digital readout of the distance, strength (audible
and visual), and in some units (i.e., dual and triple antenna),
general direction to the buried unit. The newer triple-antenna
transceivers not only provide data about distance, direction, and
signal strength, but also can more easily identify multiple burials
and their approximate location in relation to each other. The
triple-antenna transceivers reduce occasional misleading signals,
which can be a confusing issue with single-antenna and dual-
antenna devices in the final few meters of the search. Transceiv-
ers are audiomagnetic-induction devices and not radio devices;
the directional arrows point radially along a flux line of the
sending unit’s magnetic field (Figure 4-18). Likewise, the dis-
played distance represents the distance along the flux line rather
than a direct distance to the sending unit; the closer the distance
displayed, the closer the flux line from the sending unit.
Both analog and digital transceivers operate on the same
internationally standardized frequency and are compatible with
one another. However, slightly different search techniques may
be necessary to use each type most efficiently, and special train-
ing and practice are required before the user attains proficiency.
Experience has shown that digital units have a significantly faster
learning curve; these are routinely used by helicopter skiing
services and backcountry guides for clients with limited experi-
ence. Multiantenna digital transceivers have largely replaced pure
analog units because of their relative ease of use and enhanced
information regarding burial location.
53
 min
weak
max
strong
+ 5m
– –

– – min
weak

– + – max
E W
strong

A S B C
FIGURE 4-18  Induction (“tangent”) line search method. A, 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 oriented in parallel and is weakest when oriented perpendicularly.
MOUNTAIN MEDICINE

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 per-
formed when the buried person 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, Constance BB, Freer L, et al.: Field guide to wilderness medicine,
4th ed, Philadelphia: Elsevier; 2013.)
PART 1

Merely possessing a transceiver does not ensure its lifesaving an airbag, 17 died (75% survival) from complete burial. From this
capability. Experience shows that the chances of surviving full initial information, avalanche airbags provide some survival
avalanche burial with a transceiver and small-team (companion) benefit. However, the exact increase in survival benefit imparted
rescue are reported to be 27% to 45%.1,10,26 Frequent practice is by the use of an avalanche airbag device is uncertain.
required to master a transceiver-guided search, which may not Early reports found that avalanche airbag devices reduced the
be as straightforward as the directions suggest. In this regard, likelihood of critical burial from 39% to 16.2% and lowered mor-
“beacon parks” with automated practice burials have become a tality from 23% to 2.5%.11 A “critical burial” is defined as a partial
popular method for fine-tuning one’s ability. Skilled practitioners or complete avalanche burial where the victim is at risk for
can typically find a buried unit in less than 5 minutes once a asphyxiation. Among all persons caught in an avalanche, early
signal is achieved. Because speed is essential in avalanche rescue,
transceivers can certainly be lifesavers. Therefore, the minimal
rescue equipment required for a rapid small-team (companion)
recovery is a transceiver, a collapsible probe or pole to confirm
and pinpoint the suspected location of the victim, and a shovel
for extrication (Box 4-1 and Figure 4-18).
Avalanche Airbag
The primary purpose of an avalanche airbag device is to prevent
complete burial. German industrialist Peter Aschauer introduced
the backpack-integrated avalanche airbag system (ABS) in 1985
(Figure 4-19). It was designed specifically for guides and ski
patrollers but rapidly became popular in Europe for use by rec-
reationalists venturing into avalanche terrain. Accident data
involving avalanche airbag devices38 have been compiled and
analyzed since 1990 by the Swiss Federal Institute for Snow and
Avalanche Research in Davos, Switzerland. From 1990 to 2010,
295 avalanche airbag–equipped persons were caught in ava-
lanches; 255 victims survived and seven victims died with
deployed airbags (two deaths caused by full burial from second- FIGURE 4-19  The German 170-L (5.6-foot3) dual-airbag system (ABS).
ary avalanches, three deaths from full burial in large avalanches, This device utilizes two wing-like 85-L (3-foot3) balloons inflated by
and two deaths from trauma). In the other 33 victims, the airbags pulling a T-shaped ignition handle, thereby rapidly releasing nitrogen
failed to work properly, or the user did not or could not deploy from a canister that draws air into the balloons by a Venturi effect.
the airbag; of these, 10 died. Overall, of 295 persons caught in Although this configuration favors a final prone position close to the
an avalanche wearing an avalanche airbag device, 17 deaths surface of the debris, possibly compromising the airway, the manufac-
occurred (94% survival). However, it must be noted that in 67 turers suggest that the bilateral and posterior position of the balloons
persons involved in the same accidents who were not wearing affords horizontal stability in the laminar flow of the avalanche.

54

BOX 4-1  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 4-18A,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 4-18C).
2. Holding the transceiver in this position, turn until the signal is
maximal (maximum volume), then walk five to seven steps (~5 m
[16.4 feet]), stop, and turn again to locate the maximum signal
(see Figure 4-18). 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 will 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 4-18B).
studies reported that avalanche airbags reduced mortality from
18.9% without an airbag to 2.9% with an airbag.10 This apparent
dramatic reduction in mortality presumably occurs because the
avalanche airbag device effectively prevents complete or critical
burial, and very few (~3% to 5%) noncritically buried or unburied
victims die in avalanches.
Recent examination of the effectiveness of avalanche airbag
devices24 used a retrospective, multivariate regression analysis on
a comprehensive avalanche accident data set from Europe,
Canada, and the United States that included avalanches from 1994
to 2012 with the potential for mortality. Each accident in the
analysis involved at least one airbag user compared with either
nondeployed-airbag users or nonusers from the same incident.
The multivariate analysis for critical burial and mortality after
protocol exclusions included 189 seriously involved individuals
from 61 accidents. The adjusted “risk of critical burial” was 47%
with noninflated airbags or no airbag compared to 20% with
inflated airbags. The adjusted mortality was 44% for critical burial
CHAPTER 4  Avalanches
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 always to 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 the person.
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 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.
and 3% for noncritically buried victims. Finally, the adjusted
mortality reduction with an inflated airbag dropped from 22%
without use of the bag to 11% (i.e., mortality was reduced by
half with inflated airbags). Interestingly, overall noninflation rate
was 20%, the majority resulting from deployment failure by the
user. These findings, despite inherent limitations of the hetero-
geneous data set and the retrospective nature, support that
avalanche airbags are a valuable safety device, although possibly
of less impact than previously reported.
The airbag works as a result of granular convection (the
“Brazil nut effect,” similar to shaking a large bowl of mixed nuts
to have the largest nuts rise to the top) (Figure 4-20). An ava-
lanche in motion is composed of many different-sized particles
of snow and other objects moving in layers of granular flow.
When these particles and objects begin to segregate, smaller
particles sink to the lower portion of the flow and larger particles
rise to the surface. The process of granular convection depends
primarily on the relative sizes of the particles within this granular
55
 Granular convection

FIGURE 4-20  Granular convection. 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 avalanche
airbag systems. This is similar to the “Brazil nut effect,” where shaking
a bowl of mixed nuts causes the largest nuts to rise to the top.
MOUNTAIN MEDICINE
FIGURE 4-21  The JetForce Avalanche Airbag Pack (Black Diamond
Equipment) uses a battery-powered fan instead of a compressed gas
cylinder. The fan inflates a 200-L (6.9-foot3) airbag in 4 seconds, then
automatically deflates the bag after 3 minutes. This system can be
deployed, repacked, and ready for use without having to refill a com-
pressed gas cylinder.

flow. A person who is carried in an avalanche may be a medium
or small particle compared with a particulate slab and therefore
may be buried under the surface. However, the airbag device
creates a greater surface area (typically a total of 150 to 170 L
[5.2 to 6.0 feet3] when inflated) for the avalanche victim, making
the user a large enough particle to allow for greater separation
effect toward the surface, thus reducing the risk of full burial.
Buoyancy plays no role in the efficiency of this system. In addi-
tion, during partial burial, the brightly colored balloons may
be easily visible on the surface, making a transceiver search
unnecessary.
Since 1995, avalanche airbag devices have undergone signifi-
PART 1
Different avalanche airbag device configurations include a
pack with two separate airbags, a pack with a single airbag, and
a vest with a single airbag. Configurations are two approximately
75- to 85-L (2.6- to 3.0-foot3) airbags or one 150-L (5.2-foot3)
airbag. These inflate in 2 to 3 seconds with use of the Venturi
effect. In 2014, one manufacturer released a 200-L (6.9-foot3)
airbag built into a pack that inflates in 4 seconds using an electric-
powered fan instead of a compressed-gas cylinder (JetForce Ava-
lanche Airbag Pack, Black Diamond Equipment) (Figure 4-21).
Avalanche airbags may deploy as a large bag or in a horseshoe
shape around the back of the victim’s head toward the anterior
chest. Avalanche airbag systems that cover the back of the neck

cant improvements with regard to device size, balloon technol-
ogy, and cartridge weight. Avalanche airbags are available from
four companies: ABS (with partners Osprey, Dakine, Ortovox,
and The North Face), Snowpulse/Mammut, Backcountry Access,
and Black Diamond Equipment. The airbag is usually integrated
into a special backpack, and the user deploys it by pulling a
ripcord-like handle. This action releases a cartridge of com-
pressed air or nitrogen that escapes at high velocity and draws
in outside air.
and head or surround the back and sides of the head and anterior
chest (Figure 4-22) have the theoretical advantage of preventing
head trauma and may allow for a greater chance of a head-up
partial burial. However, there is no evidence to support preven-
tion of head or chest trauma with specific avalanche airbag
system configurations. This is an area for future study.
Unlike the original avalanche airbag system (ABS), none of
the new systems has been independently tested by the Swiss
Federal Institute for Snow and Avalanche Research or have a

FIGURE 4-22  Example of an airbag system that surrounds the head and anterior chest when deployed.
This configuration, unlike the ABS, seems to favor a head-up, airway-favorable final position and may afford
some theoretical protection to the head, neck, and chest. Critics of this balloon design suggest that travel
in the avalanche might be more vertical, increasing the chances of lower-extremity trauma and a possible
“straining effect” from terrain features that would disrupt the process of granular convection.

56
 CHAPTER 4  Avalanches
A

B C
d
mon
Dia
ck
Bla

FIGURE 4-23  The AvaLung is a breathing device worn over all other clothing that is intended to prolong
survival during avalanche burial by diverting expired air away from inspired air drawn from the snowpack.
The white arrows show the flow of inspiratory air; the red arrows show the flow of expiratory air. The person
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). (Courtesy Jill Rhead and Black Diamond Equip-
ment, Salt Lake City, Utah.)

documented history of use in avalanche accidents. Questions

remain about the different-shaped balloons on the market regard-
ing ease of deployment, efficacy in preventing critical burial, and
protection from head trauma. Only the German ABS has been
rigorously tested and has undergone extensive use in avalanche
accidents. The new airbag designs are too recent to make any
sound recommendations at this time.
AvaLung
In 1996, after testing a homemade prototype on himself, Dr.
Thomas Crowley received a patent for an emergency breathing
device to extract air from the snow surrounding a buried ava-
lanche victim. Black Diamond Equipment in Salt Lake City, Utah,
performed 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 4-23). The most recent version,
which is the most popular, is incorporated into various-sized
backpacks with a stowable mouthpiece kept in the shoulder strap
(Figure 4-24).
The AvaLung functions mainly by separating inhaled from
exhaled air in the surrounding burial snowpack, with a goal of
prolonging survival time by slowing the process of asphyxiation.
Ambient air is 21% oxygen (O2) and has virtually no carbon
dioxide (CO2). Expired air is 16% O2 and 5% CO2. The AvaLung
prevents rebreathing expired air, which is the major cause of FIGURE 4-24  The AvaLung backpack. A stowable mouthpiece is
asphyxiation during avalanche burial, by diverting expired air located in the shoulder strap along with the inspiratory and expiratory
away from inspired air that is drawn from the snowpack20 (see valve housing. Inspiratory air enters through a one-way valve in the
Avalanche Victim Physiology and Medical Treatment after Rescue, valve housing located in the shoulder strap and flows through respira-
later). Survival after complete avalanche burial with use of the tory tubing and the mouthpiece into the lungs. Expiratory air flows
through the mouthpiece into the shoulder strap and through a second
AvaLung has occurred in a number of cases.34
one-way expiratory valve. Expired air then travels through the respira-
The AvaLung system has proved effective in numerous simu- tory tubing and through the pack to the lower back on the opposite
lated burials by allowing persons to breathe for 1 hour in tightly side, where expiratory air is expelled. (Courtesy Black Diamond Equip-
packed snow of similar density to avalanche debris. In control ment, Salt Lake City, Utah.)
burials without the AvaLung, participants were only able to
breathe from 4 to 19 minutes using a 500-mL (30.5-inch3) air
pocket.20,35 In addition, several cases of survival have occurred,
although burial time was fairly short. In a dramatic hallmark case,
a helicopter skier survived a 120-cm (4-foot) burial of 35 to 45

57
 minutes by breathing with an AvaLung. Two other skiers buried
in the same avalanche a few feet apart at a similar depth were
not wearing the device, and both died of asphyxiation. Rescue
times were similar for the three victims, none of whom had suf-
fered any trauma.13
The ABS and AvaLung are designed as adjuncts to the basic
companion (small-team) rescue equipment, which includes a
transceiver, probe, and shovel. These devices should never be
used to justify taking additional risks. Surviving any avalanche is
always uncertain, and no equipment should ever replace sound
judgment.
AVALANCHE RESCUE
INDIVIDUAL RESCUE (SELF-RESCUE)
Escaping to the Side
During the moment that the snow around a person begins to
move, there is a split second during which that person can
potentially move off the avalanche to more stable snow (see
Figure 4-13). Escaping to the side of an avalanche is unlikely,
however, and should not be considered a viable rescue or safety
plan. If the skier happens to be next to a tree when an avalanche
begins, holding onto the tree may help prevent the person from
being carried, but the force of an avalanche usually carries the
person. As such, skiing in an area with trees should not be used
MOUNTAIN MEDICINE
as a prevention strategy. Trying to outrun an avalanche by
turning the skis or the snow machine downhill is impractical and
dangerous; an avalanche invariably overtakes its victims.
If caught, a victim should shout “Avalanche!” to alert compan-
ions, 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 impac-
tion. If the person is wearing an ABS, the ripcord should be
pulled and the airbag activated.
Actions during the Slide
PART 1
For years, it was taught to “swim to the surface” (i.e., struggling
with the arms and legs flailing) if caught in an avalanche. The
idea is that the victim may be able to climb to the surface as
well as increase the apparent surface area. The efficacy of these
actions has been questioned. The process of granular convection
(see Avalanche Airbag, earlier) rather than swimming may be
more important in keeping the victim on or near the surface.
Nevertheless, many survivors claim that “swimming” kept them
on or close to the surface. If the victim sees or feels an object,
such as a tree or rock band, the person should make every
attempt to grab and hang on, allowing some of the avalanche
forces to bypass.
Skiers should try to discard their skis and poles. With any
luck, the avalanche will strip away the skis. Backpacks should
be kept, if possible, because they make the victim a slightly larger
particle for granular convection and increase the likelihood that
the person will be closer to the surface. Packs might offer some
protection to the thoracic spine. If the victim ends up on the
surface, the equipment will be useful. However, the equipment’s
fate will usually be decided by the avalanche. Packs slide off
easily when a person is turned upside down, even with tight
straps. Snowmobile riders should try to stay on their machine.
Once separated from the machine, avalanche victims are twice
as likely to be buried than if they had stayed with the machine.
Visual clues are the quickest method to find a buried ava-
lanche victim. If the victim senses that he is close to the surface,
he should thrust a hand or a foot toward that direction. Any
visual clue on the surface will give rescuers a possible indication
of location and greatly improve odds of survival.
Creating an air pocket is a key to survival. Without an air
pocket, the time to asphyxiation is much more rapid. If the victim
is not close to the surface or the position is unknown, the person
should place one or both hands in front of the face to create a
space, or air pocket, when the avalanche is slowing. This action
should be performed early because the avalanche may stop
abruptly, at which time no movement will be possible.
58
SMALL-TEAM RESCUE (COMPANION RESCUE)
All backcountry users should carry appropriate avalanche rescue
equipment to aid a fellow group member or another group. This
includes a transceiver, shovel, and probe, as well as knowledge
of and practice using this equipment. At resorts, ski patrol
members monitor the avalanche danger and attempt to trigger
sensitive avalanches. Therefore, avalanches are rare in these
areas. However, avalanche management is not a perfect science,
and skiers have become caught, injured, and even killed at ski
resorts. Therefore, some skiers wear avalanche transceivers and
carry avalanche rescue gear inside the ski resort for increased
safety. Basic medical skills to care for and manage a partner who
has been buried in an avalanche are equally important. Every
backcountry user should attend a cardiopulmonary resuscitation
(CPR) course and wilderness-oriented first-aid course.
Calling for Help
If the accident site may be within the range of cell phones or
other communication methods, a call or text should be attempted
immediately. Search and rescue teams as well as medical assis-
tance can be summoned and can be en route during on-site
search for the victim. If team members are certain that no cell
reception or other communication is possible and that travel to
communications is more than 30 minutes away, all should remain
on-site for the search and rescue. If the accident occurs in or
near a ski area and there are several companions, one person
can be assigned to leave the scene and immediately notify the
ski patrol.
Marking the Last-Seen Area
A companion or eyewitness to an accident needs to act quickly
and positively. Rescuer actions over the next several minutes may
mean the difference between life and death for the victim. Com-
panions must assess the terrain to ensure that they and other
rescuers are safe from secondary slides. The bed surface of an
avalanche that has recently run is usually safe to enter. Occasion-
ally, however, an avalanche fracture line has broken at midslope,
which leaves a large mass of snow, sometimes called “hang fire,”
still positioned above the fracture that could avalanche onto the
rescuers.
First, the victim’s last-seen area should be fixed and marked
with a piece of equipment or clothing, tree branch, or any item
that can be seen from a distance downslope. If the victim was
seen riding the avalanche before the last-seen area, a line of
trajectory can be visualized that could narrow down likely areas
of burial. Persons equipped with transceivers should travel to the
last-seen area to begin their search (see Probing after Transceiver
Search, later). Victims who are fully buried without transceivers
likely face an unsurvivable situation.
INITIATE SEARCH AND SCAN FOR CLUES
All companions must immediately switch their units to receive
mode. At the same time as initiating this transceiver search, the
fall line (i.e., the line of trajectory) should be quickly scanned
below the last-seen area in the flow line for any clues of the
victim. A glove, ski pole, or other object could lead rescuers
directly to the victim. If an obvious clue is seen, shallow probing
should be done into likely burial spots with an avalanche probe
(i.e., spot probing). All backcountry users should carry a proper
avalanche probe. A ski, ski pole, or tree limb could be used to
search if necessary or in a ski resort, where probes may not be
carried. Likely spots are the uphill and downhill sides of trees
and rocks and benches or bends in the slope where snow ava-
lanche debris piles up. The toe of the debris should be searched
thoroughly because many victims are found in this area.
Rescue Transceivers
While making the quick visual search for clues, companions
should search the debris using their transceivers, as described in
Box 4-1 and Figure 4-18. 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.

90° 10″ 10″
25 CM 25 CM
FIGURE 4-25  Concentric probing method. Probing should proceed
from inward to outward in concentric circles spaced 25 cm (10 inches)
apart.
Probing after Transceiver Search
When the victim’s location has been pinpointed, probing should
begin. The probe should be placed perpendicular to the slope
at the location of the highest transceiver signal and pushed
deeply, usually 2 to 3 m (6.6 to 10 feet; the majority of probe
lengths). If this does not strike the victim, the probe should be
removed and probing continued in a spiral or concentric-circle
pattern until the victim is contacted (Figure 4-25). When the
victim is located by a probe strike, the probe should be left in
place and shoveling should begin.
Shoveling Techniques
Shoveling will, unfortunately, take much longer than the trans-
ceiver search. Depending on the number of rescuers and tech-
nique used, this aspect of the rescue could be the difference
between life and death. Efficient shoveling techniques can make
this process much quicker, increasing the chances of survival.
Strategic Shoveling.  During companion rescue, only one
to three shovelers might be available. The strategic shoveling
technique14 increases digging efficiency (Figure 4-26). With the
probe left in place, shovelers begin digging downslope about 1 1 2
times the burial depth, as determined by markings on the probe.
Stand away from the probe, and do not stand above the buried
victim, if at all possible. Quickly dig a waist-deep starter hole
about one wingspan wide (i.e., the distance between the finger-
tips 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.
Snow shoveled to side
Burial
depth
1.5 x burial depth
FIGURE 4-26  Strategic shoveling technique for one or two rescuers.
(Courtesy Dale Atkins and National Ski Patrol, Lakewood, Colo.)
When close to the victim, use a scraping action to clear snow.
CHAPTER 4  Avalanches
Use the first body part to estimate the location of the head, then
use the hands to clear away snow from the victim’s face and
airway, and continue to clear snow off the chest. The most
important feature of efficient shoveling is to create a ramp or
platform that leads to the probe (and the victim) instead of
digging a hole straight down around the probe. Extrication and
resuscitation of the victim are made easier by creating a flat
surface with space to work on the victim, because the air pocket
is not compromised and raising the victim is not necessary.
V-Shaped Conveyor Belt.  With a professional (organized)
rescue, when hours or days have elapsed, the debris is often
much harder as a result of age hardening. Typically, more shovel-
ers are available in a professional or organized rescue. In this
situation, the V-shaped conveyor belt method16 works effectively
to clear snow quickly (Figure 4-27). Starting downslope 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 downslope. The other shovelers use paddling-like
motions to clear out snow through the center of the V to create
a platform. When nearing the buried victim, an additional shov-
eler may join the lead to increase the working space. Shovelers
may rotate clockwise every 5 minutes to decrease fatigue. After
they reach the victim, the rescuers should locate the head and
chest and use their hands to clear a space for the airway.
Avalanche rescue courses should teach efficient shoveling
techniques, and the method should be practiced as often as
transceiver searches to reduce the total time to extrication.
Calling for Professional Resources
A cell phone or other communication method should have
already been used to alert outside agencies. If communication
could not be made, on-site rescuers often face a difficult question
of when to leave the scene to summon outside help. If only one
or two companions are present, the correct choice is more dif-
ficult. The best advice is to search the surface quickly but thor-
oughly for clues before anyone leaves to notify the patrol or
obtain outside assistance.
If the avalanche occurs in the backcountry far from any pro-
fessional rescue team (organized rescue), all companions should
remain at the site. The guiding principle in backcountry rescues
is that companions search until they cannot or should not con-
tinue. When deciding when to stop searching, safety of compan-
ions must be weighed against the decreasing survival chances of
the buried victim. If a small team (companions) rescues a team
member who has been determined to be dead, the team should
attempt to stay on scene until a professional (organized) rescue
team arrives or other appropriate arrangements are made. This
allows professional rescue teams and medical examiners to assess
the situation and assist in evacuation.
PROFESSIONAL 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 job.
No matter how an incident is managed, all avalanche search
and rescue operations have four key functional components,
which 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 who are
competent not only in avalanche rescue but also in route finding
and hazard evaluation. Basic search and rescue tools are trans-
ceivers, probes, shovels, avalanche rescue dogs, the RECCO
system (described later), 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
success, the team determines the most likely burial areas. The
59
 80 cm

A B C
MOUNTAIN MEDICINE

D E
F
PART 1

FIGURE 4-27  V-shaped conveyor belt shoveling approach. A, Positioning of rescuers, with a quick measure-
ment of the distance between shovelers. B, Working in sectors on the snow conveyor belt; snow is trans-
ported 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, Avalanche Rev 20:20, 2008, with permission.)

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 last-seen areas. 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
medical and evacuation equipment reach the site in a timely
manner.
The third component is transportation, which includes travel
for additional rescuers to and from the accident site and for
evacuation of victims. The transportation effort must begin im-
mediately so that rescuers and equipment can be moved effi-
ciently 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.
Organized Probing Search Techniques
Organized probing 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 with these methods
was thought to be about 70%. If the probe line missed the victim
on the first pass, which tended to happen, 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.
The optimal combination of probe-grid spacing and search
time, as determined by computer analysis, is a grid spacing of
50 cm by 50 cm (20 inches by 20 inches).2 This probe-grid
spacing yields the best combination of probability of detection
and fast search time. For a three-holes-per-step probe, probers
stand with their arms out, wrist to wrist. Probers first probe

60

50 cm
50 cm 50 cm
FIGURE 4-28  Three-probe spacing for 50-cm by 50-cm, three-hole-
per-step probe method.
between their feet, then probe 50 cm (20 inches) to the right and
50 cm (20 inches) to the left (Figure 4-28). 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 almost identical to
that of traditional spacing. Ski patrols and mountain rescue teams
who have adopted the three-holes-per-step style of probe with
a 50-cm by 50-cm (20-inch by 20-inch) grid have noted improved
efficiency and effectiveness of the probe line.
Because these rescuers insert more probes per rescuer, fewer
rescuers can be used on a probe line. Short probe lines are easier
to manage and work faster than long probe lines. Five rescuers
doing three holes per step at 50-cm intervals form a slightly
longer probe line than 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 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 probability of detection to 99%.
The third effective organized probe search is called the slalom
probing technique (Figure 4-29).17 In this method, organized
rescuers probe three areas in a left-to-right pattern after two
lateral steps, then step forward, and then probe three areas in a
right-to-left pattern. This pattern is repeated for the debris field
that must be searched. The main advantage of the slalom probing
method is that all probing is performed directly in front of the
rescuers, which has been determined to be stronger and more
efficient than probing to the side, as required in the three-hole-
per-step technique. Also, forward steps are more time-consuming
and variable in distance than lateral steps. The main disadvantage
is that it is surprisingly difficult to train novices to perform the
slalom probing technique well.
50 cm 50 cm
50 cm 50 cm
7 2 3 7 2 3 7 2 3 have detectors. Worldwide, more than 600 ski resorts and heli-
6 5 4 6 5 4 6 5
1 2 3 1 2 3 1 2 3 in the United States soared during the 1990s (Figure 4-31) and
FIGURE 4-29  Slalom probing technique. On direction by the incident
commander, each rescuer probes in the sites indicated by color (red,
yellow, green) in the rescuer’s respective area. (From Genswein M,
Letang D, Jarry F, et al: Slalom probing—A survival chance–optimized
probe line search strategy. Paper presented at the International Snow
Science Workshop, 2014, Banff, Alberta, Canada.)
Rescue teams use probe lines to find most avalanche victims
CHAPTER 4  Avalanches
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 (see Rescue Statistics, later).
Avalanche Rescue Dogs
Trained search dogs, which are traditionally used in Europe early
during avalanche rescues, are capable of locating buried victims
very quickly. Since 1950, there have only been nine reported live
recoveries using dogs. Six of these involved trained dogs: four
at ski areas, one along a highway, and one in the backcountry.
Three other avalanche burials involved personal dogs who found
their owners in the backcountry. Burial depths of avalanche
victims found alive ranged from 0.3 to 1.5 m (1 to 5 feet); burial
depths of victims killed ranged up to 4.5 m (15 feet).1
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 up
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 (33 feet)
deep, but have also passed over persons buried only 2 m (6.6
feet) deep. Dogs find “scent” and not people, although some-
times they find both. On numerous occasions, dogs signaled an
alert in the vicinity, which may extend out as far as 9 to 12 m
(30 to 40 feet) from a buried victim. These scent clues then led
to searchers finding victims with other technologies.
RECCO
The electronic rescue system called RECCO (www.recco.com)
enables organized rescue teams to find victims who are equipped
with reflectors (Figure 4-30). The system consists of two parts: a
detector used by the rescue team (either on the ground or from
helicopters) and a reflector 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 direc-
tional radar signal. When it hits the reflector, the signal’s fre-
quency 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, 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 using an avalanche beacon. In North America, more
than 130 ski areas, mountain rescue teams, and national parks
copter rescue teams use them.
4
THE AVALANCHE VICTIM
After reaching a 20-year low in the late 1980s, avalanche deaths
spiked twice (2007-2008 and 2009-2010) with 36 deaths, the
greatest number killed during the modern era (i.e., after 1950).
Figure 4-31 also presents the 5-year moving average. Since the
end of the 1980s, the average number of fatalities per winter rose
from 11 to 30, but decreased slightly in the mid-2000s. In recent
years, the 5-year average has edged back upward to 30 deaths
per winter. As more people head into the winter backcountry,
avalanches continue to be deadly. In the United States since 1950,
61
 A B
FIGURE 4-30  A, The RECCO reflector is a thin circuit card 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 heli-
copter. (Courtesy RECCO AB, Sweden.)

avalanches have claimed 993 lives, and 28% (281) of those riders on split boards, and snowcat skiers. In-bounds riders are
MOUNTAIN MEDICINE

victims died during the 10 winters up to 2012-2013.1 skiers and boarders who are on open terrain within the ski area
From 2004 to 2014, almost all avalanche victims (94%) were boundary that is managed for avalanches; in-area avalanche
pursuing some form of recreation at the time of the accident fatalities are rare. Among nonrecreation groups, avalanche deaths
(Figure 4-32). Snowmobilers constitute the largest group of ava- occur in residents of avalanche-hit homes, highway personnel
lanche victims, primarily because snow machines with powerful (motorists and plow drivers), and ski patrollers. Since 2004, 13
engines and better tracks can climb steep, avalanche-prone states have registered avalanche fatalities (Figure 4-33).
terrain and can cover significantly more terrain in a day than
human-powered backcountry users, thereby exposing snowmo-
bilers to greater avalanche risk. The combined “backcountry
STATISTICS OF AVALANCHE BURIALS
tourer” and “sidecountry rider” categories accounted for more Survival during avalanche burial depends on the grade and dura-
avalanche deaths than in snowmobilers (112 vs. 101). Backcoun- tion of burial and the pathologic processes of asphyxia, trauma,
try tourers and sidecountry riders are “out of bounds” skiers and and hypothermia.9 The grade of burial is defined as critical or
PART 1

snowboarders who venture into areas that are not part of a ski noncritical. Critical burials are those in which asphyxiation may
resort and thus are not managed for avalanches. The backcountry occur and include full burial or partial burial, where the head is
tourer category includes ski mountaineers, helicopter skiers, under the snow and breathing is impaired.24 Duration of burial

US Avalanche Fatalities 1950–51 to 2013–14

40
36 36
35 35
35 34
33
31
30 30
30 29
28 28 28

26
25
25 24 24 24
23 23
22 22 22
21 21
20
20
18 18
17
15
15 14 14
13 13
12 12
11
10
10 9
8 8
7 7 7 7
6 6 6 6 6 6
5 5
5 4 43 4 4
3 3
2 2
1 1
0
1951 1956 1961 1966 1971 1976 1981 1986 1991 1996 2001 2006 2011
FIGURE 4-31  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 Colorado Avalanche Information
Center.)

62
 CHAPTER 4  Avalanches
US Avalanche Fatalities by Activity 2004–05 to 2013–14
Climber 30
Hiker 13
Backcountry tourer 85
Sidecountry rider 27
Inbounds rider 11
Hybrid rider 2
Snowmobiler 101
Mechanized guide 3
Mechanized guiding client 1
Human-powered guide client 2
Hunter
Snowplayer 2
Misc recreation
Motorist
Resident 6
Ski patroller 6
Highway personnel 1
Miner
Others at work
Ranger
Rescuer
Unknown
0 20 40 60 80 100 120

FIGURE 4-32  U.S. avalanche fatalities by activity, winter 1999-2000 to winter 2008-2009. (Data from Dale
Atkins and Colorado Avalanche Information Center.)

can be influenced by depth of burial, clues on the surface that
make the avalanche victim easier to locate, available rescue
equipment, and competence of the rescuers. Body position,
traumatic injury, snow density, and presence and size of an air
pocket influence risk of asphyxiation.
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 life-and-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 hypercap-
nia 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 difficulty 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 initially might have been 80% air, it might be
less than 50% air after an avalanche and is much less permeable
to airflow, thereby making it more difficult for the victim to
breathe.

US Avalanche Fatalities by State 2004–05 to 2013–14

CO 64
UT 40
MT 40
WA 37
WY 29
ID 27
AK 25
CA 17
OR 6
NH 2
VT 1
NV 1
ND 1

0 10 20 30 40 50 60 70
Fatalities

FIGURE 4-33  U.S. avalanche fatalities by state, winter 1999-2000 to winter 2008-2009. (Data from Dale
Atkins and Colorado Avalanche Information Center.)

63

100
Survival probability (%) Swiss data 1981 to 1998 (N = 638)4
80 Swiss data 1981 to 1991 (N = 422)9
60
40
20
0 niques. Of victims (36 of 70) buried with a body part (e.g., hand)
0 20 40 60 80 100 120 140 160 180 200 220 240
Time buried under avalanche (min)
FIGURE 4-34  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.)
MOUNTAIN MEDICINE
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 4-2 shows the statistics for survival as a function
of the rescuer. Buried victims rescued by a small team (compan-
ions or groups nearby) have a much better chance of survival
than those who are rescued by professional (organized) teams.
Small teams of companions can potentially rescue a victim in
minutes, whereas it may take hours to mount a professional
rescue. Of people found alive, 78% were rescued by small teams,
and 13% were found by a professional rescue team.
Table 4-3 compares the results of rescue by different tech-
or an attached object (e.g., ski tip) protruding from the snow,
51% 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 com-
panion 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 (93%)
are recovered after they are dead.

Snow sets up hard and solid after an avalanche. It is almost TABLE 4-2  Type of Rescue for Buried Avalanche
impossible for victims to dig themselves out, even if they are
buried less than 30 cm (1 foot) deep. Hard debris also makes Victims in Direct Contact with Snow Based on a
recovery very difficult, so a sturdy shovel is essential. The pres- Sample of 360 Burials in the United States from Winter
sure of the snow in a burial of several feet is sometimes so great 2003-2004 to Winter 2012-2013
that the victim is unable to expand the chest to draw a breath.41
Warm exhaled breath freezes on the snow immediately in front Professional
of the face, eventually forming an ice lens that cuts off all air- Individual Small Team (Rescue
flow and contributes to asphyxiation in some buried avalanche (Self) (Companions) Team) Total
PART 1

victims.
Statistics regarding survival are derived from a large number Found alive 9 83 14 106
of avalanche burials (Figure 4-34). When compiling these figures, Found dead — 116 138 254
only persons who were totally buried in direct contact with the Survival 100% 42% 9% 29%
snow were included. Victims who were buried in the wreckage
of buildings or in vehicles are not included, because they can Data from Atkins D: 10 years of avalanche rescues in the United States, 2003/04
to 2012/13. Avalanche Rev 33(3):22-24, 2015.
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. TABLE 4-3  Method of Rescue for Buried Avalanche
A completely buried victim has a poor chance of survival, Victims Based on a Sample of 274 Avalanche Burials  
which is related to both time and depth of burial. Survival dimin-
ishes with increasing burial depth, because it takes longer to in the United States from Winter 2003-2004 to Winter
uncover a victim who is buried deeper. To date, no one in the 2012-2013
United States who has been buried deeper than 3 m (10 feet)
has been recovered alive; however, in Europe, two victims sur- Method Found Alive Found Dead Total
vived burials of 6 to 7 m (20 to 23 feet).1,42
Burial depth is important in avalanche survival, but time is Attached object or body 36 (51%) 34 (49%) 70
the enemy of the buried victim. Figure 4-34 shows survival prob- part
ability function calculated from European data, which has become Spot probe 3 (18%) 14 (82%) 17
a classic demonstration of decreasing survival chances with Probe line 3 (7%) 40 (93%) 43
increasing burial time. During the first 15 minutes, most people Rescue transceiver 41 (27%) 109 (73%) 150
(~90%) are found alive. At 30 minutes, an equal number are Avalanche dog 2 (7%) 21 (93%) 23
found dead and alive. After 30 minutes, more are found dead Voice 10 (100%) 0 10
than alive, and the survival rate continues to diminish with longer Digging 2 (14%) 12 (86%) 14
burial time. Speed is essential to the search. Buried victims can RECCO 0 (0%) 4 4
live for several hours beneath the snow under favorable circum- Melted out 0 (0%) 14 14
stances. A miner in Colorado who was buried by an avalanche Not found, not recovered 0 (0%) 4 4
near a mine portal was able to dig himself free using his hard Inside vehicle 0 (0%) 0 0
hat from nearly 1.8 m (6 feet) of debris after approximately 22
Inside structure 0 (0%) 2 2
hours. In 2003, two snowshoe hikers caught near Washington’s
Total 97 (28%) 254 351
Mt Baker survived burials of 23 and 24 hours. Such long survival
times are a reminder that no rescue should be abandoned pre- Data from Atkins D: 10 years of avalanche rescues in the United States, 2003/04
maturely on the assumption that the avalanche victim is dead. to 2012/13. Avalanche Rev 33(3):22-24, 2015.

64
 During the 10 years of winter 2003/04 to 2012/13, the ava-

CHAPTER 4  Avalanches
lanche transceiver was used to find more victims than any other 100
method; it is the best method for finding the completely buried Canadian sample
victim if it is carried and used correctly. The bad news is that

Probability of survival, %
80 Overall
the mortality rate over those 10 years was 73% (see Table 4-3).
Asphyxia-related deaths only
Unfortunately, most companions cannot use a transceiver fast
enough to save a life. Even in textbook rescues (i.e., signal 60 Swiss sample
quickly located and victim dug free in a short time), many victims Overall
did not survive. 40
Organized probe lines are an effective way to find a buried
victim, but because this method requires many rescuers and
much time, most victims (93%) are recovered dead. Despite the 20
sound-insulating properties of snow, 10 victims who were shal-
lowly buried were able to yell and be heard by rescuers (i.e.,
voice contact; see Table 4-3). 0
These statistics point out the extreme importance of rescue 0 30 60 90 120 150 180
skills. Professional (organized) rescue teams (e.g., ski patrollers, Duration of burial, minutes
mountain rescuers) must be highly practiced. They must have
adequate training, manpower, and equipment to perform a hasty FIGURE 4-35  Comparison of the Swiss avalanche survival curve (blue
search and probe the likely burial areas in a minimal amount of line) and the Canadian survival curve (red line) over the same 25-year
time. For backcountry rescues, the buried victim’s companions period. Note the rapid drop after 10 minutes in the Canadian curve,
(small-team rescue) remain the best hope for survival. The need although maintaining the same morphologic survival phases. (From
to seek outside rescue units means a much lower chance (but Haegeli P, Falk M, Brugger H, et al: Comparison of avalanche survival
not zero) for live recovery. patterns in Canada and Switzerland, CMAJ 183(7):789-795, 2011.)

AVALANCHE VICTIM PHYSIOLOGY

AND MEDICAL TREATMENT
AFTER RESCUE
MORBIDITY AND MORTALITY
Asphyxiation is the most common cause of death during ava-
lanche burial. More than 75% of avalanche deaths result from
asphyxiation; less than 25% result from trauma, and very few
result from hypothermia.7,22,25,28,30,41,42 Because asphyxiation is the
major cause of death during avalanche burial, time to extrication
is a major determinant of survival. In a large Swiss data set, fully
buried avalanche victims have a more than 90% chance of sur-
vival if they are extricated within 15 to 18 minutes, but this
chance drops to only 30% to 34% after about 35 minutes (see
Figure 4-34).8,15 This emphasizes the need for a swift companion
rescue at the avalanche site to avoid asphyxiation. Survival
beyond 30 minutes of burial requires a patent airway and ade-
quate air pocket for breathing. If the air pocket is large enough,
avalanche victims may survive for hours and develop severe
hypothermia.
The mortality statistics, in particular relating to trauma, vary
with geographic location and the terrain over which the ava-
lanche slides. Avalanches that run through heavily forested
regions may cause significant trauma to victims compared with
avalanches that run in open bowls above tree line. In Canada,
trauma is the primary cause of death in 24% and asphyxiation in
75% of avalanche deaths. In 13% of the primary asphyxia ava-
lanche deaths in Canada, there was evidence of major trauma,
which may have contributed to asphyxiation.7 Data from Utah
and Austria show a much lower mortality from trauma, about
5% and 6%, respectively, and a much higher mortality from
asphyxiation, about 95% and 92%.25,30 A difference in geography
between countries may be one reason why trauma mortality in
avalanche victims is higher in Canada than in the United States
and Austria.
In an example of geographic variability as it pertains to ava-
lanche survival, recent comprehensive examination of full-burial
survival patterns in Canada was compared to an updated Swiss
data set over the same 25-year period using similar statistical
methodology (Switzerland, n = 946; Canada, n = 301).23 There
was no difference in overall survival between the two countries
(46.2% in Canada, 46.9% in Switzerland). The Canadian survival
curve, however, was characterized by earlier and more rapid
drop in survival in the early stages of burial, after only 10 minutes
(Figure 4-35). Trauma accounted for more than half the deaths
in victims extricated in the first 10 minutes, and two thirds of
trauma-related deaths involved collision with trees. Overall
trauma-related avalanche mortality in Canada was 18.9%, com-
pared with about 6% in Europe and the United States.25,30
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, trauma is more likely and may
result in death. An early study of both partial and complete buri-
als in Utah and Europe reported that traumatic injuries occurred
among 25% of avalanche survivors.22 The most common trau-
matic injuries were major orthopedic, soft tissue, and craniofacial
injuries (Table 4-4). In a report of injuries in 105 avalanche vic-
tims in Austria,25 most were only minor (Table 4-5). A high inci-
dence of lower-leg fractures and shoulder dislocations occurred,
which were thought to result from attached skis and poles caus-
ing additional mechanical leverage on the extremities. Spine
fractures were found in 7% of victims.
A review of autopsy reports from 28 avalanche deaths in Utah
over a 7-year period27 showed that among 22 avalanche victims
who died from asphyxiation, one-half experienced mild or mod-
erate traumatic brain injury. The authors argued that this could
cause a depressed level of consciousness and contribute to death
from asphyxiation. All six of the avalanche deaths that resulted
from trauma involved severe traumatic brain injury. In another
review of 56 avalanche deaths in Utah, all three fatalities caused
solely by trauma showed evidence of head injury.30 Although
these studies demonstrate the role of head injury in avalanches,
TABLE 4-4  Injuries among Survivors of Avalanche
Accidents (Partial and Total Burials)
Utah Europe
Total injuries 9 (total of 91 351 (total of
avalanche 1447 avalanche
accidents) accidents)
Major orthopedic injuries 3 (33%) 95 (27%)
Hypothermia requiring 2 (22%) 74 (21%)
hospital treatment
Skin and soft tissue injuries 1 (11%) 84 (25%)
Craniofacial injuries — 83 (24%)
Chest injuries 3 (33%) 7 (2%)
Abdominal injuries — 4 (1%)
From Grossman MD, Saffle JR, Thomas F, et al: Avalanche trauma, J Trauma
29:1705, 1989.

65
 TABLE 4-5  Pattern of Injury among 105
Avalanche Victims
Trauma Frequency (n)
Cerebral trauma
Chest trauma: all 18
  Chest trauma: sternum or rib fracture (n = 16)
Chest trauma: pneumothorax or hemothorax
(n = 6)
Spinal fracture: all
  Spinal fracture: cervical (n = 3)
  Spinal fracture: thoracic (n = 1)
  Spinal fracture: lumbar (n = 3)
Abdominal trauma
Pelvic fracture
Extremity trauma: all 20
  Extremity trauma: lower-leg fracture (n = 8)
  Extremity trauma: shoulder dislocation (n = 6)
  Extremity trauma: femoral fracture (n = 4)
From Hohlrieder M, Brugger H, Schubert HM, et al: Pattern and severity of
injury in avalanche victims, High Alt Med Biol 8:56, 2007.
MOUNTAIN MEDICINE
the report from Austria of injuries in avalanche victims noted that
the two fatalities caused solely by trauma in their series resulted
from isolated fracture and dislocation of the cervical spine.25 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 stabi-
lization during the rescue and resuscitation period. Avalanche
victims can sustain virtually any type of trauma during their often
turbulent descent in the avalanche flow, and certainly if involved
in collisions with trees or rocks. The head and neck are especially
vulnerable to enormous forces, and these areas appear to be the
PART 1
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% O2 and less than
0.03% CO2; expired air contains about 16% O2 and 5% CO2.
Rebreathing expired air in an enclosed space results in progres-
sive hypoxia and hypercapnia that eventually causes death from
asphyxiation. The larger the air pocket, the greater is the surface
area for diffusion of expired air into the snowpack and for dif-
fusion of ambient air from the snowpack into the air pocket, and
thus survival time is longer before death occurs from asphyxia-
tion. An ice mask is formed when water in the warm and humid
expired air freezes on the snow surface in front of the face.
Because this barrier is impermeable to air, it accelerates asphyxi-
ation 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 where partici-
pants 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.12 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
66
10% and the FICO2 increased to about 6% (Figure 4-36). These
changes in O2 and CO2 levels in the air pocket resulted in
decreased arterial O2 saturation as measured by pulse oximeter
and increased end-tidal partial pressure of CO2. Most participants
were not able to complete the entire 30 minutes of the study and
had to stop as a result of dyspnea, hypercapnia, and hypoxia,
2
but some reached an equilibrium where FIO2 and FICO2 stabilized
and hypoxemia and hypercapnia were tolerable. These few indi-
viduals lasted the full 30 minutes of the research protocol, dem-
onstrating how breathing with an air pocket can prolong survival
during avalanche burial.
7 Hypoxemia and hypercapnia occur as expired air is rebreathed.
A smaller air pocket or lower-porosity snow (usually higher
density) causes more rapid development of hypoxia and hyper-
capnia. Larger air pockets and higher-porosity snow (usually
1 lower density) allow for more mixing of expired air with ambient
1 air within the air-filled pore spaces between grains of snow in
the snowpack. This results in longer survival times before hypoxia
and hypercapnia become severe enough to cause death from
asphyxiation. Porosity of snow, which is a dimensionless value,
refers to the volume of air within a sample of snow compared
to its total volume. It relates to the ability of gases to diffuse
through snow, and roughly correlates to snow density (i.e., the
mass per unit volume, typically kg/m3; see Physical Properties,
earlier). Higher-density snow generally, but not always, has lower
100 25
20
SpO2 (%)
FIO2 (%)
80
15
A
60
10
8
ETCO2 (kPa)
6
4 10
B
FICO2 (%)
5
0 0
0 5 10 15 20 25 30
Time (min)
FIGURE 4-36  Curves of individual respiratory parameters in persons
breathing with a tight-fitting face mask connected to respiratory tubing
running into 1- or 2-L air pockets in dense snow (n = 28). The x-axis
represents time in minutes. Some participants did not complete the
30-minute study because of dyspnea or hypoxia. A, Arterial oxygen
saturation (SpO2 [%]) as measured by a digital pulse oximeter on the
left y-axis (red lines) and fraction of inspired oxygen (FIO2 [%]) on the
right y-axis (blue lines). B, Partial pressure of end-tidal carbon dioxide
(ETCO2 [kPa]) on the left y-axis (red lines) and fraction of inspired carbon
dioxide (FICO2 [%]) on the right y-axis (blue lines). (From Brugger H,
Sumann G, Meister R, et al: Hypoxia and hypercapnia during respira-
tion into an artificial air pocket in snow: Implications for avalanche
survival, Resuscitation 58:81, 2003, with permission.)
 CHAPTER 4  Avalanches
MEAN VALUES AND RANGES FOR SpO2, ETCO2, and PICO2
100
95

SpO2%
90
85
80
75
70
60

mm Hg
ETCO2
50
40
30
20

60
50
mm Hg

40
PICO2

30
20
10
0
–10 –5 0 5 10 15 20 25 30 35 40 45 50 55 60
Time relative to burial (min)

Baseline
AvaLung
Control

FIGURE 4-37  Mean data and ranges are shown for physiologic parameters at baseline breathing ambient
air ( ), during the AvaLung burial ( ), and during the control burial without the AvaLung ( ) (n = 14). The
x-axis represents time relative to full burial in minutes for all panels. The y-axis represents percent saturation
of hemoglobin with oxygen (SpO2 [%]) for panel 1, end-tidal partial pressure of carbon dioxide (ETCO2 [mm
Hg]) for panel 2, and inspired carbon dioxide partial pressure (PICO2 [mm Hg]) for panel 3. Some mean data
points at the end of the control burial are missing or do not have ranges because of participant dropout
(i.e., burial times of 5 to 19 minutes). (Data from Grissom CK, Radwin MI, Harmston CH, et al: Respiration
during snow burial using an artificial air pocket, JAMA 283:2261, 2000; and Grissom CK, Radwin MI,
Harmston CH, et al: Respiration during snow burial using an artificial air-pocket. In Schobersberger W,
Sumann G, editors: The annual yearbook of the Austrian Society of Mountain Medicine, Austria, 2001,
Austrian Society of Mountain Medicine.)

porosity because of complex variables. Since porosity of snow
is very difficult to measure but density is frequently measured in
the field, the avalanche literature refers to snow density as a
surrogate value in relation to asphyxiation during avalanche
burial.12,20,23 An equilibrium occurs when expired air diffuses out
of the air pocket and is replaced by fresh air that diffuses in from
the snowpack, depending largely on snow porosity. This results
in FIO2 and FICO2 reaching plateaus within a physiologically toler-
able range, prolonging survival of the avalanche victim. This may
occur even with small air pockets, which has been observed
when extricating avalanche burial survivors of up to 2 hours’
duration (likely in highly porous snow).8
Even densely packed snow contains sufficient ambient air to
permit normal oxygenation and ventilation as long as all expired
air is diverted out of the snowpack. This was demonstrated in a
study of persons who were totally buried in dense snow and
who inhaled air directly from the snowpack (density, 300 to
680 kg/m3 or 30% to 68% water) through a two-way nonrebreath-
ing valve attached to respiratory tubing that diverted all expired
air to the snow surface. Participants maintained normal oxygen-
ation and ventilation for up to 90 minutes.35 This study demon-
strated 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
earlier), which has been designed to prolong survival during
avalanche burial (see Figure 4-23). Although the device prevents
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. The AvaLung has been well studied
using a human model of burial in snow of similar density to
avalanche debris.18-21 In the initial study,20 breathing with the
AvaLung while buried in dense snow was compared to 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 AvaLung 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 AvaLung (Figure
4-37). The AvaLung has resulted in survival during actual ava-
lanche burials.13,34
MEDICAL TREATMENT AND RESUSCITATION OF
AVALANCHE BURIAL VICTIMS
A published algorithm is available from the International Com-
mission for Mountain Emergency Medicine (ICAR MEDCOM) for
resuscitation of avalanche burial victims.6,9 We recommend an
algorithm for evaluating an extricated avalanche burial victim that
incorporates key decision points from the ICAR MEDCOM algo-
rithm for treatment and triage of avalanche victims in cardiac
arrest. However, our algorithm also incorporates recommenda-
tions from the Wilderness Medical Society Practice Guidelines for
the Out-of-Hospital Evaluation and Treatment of Accidental
Hypothermia.44
Figure 4-38 presents the key points regarding assessment and
treatment of an extricated avalanche burial victim. 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 should 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, the spinal column

67
 Extrication from avalanche burial
Normal Yes
mental status?
Treat for Hypothermia I (core temperature >32°C):
No Provide dry warm insulation, hot drink containing sugar,
medical transport to closest appropriate facility.
Yes
Conscious?
Treat for Hypothermia I (core temperature >32°C) or
No Hypothermia II (28 to 32°C): Clear the airway, provide
oxygen, dry warm insulation, medical transport to
closest appropriate facility.
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
No and ventilation with heated and humidified oxygen,
dry warm insulation, heated IV fluid. Package and
transport with spinal column immobilization. Transport
MOUNTAIN MEDICINE
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 with 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, 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 hypothermia and trau-
matic 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 (VF).
The medical treatment of this patient is focused on (1) ensuring
adequate oxygenation and ventilation, either noninvasively with
a bag-valve-mask device or with a supraglottic airway device or
endotracheal tube, as clinically indicated, and (2) immobilizing
the spinal column for transport and treating any obvious signs

to tertiary care facility.

of trauma. Intravenous (IV) access may be obtained and warmed
isotonic fluids infused. Treatment of hypothermia is described in
the next section.
Clear the airway, assist ventilations, provide oxygen, and intubate If a pulse is not present after opening the airway and venti-
or place a supraglottic airway. Check for pulse after ventilating lating the patient and after checking for a pulse for up to 1
and oxygenating. minute, CPR is begun.9,44 Before CPR is initiated, careful evalua-
tion for the presence of a pulse should occur. Avalanche burial
Treat for hypothermia III or IV (Core victims are hypothermic, which causes peripheral vasoconstric-
Pulse Yes Temperature <28°C): warmed IV fluids, tion and makes pulses difficult to palpate. In addition, moderate
present? dry insulation, handle gently, transport to to severe hypothermia causes bradycardia and depression of
a tertiary care facility. respiration.
No In a pulseless avalanche burial victim, electrocardiographic
PART 1

monitoring should be used to assess cardiac rhythm, or, alterna-

If rhythm is VF or VT defibrillate once if tively, an automatic external defibrillator may be applied. In the
Rhythm No core temperature <30°C, continue CPR moderately or severely hypothermic patient in VF with a core
asystole? per ACLS protocol. If PEA, continue CPR. body temperature of less than 30° C (86° F), defibrillation should
Treat for hypothermia III or IV as below. be performed according to published guidelines,3,43 with the
Yes,
or unknown caveat that, after unsuccessful defibrillation(s), further defibrilla-
tion may be deferred until rewarming is underway as chest
Death from asphyxiation
Burial No compressions continue.44 Drugs may be administered as part of
likely. Resuscitation per
>60 minutes? advanced cardiac life support in accordance with published
ACLS protocol. Cease
guidelines.43
Yes efforts when clinically
The likelihood of the successful resuscitation of an avalanche
indicated. May continue
No
burial victim who is in cardiac arrest at the time of extrication
Airway patent resuscitation and transport
depends on whether cardiac arrest occurred from asphyxiation
on extrication? to the nearest appropriate
or from hypothermia. Factors that may be used to indicate the
medical facility. A K+ of
Yes likelihood of survival in an extricated avalanche burial victim in
greater than 8 meq/liter
cardiac arrest are burial time, airway patency, core temperature,
suggests that resuscitation
Core temperature No and serum potassium level.9,43 Avalanche victims in cardiac arrest
<30°C ? may be futile and death has after burials of less than 60 minutes are unlikely to be resusci-
occurred from asphyxiation. tated, because death has most likely occurred as a result of
Yes
asphyxiation. A patent airway is essential for survival beyond 60
minutes.9 Even if duration of burial is less than 60 minutes or
Treat for hypothermia III or IV (Core Temperature <28°C): Intubation,
the airway is occluded, resuscitation should always be attempted
assisted ventilation with warmed humidified oxygen, monitor ECG,
for a limited time if feasible and safe. Avalanche victims extricated
CPR, warmed IV fluids, dry insulation, medical transport to a facility
from burials of more than 60 minutes with a patent airway, who
capable of extracorporeal rewarming.
have no signs of life but who are moderately or severely hypo-
Notes: thermic (i.e., core temperature of <30° C [86° F]), may be consid-
Burial for 60 minutes: The provider should use the 60-minute threshold as a ered for ongoing resuscitation and transport to a medical facility
general, but not absolute, guide. Circumstances such as a presumed large air that is capable of extracorporeal rewarming (Figure 4-38). Ava-
pocket could allow for a longer survival time without development of severe lanche burial victims who are extricated in cardiac arrest after
hypothermia. Core temperature: Providers may not have access to core more than 60 minutes of burial and who have an obstructed
temperature thermometers in the field. In this circumstance, the severity of airway have most likely died from asphyxiation, and continuing
hypothermia may be estimated with the use of Swiss hypothermia
stages I through IV as determined by the clinical presentation (see Box 4-2)
resuscitation efforts until rewarming occurs is unlikely to result
in survival. In one study, none of 13 avalanche victims who were
FIGURE 4-38  Assessment and medical care of extricated avalanche found in cardiac arrest after burials of 30 to 165 minutes’ duration
burial victims. survived.28 These results suggest that cardiac arrest was the result
of asphyxiation rather than hypothermia.

68
 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 discour-
age initial attempts at resuscitation, but rather to suggest that
prolonged CPR may be a futile exercise. It is always warranted
initially to 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 the importance of
immediately starting 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 potas-
sium level can be measured and used as a prognostic indicator
for avalanche burial victims in cardiac arrest.6,37,43 In a hypother-
mic adult avalanche victim in cardiac arrest, a serum potassium
level of greater than 8 mmol/L indicates that resuscitation efforts
should be terminated. If the serum potassium is greater than
12 mmol/L in an adult or a child, resuscitation efforts should be
terminated.6
HYPOTHERMIA IN THE AVALANCHE
BURIAL VICTIM
In avalanche burial victims who are extricated alive, hypothermia
is a major medical problem that requires treatment.6,9 Box 4-2
provides clinical definitions of hypothermia severity correlated
with core body temperature. As the patient is extricated from
snow burial, warm dry insulation is provided during packaging,
CHAPTER 4  Avalanches
BOX 4-2  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;
Brugger H, Durrer B, Adler-Kastner L, et al: Field management of avalanche
victims, Resuscitation 51:7, 2001; and Zafren K, Giesbrecht GG, Danzl DF, et al:
Wilderness Medical Society Practice Guidelines for the Out-of-Hospital
Evaluation and Treatment of Accidental Hypothermia, Wilderness Environ Med
25(4 Suppl):S66-S85, 2014.
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 VF. When
treatment of moderate or severe hypothermia is clinically indi-
cated, IV access is obtained, and warmed (42° C [107.6° F]) iso-
tonic 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 where definitive rewarm-
ing can occur. The shivering patient with mild hypothermia can
rewarm in the field if dry insulation is provided18 (Figure 4-39).

38.0
Extrication

37.5
Afterdrop Rewarming

37.0
Temperature (° C)

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 4-39  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 person. 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 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.)

69
 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 core
body temperature measurement in the field, preferably with 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 use of Swiss hypothermia stages I through IV, as
determined by the clinical presentation (see Box 4-2).44
Severity of hypothermia may also be estimated from the time
that the victim was buried and the average rate of core tempera-
ture cooling during burial. In a controlled experiment of human
volunteers wearing a lightweight clothing insulation system,
fully buried in compacted snow of similar density to avalanche
debris, and breathing with an AvaLung for up to 60 minutes,
core body temperature cooling rate was about 1.3° C (2.3° F) per
hour.21
Retrospective studies of core temperature on hospital arrival28
suggest that the average core temperature cooling rate is 3° C
(5.4° F) per hour in survivors (range, 0.75° to 4.75° C [1.4° F to
8.6° F]). The higher rate of cooling in this study is based on a
known time of burial and known arrival time at the hospital
where core body temperature was recorded, and it does not dif-
ferentiate between core temperature cooling rate during snow
MOUNTAIN MEDICINE
burial and afterdrop cooling rate during medical transport.
Burial cooling rates are accelerated by hypercapnia. Cooling
rates measured in hypercapnic and in normocapnic buried indi-
viduals were 1.28° C and 0.97° C (34.3° F and 33.7° F), respec-
tively,19,21 In addition, minute ventilation, respiratory heat loss,
total metabolic rate, and respiratory muscle metabolic rate were
greater for the hypercapnic persons. Afterdrop cooling rate
increases transiently after extrication from snow burial.18,19 After-
drop cooling rate increased up to fourfold for a mean of 12
minutes after extrication in those buried in snow breathing with
an AvaLung for 60 minutes18 (Figure 4-39). Accelerated cooling
rate during and after extrication places avalanche victims at
PART 1
greater risk for complications caused by hypothermia. Rescue
personnel should make every effort to prevent further heat loss
in avalanche victims 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
(Table 4-6). In one case, a 25-year-old male snowboarder with
a large air pocket in front of his body survived 20 hours of ava-
lanche burial.21 At 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
TABLE 4-6  Core Temperature Cooling Rates in Survivors of Avalanche Burial
Author (Year) Study Population
Locher and Walpoth28 16 survivors (3 cardiac arrest) of
(1996) avalanche burial
Spiegel40 (2002) Case report, 25-yr-old male avalanche
victim
Grissom et al21 (2004) 12 healthy participants with
lightweight clothing
Putzer et al33 (2010) Case report, 28-yr-old male avalanche
victim
Oberhammer et al31 Case report, 27-yr-old male
(2008)
Paal et al32 (2013) 8 piglets, anesthetized, intubated,
buried in a simulated avalanche
Boue et al5 (2014) Two case reports: first case, 17-yr-old
male; second case, 41-yr-old male
70
adequate diffusion of expired air away from inspired air and
prevented asphyxiation. In that same rescue, the survivor’s com-
panion 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 man who was buried for 100 minutes and
extricated alive with an epitympanic core temperature of 22° C.31
He was endotracheally intubated and ventilated, but went into
VF during helicopter transport and was transported with ongoing
CPR (except for 15 minutes during the initial helicopter evacua-
tion from the scene to a local hospital). He was in cardiopulmo-
nary arrest for 150 minutes before defibrillation on the fifth
attempt resulted in return of spontaneous circulation after extra-
corporeal rewarming. He made a full recovery.
These anecdotal reports demonstrate that core body tempera-
ture cooling rates during avalanche burial may vary significantly,
and that survival after long-duration avalanche burial with severe
hypothermia is possible. Survival of avalanche victims after
cardiac arrest, however, is possible when the arrest is witnessed
after extrication and caused by severe hypothermia. Resuscitation
efforts should continue, and these victims should be transported
to centers capable of extracorporeal rewarming. Avalanche
victims extricated after unwitnessed cardiac arrest most likely
were asphyxiated, and resuscitation to a perfusing rhythm is very
unlikely.29
SUMMARY
Asphyxiation is the major cause of death during avalanche burial
and is time dependent. Traumatic injuries can be immediately
fatal or can shorten the time for asphyxiation to occur. Avalanche
victims who have not succumbed to a traumatic fatality and who
are extricated within 15 minutes have a greater than 90% chance
of survival. However, this “survival phase” decreases to about
30% if they are extricated after 30 minutes, thus emphasizing the
need for small-team (companion) rescue with use of avalanche
transceivers, probes, 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 survival is pos-
sible during burial. 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, 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 providing warm, dry insulation and
Conditions Cooling Rate
Retrospective review, avalanche 2.9° C/hr (range, 0.75°-4.75° C/hr),
burial victims burial to hospital arrival
20-hr avalanche burial with a large air 0.6° C/hr
pocket
Simulated avalanche burial for up to 1.3° C/hr (range, 0.6°-2.4° C/hr)
60 min
90-min avalanche burial; 25-min 5° C/hr, burial to hospital arrival
transport
95-min avalanche burial; cardiac 9° C/hr tympanic membrane
arrest after extrication temperature, burial to extrication
Breathing into an air pocket or 4.6° C/hr with air pocket and
ambient air 4.8° C/hr with ambient air
First case, complete burial for 6 hr First case, 2.3° C/hr
Second case, complete burial for 7 hr Second case, 1.8° C/hr
warm, sugar-containing liquids. Rewarming will occur through should be anticipated, although any injury pattern can occur.
shivering. Avalanche burial victims who are not shivering have Many avalanche victims have no traumatic injuries.
progressed to moderate or severe hypothermia and require
medical transport to a hospital for definitive rewarming. Uncon-
scious avalanche burial victims who are breathing may require
ACKNOWLEDGMENTS
endotracheal intubation for airway control and assisted ventila- The authors thank Betsy R. Armstrong, Richard L. Armstrong,
tion and are most likely moderately to severely hypothermic. and Knox Williams for their contributions to previous editions
Victims who are extricated in asystolic cardiac arrest have most of this text.
likely died from asphyxiation, and resuscitation to a perfusing
rhythm is very unlikely. Avalanche victims extricated with a
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71.e1

CHAPTER 5 
Lightning-Related Injuries and Safety
MARY ANN COOPER, CHRISTOPHER J. ANDREWS, RONALD L. HOLLE,
RYAN BLUMENTHAL, AND NORBERTO NAVARRETE ALDANA
HISTORICAL OVERVIEW104,155,325,381
Lightning has caused injuries to people since humans evolved
on Earth. It has played a major part in almost every ancient
religion and culture. Priests, some of whom were the earliest
astronomers, also became proficient at weather prediction, inter-
preting changes in weather as omens of good or bad fortune,
sometimes to the advantage of their political mentors. To this
day, lightning continues to engender stories, perceptions, and
myths and is a popular topic for the press and science and
weather documentaries.155,325
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 5-1).
Beginning around 700 BC, Greek artists began to incorporate
lightning symbols representing Zeus’s tool of warning or favor.
Zeus, the king of the gods, could control the weather. Early
Greeks believed that lightning was his weapon and that lightning
striking the Earth was a direct sign of Zeus’s presence or influ-
ence. The ancient Greek poet Hesiod called Zeus the “cloud-
gatherer” and the “thunderer.” Zeus was also concerned with
hospitality; if you treated a guest or stranger badly, you could
outrage him (Figure 5-2).
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 regarded lightning as more ominous than
did the Greeks, with Jupiter using thunderbolts as tools of ven-
geance 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
CHAPTER 5  Lightning-Related Injuries and Safety
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 caused
by the flashing feathers of Impundulu, the lightning bird-god,
whose flapping wings produced the sound of thunder (Figure
5-3). 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. Different charms, herbs, or other
materials may be buried under a house to protect it from light-
ning. 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.
Their lightning spirit is depicted as having axes attached to his
joints, which 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 was the god of
heaven, lightning, rain, storms, and thunder (Figure 5-4). 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 pow-
dered 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 Thun-
derstorms” of ancient Chinese religion.
Scandinavian mythology alludes to Thor, the thunderer, who
was the foe of all demons (Figure 5-5). 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 holy dwellings, because steeples were struck frequently
71
 uncontrollable, and unmanageable. Cambodians 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 of lightning strike, 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 underneath it.
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
use gasoline (petrol) to bomb the house of an enemy whom 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 hippopota-
mus hide 2.4 m (8 feet) underground will protect their area.
Wearing red is believed to be protective, but mirrors are thought
to attract lightning, not only in Africa but in other cultures, includ-
ing the United States.
South Africans believe that the Syringa tree attracts lightning
(Figure 5-6). So strong is this belief that some farmers will cut
down every Syringa tree on their property. Other trees are
believed to be protective and homes are preferentially built under
or near these trees.
In “civilized” Western societies, lightning can take on mystical
significance. When lightning struck an English cathedral just
MOUNTAIN MEDICINE

FIGURE 5-1  Teshub, the Syrian weather god.

PART 1

FIGURE 5-4  Indra, the Hindu god of heaven, lightning, rain, storms,
and thunder.
FIGURE 5-2  Zeus, king of gods who hurls the lightning.

FIGURE 5-3  Impundulu, the lightning bird. (Copyright artbybluedaisy.)

by lightning. French peasants carry a pierre de tonnerre, or light-

ning 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 great fear as mysterious, FIGURE 5-5  Thor, the Norse god of thunder.

72

FIGURE 5-6  So strong is the belief among South Africans that the
Syringa tree attracts lightning that farmers will cut down every Syringa
tree on their farms. (From http://www.bushveld.co.za/wildsyringa-
tree.htm.)
before enthronement of a controversial bishop in the late 20th
century, some regarded it as an omen. Bullock53,54 advances a
case that the conversion of Saul on the road to Damascus resulted
from a lightning strike.
MODERN LIGHTNING MYTHS AND
MISCONCEPTIONS
Medicine and meteorology are replete with myths, false impres-
sions, and misunderstandings. In meteorology, these are based
on a combination of lack of insight and understanding, limited
personal experience, wishful thinking, and faulty outside opinion.
This problem exists with regard to tornadoes, hurricanes, winter
storms, perceived local effects, rare-event frequency, apparently
cyclic storms, and so forth. Lightning is among the worst phe-
nomena in this regard. These myths and misunderstandings
are not idle issues; they can result in fatalities, maltreatment
of patients, and erroneous court testimony. Therefore, some
common misconceptions are worth addressing.
LIGHTNING LORE
To dispel myths and misconceptions, it is helpful to understand
the basic facts: lightning appears during thunderstorms that are
often small and local, so the related time and space scales are
short and limited. The effect of lightning begins with a 1-inch-
diameter channel that has an extreme but spatially limited area
of influence in most cases and only lasts a fraction of a second.
As with other environmental threats, avoidance activities often
need to be taken before lightning appears a certain threat.
The most important myth is that something can be done to
make people completely safe from lightning wherever they may
be. In more developed countries, almost 100% of lightning casu-
alties occur because people do not take advantage of two gener-
ally safe locations: (1) a large, substantial, and enclosed, frequently
occupied structure and (2) a fully enclosed, metal-topped vehicle.
In the event of lightning strike, these locations conduct energy
around the person to the ground through structural metal (e.g.,
plumbing, wiring, metal vehicle body). If a person is not inside
one of these two reliably safe places, lightning becomes a threat.
Outside these places, no posture, location, or action will make
a person completely safe. In developed areas, these safe places
are available to most people most of the time. When people
choose to be away from these safe places, they have put them-
selves at risk for lightning injury. Thus, proper planning is
important.
It is nearly impossible to protect all people in developing
countries because there are times when lightning-safe structures
or vehicles are unavailable. At night, homes may provide no
lightning protection because of rudimentary construction. During
the day, people may be at risk because schools, markets, and
work structures may not be safe. Workers are also vulnerable
because of labor-intensive manual agriculture, mining, and other
CHAPTER 5  Lightning-Related Injuries and Safety
unprotected work situations.
A second safety myth is that a person is safe if it is not raining
hard or thundering frequently. Most people seek shelter from
rain when storm clouds roll overhead. However, if shelter is not
sought, injuries occur even in locations where there are relatively
low flash rates. Protection from the rain is not the same as pro-
tection from lightning. Approximately 10% of cloud-to-ground
strikes occur when no rain is falling at the time or location of
the ground strike.
At least one-third of lightning casualties occur as the thunder-
storm is approaching, because people misjudge its location or
speed of approach, do not pay attention to warning signs, or
want to finish an activity before seeking shelter.89,190 Lightning
may travel horizontally as far as 16 km (10 miles) or more in
nearly any direction from the edge of a thunderstorm. As a result,
when the sun is shining where the person is located, lightning
may flash “out of a clear blue sky.” Approximately one-third of
victims are struck at the end of a thunderstorm because they
have gone outside too soon.
One of the most consistently dangerous locations of injury is
standing near a tree or other tall object. Tents, regardless of their
construction, do not prevent 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. The takeaway is that no place outside is
safe from lightning threat when thunderstorms are in the area.
Small structures are almost always dangerous. It should be
assumed that a small structure is not lightning safe, although it
provides rain or sun protection. Although beach, sun, rain, bus,
and golf shelters and sheds, including a hiker’s lean-to, can be
protected to some extent against lightning strikes by adhering to
National Fire Protection Association (NFPA) lightning codes
(NFPA780), this does not mean the people inside are safe.229,291,292
In fact, it is likely that using such shelters may actually increase
a person’s risk for injury because of side flash and ground
current. One should think of these shelters as capacitors with air
insulation between the capacitor plates (roof and floor). It is easy
to understand that someone standing inside the shelter decreases
the amount of energy needed to discharge the capacitor and send
lightning energy through the occupant. Sheltering within a
shallow cave on a mountainside may protect from rain but may
be very dangerous from a lightning perspective.
“When thunder roars, go indoors” is a primary teaching phrase
in many lightning safety education efforts, including for the
National Weather Service’s Lightning Safety Awareness Week
(http://www.lightningsafety.noaa.gov).295 Although one might
suppose that seeing lightning is a reliable warning, this is not
always the case. On the Great Plains and in the western United
States, lightning may be seen up to 160 km (100 miles) away,
but in a forested area, lightning may not be seen at all before
people are in danger. Seeing lightning is highly variable and may
overestimate or underestimate the risk. Thunder is a more reliable
tool for estimating distance and danger, because it is seldom
audible from more than 16 km (10 miles) away. Unfortunately,
in many cases, such as in a city, heavy traffic area, or noisy sports
stadium, thunder may be inaudible.
The flash-to-bang method refers to seeing lightning, then
hearing thunder. It is useful to understand in concept, even
though it is decreasingly used by the general public, The rule is
frequently misremembered, and there may be substantial uncer-
tainty in linking flashes to thunder. The 30-30 rule from the late
1990s addresses the beginning and end of thunderstorms from a
lightning safety point of view.43,295 The first “30” is for counting
the seconds from seeing lightning to hearing its thunder at the
beginning of a storm. If the count to thunder is 30 seconds or
less, lightning is 10 km (6 miles) distant or closer, indicating that
a person is in danger and should be seeking safe shelter. U.S.
Lightning Safety Week leaders replaced the first “30” for the
general public with the phrase, “When thunder roars, go indoors,”
because they realized that people were using this time first to
count rather than simultaneously seek shelter.295 The second “30”
indicates the minutes elapsed to reach the conclusion of the
storm after seeing the last lightning or hearing the last thunder.
One should wait these 30 minutes before going outside and
73
 resuming activity. Although the 30-30 rule is not used as often
as previously, the concept of a rule for both the beginning and
end of a thunderstorm is the basis for safety rules used at many
large venues, such as airports, mines, sports stadiums, and indus-
trial sites. When objective lightning detection network data
provide accurate information on lightning times and locations for
large venues, these data should be used instead of imprecise
colloquialisms.292,295
In developed countries, lightning injuries may occasionally
occur indoors, but they are rarely, if ever, fatal. The causes are
contact injury or side flashes from plumbing fixtures, computers,
hard-wired telephones or electronic devices, and other appli-
ances.11,125,126 With a hard-wired phone, persons may suffer acous-
tic damage, neurocognitive deficits, death, or other lightning-related
problems.32,277 These occur because the telephone system in most
houses is not grounded to the house’s electrical system, but rather
acts as a conduit for lightning either to come into or to exit
from the home. Cell phones and cordless indoor phones offer
complete protection from indoor electrical effects of light-
ning.6,25,140,173,174,274,295 In developing countries where safe housing is
not available, a dozen or more people may be killed indoors
during a single incident.
MEDICAL MYTHS AND MISCONCEPTIONS
A persistent myth is that lightning strikes are invariably fatal (Box
MOUNTAIN MEDICINE
5-1). In truth, mortality rate may be as low as 5% to 10%.67 One
study of lightning cases occurring since 1900 found that lightning
BOX 5-1  The Most Common Myths and Facts about Lightning
No Truth
• Lightning injuries are always fatal.12,26,33,87
• Lightning is spelled with an e, “lightening.”
• The cause of death from lightning injury is burns.12,26,33,87
PART 1
• Burns are a major component of lightning injury.12,26,33,87
• Nothing is left of a person after a lightning strike except a pile of
ashes.87,88
• Lightning victims have “entry” and “exit” points.33,88
• Lightning victims have internal burns.88
• 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.295
• It is safe to wait until the rain arrives to evacuate.295
• It is safe to finish the game if lightning is nearby.190,295
• As soon as the rainstorm passes and rain stops falling, it is safe to
resume activity.190,295
• 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.295
• Tall objects provide a 45-degree “cone of protection.”
• The majority of persons injured are golfers.190,295
• Lightning injuries cannot occur inside a building.
• Rubber tires (shoes, raincoats, sitting on a backpack) protect a
person from lightning.295
• Cell phones, iPods, and other electronic devices attract
lightning.6,25,140,173,174,274,295
• Golf, picnic, bus, rain, beach, and other shelters are safe.229,295
• Grounding a building or shelter makes it safe for people from
lightning injury.229
• Grounding a building makes it safe from structural
damage.229,292,325
• Lightning victims remain electrified and dangerous to touch.
• Lightning victims are easier to resuscitate than other cardiac
arrest victims.372
• If there are no outward signs of lightning injury, the damage
cannot be serious.89,90
• Lightning victims usually require treatments similar to those for
high-voltage electrical injuries, with aggressive fluid resuscitation,
alkalinization, and fasciotomies.88,93
• Lightning survivors have few permanent problems.90,105,281,320
74
strike carries a mortality rate of 30% and morbidity rate of 70%.87
A slightly different interpretation of the same data yielded a
mortality rate of 20%.33 Because peer-reviewed publications tend
to reflect severe or interesting cases, case reviews likely overes-
timate mortality rate.
A prevalent myth is that the lightning victim retains an electri-
cal charge and is dangerous to touch because the person is still
“electrified.” This myth may have led to unnecessary deaths by
delayed resuscitation.89 A person does not retain a charge like a
battery or a capacitor. However, a person in contact with a live
electrical power wire may transmit electricity.
A myth regarding treatment is that lightning injuries should
be treated as are other high-voltage electrical injuries. In devel-
oped countries, 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.23,88
Although burns are commonly thought to be the major cause
of death, this is not the case. Less than one-half of lightning
survivors have any signs of burns or marks on their skin. The
“crispy critter” myth, where someone struck by lightning bursts
into flames or is reduced to a pile of ashes, is science fiction,
not fact.89 Lightning frequently flashes over the outside of a
victim, sometimes damaging or disintegrating clothes, but leaving
few external signs of injury and few, if any, burns. The only
cause of immediate death is from cardiac arrest, sometimes fol-
lowing respiratory arrest.87 Persons who are stunned or lose
consciousness without cardiopulmonary arrest are highly unlikely
to die, although they may have serious long-term sequelae.90,97,281,320
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 when thunderstorms are in the area.295
• It is better to be “proactive” rather than “reactive” with lightning
injury avoidance.295
• The top activities and places for lightning casualties in the United
States are all outdoors295:
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.295
• Another safe shelter is a fully enclosed, solid, metal-topped
vehicle, such as a car or bus.90,105,281,295,320
• 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.229,292,295
• Having and following a lightning safety plan can decrease the
number of lightning deaths and injuries.295
• 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.295,342
• 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.104
• The primary cause of death is cardiac and respiratory arrest at the
time of the injury.87
• Ninety percent of lightning victims survive, but often with
disability.90
• Lightning victims are safe to touch and do not retain an electrical
charge.292,295
• Automated external defibrillators (AEDs) have been useful in
some resuscitations.103,106,290
• Cell phones, iPods, and other small electronic devices do not
attract lightning.6,19,25,140,173,174,274,295
• Lightning can strike the same place more than once.

BOX 5-2  Lightning Myths Commonly Cited as Facts
in Litigation
These myths apply to electrical injury as well as lightning injury.
Behavior of Current in the Body
• Current seeks the 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).
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 experiencing 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, posttraumatic stress disorder,
adjustment disorder, or other psychological problem negates
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.
Delayed causes of death include suicide induced by depression,
perhaps related to disabilities wrought by lightning.90,97 Unfortu-
nately, burns in developing countries seem to be more severe in
nature, perhaps because victims suffer temporary paralysis from
lightning (keraunoparalysis) and may not be able to escape from
falling, burning thatch.
Two other myths are, “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”89 (Box 5-2). Older medical literature,
lacking longitudinal or follow-up reports, implies that there are
few permanent sequelae of lightning injury. However, reports in
the last two decades consistently document several permanent
sequelae, including nervous system injury (e.g., peripheral neu-
ropathy, chronic pain syndromes) and neuropsychological symp-
CHAPTER 5  Lightning-Related Injuries and Safety
toms (e.g., severe short-term memory difficulty, difficulty
processing new information, attention deficit, depression, post-
traumatic stress disorder (PTSD).297,315,319,320,323,326,330
Medical literature and practice are plagued by myths that arose
from misread, misquoted, or misinterpreted data. These myths
continue to be propagated, such as the “suspended animation”
tenet that lightning victims who have resuscitation for several
hours or who have been in cardiac arrest for a prolonged period
without resuscitation may still successfully recover. This concept,
credited to Taussig,372 appeared some time before her article. The
case reports a longer resuscitation period than usual, but not as
miraculous as reported in Taussig’s paper or as mentioned in
subsequent references to her article.
A study of lightning survivors showed prolongation of the QT
interval, raising the theoretical possibility of torsades de pointes
as a mechanism for the suspended animation reports.23 There is
evidence from animal experiments to support the teaching that
respiratory arrest may persist longer than does cardiac arrest.12,108,109
A study of Australian sheep struck by simulated lightning showed
histologic evidence of damage to respiratory centers located
beneath the fourth ventricle.12 Prolonged assisted ventilation may
be successful after cardiac activity has returned, but this is obvi-
ously difficult to test in a human clinical study.92,95,301
Another series of animal experiments with simulated lightning
strikes to hairless rats showed that it is possible to obtain skin
changes (keraunographic markings), primary and secondary
cardiac arrest with prolonged respiratory arrest, and temporary
lower-extremity paralysis.108,109,111
METEOROLOGIC LORE
Some people believe that small rivers, lakes, buildings, and hills
can influence the formation or path of thunderstorms. Cumulo-
nimbus clouds that produce lightning are, at the very least,
several miles high and wide, and usually much larger. They move
and transform because of large-scale factors exerted on the local
atmosphere from great distances. Winds aloft arrive from various
directions and usually are sufficiently strong that air within a
thunderstorm may well have originated in another state or even
country as recently as within the past 6 hours. A natural feature
such as a small lake that is 1 km (0.6 mile) wide will have a
thunderstorm traverse it at a typical velocity of 30 km/hr (18
miles/hr) over approximately 2 minutes. A very large mountain
or ocean shoreline poses a different situation because of station-
ary large surface temperature contrasts.
“Lightning never strikes the same place twice,” noted Benja-
min Franklin in the late 1700s. In fact, tall buildings, communica-
tions towers, and wind turbines are struck many times a year. If
the same meteorologic circumstances that caused the original
lightning strike to occur are present, it is likely that lightning will
strike repeatedly in the same place.
MYTHS REGARDING ELECTRIC
CURRENT CONDUCTION
The myth that “electricity seeks the least resistant path between
two points” leads to the conclusion that there is only one line
or tissue in which current will travel and produce damage. To
the contrary, electric current is carried along all tissues and
paths in inverse proportion to the resistance within the tissue/
path. All structures between contact points are at risk, and there
may be multiple paths between any two points traversed within
a human.
Another myth is that lightning always seeks the earth, and
furthermore, seeks the shortest path to the earth. Electrical energy
may be conducted between two points on a body, neither of
which needs be connected to the earth (e.g., the shock delivered
to a person with each hand touching separate conductors). When
a person is touching the earth, part of the current may flow
through the person to earth and part may flow between two
conduction points.
People commonly assume that no psychological effect will
occur if lightning/electric current does not transit the brain. This
75
 argument ignores the fact that multiple pathways exist for current
conduction. Current conducted between two hands will be
accompanied by electricity in the head and brain as a parallel
pathway. In addition, there may be PTSD from the injury, blunt
injury, and other factors (e.g., cortisol release) that can cause
profound effects on the brain. Certainly, peripheral electric
shocks have been shown to have effects on brain tissue.241
Many people try to simplify a complex phenomenon by using
a much simpler phenomenon as an analogy. For instance, they
may use a household circuit to explain lightning or electricity
and assume that the effects are linear and scalable. Persons with
knowledge of physics may insist on using Ohm’s law. Lightning
and electric currents are highly nonlinear and not amenable to
simple circuit analysis. Lightning stroke current is probabilistic.
It cannot be modeled using ordinary electrical components and
principles and should not be analyzed in this way. Furthermore,
the body and its tissues do not support this approach.
MISCELLANEOUS LORE
Innumerable myths, superstitions, and misconceptions about
lightning based on local customs, beliefs, and stories exist. An
example is that using a cell phone increases a person’s risk of
lightning injury. With almost universal use of cell phones, it is
common for people to be injured while using them (Figure 5-7).
There is no scientific evidence that electromagnetic waves, the
MOUNTAIN MEDICINE
metal in a phone, or any other factor increases the risk for light-
ning strike. Injury probably occurs because people who should
be seeking safety inside a substantial building or fully enclosed
metal vehicle are outside and distracted from paying attention to
the weather while they are talking or texting.
Other Specific Myths and Misconceptions
• Victims may have internal burns. False; there may be cellular
and nervous system damage, but rarely, if ever, internal burns
typical of high-voltage electrical injuries.
• Wearing rubber-soled shoes is protective. False; similar errone-
ous concepts include wearing a raincoat or sitting on a foam
PART 1
pad or backpack. These do not protect a person or reduce
the severity of the injury.
• The rubber tires on a vehicle protect a person. False; electrical
energy travels along the outside of a metal conductor (the car
body). It dissipates through the rainwater to the ground or
flashes off the axles or bumper of the car (Figure 5-8). Tires
may be torn or exploded.
• Metal attracts lightning. False; wearing metal does not attract
lightning or increase one’s risk. Metal objects, such as fences
and bleachers, conduct electricity and lightning after they
have been struck, but do not inherently attract lightning. Metal
objects worn by a victim may become heated and thereby
cause burn injuries. Tall objects tend to be made of metal,
which are tall, isolated, and pointed. Their composition is not
FIGURE 5-7  Warning on the Great Wall of China.
76
FIGURE 5-8  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.
itself a significant factor for the propensity to be struck. The
primary factors that affect where lightning will strike follow:
1. Height of an object
2. Isolation of an object from taller objects
3. Pointed object (not a factor for people)
• Lightning always hits the highest object. False; lightning is only
affected by objects within approximately 30 to 50 m (98 to
164 feet) from its leading tip. In addition, several pictures exist
of lightning striking halfway down a flagpole or in a parking
lot next to tall, isolated, and pointed light poles. Someone
standing in the middle of a football field will not be protected
by the goalposts if lightning is coming down directly over-
head. There are many photographs of lightning branching to
meet the earth in several places. These images portray the
immense difficulty in being sure of the path of a cloud-to-
ground lightning event.
• Carrying an umbrella increases risk. False; compared with the
mile or two that lightning has already traveled to reach a
person, increasing or decreasing one’s height by a foot or two
has a very minor effect.
• The lightning “crouch” position can be used to significantly
protect someone caught in a thunderstorm. False; the change
in height by approximately a foot has a very minor effect. A
statistical evaluation indicated that it may decrease risk of the
very infrequent direct strike by approximately 50%, but sub-
stantial risk remains from mechanisms of ground current, side
flash, direct contact, and upward streamers.341 The crouch
cannot offer the almost complete protection afforded by pre-
planning, proactive avoidance of lightning, and staying in a
substantial building or completely enclosed metal vehicle.
• Lightning may occur without thunder. False; whenever there
is lightning, there is thunder, and vice versa. Sometimes it will
appear that lightning is visible without thunder, since thunder
is seldom heard more than 16 km (10 miles) from the light-
ning stroke. Thunder can be difficult to hear because of wind,
trees blowing in the wind, noisy activities, and sound being
blocked by buildings or mountains. There is also distraction
from conversation, mobile phones, and other electronic
devices. Survivors who are very close to a strike may not hear
or remember the thunder, but it was there.
 awareness campaign has been sustained across the United States

CHAPTER 5  Lightning-Related Injuries and Safety

7 for more than a decade.100,213
70 On average, 10 lightning-related injuries require medical treat-
Deaths per million
6 ment per lightning fatality over a large geographic area and a
% Rural

% Rural of total population

5
Deaths per million
4
3
2 30
1 20
0 10
1900 1920 1940 1960 1980
FIGURE 5-9  U.S. lightning deaths per million people from 1900 to
2013 (red). Percent rural population (blue). (From Lopez RE, Holle RL:
Changes in the number of lightning deaths in the United States during
the twentieth century, J Climate 11(8):2070-2077, 1998.)
INCIDENCE OF INJURY
The number of lightning fatalities in the United States and other
developed countries is well known, but the global figures are
not reliable. The basis for global estimates comes from well-
studied data from the United States and other developed coun-
tries that can be extrapolated. The U.S. lightning casualty history
is an instructive example of what might be achieved globally,
recognizing the trend from an agricultural to urban economic
milieu.
U.S. LIGHTNING CASUALTIES AND LIGHTNING
The number of annual lightning fatalities in the United States
decreased greatly from a maximum of more than 400 deaths early
in the 20th century to less than 30 deaths in recent years.114,199,259,291,340
Figure 5-9 shows that the lightning fatality rate decreased from
as high as six fatalities per 1 million people per year early in the
20th century to less than 0.1 per 1 million people per year at
present.259 This trend occurred simultaneously with a decrease
from a 60% rural population in 1900 to the current rural popula-
tion below 20%.
During this period, in addition to the rural to urban shift,
there was also a significant increase with respect to lightning
safety in the quality of dwellings, workplaces, schools, and
other public and private buildings.192 Also important was a huge
increase since the early 20th century in availability of fully
enclosed, metal-topped vehicles that provide safety from light-
ning.192 Additionally, a significant lightning safety education and
60 long period.67 Males (84%) account for a much higher number
of fatalities in the United States than do females.114 This male
50 majority has been found in most regions of the world over the
last two centuries. The most common situation is for a single
40 victim to be involved in a lightning incident.
Lightning deaths by U.S. state for the decade from 2005 to
2014 are shown in Figure 5-10, left. The general pattern is some-
what similar to the distribution of lightning in Figure 5-11. In
general, there are more fatalities in the southeast, but more
populous states also have larger total numbers of fatalities. Fatal-
ity information, rather than injuries, is used for these maps,
2000
because of greater uncertainty due to injury underreporting.260
The lightning hazard is shown more clearly when population is
taken into account (Figure 5-10, right). There are two maxima,
one in the southeast and the other in the northern Rocky Moun-
tain states. The most populous states, such as Pennsylvania, no
longer necessarily have high ranks. Similar tabulations were
recently made by Ashley and Gilson,35 and maps by U.S. state
have been published for earlier years.114
A large number of maps of cloud-to-ground lightning
flashes for the U.S. have been prepared for three decades from
data collected by the National Lightning Detection Network
(NLDN)113,286 (Figure 5-11). More than 20 million cloud-to-ground
flashes occur annually in the lower 48 states.304 Existing technol-
ogy detects more than 90% of all cloud-to-ground flashes within
the contiguous United States.113,286 The most recent detailed 10-
year climatology of cloud-to-ground lightning from the NLDN
shows three locations on peninsular Florida, with the largest
density of flashes per area in the United States. Flash density
decreases northward and westward from Florida, although there
are many variations that depend on well-identified meteorologic
factors of strongly heated land surfaces producing strong upward
atmospheric motions. Similar important features occur along the
coast of the Gulf of Mexico. In the mountainous western states,
where there are large changes in elevation, strong upward atmo-
spheric motions are produced during many summer days.188
A series of NLDN studies has explored monthly and diurnal
distributions of lightning, so these aspects of the lightning threat
are well known across the continental United States. Approxi-
mately two-thirds of cloud-to-ground lightning flashes and casu-
alties occur between noon and 1800 Local Standard Time.114
Similarly, approximately two-thirds of cloud-to-ground lightning
flashes, as well as lightning casualties, occur during the summer
months of June, July, and August.114,195 However, there are sig-
nificant and sometimes unexpected variations from these general
results.
The first steps to combining population with lightning data
were made by noting that U.S. lightning fatalities tend to be
concentrated in urban areas.35 A new study of lightning fatality

Fatalities Fatality rate

0 3 0 2005–2014 2005–2014
1 0
4
1 5 8
1 1 2 7 4 6
1 2
9 12
7 1 6 17 7 4 23
5 13 1 13
3 0
10 3
14 3 2 7 6 12
9
20 9 8 10 13 Rank Rank
Source: Storm Data 1–10
Alaska: 0 Hawaii:0 1–10
American Samoa: 1 47 11–20 Source: Storm Data
11–20
D.C.: 0 Guam: 1 21–30 Ranks include 50 states, 30 March 2015
21–30
Puerto Rico: 0 Virgin Islands: 0
30 March 2015
31–52 D.C., and Puerto Rico 31–52

FIGURE 5-10  Lightning fatalities (left) and fatality rate (right) by U.S. state from 2005 through 2014.

77
 Flash Density
Flashes/sq km/year
12 and up
8 to 12
4 to 8
2 to 4
1 to 2
0.5 to 1
0.25 to 0.5
0+ to 0.25

FIGURE 5-11  Cloud-to-ground flash density at 2-km resolution from 2006 through 2015, based on the U.S.
National Lightning Detection Network. (Courtesy Vaisala Inc.)
MOUNTAIN MEDICINE

risk combines lightning frequency from a detection network with
U.S. population data.347
GLOBAL LIGHTNING CASUALTIES AND LIGHTNING
No reliable complete global information exists regarding fatalities
or injuries. Two recent global lightning fatality studies estimate
6000 fatalities and 24,000 fatalities per year.59,198 Underreporting
of lightning fatalities, and especially injuries, results from a
number of factors, including the situation that many events
involve only one person and may not be reported or considered
newsworthy.260 In past population studies, the practice has been
PART 1
recent years that summarize lightning fatalities on national scales.
Even though single-incident cases dominate data sets from more
developed countries, events with large numbers of deaths and
injuries that may be more common often occur in developing
countries. In addition, it is not uncommon in developing coun-
tries for multiple fatalities to occur in what would be considered
an ‘indoor’ environment.
Figures 5-12 through 5-17 summarize all published national
studies of fatality rates, with low lightning fatality rates in yellow,
medium in orange, and red for highest. Fatality rates by decade
since the 1800s have been published,189 but no summary over
recent years has been made. The most common shading is white,

to assume that injuries are 10 times as frequent as are fatalities,67 which indicates that no national lightning casualty summaries
although this may not be the case in developing countries. There have been published. It is apparent that the highest rates are in
is a limited number of published formal and informal papers in Africa and South America. The lowest rates are evident in North

Oman
Mali Niger
Chad Eritrea Yemen
Burkina Sudan
Faso Djibouti
Benin Nigeria Ethiopia
Central African
Cameroon Republic
Somalia
Equatorial Uganda
Guinea Congo Kenya
Sao Tome Congo, DRC Rwanda Seychelles
and Principe
Burundi
Tanzania

Angola Comoros
Malawi
Zambia
Juan De Nova I.
Zimbabwe Madagascar Mauritius
Namibia
Botswana

Mozambique
South
Africa Swaziland
Lesotho

FIGURE 5-12  Lightning fatality rate per million people per year in Africa. Red shading indicates rate >5.0
fatalities/million/yr, and orange is 0.6 to 5.0. White indicates no national summaries have been published
for data sets ending in 1979 or later.

78
 CHAPTER 5  Lightning-Related Injuries and Safety
Russia

Kazakhastan
Mongolia
Kyrgyzstan North Korea

Tajikistan
Japan
China
Afghanistan
South Korea
Pakistan India
Laos

Vietnam
Nepal Philippines Northern Mariana Is.
Bhutan
Guam
Bangladesh Sri Lanka Palau
Myanmar Maldives

Cambodia Singapore Indonesia

Malaysia Brunei
FIGURE 5-13  Lightning fatality rate per million people per year in Asia. Orange shading indicates rate of
0.6 to 5.0 fatalities/million/yr, and yellow shading indicates <0.5. White indicates no national summaries
have been published for data sets ending in 1979 or later.

America, Western Europe, Japan, and Australia. This is probably
because of the availability of more substantial housing, metal
vehicles, lightning education, and lower lightning density in
temperate zones. Regional, local, short-period,1 and Internet-
based reports are not included. The most recent published results
include the following:
• Africa: South Africa,47 Malawi,282 Swaziland,128 Uganda,5 and
Zimbabwe81,376
• Asia: China,262,398 India,207 Japan,224a Malaysia,2 and
Singapore306
• Australia84
• Europe: Austria,231 France,159 Greece,311 Lithuania,149 Poland,256
Turkey,371 and United Kingdom (including Ireland and
Wales)133,134
• North America: United States,114,200,259 Canada,275 and Mexico322
• South America: Brazil59 and Colombia288
Timor Leste
Solomon
Australia
FIGURE 5-14  Lightning fatality rate per million people per year in
Australia. Yellow shading indicates rate <0.5 fatalities/million/yr. White
indicates no national summaries have been published for data sets
ending in 1979 or later.
Figure 5-18 shows Global Lightning Network (GLD360) strokes
for 2011 to 2014.317,318,351 Unlike prior lightning detection net-
works, which did not provide good data over large bodies of
water, GLD360 is a real-time network that seamlessly covers
continents as well as oceans to show lightning on monthly,
regional, and annual scales. Because 80% of GLD360 lightning
events are cloud-to-ground strokes, the actual lightning threat
is now much better known around the globe. Land areas
clearly comprise most of the lightning threat to people and
infrastructure.
Lightning is not uniformly distributed. Some locations on land,
especially along the slopes of tall mountains and along tropical
coastlines, have much more lightning at certain times of day and
year than do others. This knowledge can be useful to improve
understanding of lightning threat. Studies have been made in a
number of countries of the variability of lightning in time and
space. The opportunity now exists for global studies using light-
ning detection data sets with substantially uniform areal
detection.
TRENDS IN LIGHTNING FATALITIES
The maps show that the highest population-weighted annual
rates of lightning fatalities occur in countries with the following
features:
• Fewer lightning-safe dwellings, workplaces, school, and other
facilities than in more developed countries
• Fewer easily available, fully enclosed, metal-topped vehicles
• High rate of labor-intensive manual agriculture, mining, and
other activities
• Lack of awareness or data about the lightning threat and its
avoidance
• Unavailability or delay in medical treatment
The global population living in these situations may be
increasing in absolute number, but statistics are difficult to obtain.
Also, the trend toward a reduced percentage of the population
in rural areas has not occurred in many areas of the world. For
example, it has been reported that 97% of lightning fatalities in
China occur in rural areas.262 As a result, it is likely that the
number of lightning fatalities and injuries globally is steady or
may be increasing, which will continue until more people have
ready access to safe dwellings, structures, and vehicles and spend
less time in labor-intensive agriculture and other outdoor occupa-
tions. The lightning fatality and injury rates per population are

79
 Faroe Is.
Sweden

Estonia

Isle of Man Latvia

Denmark
Lithuania
Netherlands

Ireland Belarus
Poland
Germany
Belgium
Czech
Guernsey Republic
Slovakia Ukraine

Austria Hungary
Monaco France Liechtenstein
Romania
Andorra Italy
Moldova
Bulgaria
Georgia
MOUNTAIN MEDICINE

Albania
Armenia
Portugal Spain
Greece
Turkey

Gibraltar Malta
Syria
Iraq
Tunisia Cyprus
PART 1

Croatia Montenegro Lebanon

Slovenia Bosnia and Herzegovina
FIGURE 5-15  Lightning fatality rate per million people per year in Europe. Yellow shading indicates rate
<0.5 fatalities/million/yr. White indicates no national summaries have been published for data sets ending
in 1979 or later.

El Salvador
Costa Rica
Panama Aruba Barbados

Trinidad and Tobago

Canada
Venezuela Guyana

Columbia French Guiana

St. Pierre
and Miquelon
United States Bermuda
The Bahamas
Turks and
Ecuador
Caicos Is.
Mexico Peru Brazil
Anguilla
Guatemala Montserrat Bolivia
Johnston El Salvador Aruba Barbados
Atoll Cayman Is. Haiti
FIGURE 5-16  Lightning fatality rate per million people per year in
North America. Orange shading indicates rate of 0.6 to 5.0 fatalities/
million/yr, and yellow is <0.5. White indicates no national summaries Paraguay
have been published for data sets ending in 1979 or later.
Chile Argentina Uruguay

FIGURE 5-17  Lightning fatality rate per million people per year in
South America. Orange shading indicates rate of 0.6 to 5.0 fatalities/
million/yr. White indicates no national summaries have been published
for data sets ending in 1979 or later.
80

GLD360 Data
strokes/sq km/year
32 and up
16 to 32
8 to 16
4 to 8
2 to 4
1 to 2
0.5 to 1
0.25 to 0.5
0+ to 0.25
FIGURE 5-18  Map of 3,639,467,075 Global Lightning Dataset GLD360 strokes for 3 years through Decem-
ber 2015. (Courtesy Vaisala Inc.)
thought to be very high in many of the countries that have no
published national fatality data shown in Figures 5-12 through
5-17. For example, India is documented to have an average of
1755 deaths per year from 1967 to 2012,207 which represents
78,975 fatalities during this period.
CONCLUSIONS
The impacts of lightning vary greatly between developed and
less developed countries. In the United States the population-
weighted rate of lightning fatalities and injuries has greatly
decreased from a maximum approximately a century ago. The
two priorities in less developed countries to achieve a decrease
in lightning deaths and injuries are protecting people working in
labor-intensive agriculture and providing lightning-safe dwell-
ings, buildings, and vehicles. Data from global lightning detection
networks can help identify areas with the highest density of
lightning. Through a combination of sound science, education,
and uniform global lightning data, advances can be made to
reduce the impacts of lightning on people and assets. To achieve
improvements, the infrastructure of these countries likely must
be significantly improved, accompanied by inexpensive lightning
protection systems that can be easily installed and maintained.
Initial activities have been taken with regard to education and
awareness of lightning threat in several Asian countries through
the Centre of Excellence on Lightning Protection (CELP)96,156,157,212
and are beginning in Africa by the newly formed African Centres
for Lightning Electromagnetics (ACLE).
EARLY SCIENTIFIC STUDIES AND
INVENTION OF THE LIGHTNING ROD
The study of electrical phenomena is often traced to 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 elec-
tric science and during his lifetime was known as the American
Newton. He was accepted into the French and English courts
around the time of the American Revolution not because he was
an ambassador from America but because he was considered 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 contribu-
tions.83,325 Before his work, it was thought that two distinct types
of electrical phenomena existed. Franklin’s work148 unified these
two aspects and is responsible for renaming them “positive” and
CHAPTER 5  Lightning-Related Injuries and Safety
“negative.” He went on to prove that lightning is an electrical
phenomenon and that thunderclouds are electrically charged, as
demonstrated by the famous kite and key experiment.147 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 the Shrouds, to
the Water, will not be hurt by Lightning.
In the 1750s and 1760s, use of lightning rods became preva-
lent in the United States for protection of buildings and ships.
Some scientists in Europe urged installation of lightning rods on
government buildings, churches, and other tall buildings. Reli-
gious 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.58
At one time (and still believed by some laymen today), light-
ning rods were theorized to diffuse electrical 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 aircraft, 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 providing a preferential attachment
81
 FIGURE 5-19  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.) FIGURE 5-21  Damage to curtaining material covering a window of the
clubhouse in Figure 5-19. (Copyright Ian R. Jandrell.)

point for the lightning stroke, allowing the current to be harm- is a storage shed, house, school, hospital, or munitions factory.
lessly directed through the system to the ground.52,291,295 Lightning In cases not covered by code, a lightning protection system,
MOUNTAIN MEDICINE

can otherwise travel into or through the building and cause
extensive damage (Figures 5-19 to 5-21).
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).115 In the past decade,
NFPA 780 (U.S. National Fire Protection Act) has been accepted
worldwide as a reliable standard.291
Building codes and industrial standards may require particular
structures to have lightning protection systems.52,291 Including a
system in the initial design and construction is always easier
PART 1
despite high exposure to lightning, may not be worth the
expense, such as for a mountain cabin that is seldom visited.228,295
At present, the most important economic impacts from light-
ning include electrical utility interruption; interruptions at airports
and other outdoor locations; loss or corruption of financial,
security, and other databases and control systems; and downtime
of industrial equipment. For humans, the impact of being struck
by lightning includes loss of work ability, unemployment, rela-
tionship decay, depression, anxiety, and loss of cognition, and
this is of economic importance as well. Lightning may pose sig-
nificant danger not only to individuals, but also to larger groups,
such as when hundreds of miners are trapped deep underground

and less expensive than modifying a completed building. Other after lightning has made elevators, ventilation systems, and water
factors to be considered include relative frequency of strikes in pumps nonoperational.295
an area; height, construction, and design of the building; and At home, the most reliable way to protect electronic equip-
degree of protection desired, depending on whether the building ment is to unplug it from the wall before arrival of a

A B
FIGURE 5-20  Damage to the ceiling (A) and internal wall (B) of the clubhouse in Figure 5-19 with resultant
damage to the electrical and electronic devices connected to the electrical system. (Copyright Ian R.
Jandrell.)

82
thunderstorm. Surge protectors, which may be effective for minor have ice aloft at temperatures colder than freezing; at these tem-

CHAPTER 5  Lightning-Related Injuries and Safety

household electrical surges, are seldom completely effective
in eliminating the effects of lightning, despite manufacturers’
claims. Lightning protection needs to be done correctly, and it is
recommended that it be installed by a licensed, bonded, insured,
and experienced specialist using proven methods according
to accepted codes. The best source of information on lightning
risk for people is the Lightning Protection Institute (www
.lightning.org).
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 This section describes the simplified and most
common mechanisms of thundercloud formation and lightning
strike.
Thunderstorms can be formed in a number of ways to produce
the necessary vertical updrafts. These ingredients are afternoon
heating of warm moist air, large-scale upward atmospheric
motions (Figure 5-22A), sea and lake breezes, lifting of deep
layers of the atmosphere by mountains, and cold fronts.188,194
As warm air rises, turbulence and induced friction cause
complex redistribution of charges within the cloud (Figure
5-22B). 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
peratures, 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 between
layers as a result of 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 cloud generally become
negatively charged relative to the earth. The earth, which nor-
mally is negatively charged relative to the atmosphere, has a
strong positive induced charge as the negatively charged thun-
derstorm 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
upward-propagating leaders.325
Normally, the discharge of the potential difference is discour-
aged 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 5-22C  ). Although the

High-altitude winds

40,000 Ice –60

35,000 –36
Snow
30,000 –16
Altitude (feet)

Temperature (° F)
25,000 Snow –3

20,000 18
Freezing
air

15,000 32
m

level
ar

10,000 Rain 46
W

5000 63

A B Heavy surface rain

Downward
leader

Return
stroke
Upward
streamer

C D E F
FIGURE 5-22  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.

83
 tip of the leader may be luminous, the stepped leader itself is
barely discernible with the unassisted eye. Very-high-speed video
has shown this bright tip and a more faint trailing leader as it
travels to the ground.349,353 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 (V). 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 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 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, 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 extremely unsafe.
DIAMETER AND TEMPERATURE OF LIGHTNING
Although many techniques have been used to measure the diam-
eter and temperature of lightning, all measurement techniques
MOUNTAIN MEDICINE
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. Measure-
ments 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 do 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
PART 1
of 3 to 20 m (9.8 to 66 feet).
The temperature of the lightning stroke varies with the diam-
eter of the stroke and has been calculated to be approximately
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 tem-
perature 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 (intra-
cloud) flashes (Figure 5-23). Cloud-to-ground flashes contain one
or more return strokes. The flickering often seen in a cloud-to-
FIGURE 5-23  Cloud-to-ground flash (right) and cloud flash (center).
(Copyright Ronald Holle.)
84
ground flash is caused by 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 subse-
quent return strokes often takes a different path to the surface,
up to a few kilometers from the first return stroke; the average
is 1.47 ground contact points per flash.367 The term total lightning
describes the sum of cloud-to-ground and cloud flashes. An
extremely small portion (<0.01 of 1%) of all lightning travels from
ground to cloud when this is induced by the special circum-
stances 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 (Figure 5-23). There are
several times as many cloud flashes as those that reach the
ground. Cloud flashes have been measured to extend 305 km
(189 miles) in horizontal length and last 5.7 seconds.244 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.
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 to travel down
narrow spaces such as hallways. Ball lightning very infrequently
injures people and objects and often exits through a door,
chimney, or window.313 It may explode with a loud bang or
exhibit other bizarre behavior.
Cloud-to-ground lightning flashes usually lower negative
charge to the ground.325 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, or 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 tend more 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 impor-
tant because of its usefulness in many lightning safety recom-
mendations.295,384 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, because the sound travels at a
rate of 3 sec/km (5 sec/mile).
• Wind, rain, man-made noise such as traffic, vegetation, and
intervening buildings, hills, and mountains reduce audibility
of thunder.
• The pitch of thunder deepens as the rumble persists, because
only lower-frequency sounds remain at greater distances.
• Atmospheric turbulence reduces 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. Because
there is a large difference between the speed of light and 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 later in Precautions for
Avoiding Lightning Injury.
MECHANISMS OF INJURY
BY LIGHTNING*
ELECTRICAL INJURY PHYSICS REVISITED
In many texts dealing with electrical injury, Kouwenhoven’s six
factors (AC vs. DC, voltage, amperage, duration, pathway, and
resistance) are often discussed. However, these factors are neither
useful clinically nor useful predictively and have led more to
confusion and misunderstanding of electrical and especially light-
ning injuries than to understanding or usefulness in the medical
setting. In addition, simplistic application of this list leads to even
more misunderstanding by attorneys, insurance companies, and
others regarding the disabilities that typically occur, with the
unfortunate outcome of denial of legitimate claims for real inju-
ries and their sequelae.
CONCEPTS IN ELECTRICITY
Voltage can be regarded as an external force or pressure applied
to an object to force it to conduct electric current, like water
pressure applied at one end of a pipe to cause water flow
through the pipe. When voltage is applied, a current (measured
in amperes) flows through the conductor (i.e., the object). The
amount of current is inversely proportional to the resistance of
the object. For a given applied voltage, the higher the resistance
of the object, the smaller the resulting current. For technical or
generated electrical injuries, the voltage is externally selected, the
resistance of an object is a given, and the current is the result.
Resistance is a given property of an object. It can be thought
of as the ease or difficulty with which something flows through
the object and is analogous to the diameter of the water pipe or
the friction within the pipe. Resistances of various tissues in the
body have been measured, but these change as integrity of the
tissue changes. 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, as tissue reacts to injury, resistance changes.
Although theoretically these changes can be modeled for tissues,
the uncertainty that creeps into nearly every clinical situation
makes application of these calculations to explain or predict
injury to an individual patient much too complex and fraught
with error to be used on a day-to-day basis. Even worse, complex
calculations such as these can easily be misapplied in a court of
law, taking the focus away from objective clinical evidence of
injury and disability.
Another treatment of Ohm’s law would be to specify current
and resistance, making voltage the calculated or measured
outcome. Generated electricity is in the first category, a “voltage-
driven” phenomenon, where the equation is driven by voltage.
Resistance changes as injury occurs, and current is the calculated
or measured dependent variable. Lightning is quite different and
in the second category, a “current-driven” phenomenon. Although
the simplest form may be governed by Ohm’s law, the resistance
of the body is not uniform. The result is that advanced calcula-
tion methods must be used to find the voltage across the body
when struck and subjected to lightning current, including the
phenomenon of flashover. To make the situation even more
complex, once lightning attachment occurs and an open channel
is made, the voltage drops to zero, making Ohm’s law meaning-
less as an avalanche of current begins to flow.
Another concept to consider is that of an electric field. When
a voltage is applied across a definite area of space (e.g., the
“gap” between a cloud and the ground), an electric field results.
Air generally has a high resistance and is a good insulator, con-
ducting very little current under these circumstances. 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.”
That is, an avalanche of electrons will occur in the gap. Before
*References 8, 10, 26, 27, 41, 63, 75, 91-93, 99, 104.
this happens, a minor amount of current will be conducted
CHAPTER 5  Lightning-Related Injuries and Safety
under the influence of the field. Beyond this point, new pro-
cesses come into play, causing the physical structure of the
conducting medium to be disrupted. The actual moment that this
disruption occurs varies with the voltage applied and width of
the gap. The voltage necessary to flash over an air gap is about
4000 V/cm (10,000 V/inch), depending on humidity and other
factors. A large, noisy flashover may be observed if the gap is
sufficiently large and rapid expansion of superheated air forms
the thunderclap.
Technical Electricity Supply vs. Lightning Current
Technical electricity is provided to a household at a constant
voltage; current flows in devices connected to this supply. Flash-
over is rare at relatively low voltage in domestic use. The behav-
ior of any current that results is much more linear, although not
perfectly so when it involves the human body. The possibility
for conduction of large internal currents exists, and for longer
periods of time, because flashover is absent. Heat generated by
this current is much more likely to result in burning. Conduction
is likely to be much more prolonged. Resultant muscular reac-
tions for a prolonged period locks muscles through contraction
to the source, prolonging the contact. Prolonged conduction
internally can expose the heart to prolonged, damaging passage
of current. Ventricular fibrillation (VF) arises proportionate to the
amount of conducted current and the duration of time over which
it is conducted. The current flowing for a given time allows one
to estimate the likelihood of VF.205 A victim who is still in contact
with the electrical source continues to be dangerous for the
human rescuer to touch.
Lightning current, on the other hand, is of very short duration
(microseconds). Burning is therefore minimal. Flashover is highly
likely, making internal conduction minimal. Once the discharge
is completed (fractions of a second), a victim is safe to touch.
Current, though short-lived, is large. Some sequelae of both types
of current passage are similar otherwise, particularly the psycho-
logical sequelae.
MECHANISMS OF INJURY
General Conduction Effects
Lightning is dangerous to humans predominantly because of heat
and less because of concussive force. Lightning may injure indi-
rectly through forest fires, house fires, explosions, or falling
objects. Only injuries directly caused by lightning are discussed
here. When lightning current is injected into an individual,
current is initially transmitted directly through the individual for
microseconds until internal structures (capacitances) become
charged, and flashover occurs over the surface of the individual
as the breakdown field is reached. After that, internal current
reduces dramatically.301
Lightning current may initially be inflicted on a person in
several ways, described in more detail later (Box 5-3 and Figure
5-24).226 The internal current phase may cause cardiac and respi-
ratory arrest, particularly if the pathway primarily includes the
heart. As the body’s electric potential builds up in response to
BOX 5-3  Mechanisms of Lightning Injury
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 current3,75 (also called fifth mechanism)
Blunt Force Trauma Effects
6. Barotrauma
7. Concussive injury
8. Musculoskeletal injury from muscle contraction; falls
85
 Contact voltage

Side flash
MOUNTAIN MEDICINE

A Direct strike B C
PART 1

Upward streamer
Ground
current

D2

Step voltage Step voltage

D1

D3 E
FIGURE 5-24  Mechanisms of lightning 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.

internal current, it produces an electric field over the surface of
the body. Our understanding of what happens to a lightning-
struck human is assisted by what happens with conduction in
wood on telephone and electrical supply poles.118 The consis-
tency and resistance of wood are much closer to that of the
human body than one might expect. This allows us to conclude
that after flashover occurs, internal current drops dramatically.
Current can be directed to be conducted within the wood or
conducted externally over the wood, but not both ways. In wood
pole design, metal implants from outside to inside the wood
enhances the ability to swap between these routes. As the current
continues to increase, the surface flashover bridges the strike

86
point and the ground. When this happens, most of the lightning
current flows as an arc current through the air outside the body
(flashover effect). Only a tiny fraction flows through the body
and may not be sufficient to cause cardiac and respiratory arrest
unless it has already done so.
Specific Strike Mechanisms
There are five mechanisms by which lightning current may
impinge on a body. Several authors have attempted to estimate
the percentage of injuries connected with each mechanism; this
is speculative28,102,104 Similarly, mortality attributed to each mecha-
nism is speculative and not derived from studies.
Direct Strike.  A direct strike occurs when the lightning
stroke attaches directly to the victim (Figure 5-24A). This most
often occurs in the open when a person has been unable to find
a safe location and occurs in no more than 3% to 5% of fatalities
in developed countries. Even though it seems intuitive that direct
strike would 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 examina-
tion of thousands of cases (Figure 5-25).101
Contact (Touch Potential) Injury.  Contact injury, or touch
potential injury, occurs when a person touches or holds onto an
object to which lightning attaches. A voltage gradient is created
on that object from strike point to ground or to another point of
contact, and the individual in contact with the object is subject
to the voltage between his or her contact point and the earth
(Figure 5-24B), resulting in a current flowing through them.
Contact injury probably occurs also in about 3% to 5% of strikes.
Static electricity may be discharged when a person reaches
for a car door or stands close to a metal window or door frame
during 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 dis-
charges are unlikely to be any more dangerous than static elec-
tricity discharges experienced in the winter months from shuffling
across the carpet and reaching for a door handle.
Side Flash.  A more frequent cause of injury, accounting for
as many as 30% of lightning-related fatalities, is a side flash, also
termed “splash.” Side flashes occur when lightning that has hit
an object, such as a tree or building, travels down that object
before a portion “jumps” to a nearby victim (Figure 5-24C). Safety
protocols stress that standing under or close to trees or other tall
objects is dangerous and to be avoided. Current divides itself
between the two paths in inverse proportion to their resistances.
Side flash may also occur from person to person.
Contact Direct Blunt
injury strike injury
3–5% 3–5% ?
Upward
streamer
10–15%
Ground
current
50–55%
Side
splash/flash
30–35%
FIGURE 5-25  Chart showing the frequencies of primary lightning fatal-
ity mechanisms. (From Cooper MA, Holle RL: Mechanisms of lightning
injury should affect lightning safety messages. Preprints, International
Lightning Meteorology Conference, Orlando, Florida, Vaisala, 5 pp.)
Earth Potential Rise.  Also called “step potential,” “ground
CHAPTER 5  Lightning-Related Injuries and Safety
current,” and a number of other similar terms, 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 within
any other conductor. Earth has a defined resistance, and thus
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, thus the term. EPR can damage a person in several ways.
If a person is standing in an area where EPR is active, that is,
near the location of a cloud-to-ground lightning strike, a voltage
will appear between the feet, and current will flow through the
legs into the lower part of the body. Four-legged animals are
likely to sustain even more serious damage if the current goes
between back and front legs, where the path may involve the
heart (Figure 5-24D1,D2).
A special case occurs when a person is injured inside a build-
ing as lightning strikes nearby.11,30,125 The person, along with the
environment (including the dwelling) around the person, is
raised in potential via EPR. For example, if a telephone line is
not locally earthed (grounded), the person touching the tele-
phone is at the same voltage as the environment. Current is
transmitted from the local EPR-raised environment to the remote
unaffected earth using the human as the medium between the
local environment and the distant earth.
All local electrical apparatuses, including telephones, should
be well grounded locally. The grounds of all local structures (e.g.,
power, telephone, plumbing, structural steel) should have a
common grounding point (i.e., should be bonded) to eliminate
any voltage differences developing between separated ground
points for each system. For the special case of indoor or tele-
phone injury, EPR may account for 80% or more of the injuries;
all these relate 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. Any practices that
bring earth voltage more easily inside a dwelling will make this
worse: plumbing, house base metal reinforcing, and high earth
resistivity.
Kitagawa and colleagues226 have identified further subdivi-
sions of the EPR phenomenon. Not only can EPR occur as dis-
cussed, but it can also occur in a manner similar to the surface
flashes over a body, with arcs developing over a ground surface
(Figure 5-26). Despite mathematic modeling that assumes the
earth is homogeneous, the grounding earth is not homogeneous
and provides arc generation points.
Irregularities occur on mountainsides. If the terrain is mark-
edly irregular, spreading lightning current may reach the surface.
A surface arc discharge may develop along with flow of the
conduction current in the ground. Because arcs carry consider-
able energy, a person exposed to a surface arc discharge is more
likely to sustain a more severe effect, including thermal injuries,
temporary 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 outcrop-
ping of terrain, where surface arcing is much more likely to
occur, injuring the person just as the person thinks some degree
of safety has been achieved (Figure 5-24D3). All these factors
illustrate the danger of being outdoors in the presence of
lightning.
Ground current effects are more likely to be low level and
less likely to produce fatalities. However, multiple victims with
injuries are frequently found in an arc around the strike point
to earth. Large groups have been injured on baseball fields,
at racetracks, while hiking or camping, and during military
maneuvers.34,58,61 Shocks via telephones can produce significant
long-term medical problems, and the majority of these are via
EPR.30,125,281
Upward Streamers.  Upward streamers generate the fifth
mechanism of lightning injury.8,61,91 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 (Figure 5-24E). Streamers occur even when there is no
attachment between them and the stepped leader. Although one
might think that these streamers are weak in energy compared
87
 watches, and other objects worn by the victim. Torn clothing
may raise the suspicion of foul play if the incident was unwit-
nessed. The clothing is typically ripped as if by some internal
explosion. Similarly, belts and boots may be ruptured from the
inside by vapor explosion of sweat or water in socks.355 There
are two theories to explain this:
1. Flash moisture vaporization theory.227,300,301 Blast injury results
from the explosive vaporization of superheated water along
the path of the surface flashover. Lightning blast injury to
the skull, brain, and viscera has been demonstrated in
animals.300
2. Concussive/explosive force, from being close to the lightning
channel. As lightning superheats and the air expands explo-
sively, a “pressure-shock wave” can occur. One can hear
thunder from as far away as 14 km225 to 25 km325 (8 to 15
miles), indicating a tremendous amount of energy is involved
in generation of thunder. Even before the noise is produced,
a pressure blast wave can affect people close by the lightning
channel. During a lightning strike, the channel temperature
will be raised to about 25,000 kelvins (K) (24,727° C [44,541° F])
in a few microseconds, and as a result, the pressure in the
channel may increase to several atmospheres (atm). The
A resulting rapid expansion of the air creates a shock wave. This
shock wave can injure a person in the vicinity of the lightning
flash.112
Halldorsson and Couch169 believed that this explosion/
MOUNTAIN MEDICINE

implosion phenomenon may cause trauma that mimics blast

injuries seen in bomb blast victims. The sudden, cylindrical-
shaped pressure shock wave that arises from the rapid volume

B
PART 1

FIGURE 5-26  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.

with the full lightning strike, they may carry significant and dan-
gerous current through or around the victim. Upward streamer
injury is probably the most underestimated mechanism of light- FIGURE 5-27  Example of contact and side flash lightning casualties.
ning injury.
It is difficult to separate the incidence of injury due to EPR
from that attributed to upward streamers. Where direct strike may
account for 5% of individual strikes, contact potential approxi-
mately 5%, and side flash approximately 30%, the combined
incidence of EPR and streamer shock may be up to 60%. There
are no better figures in the literature, and these represent a con-
sensus, at least in terms of relative rankings. Many cases with
multiple casualties are likely a combination of many of these
effects, with the majority of them from EPR and upward stream-
ers, sometimes complicated by side flashes if people or animals
are standing too close together (Figures 5-27 and 5-28).
Barotrauma and Blunt Injury from Lightning
The prior five mechanisms are strictly electrical mechanisms.
Injuries may also be characterized by more indirect, nonelectrical
mechanisms, such as concussive injuries, blast injuries, and blunt
force injury from being thrown.
Persons may sustain 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. Witnesses have reported victims
being thrown tens of yards by either mechanism.
A curious but common and often diagnostic finding is the
tearing, melting, magnetizing, or signs of arcing seen in clothing, FIGURE 5-28  Example of side flash or “splash” lightning casualties.

88
 CHAPTER 5  Lightning-Related Injuries and Safety
A

FIGURE 5-29  Mechanism of concussive, explosive barotrauma.

expansion may reach pressures of more than 10 to 20 atm (1013

to 2026 kilopascals [kPa]) in the vicinity of the lightning bolt
channel112,180,245,265,335,400 (Figure 5-29). It has been known to cause
shrapnel injury; one victim had multiple small fragments of shat-
tered concrete pavement embedded in her skin49 (Figure 5-30). B
Lightning’s pressure blast wave has been reported to tear and
tatter clothing, fracture bones, and cause tympanic membrane FIGURE 5-30  A, Concrete pavement that was struck by lightning.
rupture and lung contusions. Tympanic membrane rupture may B, Secondary missile injury caused by lightning striking concrete pave-
make the diagnostic difference in difficult cases. A study by ment. (Copyright the American Journal of Forensic Medicine and
Richmond and colleagues334 suggests a minimum threshold of Pathology; from Blumenthal, R: Secondary missile injury from lightning
about 20 kPa to produce minor eardrum rupture. The threshold strike, Am J Forensic Med Pathol 33(1):83-85, 2012.)
for lung damage occurs at about 103 kPa of blast overpressure.152
Pneumomediastinum and bleeding lung in a tracheostomized
patient have both been reported.50,169,280,365 As the blast wave
impacts the human body surface, a pressure differential is gener-
ated at that surface, resulting in rapid acceleration and move-
ments of the body surface, with propagation of shear and stress
waves through the tissue390 (Figure 5-31). The force of the pres-
sure blast wave may be another mechanism that causes falls, in
addition to head, brain, and other blunt trauma.
No evidence suggests that lightning victims sustain severe
blast-related disfigurement, such as blast-related cavitation. About
690 kPa is the minimum threshold for serious damage to
humans,152,223,355 although, paradoxically, the human body can at
other times survive relatively high blast overpressure without
experiencing barotrauma.266
Theoretically, it is possible to estimate the distance from which
a human could be at risk from lightning’s pressure blast wave.
A 4.5-kg TNT–equivalent bomb would rupture the eardrum of a
70-kg (154-lb) person within approximately 10 m (33 feet); lung
damage would occur at about 5 m (16.5 feet), and the body
would be injured at about 3 m (10 feet).152

PATHOPHYSIOLOGY OF
LIGHTNING INJURY
This section describes the way in which lightning and electric
current produces alterations in human physiology.

ELECTRICAL INJURY PHYSICS REVISITED

This section examines the voltages, currents, and pathways that
are estimated to occur in a lightning strike by the five mecha-
nisms referred to above.26,87,104,208
Electric Field Effects
Figure 5-32 shows 20 kilovolts (kV) applied to a 1.8-m (6-foot)
man, causing current to traverse source to ground. This produces
FIGURE 5-31  Graphic representation of the pathogenesis of traumatic
emphysema (pneumomediastinum): Lightning’s blast wave may cause
widespread distribution of fine air bubbles within the mediastinal soft
tissues, extending around the esophagus and pericardial sac. The
theory is that barotrauma may cause disruption of the normal architec-
ture of the pulmonary parenchyma, which may then cause air to dissect
into the surrounding soft tissues. (Graphic courtesy Ryan Blumenthal,
Department of Forensic Medicine, University of Pretoria.)

89
 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 (0.4 inch) of a child’s lip and generates a field strength of
11 kV/m. Even though no one would classify the child’s injury
as being caused by “high” voltage, it is from a high electric field
strength and produces the same tissue destruction in a small
localized area, much as would a high-voltage injury to the stand-
ing man. In both cases, the voltage can be applied for an arbitrary
amount of time. The difference is the distance over which the
field is applied and the localization of the field. High electric
6 feet 20 kV fields of approximately this size, if applied for a sufficiently long
period, can rupture cell membranes by generating pores in cell
membranes (electroporation). Cell death, or at least dysfunction,
results. Although Lee247 has discussed the importance of internal
electric field calculations in describing electroporation damage,
this has not been studied for lightning injury, and the time scale
is quite different.
Characteristics of Lightning Current vs.
Industrial Electricity
The danger of industrial electrical current versus lightning current
= Electric field is discussed earlier.
approx. 10 kV/m Industrial current is usually inflicted at low voltage, although
voltage is a poor predictor of injuries.82 It is usually alternating
current (AC). If the supplied voltage is measured at any one
MOUNTAIN MEDICINE

20 kV location, the voltage swings negative and positive in a sinusoidal

= 10 kV/m manner. Long ago, AC was chosen for electrical distribution
A 2m
because of ease of generation and transmission. Current flowing
constantly in one direction is called direct current (DC) and is
the current one encounters from a DC battery.
Lightning is neither direct nor alternating current. The best
110 V
description of lightning is that it 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 disap-
pears, and a large current flows largely in a single direction
PART 1

impulse over a very short time. The study of massive electrical

1 cm
1 cm
= 11 kV/m
B current flowing through the tissue and its resistance:
110 v/1 cm = 11 kV/m
C frequently causes only superficial streaking burns. Burns, dis-
FIGURE 5-32  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 pro-
duced. 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.  understood factors may contribute to the formation of deep
C, This explains the deep full-thickness burns the child receives, which
one would not predict given the “low-voltage” source.
discharges of such short duration, particularly their effects on the
human body, is not well advanced, although recently the thresh-
old for VF induction for short duration impulses has been
addressed.22 Linear equations, such as Ohm’s law (V = I × R) and
power calculation (P = V × I), do not apply.
Energy dissipated in a given tissue is determined by the
Energy ( heat ) = Current 2 × Resistance × Time
where a current flows through a resistance for a period of time.
The energy is produced in the tissues, subject to the current, and
largely appears as heat. This is often referred to as joule heat but
is seen as temperature rises in the tissues if current is applied
for a sufficiently long time.
As resistance increases, such as in the high resistance of skin,
so does the heat generated by passage of the same current. In
humans, when low current levels are encountered for a given
time, much of the electrical energy may be dissipated by the
skin, so that superficial burns are often not accompanied by
internal injuries. Similarly, high-level current injuries, such as
lightning, applied for a very short interval will cause little burn
damage.
Although lightning occasionally creates what appear to be
discrete entry and exit wounds, these are less severe and exten-
sive than one would expect from a “high-voltage” injury. There
is no voltage after lightning attachment occurs. Lightning more
cussed later, are a most important distinction between lightning
and industrial electric shocks. The exception to this is when a
long, continuing current stroke occurs. 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
burns, although deep burns similar to those seen with high-
voltage electrical injuries are quite rare with lightning. Skin at the

90
site of a direct strike can also be mechanically or electrostatically
disrupted. However, skin breakdown should not be the expecta-
tion for all lightning strikes, because direct strikes occur in only
3% to 5% of cases.102 The absence or presence of skin breakdown
should not be used to deny that injury occurred or to diagnose
a direct strike clinically.
ESTIMATION OF LIGHTNING CURRENTS
It takes a finite amount of time for skin to break down when
exposed to heat or energy. Generally, lightning is not present
long enough to cause skin to break down. A large portion of
current travels along the outside of the skin as “flashover.” Some
experimental evidence indicates that a portion of the current may
enter cranial orifices: the eyes, ears, nose, and mouth.14 This
pathway would help explain the myriad eye and ear symptoms
reported with lightning injury.
Functional consequences of lightning on cardiorespiratory
function showed that entry of current into cranial orifices allows
passage of current directly to the brainstem. In a sheep study,
specific damage to neurons at the floor of the fourth ventricle
was demonstrated in the location of the medullary respiratory
control centers.12 Blood and cerebrospinal fluid (CSF) are pref-
erential paths that conduct current to impinge directly on the
myocardium. Histologic damage to the heart, consistent with a
number of autopsy reports of inferior myocardial necrosis, was
demonstrated in similar experiments.12,32
An alternative hypothesis can be tested with a mathematic
technique.26 Certain assumptions are made in any model, usually
based on accepted principles. Figure 5-33 shows a model for
skin resistance (A) and its connection to the internal body milieu
(B). The internal body structures are regarded as purely resistive,
whereas the skin contains significant elements of capacitance.46
In the model, for the infrequent direct strike, the sequence
of events during the strike begins with the stroke attaching ini-
tially to the victim’s head. For a brief moment, current flows
internally as the skin becomes charged. At a voltage taken as
5 kV, the skin was assumed to break down. Once the internal
current increased, the voltage across the body to the earth
built up, and external flashover across the body occurred when
10 kW
0.25 mF
A 300
10 k
B
FIGURE 5-33  A, Electrical model for human skin impedance. B, Model of human body for the purpose of
examining current flow during lightning strike.
the field reached the breakdown strength of air, 4000 V/cm
CHAPTER 5  Lightning-Related Injuries and Safety
(10,000 V/inch).
The results of modeling these events are shown in Figure 5-34,
and the relative magnitudes of the various voltage components
can be seen with their time scale. On this 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, and then skin breaks down quickly and external flash-
over occurs. Support for this model is shown in waveforms
recorded from measurements in the experimental application of
lightning impulses to sheep.12 Further modeling of step voltage
injury verified that, for the erect human, this mechanism is less
dangerous than direct strike.226
Further experimental evidence suggests that “a fast flashover
appreciably diminishes the energy dissipation within the body
and results in survival.”301 In addition, Ishikawa and colleagues208
obtained experimental results with rabbits similar to the human
data noted in Cooper’s study.87 Cooper and associates107-109 carried
her studies to animals in developing a model of lightning injury
and successfully showed primary cardiac arrhythmias, prolonged
ventilatory arrest, secondary cardiac arrest, keraunographic skin
changes, and temporary lower-extremity paralysis.
As current flashes over the outside of the body, it may vapor-
ize moisture on the skin and blast apart clothes and shoes,
leaving the victim nearly naked, as noted by Hegner 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 par-
tially 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. The soles may disappear with
or without the heels. Any of the foregoing may occur and the person
not injured or only slightly shocked.175
10 k 0.25 m
10 k
200
200
Key 0.25 m
300
300
0.25 m 10 k 0.25 m
91

Response
No flashover
5 MV VAC
VAB
4 MV
5 kA
VAF IFH
VEB,DB
1.11.7 50 Time
(msec)
With flashover
D E
G2
VAB 500 kV
5 kV
IFH 800A
MOUNTAIN MEDICINE
<<5 kV
VAF
VDB
340 nsec Time
FIGURE 5-34  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.
The amount of damage to clothing or the surface of the body
is not an index of the severity of injuries sustained within a
PART 1
human. Either may be disproportionately great or small. However,
in unwitnessed situations, forensic evidence of damage to shoes
and clothing, sometimes accompanied by tympanic membrane
rupture, may be the most important and reliable indicator in
determining whether lightning caused a healthy person’s death
when no other cause is apparent.47,218,389
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. This conclusion is reached both
because lightning is not present long enough to cause tissue
breakdown in the classic burn sense and because of the results
of the mathematic modeling describing the path of the energy
and how long it is in contact with the body.
ESTIMATES OF STREAMER CURRENTS
Upward streamer mechanism currents have been estimated.8-10,91
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 from perhaps 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, current must flow
through the person. If this streamer meets the downward leader,
a direct strike results. If attachment does not occur, then once
the return stroke is established through another upward streamer
elsewhere, the subject upward streamer collapses back through
the victim. Thus an initial unidirectional current occurs in this
case, followed by a reverse collapse.
Becerra and Cooray41 studied the amount of current to which
a victim of upward leader current may be exposed. They identi-
fied two processes that are important to model. First, current
flows through a victim to establish the upward streamer and
92
A
G4
5 kV
F
G1 5 kA peak
500 kV
8/20 msec wave
H
G3
5 kV
B
Physical Earth
150
C
True Earth
space charge around the victim’s head, under the influence of
the electric field resulting from the stepped leader’s downward
path. Second, once a separate leader from the one affecting the
person makes connection with the stepped leader, 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-kiloampere (kA) lightning strike grounding just
beyond the striking distance, current rises to approximately 20
amperes (A) over 150 microseconds (µsec). At the start of this
rise, there is an extremely short pulse of about 5 A. This repre-
sents 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 potentially 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, which again is 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 time constant. The least peak current is computed
at about −600 kA, with the least energy deposited being 0.22
kilojoule (kJ). Again, these are highly significant currents that are
large enough to produce significant injury and death.
BEHAVIOR OF ELECTRIC CURRENT IN TISSUE
High-voltage or low-voltage electric current may be carried
through tissue in a direct conduction manner, 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.248 It is a feature of the nonlinearity of tissue
that as conduction takes place, tissue modifies and its properties
change. Conduction in a biologic material such as wood is dis-
cussed earlier, and the various tissue dispersions in operation
during conduction are examined later with current research.
MAGNETIC FIELD EFFECTS
It has been stated that some effects of lightning might be mag-
netically mediated.27,75 A case cited in support of this involved 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 was
also stated that three methods of lightning shock may have
existed—direct strike, side flash, and ground potential/streamer
potential—but no evidence of any was seen. It is uncertain what
evidence may have been expected from the latter two mecha-
nisms, which may have been more likely causes. Contact poten-
tial was not considered relevant. In this case, with persons under
a tree, it would seem possible to explain deleterious effects
without resorting to a magnetic hypothesis, but this bears exami-
nation if only because it is a recurrent question. In the case under
consideration, the stroke was considered as a line current 1 m
(3.3 feet) distant from the victim, and peak fields and their effects
were calculated.
In considering this contention, it is useful to consider the
stroke as a single line current; however, one must also have an
idea about how far from a victim such a stroke will act. If the
stroke is close to a victim, attachment to the victim takes place
and electrical effects apply as described earlier. If farther 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 dis-
tance 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 mag-
netic field acts without lightning attachment and its electrical
effects. The standard striking-distance formula gives such a dis-
tance,120 as follows:
d s = 10 × I0.65
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, assume a stroke has a peak current
of 18,000 A (50th percentile of lightning strike currents) so that
ds is 65.5 m (215 feet). Pure magnetic effects are applicable at
this distance and beyond. Inside this distance, the victim is
subject to electric 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 resis-
tivity 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 influ-
ence) is:
µ 0 I peak
B peak =
2πd 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. (Magnetic field strength is measured in
Teslas [T], with 1 µT being 1 × 10−6 T.) The magnetic fields used
in magnetic resonance imaging (MRI) are 2 to 5 million times
these levels. As with other exposures, effects from chronic expo-
sures may be quite 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,
CHAPTER 5  Lightning-Related Injuries and Safety
where to 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, the time rate of change for
the B field is about 22 T/sec. Andrews and colleagues27 applied
this field to a model heart and found that an entirely noninjurious
current resulted.
It is concluded that magnetic field danger in normal circum-
stances does not seem to exist.27 Certainly, special circumstances,
such as the presence of a pacemaker or of an arrhythmic pathway,
might exist, but in normal terms, magnetic effects would not
seem to be clinically significant during occurrences of lightning
strike.
X-RAY AND GAMMA RAY EFFECTS
In recent years, both x-rays and gamma rays associated with
lightning have been detected. As with magnetic effects, when
calculated, both x-rays and gamma rays are much too small,
short-lived, and usually far too distant to cause harm to people.
THE FARADAY CAGE
It has been stated that the safest place for personal protection
from lightning is in a solid vehicle or enclosure. This is a specific
example of the general Faraday cage.
Any hollow symmetric shape made of conducting material is
such that charge introduced at any one point of its surface will
distribute quickly over the entire surface. The surface, by virtue
of its conduction properties, remains at a constant potential
(voltage). The potential of one side of the shape will be the same
as that of the opposite side. Because current flow depends on a
difference of potential, there can be no internal current flow. A
person inside such a container is safe from whatever impinges
on the outside, with the following conditions:
1. Provided the shape is surrounded by conducting material, the
same principles apply to a nonsymmetric shape, such as a car
body.
2. Provided the walls of a building or structure are sufficiently
conductive, the same principles apply to a solid building, but
not an open-sided building.
3. Full metal will form such a cage; however, wire meshing or
metallic framing is sufficient to achieve the same end.
Conductivity of building walls is enhanced by metal internal
wall framing and addition of metal piping, external down-piping,
metal roofing, and any continuous metal or framing enclosing
the space. These principles can be applied to other structures to
assess their protective ability.
INJURIES FROM LIGHTNING26,68,88,104
There are marked differences between injuries caused by high-
voltage electrical accidents and lightning (Table 5-1). Exposure
to high-voltage–generated electricity tends to be more prolonged,
particularly if the victim “freezes” to the circuit. In this context,
“long” could 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 require major amputations. Myoglobin release
may be pronounced, and renal failure may occur. In addition,
compartment syndromes requiring fasciotomy may occur. Burns
may be severe.88,234a
In contrast, lightning contact with the body is almost instan-
taneous, often leading to a 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. Serious burns and deep injury are uncommon. Fluid
restriction and expectant care are usually the standard.88 Light-
ning injuries are primarily neurologic, not burns.
There have been at least two useful categorizations of light-
ning injuries by severity of injury, based on (1) the initial pre-
sentation and (2) the neurologic outcome (Box 5-4).
93
 TABLE 5-1  Lightning Injuries Compared with
paralysis, particularly of the lower extremities, with mottled skin
and diminished or absent pulses. Nonpalpable peripheral pulses
High-Voltage Electrical Injuries may indicate arterial spasm and sympathetic instability, which
should be differentiated from hypotension. If true hypotension
Factor Lightning High Voltage
occurs and persists, the victim should be scrutinized for fractures
and other signs of blunt injury. Spinal shock from cervical or
Energy level 30 million volts (V), Usually much lower*
other spinal fractures, although rare with lightning, may also
50,000 amperes (A) account for hypotension.
Time of Brief, instantaneous Seconds Occasionally, victims have suffered temporary cardiopulmo-
exposure nary standstill, although it is seldom documented. Spontaneous
Pathway Flashover, orifice Deep, internal recovery of the pulse is attributed to the heart’s inherent auto-
Burns Superficial, minor Deep, major injury maticity. However, respiratory arrest that often occurs with light-
Renal Rare myoglobinuria or Myoglobinuric renal ning injury may be prolonged and may lead to secondary cardiac
hemoglobinuria failure common arrest from hypoxia or some other, yet-to-be-elucidated cause.
Fasciotomy Rarely if ever necessary Common, early, and Seizures may occur.
extensive Burns are uncommon in lightning victims. First- and second-
Blunt injury Explosive thunder effect Falls, being thrown degree burns not prominent on admission may evolve over the
first several hours. Rarely, third-degree burns may occur. Tym-
*Range is 500 V up to millions of volts in transmission lines. panic membrane rupture should be anticipated and, along with
hemotympanum, may indicate a basilar skull fracture.
Whereas the clinical condition often improves within the first
INITIAL PRESENTATION MODEL few hours, victims are prone to permanent sequelae, such as
sleep disorders, irritability, difficulty with fine psychomotor func-
Minor Injury tion and attention, chronic pain and dysesthesia, generalized
These patients are awake and may report symptoms such as weakness or easy fatigability, sympathetic nervous system dys-
dysesthesia in an extremity or a feeling of having been hit on function, chronic headaches, and sometimes PTSD. A few cases
MOUNTAIN MEDICINE

the head, or they may recall having been in an explosion. They
may or may not have perceived lightning or thunder. At the
scene, they often suffer confusion, amnesia, temporary deafness
or blindness, or temporary unconsciousness.88 They seldom dem-
onstrate 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 sustain tympanic membrane rupture from the explosive
force of the lightning shock wave. Vital signs are usually stable,
although occasionally, victims demonstrate transient mild hyper-
tension. They may experience soreness for a few days; recovery
is usually gradual and may or may not be complete. Permanent
PART 1
of atrophic spinal paralysis have been reported.26,68,88,104,390a
Severe Injury
Patients with severe lightning 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
sustained 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,
worsening further with any delay in initiating cardiopulmonary

neurocognitive damage may occur. Some victims may suffer
PTSD and other psychological sequelae.
Moderate Injury
Moderately injured lightning victims may be disoriented, combat-
ive, or comatose. They often exhibit keraunoparalysis (a term
introduced by the French neurologist Charcot), which is motor
BOX 5-4  Lightning Injuries
resuscitation (CPR), thus causing anoxic injury to the brain and
other organ systems. There are anecdotal reports of successful
resuscitation of lightning victims with automated external defibril-
lators (AEDs).159a,290,364
NEUROLOGIC OUTCOME MODEL
Cherington66,68,80 proposed a classification of lightning injury
focusing on neurologic complications. The classification consists
of four groups, based on time of onset, duration of symptoms,
and severity of the clinical situation.

Immediate Immediate and Transient Symptoms

• Cardiac arrest and cardiac injuries These transient symptoms may include loss of consciousness,
• Pulmonary injuries amnesia, confusion, headache, paresthesias, and weakness. Many
• Neurologic signs patients experience temporary paralysis of their limbs; kerauno-
• Seizures paralysis is a brief paralytic state with loss of sensation that affects
• Deafness the lower more than the upper limbs. Muscle strength and sensa-
• Confusion, amnesia tion usually return to normal within a few hours. Paralysis is
• Blindness accompanied by pallor, severe vasoconstriction, and hyperten-
• Dizziness sion. Some have suggested that this peculiar state is caused by
• Contusion from shock wave transient outpouring of catecholamines.
• Chest pain, muscle aches
• Tympanic membrane rupture Immediate and Prolonged or Permanent Symptoms
• Headache, nausea, postconcussion syndrome
Patients have structural lesions that may be seen on imaging
Delayed studies or on postmortem examination. The great majority of
• Neurologic symptoms and signs these neurologic complications involve the CNS, including post-
• Neuropsychological changes hypoxic ischemic encephalopathy, intracranial hemorrhage, cere-
• Memory deficits bral infarction, cerebellar syndromes, and spinal cord injuries.
• Attention deficit
• Coding and retrieval problems Possible Delayed Neurologic Syndromes
• Distractibility
Delayed neurologic disorders attributed to lightning include motor
• Personality changes
• Irritability
neuron disease and movement disorders. These sequelae have
• Chronic pain followed lightning strikes from days to years, although the cause-
• Seizures and-effect relationship between lightning and all subsequent
delayed neurologic complications remains open to question.

94
Lightning-Linked Secondary Trauma from Falls or Blast
Lightning can cause trauma when the patient is thrown or falls.
Injuries include epidural, subdural, and subarachnoid hemor-
rhages. Blunt and blast effects can damage the brain and other
organs and cause tympanic membrane rupture, the most common
blast effect seen in victims of lightning strike.
CARDIOPULMONARY ARREST AND
CARDIAC INJURIES*
Cardiac Arrest
The most common cause of death in a lightning victim is cardio-
pulmonary arrest. In fact, a victim is highly unlikely (p <0.0001)
to die unless cardiopulmonary arrest is sustained as an immediate
effect of the strike. In the past, almost 75% of persons who sus-
tained cardiopulmonary arrest from lightning injuries died, mainly
because CPR was not attempted.87
A primary cardiac arrest occurs immediately after the lightning
discharge and is manifested as asystole and respiratory standstill.
Because of the heart’s automaticity, myocardial contractions gen-
erally resume, and return to a spontaneous circulation is possible
within a short time. Unfortunately, respiratory arrest caused by
unknown factors may persist, and unless the victim receives
immediate ventilatory assistance, attendant hypoxia may induce
arrhythmias and secondary hypoxic cardiac arrest.29 Primary and
secondary cardiac arrests had previously been hypothesized and
confirmed in animal studies.12,99,107-109 For example, sheep sustain
initial asystole followed by resumption of a short run of brady-
cardia, then tachycardia, followed by atrioventricular block or
bradycardia, and finally asystolic cardiac arrest.12 Prolonged respi-
ratory arrest has been confirmed in hairless rats.107,234
It is unknown whether cardiac arrest and arrhythmias induced
by lightning are a result of damage to central cardiac and respi­
ratory centers in the brain, to the carotid body and other pace-
makers along the cardiac control paths, to feedback control
mechanisms within the autonomic nervous system (ANS), to the
heart, or to a combination of these.95,107 Certainly, clinical evi-
dence of general damage to ANS regulation has been well docu-
mented and confirmed in the laboratory.107
Asystole and ventricular fibrillation have been reported with
lightning strike.14,159a,170,222,232,275a,396 As noted in animal studies, asys-
tole seems to be both the first and the last response to the strike,
as the secondary agonal arrest rhythm of VF deteriorates.
Other Cardiac Injuries
Multiple mechanisms, such as direct thermal damage, coronary
artery spasm, increased circulating catecholamine levels, myo-
cardial ischemia secondary to arrhythmia, and coronary artery
ischemia as part of a generalized vascular injury, have been sug-
gested to explain the cardiovascular events following lightning
strike.172,269
Immediate prolongation of the QT interval has been shown
in up to 64% of cases evaluated, with consequent predisposition
to arrhythmias.24 In the study by Lichtenberg and colleagues253
of four patients with direct injuries, three had a prolonged QTc,
whereas none of the patients with splash or ground strike had
a prolonged QTc.
The electrocardiogram (ECG) pattern after initial shock may
show tachycardia or bradycardia and the pattern of myocardial
infarction. In the months and years following lightning strike,
arrhythmias, such as tachycardia, bradycardia, premature ven-
tricular contractions, and atrial fibrillation, have been re-
ported.106,130,249,253,305,363 Postural tachycardia also has been reported,
implicating the ANS.166
Although the initial ECG may be unreliable for reasons
given next, it is not uncommon to find ST changes consistent
with ischemia and myocardial injury compromising any coro-
nary vascular segment.209,253,272 However, the ST-segment and
T-wave changes generally occur on the inferior side of the
heart.7,26,135,170,209,220,253,350 Creatine phosphokinase (CPK), MB isoen-
*References 39, 87, 93, 96, 103, 106, 112, 232, 396.
zyme, and troponin are used as markers of myocardial damage.
CHAPTER 5  Lightning-Related Injuries and Safety
The first report of troponin level elevations and cellular damage
in a lightning survivor was published by a high-altitude pul­
monary physiologist who was injured while climbing in the
Alps.40
Saglam and associates350 presented a typical case of infarct
changes with normal coronary angiography, summarizing the
widespread cardiac consequences of lightning strike: “the vic-
tim may develop hypertension, tachycardia, nonspecific elec-
trocardiographic changes (including prolongation of the QT
interval and transient T-wave inversion), and myocardial necro-
sis 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.160,348 Many of these abnormalities are accompa-
nied by normal coronary angiography and nuclear medicine
scans.209,220,350,396
The ECG changes may not occur until the second day follow-
ing the strike,307,337 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.209,307
Several reports of cardiomyopathy exist. Rivera and associ-
ates337 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. The authors 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 myofila-
ment sensitivity to calcium.” There was a similar case in a 36-year-
old man who presented with severe compromise of ventricular
function with ejection fraction of 15%, and rapid recovery during
a 10-day hospitalization.364
Takotsubo-shaped hypokinesis with aneurysmal dilation (tran-
sient left ventricular apical ballooning syndrome) with associated
cardiomyopathy has been described.172 This is noted in the setting
of ECG changes mimicking myocardial infarction, but with
minimal enzyme release.131,160 Recovery from dramatic dysfunc-
tion is completed over days to weeks.
Some clinicians have theorized that vascular spasm is a cause
of cardiac damage not dissimilar to keraunoparalysis.306 However,
ECG changes are not always consistent with cardiovascular
supply patterns. Areas of focal cardiac necrosis have been
reported in autopsies, and histologic changes have been shown
in sheep hearts.14
PULMONARY INJURIES
Pulmonary edema may accompany severe cardiac damage.124a,131
Pulmonary contusion, with hemoptysis and pulmonary hemor-
rhage, may result from blunt injury or direct lung damage.365
Blunt thoracic trauma may also cause pneumomediastinum.169
NEUROLOGIC INJURIES37,68-71,90,217,224
Lightning injury is primarily neurologic, 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 for survivors. Tools commonly used in
evaluation and treatment include functional scans, such as single-
photon emission computed tomography (SPECT, usually demon-
strating an abnormality); positron emission tomography (PET);
anatomic scans such as computed tomography (CT) and MRI
(rarely demonstrating gross abnormality); neuropsychological
assessment; cognitive retraining; pharmacotherapy; and psycho-
therapy. Electroencephalography is often mentioned in the litera-
ture but is seldom helpful.32,88
95
 Central Nervous System Injury37,68-71,76-80,90,224
Almost 72% of victims in one study had loss of consciousness.87
Nearly three-fourths of these victims also suffer cardiopulmonary
arrest. Persons with cranial burns are two to three times more
likely to sustain immediate cardiopulmonary arrest and have a
three to four times greater probability of death. Persons who are
stunned or lose consciousness without cardiopulmonary arrest
are highly unlikely to die, although they may still have serious
sequelae.
The victim of prolonged cardiopulmonary arrest may suffer
anoxic brain injury that is not specific to lightning injury.80a
Whether by this mechanism or others, cell loss and infarction
of various CNS areas (e.g., cerebellum,37 cerebrum) have been
reported. Autopsy findings include meningeal and parenchy-
mal blood extravasation, petechiae, swelling and herniation
of the brainstem, dural tears, scalp hematomas, and skull
fractures).170,265a,284,300,374
Gross structural changes to the brain have been reported,
including coagulation of brain substance, formation of epidural
and subdural hematomas, paralysis of the respiratory center, and
intraventricular hemorrhage. In hemorrhagic injuries, there is a
pattern of compromise to the basal ganglia.4,60,167,305,368 Intracranial
hemorrhages related to blunt trauma do not tend to occur in the
basal ganglia, and therefore mechanical trauma is a less likely
explanation. Studies in animals suggest that direct cellular damage
occurs to basal ganglia, the respiratory center beneath the fourth
MOUNTAIN MEDICINE
ventricle, and the anterior surface of the brainstem. This occurs
because the path of current flow in direct-strike patients is
through orifices of the head (eyes, nose, ears), and the current
travels caudally from the neocortex toward the basal ganglia,
pituitary, hypothalamus, and brainstem.12,14 As a result, signs
and symptoms of endocrine dysfunction, respiratory or cardiac
arrest, and sleep disturbances can be reasonably expected to
occur. Cerebellar compromise may eventually manifest as par-
kinsonism, extrapyramidal syndrome, or other involuntary move-
ment disorders.37,66,69,79,80,297
Although MRI or CT may show diffuse edema, intracranial
hemorrhage, or other injuries, they are most often normal.79,80,124
PART 1
Hemorrhage has been found on MRI in a few acutely injured
victims.79,383
Seizures may accompany initial cardiorespiratory arrest as a
result of hypoxia or intracranial damage. Electroencephalography
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 hos-
pitalization. Some victims, including children, develop delayed
seizures (months to 1 or 2 years later), some of which manifest
as “absence spells,” memory loss, or blackouts that are often
diagnosed as “pseudoseizures.”
In Cooper’s study87 of severely injured victims, nearly two-
thirds had some degree of lower-extremity paralysis (keraunopa-
ralysis), usually demarcating around the waist or pelvis, and
approximately one-third had upper-extremity paralysis. The
affected extremities appear cold, clammy, mottled, insensate, and
pulseless.26 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.26,88 Fascioto-
mies 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
(immediate or delayed), and progressive muscle atrophy of the
upper extremities.
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 victims may carry on a conversation
and remember their actions before the strike, they are often
unable to assimilate new experiences for several days, even
when there is no external evidence of lightning burns on the
head or neck. Early after the strike, symptoms resemble postcon-
cussion syndrome.
96
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 PTSD.90 Centrally derived pain and psy-
chological syndromes have been reported.66,69,79,80,297
Spinal cord injury developing over months after the injury has
been reported.242,243 Paresthesias are frequently seen, often in the
area of keraunoparalysis. There may be evidence of autonomic
neuropathy.
Peripheral Nerve Injury*
The peripheral nervous system may be affected. Pain and pares-
thesias are prominent features of lightning 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. Any peripheral nerve can be
involved.
Autonomic Nervous System Injury85,176,177,323,357,358
Central hyperadrenergic state with superimposed autonomic
storms and diffuse degeneration of the peripheral autonomic
system have been reported.309,387 Autonomic dystrophy, also
called sympathetic dystrophy or sympathetically mediated pain
syndrome, may occur. Such chronic pain syndromes are now
subsumed under the classification of complex regional pain syn-
dromes, which are of type 1 (reflex sympathetic dystrophy) or
type 2 (previously causalgia).
Complex regional pain syndromes are long-term neurologic
sequelae that may be caused by even minor injuries to nerves.
These are characterized by pain, edema, autonomic dysfunction,
trophic changes (including atrophy secondary to disuse from
pain), and movement disorder.
Posttraumatic Headache93,375
Many victims of lightning injury exhibit severe, unrelenting
headaches for the first several months, along with other symp-
toms, including gastrointestinal distress, that resemble postcon-
cussion symptoms. Acupuncture may be effective. Many patients
complain of nausea and unexpected, frequent vomiting spells
early in the recovery period. Dizziness and tinnitus from eighth
cranial nerve injury are also common complaints, especially with
telephone-transmitted lightning strikes.30,90,104,388,392
BURNS†
Most people assume that because of the tremendous energy
discharge involved, a lightning victim will be “flash-cooked.”58,89
Fortunately, the physics of lightning flashover, as well as the vast
majority of injuries occurring from indirect strikes, spares 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. Burn location provides a prognostic indi-
cator. Cranial and lower-extremity burns are associated with a
fourfold and fivefold increase in mortality, respectively, com-
pared to burns in other locations.87
Skin injuries are influenced by amount of moisture on the
surface, type of clothing, and presence of metal objects worn or
carried during the strike. Superficial partial- or full-thickness
burns can be isolated or combined. The morphology can be
linear, punctuate, flower-like, tattooing, or imprint burn mark
from contact with metal objects; feathering; fern-leaf mark; or
classic first, second, or third degree.74,272,385
Entry, Exit, and Types of Burns
Discrete entry and exit points are uncommon with lightning. The
burns most frequently seen may be divided into five categories:
*References 66, 68-70, 85, 176, 177, 217, 315, 319, 320, 323, 330, 357,
368, 378, 384, 392.
†
References 38, 61, 86, 93,104, 181, 206, 268, 283, 284, 360, 366, 380.
 CHAPTER 5  Lightning-Related Injuries and Safety
A B C

D E F

G H I J
FIGURE 5-35  Linear burns from a fatal 1977 lightning injury to 22-year-old baseball player. Most of these
marks (those with small eschar) did not appear until a few hours to a few days 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 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 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 electri-
cal 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 contu-
sion 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 (H). I and J, Damage to the left lower leg and foot. (Copyright Mary
Ann Cooper.)

linear; punctate, full thickness; feathering, or flowers; thermal
from ignited clothing or heated metal; and combinations.
Linear burns often begin at the victim’s head and progress
down the chest, where they split and continue down both legs
(Figure 5-35). The burns generally are 1 to 4 cm (0.5 to 1.5
inches) wide and tend to follow areas of heavy sweat concentra-
tion, such as beneath breasts, down the middle chest, and in the
midaxillary line.88 Linear burns are usually first- and second-
degree burns that may be present initially or may develop as late
as several hours after the lightning strike. They are not primary
lightning injuries, but more likely steam burns caused by vapor-
ization of sweat or rainwater on the victim’s skin as flashover
and current flow occur around the body. In patients wearing thin
or cotton clothing, the steam tends to escape through the cloth-
ing, causing less damage than in areas where the clothing is
bunched (e.g., axilla, antecubital fossa [see Figure 5-35C], groin)
or under nonporous material, such as leather jackets or belts
(Figure 5-36).
Punctate burns are discrete circular burns that individually
range from a few millimeters to 1 cm (0.4 inch) in diameter, and
may be multiple and closely spaced (Figure 5-37). 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 5-35H). Examina-
tion of clothing may show singed fibers at the edge of the
damage and absence of very fine fibers on material, such as
cotton, because these were vaporized or burned away (Figures
5-38 and 5-39; see also Figure 5-33B). 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 joining pieces at the seams
will often show a tiny droplet of plastic, because thread contains
a polyester or nylon core for strength and durability.
Feathering or fern-leaf mark figures are pathognomonic of
lightning and known by such names as Lichtenberg flowers or
figures, filigree burns, arborescent burns, ferning, and kerauno-
graphic markings73,74,86,129,203,239,263,332,380 (Figures 5-40 and 5-41). These

97
 A B
FIGURE 5-36  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 5-35. A, Note the more exten-
sive 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.)

markings are not true burns, usually appearing as transient pink with their rapid resolution and pattern of color changes. Experi-
to brownish, sometimes lightly palpable, arborescent marks that mentally, these marks follow the flashover current lines seen in
follow neither the vascular pattern nor nerve pathways. The Cooper’s animal model.102,104
MOUNTAIN MEDICINE

pattern found is similar to that on a photographic plate exposed
to a strong electric field and has been compared with fractals.181
Sometimes the most superficial skin over the areas will slough
or flake off after a few 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 contract-
ing capillaries, similar to a superficial bruise, which is consistent
PART 1
Deep burns may be caused by metal worn close to skin.104,215,385
Figure 5-35E shows a burn resulting from a metal belt buckle or
athletic supporter worn by a young man who was struck by
lightning while playing softball. Figure 5-42 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 light-
ning, causing severe thermal burns.26,88 Victims of lightning
may exhibit various combinations of burns, as demonstrated in
Figure 5-35.
In developing countries, reports often describe lightning
victims as “charred” or “burned beyond recognition.”94 Since

these reports are frequently written with no first-hand knowledge

or investigation, it is unclear if these are from the reporter’s
expectations or if the character of burns from lightning in devel-
oping countries is different or more severe. Recent newspaper
reports accompanied by pictures or YouTube documentation
show that buildings where people were injured have been almost

B
FIGURE 5-37  A, Punctate burns to the shoulder and arm of a 12-year-
old 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 FIGURE 5-38  Damage to the socks of a fatally injured farmer. (Copy-
right arm burn. (Copyright Mary Ann Cooper.) right Mary Ann Cooper.)

98
 CHAPTER 5  Lightning-Related Injuries and Safety
A B
FIGURE 5-39  A, Melting of synthetic clothing material from lightning damage. B, Underlying damage to
skin from zipper and melted material. (Copyright Ryan Blumenthal.)

completely destroyed. Most homes and businesses in developing lightning has been well described and includes pulmonary
countries have no protective Faraday cage effect and do not effects,221,280,365 pneumomediastinum,169 gastrointestinal perfora-
provide safe shelter from lightning. Because of the high incidence tion36,142,221 or contusion,170 and tympanic membrane damage (see
of acute keraunoparalysis, it is hypothesized that even young Ear Injuries, later). Injuries caused by fragments that impact and
healthy victims may be paralyzed temporarily after lightning penetrate the body are similar to injuries secondary to explosion,
injury and unable to evacuate from mud and thatch structures but are rare in lightning injury.377 Tertiary injuries from explosion
(Figure 5-43). are closed and concussive, and usually produced by falls.
Back and spinal injuries unrelated to the electrical effects of
BLUNT, CONCUSSIVE, AND EXPLOSIVE lightning injury may result from these mechanisms. A variety of
(BLAST) INJURIES
As with explosive injuries, lightning may cause several types of
injuries, which can be similarly classified. Primary explosive
injuries, similar to the shock wave formed on a battlefield, an
explosion, or barotrauma, mainly manifest with damage to organs
containing air or gas in their interior (ear, lungs, intestines), or
in areas with air-liquid and air-solid interphases. Barotrauma from

FIGURE 5-41  Lichtenberg figures in a teenager who survived lightning

strike. (Courtesy/copyright Mary Ann Cooper.)

B
FIGURE 5-40  A, Feathering marks. B, Ferning developed after the FIGURE 5-42  Metal necklace burned into skin by lightning with per-
victim received a side flash lightning strike. (A courtesy Mary Ann manent tattooing (nonfatal injury). (Copyright Mary Ann Cooper; cour-
Cooper; B courtesy Sheryl Olson, RN.) tesy R. Washington.)

99

FIGURE 5-43  Rondavel in South Africa where this woman’s family
member died by fire. (Courtesy Ronald Holle.)
fractures, including skull, ribs, extremities, and spine, have been
reported in lightning victims.219,255 Unfortunately, these are often
missed, particularly in the workup of persons with chronic pain.
Rarely, a burst-like injury of soft tissue occurs and discloses
MOUNTAIN MEDICINE
extensive underlying injuries, especially in the feet, where boots
or socks may explode as a result of vapor expansion (Figure
5-44; see also Figures 5-35H and 5-38). 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,365 heart failure, and isch-
emic bowel.
Other findings, such as hemoglobinuria and myoglobinuria,
are seldom reported.312,314 Multifactor rhabdomyolysis may be
PART 1
A
B *References 56, 62, 127-126, 137, 165, 204, 216, 230, 276, 293, 294, 336,
FIGURE 5-44  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.)
100
diagnosed due to elevation of CPK.287,289,386 When these occur,
they are usually transient. Myoglobinuric renal failure is quite
rare.171,269,302,314
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*
Ocular injuries may be caused by direct thermal or electrical
damage, intense light, contusion from the shock wave, or com-
binations of these factors.
Although cataracts most often develop within the first few
days, they may occur late and are often bilateral.† While the cata-
racts may be the typical anterior midperipheral type, posterior
subcapsular opacities and vacuolization seem to occur more
often with lightning injuries.56 Corneal lesions, hyphema, uveitis,
macular holes, iridocyclitis, vitreous hemorrhage, choroidal
rupture, chorioretinitis, retinal detachment, macular degenera-
tion, macular hole,61,327 optic atrophy, diplopia, loss of accom-
modation, and decreased color sense have been reported.
Autonomic disturbances of the eye, including mydriasis, Horn-
er’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
conversion of St Paul on the Damascus road and his subsequent
blindness were caused by lightning.53,54
Dilated or nonreactive pupils should never be used as a
prognostic sign or criterion for brain death in a lightning victim
until all anatomic and functional lesions have been excluded.64,65
EAR INJURIES‡
Between 30% and 50% of more severely injured lightning victims
may have ruptured 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.26,87 Otor-
rhea of CSF or hemotympanum rarely occurs. Disruption of the
ossicles and mastoid has been reported. All these injuries are
manifested as conductive hearing loss. Many cases of permanent
deafness are noted in older literature and are seldom found
today. The mechanism of sensorineural hearing loss may be
explained by microhemorrhage and microfracture in the cochlea
or by the hypoxia theory.285
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 nystag-
mus and ataxia may occur. Otologic injury from hard-wired
telephone–transmitted lightning strikes is common, but probably
occurs less often now with the advent of mobile phones.11,30,31
FETAL SURVIVAL
The fetus of a pregnant woman struck by lightning has an unpre-
dictable 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 was
stillbirths or deaths in utero. There has been one report of rup-
tured uterus after lightning strike.87,144,150,329
366, 395.
†
References 56, 126, 127, 137, 165, 168, 230, 276, 336, 366.
‡
References 42, 44, 57, 141, 153, 158, 163, 216, 238, 277, 285, 298,
299, 328, 369, 388.
 CHAPTER 5  Lightning-Related Injuries and Safety
HEMATOLOGIC ABNORMALITIES TABLE 5-2  Frequent Complaints of Lightning Survivors
Several unusual hematologic complications have been attributed Symptom %
to lightning injuries in isolated case reports. These include dis-
seminated intravascular coagulation (DIC), transiently positive Memory disturbance 71
Coombs test, and Di Guglielmo syndrome, a type of erythroleu- Concentration disturbance 63
kemia characterized by erythroblastosis, thrombocytopenia, and Aggression and irritation 67
hepatosplenomegaly. Although there have been anecdotal reports Wariness and phobia 58
of increased hypersensitivity, development of allergies, and
Loss of mental powers 50
increased risk for cancer in lightning victims, perhaps indicating
Social isolation 38
an immunologic component to lightning injury, these have not
been studied or validated with controlled longitudinal studies. Sleep disorder 38

ENDOCRINE AND SEXUAL DYSFUNCTION

Other neurologic-endocrine findings have anecdotally been
reported, including cerebral salt wasting syndrome and inappro-
priate secretion of antidiuretic hormone (SIADH).136,303
Decreased libido for both men and women and impotence
for men are common complaints. Sexual dysfunction may be
caused by neural, spinal cord, endocrine (including hypoadrenal-
ism and hypogonadism), 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 by a specific brain injury mechanism. Some patients
have reported amenorrhea or menstrual irregularities lasting up
to 2 years.
PSYCHOLOGICAL AND NEUROCOGNITIVE
DYSFUNCTION*
A person hit by lightning may 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. Neurocog-
nitive deficits may not become apparent until a victim attempts
skilled mental functions or returns to work. Often the person
returning to work, because of decreased work tolerance, short-
term memory problems, easy fatigability, and difficulty assimilat-
ing new information, will be unable to continue the prestrike
occupation. Chronic pain syndromes are cited as commonly
overlooked diagnoses in psychiatric and functional terms and can
lead to depressive symptoms.24,177 If the survivor does not obtain
useful medical and psychological help, the person often lapses
into a low-functioning state, unable to work and with multiplying
psychological dysfunctions.
Although some medical clinicians have been historically suspi-
cious of victims’ complaints of psychological and neurocognitive
dysfunction, evaluation of many such patients shows a vast com-
monality of psychological symptoms. Although every syndrome
has its pretenders, there is a tendency, both medically and legally,
to discount survivors’ complaints as evidence of malingering,
excessive reaction, conversion reaction, personality problems, or
manifestations of “weak” coping strategies. The psychological
disability has been examined for its depth and pervasive-
ness.17,279,315,316,320,321 Patients are often young, previously healthy,
and generally productive, with young families. Serious injury may
change the family structure, family economic expectations, social
structures, and future planning. As with other serious illnesses,
relationship breakdown may occur. There is both economic and
social cost to society, the workplace, and the home.
Survivors often complain of symptoms listed in Table 5-2 and
others, including anxiety, depression, and learning disorder.17 In
a long term study, Andrews18 noted problems with learning and
executive function (Table 5-3).
Functional Issues
Memory Disturbance.  Individuals show marked diminu-
tion of short-term memory ability. They require shopping lists
*References 69, 70, 104, 315, 319, 320, 326, 378, 393, 394.
and reminder lists. Memory for recent names and places is dimin-
ished to the point of disability. Individuals tend to self-isolate,
stop mixing socially, and avoid new circumstances.90
Concentration Disturbance (Adult Attention Deficit Dis-
order).  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. Calculation, estimation, and managing accounts and tele-
phone calls become erratic. This affects both family and work
performance. Ability at mental manipulation and problem solving
is greatly 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 patient 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 may 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 after injury) is common and may
last for years. Flashbacks and nightmares may be experienced as
part of PTSD.
Phobic Behavior.  Avoidance of thunderstorms and electric-
ity is common, along with other, less specific phobias.
Depression.  Depression, both from biologic injury and sec-
ondary to chronic pain, loss of work, sleep deprivation, decreased
TABLE 5-3  Learning Deficits in Lightning Survivor
Findings %
Memory and Learning Deficits
Globally 19
Visual 35
Visuospatial 38
Auditory 62
Other Deficits
Verbal learning 54
Verbal fluency 46
Concentration 46
Attention 42
Executive function 38
Reduced executive speed 62

101
 mental abilities, or changes in family dynamics, is almost univer-
sal and should be anticipated. 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.320,378 Primeau and co-workers320,321 point to research
difficulties, including sample bias and heterogeneity, methodol-
ogy (cross-sectional rather than longitudinal or prospective), and
the essential difficulties of determining premorbid status or
current independent psychiatric status. The authors considered
somatoform disorders as a cause, noting patients’ tendency to be
preoccupied with the injury and to overattribute subsequent
symptoms to lightning injury. This may result partly from physi-
cians’ general lack of knowledge of the problems and the lack
of longitudinal controlled studies, so victims do not know what
to expect in the future.
Other Behavioral Issues.  Conversion reaction may also be
considered, although it cannot account for the symptomatology
of lightning and electrical disability.90 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 pre-
occupation with physical complaints. It should surprise no one
MOUNTAIN MEDICINE
that a person suffering from chronic pain and neurologic injury
that hampers normal preinjury activities will rank higher on the
“preoccupation with physical complaints” and “conversion”
scales than will uninjured normal individuals.
Andrews and Darveniza30 recognized three postinjury syn-
dromes in telephone-related lightning injury and correlated these
with the postinjury periods of 1 week, 1 week to 3 months, and
3 months to 3 years. Primeau and co-workers320 add a fourth
syndrome, in persons experiencing longer and perhaps lifetime
dysfunction.163 Cherington68 and colleagues80 have further classi-
fied lightning injury by its permanent sequelae.
The first 12 months after injury are crucial to recovery. It is
PART 1
during this period that the most recovery is seen, with possible
mild improvement up to 3 years after injury. Van Zomeren and
associates378 provide one of the few thorough examinations of
the syndrome in lightning-injured patients. The main complaints
were fatigue, energy loss, poor concentration, irritability, and
emotional lability. Impairment of memory, attention, and visual
reaction times as well as depression and PTSD were documented
(p <0.001). The authors stated that the lasting complaints and
mild cognitive impairments could not be explained on the basis
of anxiety reactions or depression, and summarized their findings
under the heading of “vegetative dystonia.”
RECOGNITION AND ACUTE
TREATMENT OF LIGHTNING
INJURIES88,90
DIAGNOSIS
Diagnosis of lightning injury may be difficult. The history of
thunderstorms, 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 history taking and careful physical examina-
tion at the earliest opportunity may help determine the true
cause. Any person found with linear burns, mental status
changes, ruptured tympanic membrane, and clothes exploded
off should be treated as a victim of lightning strike. Tympanic
membrane rupture may make the diagnostic difference in diffi-
cult cases.
Diagnosis is made doubly difficult because burns, which most
people expect to accompany lightning injuries, are often absent.
Feathering marks, also called Lichtenberg flowers, are pathogno-
monic of lightning strike but are rare.73,74,86,129,332,380 Other signs or
102
symptom complexes include linear or punctate burns, tympanic
membrane rupture, confusion, and outdoor location. Because
several cases of side flash or contact injury from indoor plumbing
and telephones have occurred, the physician should suspect
lightning strike in persons found confused and unconscious
indoors after or during a thunderstorm.11,26,30,88
Documentation of lightning activity to support legal or insur-
ance claims is available from commercial sources.
INITIAL FIRST AID AND TRIAGE
OF VICTIMS26,88,103,106
Ensuring scene safety is paramount. Rescuers are at risk if thun-
derstorms are in the area.373 If the situation makes it possible,
the victim is transferred to a safe area quickly, or to a location
under lesser risk.
If the victim is unresponsive with no breathing or no normal
breathing (i.e., only gasps), the person has suffered a cardiac
arrest. Rescuers should immediately activate the emergency
response system, if possible. CPR should be started immediately
with a CAB (chest compressions, airway, breathing) sequence.
AEDs have been helpful in some cases.159a,290 Cardioversion,
defibrillation, and medications should proceed according to the
most recent advanced cardiac life support (ACLS) guidelines.379
The victim will probably die unless pulse and respirations
resume spontaneously in a short time. The heart may resume
activity but may slip into secondary cardiac arrest. It is unknown
whether the secondary arrest is caused by primary brain damage,
hypoxia from prolonged respiratory arrest, primary cardiac
damage, autonomic nervous system damage, or any of a number
of other mechanisms. If no pulse is obtained within 20 to 30
minutes of starting CPR, it is reasonable to stop further resuscita-
tion efforts; 77% of victims do not respond to CPR.87 If a pulse
is obtained, ventilation should be continued until spontaneous
adequate respirations resume, the victim is pronounced dead,
continued CPR is deemed unfeasible because of rescuers’ exhaus-
tion, 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,120a,397
because victims who show some return of consciousness, or who
have spontaneous breathing, are already on the way to recovery.
The most vigorous CPR attempts should be directed to the victims
who appear to be dead, because they may ultimately recover
if properly resuscitated.106,159a,379 Survivors should be routinely
stabilized and transported to the hospital for more thorough
evaluation.
The probability that lightning victims can recover after pro-
longed CPR is low. No evidence suggests that survival after a
longer period than normal without resuscitation is possible in the
victim 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 pro-
nouncing a victim dead, the rescuer must ensure that other
problems, such as hypothermia, are not contributing to the vic-
tim’s response to CPR efforts.
Other procedures, such as airway control or intubation, and
institution of intravenous (IV) fluids and oxygen may be required.
Because lightning victims may suffer traumatic blunt injuries,
rescuers may need to perform spinal immobilization and splinting
of fractures, if possible, before transport.
Most lightning injury victims can be treated and discharged
from the emergency department (ED), but more complex light-
ning injuries are considered one of the criteria for being referred
and assessed at a burn unit. If this is not possible because of
geographic location or distance, the receiving institution must
have the capacity to treat victims with complex trauma, promptly
assemble a multidisciplinary group of specialists and paramedical
staff with experience in these types of injuries, and access a
consolidated group of rehabilitation, physical, and occupational
therapists.

HISTORY AND PHYSICAL EXAMINATION
An eyewitness report is helpful because lightning victims are
often confused and amnestic.87,88 History that includes a descrip-
tion of the event and the victim’s behavior following the strike
may be helpful.
After scene safety has 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 con-
sciousness. Because many victims are struck during a thunder-
storm, they may be wet and cold. Hypothermia should be
anticipated and treated appropriately (see Chapter 7).
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 assimi-
late information, perseverates, or asks repetitive questions.
The scalp should be meticulously checked for hidden lesions.
The victim’s eyes should be examined for pupillary reactivity and
ocular injury. Pupillary dilation or lack of pupillary reaction
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.
The cardiovascular examination should include distal pulses
in all extremities, because assessment of just one extremity,
usually the one most compromised, can result in the examiner
considering the absence of distal pulses a sign of poor hemody-
namic state. Cool, mottled, and pulseless extremities as a mani-
festation of keraunoparalysis may occur in up to two-thirds of
victims.87 Evaluating proximal pulses (femoral and carotid) may
help avoid confusion. In the setting of an overall absence of
distal pulses, cardiogenic, hypovolemic, and spinal shock should
be ruled out.106 Detecting arrhythmias may be difficult in a wil-
derness setting far from clinical resources. Repetitive evaluation
of pulses and auscultation may determine the presence of some
arrhythmias. 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 victim’s abdominal examination occasionally demon-
strates absent bowel sounds, which suggests ileus or indicates
acute traumatic injury, such as contusion of the liver, bowel, or
spleen.
The examiner should document skin changes. The victim’s
skin may show mottling, especially below the waist. Burns may
be present or may require hours to evolve. However, most are
minor injuries. Notation of pulses, color, and movement and
sensory examination of the victim’s extremities are important.
Keraunoparalysis is common, but usually improves or resolves
in a few hours.
The physical findings and mental state of minimally and mod-
erately 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 ven-
tilation, antiarrhythmic medications, and invasive interventions
and monitoring techniques, or referral to a burn center.
LABORATORY TESTS AND
RADIOGRAPHIC EXAMINATION
The more severely injured victim may require tests such as com-
plete blood count, electrolytes, blood urea nitrogen, creatinine,
testing for cardiac damage, and urinalysis. If the victim is to be
placed on a ventilator, arterial blood gas (ABG) determinations
will be necessary. If intracranial pressure monitoring is used,
determination of serum osmolality may be required.
An ECG is desirable for evaluating most lightning victims.
Although several types of acute arrhythmias have been reported,
they are uncommon. QT prolongation is an abnormality
associated with lightning injury.24,253,307,350 The increased risk of
developing torsade de pointes ventricular tachycardia (VT) must
CHAPTER 5  Lightning-Related Injuries and Safety
be considered, so monitored admission of lightning strike victims
with QT prolongation is probably prudent. Cardiac enzyme ele-
vations have rarely been reported with lightning injury, but
measurement is recommended with any cardiac symptomatology
or abnormal ECG.
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 conscious-
ness requires brain CT or MRI to identify trauma or ischemic
injury. Other studies to rule out fractures, dislocations, and other
bony abnormalities may be obtained as clinically indicated.
The serum creatine kinase (CK) level is typically used as a
biochemical marker of rhabdomyolysis and prognosticator of the
risk for acute renal failure, even though CK shows a wide range
among individuals. Although measurement of plasma or urine
myoglobin can also be used as a confirmatory test, these are not
widely used in clinical practice.
TREATMENT87
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. Fluid restriction in normoten-
sive or hypertensive victims is recommended because of the risk
for cerebral edema, particularly if intracranial injury is suspected.
In seriously injured or unstable patients, intensive care unit
(ICU) types of monitoring, including arterial or central venous
pressure, may be indicated. Careful intake and output measure-
ments 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. There are no reports in the
literature of investigations about the usefulness of mannitol-
induced diuresis, alkalinization, or aggressive fluid therapy in
lightning injuries, unlike what is known about the treatment for
high-voltage electrical injuries. However, if burns are severe and
extensive, which is rarely the case in developed countries, fluid
resuscitation may be required.
Fasciotomy Not Needed
Intense vascular spasm with lightning is usually transient and
caused by sympathetic instability. The presence of keraunopa-
ralysis should not be treated like similar-appearing traumatized
extremities caused by high-voltage electrical injury.26,88,267 Steady
improvement in the mottled and 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 increased intracompartmental tissue pres-
sures are documented.
Antibiotics and Tetanus Prophylaxis
Prophylactic antibiotics are not indicated. Antibiotic therapy
should 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 Therapy103,106,144,232,253
Management of cardiac arrest, including use of an AED, is stan-
dard. In the lightning victim who is not in cardiac arrest, vaso-
spasm may make peripheral pulses difficult to palpate. When
pulses are present, it is usually easiest to feel them in the femoral,
brachial, or carotid arteries. 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 perfu-
sion. Causes of hypotension include major fractures, blood loss
103
 from abdominal or chest injuries, spinal shock, cardiogenic
shock, and occasionally deep burns similar to high-voltage elec-
trical burns. As soon as an adequate central blood pressure is
achieved, 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.
If lightning did not cause immediate cardiac arrest, there is
very low risk of death. However, observation, cardiac monitoring,
and serial cardiac marker (e.g., troponin) measurements are in-
dicated if there is any sign of cardiac ischemia or arrhythmia, or
if the victim complains of chest pain. The indications for antiar-
rhythmic drugs and pressor agents are the same as for suspected
myocardial infarction.88 No systematic study has addressed proper
duration of observation for lightning survivors.
Transient hypertension may be so short-lived as not to require
acute therapy. However, several victims developed hypertension
12 to 72 hours after lightning strike and seemed to respond well
to antihypertensive medications. No systematic study of antihy-
pertensive agents has been undertaken for lightning survivors.
Central Nervous System Injury*
Every lightning victim should have a screening neurologic exami-
MOUNTAIN MEDICINE
nation. If there is 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 con-
sciousness, or who shows decreasing level of consciousness,
should undergo cervical spine imaging, brain CT, and possibly
brain MRI.
Cerebral edema may be managed with standard therapies,
which may include mannitol, furosemide, fluid restriction, and
cerebral pressure monitoring. Although hypothermia prior to
resuscitation efforts was reported to contribute to complete
recovery in one victim, there is no evidence that this would
benefit all victims.222
PART 1
Early seizures are probably caused by anoxia. If there is evi-
dence of CNS damage, or if seizures continue after adequate
oxygenation and perfusion have been restored, standard phar-
macologic intervention with diazepam, fosphenytoin, phenobar-
bital, and other anticonvulsants should be considered. The
response to specific individual 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.
Burns†
Lightning burns may be apparent at admission but more often
develop within the first few hours. Burns 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, the decision must be made by
the treating physician, according to the case. Overzealous hydra-
tion with resultant cerebral edema following presumption of
similarity to high-voltage injuries has probably harmed more
lightning victims than has myoglobinuric renal failure.
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 light-
ning burns are superficial and do not require active surgical
intervention is reinforced by Matthews and Fahey.268 Their paper
*References 26, 66, 68, 71, 78-80, 89, 90, 393, 394.
†
References 38, 86, 93, 104, 129, 181, 206, 268, 283, 284, 359, 360,
366, 380.
104
provides a useful guide to the remote need for surgical interven-
tion 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 exist of successful treatment of optic neuritis with
high-dose corticosteroids similar to those used with spinal cord
injury, but because there were no controls, it is not known if
recovery would have occurred without drug 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 vic-
tim’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. Otor-
rhea and hemotympanum suggest basilar skull fracture. Com-
plaints of pain around the angle of the victim’s jaw may indicate
occult fracture of the styloid process and other musculoskeletal
damage.
Pregnant Victims144,150
If a pregnant woman is struck by lightning, 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.146 A nasogastric tube is
appropriate if ileus or hematemesis occurs. Extended Focused
Assessment with Sonography for Trauma (EFAST) is indicated in
comatose patients who remain hypotensive. Abdominal CT scan
is preferred in hemodynamically stable patients, because intesti-
nal 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, hypo-
gonadism, 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 light-
ning injury.
Pronouncing the Victim Dead55,64,65,101,103,106
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 pupillary 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 CPR.
Long-Term Care‡
In the long run, there is no specific treatment for lightning
injury. Lightning is a nervous system injury that can involve
chronic pain, neuropathy, and brain injury, sometimes compli-
cated by initially unrecognized musculoskeletal injury. Most
symptoms can be treated in standard fashion, including cogni-
tive therapy, pain management, job retraining, and counseling,
as indicated by the survivor’s signs and symptoms. As with any
*References 56 ,62, 126, 127, 137, 165, 166, 204, 216, 230, 276, 293, 294,
336, 366, 395.
†
References 14, 42, 44, 57, 153, 158, 164, 216, 239, 277, 298, 299, 328,
369, 388.
‡
References 69, 107, 111, 243, 319, 359, 393, 394.

TABLE 5-4  Drugs That May Be Useful in
Lightning Patients
Symptoms Suggested Drugs
Pain Nonsteroidal antiinflammatory drugs
Acetaminophen
Duloxetine
Gabapentin and similar drugs
Social avoidance Venlafaxine
Desvenlafaxine
Duloxetine
Older tricyclic antidepressants, including
clomipramine
Others Fluoxetine
Paroxetine
Escitalopram
Resistant cases Monoamine oxidase inhibitors
serious illness, the caregiver and family may be the unsung
heroes and need support, recognition, and counseling, as well
as respite.
Pain Control
Neuropathy and autonomic pain syndromes may develop in
survivors. These may respond to chronic pain management thera-
pies, such as combinations of nonsteroidal antiinflammatory
drugs (NSAIDs), antiepileptic agents, antidepressants, and gan-
glionic blocks26,30,176,177,320 (Table 5-4). Acupuncture may be helpful
for resistant posttraumatic headaches that often accompany light-
ning injury.
Psychological Problems and Cognitive Deficits
In recent years, neuropsychological deficits from lightning have
become better appreciated.17,230,315,319,320,378 Heightened anxiety
states, hyperirritability, memory deficits, attention deficit, aphasia,
sleep disturbance, PTSD, and other evidence of brain damage
should be assessed.30 Some of these deficits are similar to 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.69,319,394,395
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 pre-
dispose to more pronounced neuropsychological symptoms.
Other aids in assessment may include occupational therapy and
psychiatric evaluation.
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 poorly 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. Although it is helpful if the specialists have famil-
iarity with lightning survivors and the literature, it is not manda-
tory if they are willing to work with the survivors and their
families and read the lightning literature.
It has been shown that clinical depression and electrical inju-
ries are associated with decreased hippocampal mass and hip-
pocampal cell atrophy.51,116,241,352,362 The conclusion that untreated
depression can cause brain damage necessitates almost manda-
tory antidepressant use. In electrical injury survivors, litigation
has not been shown to be a factor,178,179,370 but similar studies
have not been done in lightning survivors. Regardless, treatment
should not be delayed until litigation is complete. Depending on
the symptomatology, some pharmacologic recommendations are
included in Table 5-4.
A mainstay of treatment is ongoing psychologist consultation
CHAPTER 5  Lightning-Related Injuries and Safety
and support.319,393,394 Therapy should be multifactorial and guided
by the individual’s symptomatology, as follows:
• For reestablishment of personal image and personal integrity
in the face of lost function
• Aids and techniques for living with memory dysfunction
• Aids and techniques for concentration and motivation
assistance
• Consideration of adapting to other limitations
• Social support
• Family and relationship counseling
• Adjunctive treatment for depression and anxiety
Treatment may also be needed to address adaptation to a new
life circumstance if the injury is severe enough that the individual
cannot return to previous employment and family situation.
Less conventional treatment methods, such as eye movement
desensitization and reprocessing (EMDR) therapy, may have a
place, but these should be performed in the hands of an expe-
rienced practitioner and tailored to the individual.
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 numer-
ous materials for survivors and their families (PO Box 1156,
Jacksonville, NC 28541-1156; Tel: 910-346-4708; http://www
.lightning-strike.org).110,111 Other useful websites are http://www
.uic.edu/labs/lightninginjury and http://www.lightningsafety
.noaa.gov.
FORENSIC INVESTIGATION
An unwitnessed lightning event can be one of the most
difficult clinical presentations to diagnose.72,148 The forensic
examination of a critical lightning event can be divided into
five stages48,261,356,391:
1. Case history
2. Scene investigation
3. Physical and/or autopsy examination
4. Special procedures
5. Collation
CASE HISTORY
If a witness is available, it is important to answer the following
questions:
• 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 person 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 person 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 person? Specifi-
cally, 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.138
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 inves-
tigating officers will be called to review the scene of a light-
ning strike. Signs of lightning strike on the scene can be subtle
or blatant.210
105
 Lightning scene investigation can be divided into the
following:
1. Environmental signs of direct lightning strike
2. Structural signs of direct lightning strike
3. 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.
• Soil may show fulgurite formation—bore or tube-like struc-
tures 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 m (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 be
advised of the incident, particularly if there is any indication
of intent to file a lawsuit by a surviving party.
Structural Signs of Direct Lightning Strike
Jandrell and associates210 described the effects of direct lightning
strike to housing structures in southern Africa.161,270,271 Figure 5-19
shows damage to the roof of a clubhouse from direct lightning
MOUNTAIN MEDICINE
strike. The damage was extensive and included structural and
internal damage (see Figure 5-20). Figure 5-21 shows damage to
curtaining material covering the window. Thatched structures
have been known to ignite following lightning strike. Thatch is
very combustible, so inhabitants are at greater risk for severe
injury and burns.161,187
Trace Evidence Signs of Direct Lightning Strike
A direct strike can be very difficult to prove. Cindering on cloth-
ing or arc marks on metallic structures may be seen. In “zincifica-
PART 1
A B
FIGURE 5-45  Simulated lightning strike applied on one dummy coated with metal and the other without.
Discharges ran from an electrode equidistant from both and hit each dummy an equal amount of times,
showing that metal does not attract lightning, including anything a person wears. (Copyright Nobu Kitigawa;
courtesy Mary Ann Cooper.)
106
tion” and “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 may 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 of a lightning victim should
be performed.
• The external examination should include a meticulous descrip-
tion of clothing and any evidence of resuscitation (Figure 5-38).
• Metal objects may have burned underlying skin or may have
been marked by the heat of electrical arcing but did not attract
the lightning strike (Figure 5-45). Figure 5-39 shows damage
to clothing and underlying burns. Figure 5-42 shows perma-
nent tattooing from a metal necklace burned into skin in a
nonfatal injury.215
• Metal objects may show signs of fusing, zincification, or cupri-
fication. 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 5-44 shows damage
to a hiking shoe with underlying damage to the skin of the
foot.26
• Determine if there has been tympanic membrane rupture.
Barotrauma, including pneumomediastinum, has been cited
as one of the injuring mechanisms of lightning.169
• Note singed or scorched hair.
• Ocular injuries, such as retinal detachment, should be deter-
mined. Cataracts may be difficult to demonstrate postmortem.
• Unique arborescent or fern-like injuries (Lichtenberg figures)
should be noted (see Figures 5-40 and 5-41).
• Determine if there are lightning wounds on the bases of the
feet—the “tiptoe” sign typically on the base of the foot.283
• The procedure for internal examination is identical to that for
any forensic autopsy.
• In female victims, ascertain if the victim was pregnant, and if
so, carefully examine the fetus macroscopically and micro-
scopically for injuries.150
SPECIAL PROCEDURES
Diagrams and Photographs
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 electro-
thermal injury patterns. Close-up and distance photographs
should be taken to document all injuries.
Radiographs
Radiographic examination may be helpful. Certain fractures, dis-
locations, and subluxations may be missed at autopsy.211 CT or
MRI might add to the body of knowledge that constitutes post-
mortem, noninvasive, and virtual analyses. Certain keraunopatho-
logic findings, such as pneumomediastinum, may be missed at
autopsy.169
Histologic Examination209,213
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
nuclei in the lower epidermis. Histologic staining of the heart
with hematoxylin and eosin may prove useful. The heart should
also be carefully examined microscopically for signs such as
“waviness” of the myofibers,211 necrosis, and contraction bands.396
Special preparation of the heart with each of Mallory, Weigert
elastic, Movat pentachrome, and acid fuchsin orange stains, as
well as immunohistochemical staining with monoclonal anti–
complement C9 antibodies, may aid the diagnosis of myofiber
breakdown, an antemortem change that may be a distinct finding
in electrothermal injury cases.143 Any neuropathologic condition
should be specifically investigated and addressed.
Toxicologic Studies
Ethanol, recreational drugs, and carbon monoxide (CO) levels
are the minimum toxicologic investigations required in lightning
cases. From a mitigating-circumstance point of view, ethanol and
recreational drugs are always important to know. CO levels will
be valuable, especially if there is a thermal component to the
injuries.
Collection of Evidence
Investigators should collect and preserve evidence or specimens,
because equivocal cases may require electrical testing of equip-
ment by an expert. Nearby damaged electrical equipment should
be sent to an electrical engineer for testing. Unwitnessed light-
ning cases are typically complex, and unusual situations may
arise occasionally. The approach to all these cases should be
multidisciplinary. Only by means of a careful forensic investiga-
tion, with strict adherence to guidelines, will the truth be revealed.
This becomes even more important in determining whether 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 experi-
ence, cognitive ability, and facts. At the end of the investigation,
investigators should collate their findings with the known physics
and effects of lightning.325
PRECAUTIONS FOR AVOIDING
CHAPTER 5  Lightning-Related Injuries and Safety
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, sport-
ing events, concerts, and similar situations. Lightning injury pre-
vention behavior should be proactive, rather than reactive, after
the threat becomes imminent. Clearly defined education is impor-
tant, in advance, 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
20 to 25 million cloud-to-ground lightning flashes in the United
States every year, and one-half have a subsequent return stroke
coming to ground at a different location up to a few kilometers
from the first stroke.367 For this reason, it is impractical for the
National Weather Service (NWS) to warn of every potentially
dangerous lightning flash, so the key to safety is individual edu-
cation and responsibility.84,250,252,384 Only one-quarter of U.S. light-
ning fatalities are associated with tornado or severe thunderstorm
warnings issued by the NWS.35 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 NWS295 at http://www.lightningsafety.noaa.gov.
Cloud-to-ground lightning data from the NLDN have shown
that lightning deaths and injuries occur in generally equal por-
tions before, during, and after the strongest lightning activity in
a thunderstorm.201,250 Weak thunderstorms are at least as likely to
result in casualties as are moderate or strong storms.193 A detailed
study by Lengyel and associates250 found that almost half of
lightning victims had enough warning to reach safety from nearby
lightning before they became a lightning casualty, so that antici-
pation would have been beneficial. A recent publication docu-
ments in detail two cases in Rocky Mountain National Park
involving low-flash-rate storms that killed people on successive
days.183
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.201,399 Development of
national lightning detection networks and availability of other
meteorologic data sets had caused major rethinking of existing
guidelines. Since 1998, most of the guidelines have been sup-
ported, 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 considered to be based on false
assumptions and have become obsolete.
LIGHTNING SAFETY PLAN†
For a person watching the sky who is prepared by being aware
of the forecast, lightning rarely appears so suddenly that precau-
tions could not have been taken to minimize the risk. Thunder-
storms take tens of minutes to develop or move into an area. A
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 people or
situations change. The National Athletic Trainers’ Association
(NATA) has recently published a full description of how to make
such decisions.384 The National Collegiate Athletic Association
(NCAA) website has a succinct version at http://www.ncaa
publications.com/productdownloads/MD10.pdf.43 A checklist for
lightning safety has been developed for large venues, stadia, and
other situations and can be accessed via a toolkit at http://
www.lightningsafety.noaa.gov/more.htm. The NWS works with
groups to tailor large-venue situations to their setting. Their Storm
*References 43, 104, 105, 117, 132, 196, 201, 251, 295, 338, 344-346, 384,
399.
†
References 43, 105, 117, 132, 201, 295, 343, 346, 344, 384, 399.
107
 Ready Program covers most outdoor storm threats and is useful
for camps and hiking programs and in planning for many other
wilderness or near-wilderness situations (http://www.nws.noaa
.gov/stormready/).296
Before working in the outdoors or going on a recreational
trip, be aware of weather forecasts and conditions. If thunder-
storms are forecast for later in the day, pay attention to updates
by using National Oceanic and Atmospheric Administration
(NOAA) weather radio, cell phone lightning 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 weather data, particularly free
ones, may be delayed by several minutes.
Thunderstorm and tornado warnings issued by the NWS indi-
cate 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 appears in less intense,
yet frequently nonsevere, thunderstorms.35
Most lightning occurs during the summer months of June,
July, and August (Figure 5-46A).188 Furthermore, most lightning
occurs between noon and 6 PM (Figure 5-46B).187 These general
figures make it much more apparent when to avoid long, risky
exposure to lightning. Storms begin before noon on some days,
particularly in locations such as over the high mountains of Colo-
MOUNTAIN MEDICINE
lightning.186,397 Summer lightning may linger into the evening in
almost all regions of the country; unfortunately, this is the time
of day when sports and recreation users are more likely to be
outdoors.43
AN APPROACHING THUNDERSTORM
Pay more attention to lightning than rain. Approximately 10% of
all cloud-to-ground lightning strikes occur without rain at the
location of the ground strike, so waiting for rain to arrive does
not provide certain protection from lightning when a thunder-
storm approaches. Thunder can be heard up to about 10 miles
away in quiet conditions, but not nearly that far in the presence
of wind or traffic, or when inside a structure.
A simple rule at the beginning of a storm is, “When thunder
roars, go indoors.”182,292,-342-344,346 This rule removes any doubt
about whether it is time to take action and is effective as a thun-
derstorm 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.43,105,132,193,264,384,399 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 interval from flash to bang is 30
seconds or less, people are in danger from lightning and should

rado, where a few flashes can occur by 10 AM on active days. In actively seek a designated safe place. This count of 30 seconds
such a location, starting hikes very early in the morning helps to indicates lightning to be no more than 10 km (6.2 miles) away,
eliminate lightning threat, while beginning a hike in late morning using the speed of the sound of thunder of 5 sec/mile. Ten
on active thunderstorm days results in increased vulnerability to kilometers (6.2 miles) includes about 80% of all subsequent

35

30
PART 1

Percent of fatalities

25

20

15

10

0
J F M A M J J A S O N D
A Month

16

14

12
Percent of fatalities

10

0
00 06 12 18 23
B Local standard time

FIGURE 5-46  A, Lightning fatalities per month from 1959 through 1994 for the United States. B, Hourly
distribution of U.S. lightning fatalities. (From Curran EB, Holle RL, López RE: Lightning casualties and
damages in the United States from 1959 to 1994, J Climate 13(19):3448-3464, 2000.)

108
cloud-to-ground lightning flashes in a storm.202 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 situations, too many warnings from a large radius
around a point may 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 downtime 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 lightning rather than 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.202,250 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.187,191
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.43,105,132,201,399 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.202 In a large-group
situation, however, where a long evacuation time is required, the
full 30 minutes is needed to avoid returning people to a field or
stadium too soon, then needing again to send them to safety 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
return to a dwelling in a matter of a few seconds if necessary.
In practice, most airports and other industrial situations use a
warning expiration time of 15 minutes, although local high levels
of safety concerns may make 30 minutes preferable. Less than a
10-minute wait time is not recommended. There are exceptions
to all rules when a large, overhead thunderstorm lingers for hours
over a location.214 In such a situation, any policy may need to
balance between efficiency and safety of outside workers.
SAFE PLACES INSIDE
There are two reliable places to be safe from lightning: inside a
large, substantial building and 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, almost always at night.187 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.292
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
CHAPTER 5  Lightning-Related Injuries and Safety
FIGURE 5-47  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.”
around people and into the ground. Contact with conducting
paths of wiring, plumbing, corded telephones, and large open-
ings, 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.
Unsafe indoor locations are small structures such as those
used as golf, beach, sun, rain, school, agricultural, or bus shel-
ters (Figure 5-47). All these structures should 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, installed, and approved by a knowledgeable,
experienced, bonded insured lightning protection specialist.229
Also on this list of unsafe structures are all tents that only pro-
vide rain protection but no barrier to lightning.190 Pads on the
ground surface inside a tent are of no value for lightning protec-
tion; composition of the tent structure and poles provides no
protection.
In less developed countries, dwellings and workplaces may
be thatched-roofed huts that provide no protection from lightning
because they are often ungrounded and made with nonconduct-
ing material.187 Note that it is possible to provide low-cost light-
ning 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 using internationally accepted, scientifically based
standards to ensure their efficacy.240
Vehicles191,214,292,399
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 the cases;
the majority said the experience was frightening, but they
emerged unscathed. There have been no documented “electrical”
injuries to occupants, with the exception of those involving direct
wiring, such as from older handheld police radios.191 The only
unambiguous fatality was an older adult who was startled or
incapacitated by a nearby flash and drove into oncoming traffic.
Damage to vehicles ranged from minor, such as antennas vapor-
izing, to a few cases of major engine failure and electrical fires;
nevertheless, all passengers escaped the vehicles.
Unsafe vehicles are those without the safety of fully enclosed
metal surroundings that would otherwise act in a manner con-
sistent with a Faraday cage.99 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
109
 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 include those with cloth tops (convert-
ibles) or fiberglass or plastic bodies. Others include golf carts
and four-wheeled conveyances with open sides. Strikes to such
vehicles have no defined path to ground, and it is not safe for
people to be inside them. Although it is possible to design light-
ning protection for unsafe golf carts and other open-sided vehi-
cles, there is no such commercially available product; such an
approach requires a specific configuration and correct behavior
of people inside them.119
Any place outside such a vehicle is as unsafe as anywhere
else outside.191 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 in
parking lots, waiting for buses, and law enforcement and other
people near but not inside disabled vehicles.
A fully enclosed, metal-topped vehicle can be used as a safe
place at a school or sports event. If flashes will strike the ground
MOUNTAIN MEDICINE
at such a venue, it is an easy choice to be inside such a vehicle
rather than outside at the same location.
ALWAYS UNSAFE OUTSIDE281
There are no reliable places outside to be safe from lightning.
Almost complete safety can be achieved by being inside a large,
safe building or a fully enclosed, metal-topped vehicle, as
described in the previous two sections. Some recommendations
continue to emphasize the speculative and ultimately unsuccess-
ful safety approaches outside, at the expense of noting the reli-
able safety that is often present in more developed countries in
PART 1
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. As described earlier, it
is estimated that only about 3% to 5% of lightning injuries and
deaths are caused by direct strikes. The result of this mistaken
direct-strike approach is the recommendation that lowering one’s
height is sufficient to be safe, rather than recognizing the other,
more likely mechanisms and using 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 build-
ings and vehicles. 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 a safe
building or vehicle is located and how long it will take to reach
that location, and complete the plan by reaching safety before
lightning arrives.
Lightning is not predictable in its path to ground, and exactly
what it strikes is not predictable with any certainty. Case reports
have indicated that the prior speculative 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 branches reach the surface appears to be random within
the flash.354
Roeder342 examined the relative value of common advice on
outdoor lightning avoidance according to the five mechanisms
of lightning injury (see Specific Strike Mechanisms, earlier). It
was found that if every precaution were to be followed, and
some are quite difficult, only a 50% reduction in risk would be
achieved. The other 50% of the time would result in an injury
or fatality. As mentioned, one of the least effective approaches
110
is to stress the direct strike by lowering one’s height, because
the direct-strike situation is scarce.
The Difficulty of Wilderness Situations
No action will achieve certain safety from lightning in the wilder-
ness away from a substantial building or fully enclosed, metal-
topped 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 a day or less, often on a weekend day.190 For
this common situation, the first approach of avoiding the risk is
most manageable, since a vehicle or sometimes a sufficiently
large building is likely to be 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
western United States, for example, storms start as early as 10 or
11 AM local time, 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 necessarily preclude hiking on
most days; a study over Colorado’s Rocky Mountains271 showed
that no location had lightning on more than one-third of summer
days, and almost none during spring and fall months.194,258 There-
fore, hikers can manage the risk by choosing the time and place
of a day hike. Once the hike is underway, they should pay atten-
tion to evolving cloud formations that indicate future lightning,
stop the hike or climb, and return to safety when indicated (see
An Approaching Thunderstorm and End of Thunderstorm,
earlier).
The pressure of a schedule or other factors may be such that
a wilderness activity will take place despite the possibility of a
very real lightning threat. Thus, a hiker or climber has accepted
the personal risk in the same manner as risks from dangerous
animals, falls, or other natural hazards. Roeder342 analyzed the
relative risk when no acceptable buildings or vehicles are nearby.
The five mechanisms of lightning injury discussed earlier help to
identify actions that can 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 the
full lightning exposure. In other words, following all precautions
does not prevent half the lightning risk. Because the steps must
be performed correctly, remembered under duress, and reduce
the risk for death or injury by only one-half, they are not to be
considered when lightning safety can be readily attained by
entering a safe building or vehicle.
SAFETY OF LARGE GROUPS
An individual can respond to lightning threat quickly by going
inside a large, substantial building or fully enclosed, metal-
topped vehicle. In less than a minute in the backyard of a dwell-
ing, for example, quick action places the person in safety. When
the threat is over, using a rule such as 15 minutes for the cessa-
tion 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 passes.
For larger crowds, all these steps are more difficult. Steps
include accepting that lightning threat is important, knowing how
to identify lightning threat, where safe locations are located and
how long it will take to reach them, recognizing when the threat
is over, and who makes important decisions.43,105,117,201,258,264,295,384
In the case of a neighborhood youth soccer game, for example,
safety can be reached in minutes inside nearby fully enclosed,
metal-topped vehicles. When game officials or others make the
decision to go to safety, players and spectators need to go imme-
diately 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 commonly located in
parking lots around the field (see Buildings section of Safe Places
Inside, earlier). 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 be available to open doors when
players and spectators need to get inside in a hurry.
When the crowd is large at a sporting or other outdoor event,
the situation becomes more complex. Advance planning is essen-
tial. 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 thun-
derstorm threat may be more acceptable. In the United States,
the lightning threat at collegiate football games was examined
by Gratz and Noble,162 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. Holle and Krider196 present a case study of an individual
game’s response to the lightning threat. Edwards and Lemon132
emphasized the potential for major storm-related disruptions at
auto, dog, and horse races; professional and collegiate sporting
events; and outdoor concerts, examining situations such as close
calls of tornadoes passing near large crowds. However, their
warnings have often been met with silence, skepticism, or limited
positive responses.
There are now lightning safety recommendations for schools
and U.S. athletic programs from the NCAA and NATA.43,378 Nearly
all institutions follow these recommendations, so it has become
common for all types of U.S. collegiate sporting events, as well
as many professional sporting events, to be delayed, suspended,
or canceled. This wisdom has spread worldwide such that light-
ning safety policies are now followed globally in athletic events,
at least to some degree. There have been almost no lightning
casualties over the last decade 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 and NATA 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,
proven, and accurate cloud-to-ground lightning data are available
on cell phones, websites, and other portable devices that objec-
tively measure the presence of lightning. Any purchaser or user
of these devices should be certain that lightning data are real
time. Rules need to be established for behavioral triggers 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 approach-
ing lightning for action to be taken. The rule needs to be fol-
lowed objectively on days when the threat exists. Programs may
choose to use the checklist for lightning safety that has been
developed for large venues, stadia, and other situations by invok-
ing a toolkit at http://www.lightningsafety.noaa.gov/more.htm.
The NWS has worked with many groups to tailor large-venue
lightning safety to their settings.
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 impres-
sion 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.196 At
other locations, a nearby gymnasium or school building 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, so warning horns or
message boards may be the best approach. Informing people
waiting in diverse locations involves complete and active plan-
ning 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
CHAPTER 5  Lightning-Related Injuries and Safety
safety information in event programs may also be useful in com-
municating safety information.
The “all clear” at the end of the lightning threat needs to be
identified as objectively as is the warning at the beginning (see
End of Thunderstorm, earlier). As crowds become larger, a longer
wait time until 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 well be needed to avoid 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
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.15 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 infra-
structure. This approach has long been used for space vehicles
and other critical activities and structures. There are great 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 loca-
tions 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 pos-
sible for the crowd and media (Figure 5-48).
Lightning Protection in Situ15
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. It is emphasized
that the following examples are illustrative only, and proper
design is needed when these are being implemented.
Figure 5-49 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 5-48A shows the “natural” protected zone around a
temporary stand that might form an evacuation region if other
risks are accepted. Franklin rods added along the back of the
stand extend this zone and also add some in situ protection
(Figure 5-48B). 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 (Figure 5-48C).
These can be made almost unnoticeable, especially to media
cameras. Alternatively, they can carry banners, lights, or media
cameras.
Figure 5-50 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 5-51 shows a stadium for a field game (e.g., baseball),
where an existing stand provides some protection, as do light-
ning pylons. The addition of overhead wires can complete the
coverage.
Figure 5-52 shows the main stadium stylistically and how open
stands at either end of the stadium can be protected by fine
wires, which are all but invisible.
CONTROVERSIES AND ONGOING
RESEARCH IN LIGHTNING INJURY92,95
Much remains to be learned about lightning injury, and knowl-
edge at present remains partial. Specific areas of controversy,
111
 A
B
MOUNTAIN MEDICINE
C
FIGURE 5-48  A, Natural protection zone of a stand. B, The effect of
Franklin rods disguised as flagpoles. C, The added effect of a catenary
PART 1
added to a stand. (Redrawn from Crowd protection strategies: Experi-
ence from the Sydney Olympic Games, 2000. Presented at Interna-
tional Conference on Lightning and Static Electricity, Blackpool, UK,
2003.)
FIGURE 5-50  Use of catenaries to protect several stands. (Redrawn
from Crowd protection strategies: Experience from the Sydney
Olympic Games, 2000. Presented at International Conference on Light-
ning and Static Electricity, Blackpool, UK, 2003.)
112
FIGURE 5-49  Protected zones on a pathway from light poles of
varying height. (Redrawn from Crowd protection strategies: Experi-
ence from the Sydney Olympic Games, 2000. Presented at Interna-
tional Conference on Lightning and Static Electricity, Blackpool, UK,
2003.)
Covered
stand
FIGURE 5-51  Effect of existing covered stands and lighting stan-
chions. (Redrawn from Crowd protection strategies: Experience from
the Sydney Olympic Games, 2000. Presented at International Confer-
ence on Lightning and Static Electricity, Blackpool, UK, 2003.)
Covered stand
Open stand Open stand
Open field—overhead is a network
of cables along which cameras
travel—providing adequate protection.
Covered stand
FIGURE 5-52  Open field—a properly installed network of overhead
cables that can double for movable 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.)
limitations of present research, and currently debated features
point the way for future research.
There are presently two major thrusts in keraunomedicine,13
the interaction of lightning with humans and their protection: (1)
the interaction between electric current and humans—the patho-
physiologic changes that are induced and how they underlie
lightning injury symptomatology—and (2) the protection of indi-
viduals and crowds from lightning injury. Lightning experts note
the significant reduction in strikes and morbidity/mortality as
good indices of success in this area. An entirely uninvestigated
area is whether there are ways to mitigate the process of injury
once it has occurred so that common sequelae can be avoided.
PROBLEMS WITH EXPERT REPORTING92,98
At regular stages, medicolegal reporting, including to workers’
compensation entities, is required for documentation and evalu-
ation of an injury.
Totality of the Injury
Rarely is there a report on the totality of an electrical or lightning
injury. Most reports focus only on the section of an injury that
is in a particular medical specialist’s realm. The orthopedic
aspects are often reported by an orthopedic surgeon as if the
injury was the result of simple trauma rather than a complex
electrical injury. Similarly, neurologists may report on neurologic
aspects, rarely giving a view of the entire injury complex. They
may take their knowledge from neurologic trauma coupled with
misguided assumptions about neural vulnerability. There are
three consequences:
1. There is seldom expert assessment of the physical/engineering
aspects of the injury.
2. There is little perception of the total injury complex and its
nuances.
3. There is an assumption, often erroneous, as to the precise
physical aspects of the injury.
Recent vascular research308 has demonstrated the importance
of vascular damage in contrast to more commonly assumed
neural damage. Current passage through body fluid (blood and
CSF) is important and is much more supportable in theoretical
terms than is neural transmission. In addition, release of humoral
factors may well affect brain functions, with the cortisol-HPA
(hypothalamic-pituitary-adrenal) axis particularly implicated (see
next).
Presumption of Site of Injury
Electrical injuries are uncommon and lightning injuries rare in
most practices. Unless the physician has a special interest in
them, they will usually make up only a tiny part of any physi-
cian’s work. Because of unfamiliarity with the overall picture,
physicians, both general practitioners and specialists, will often
and quite naturally default to diagnostic tests with which they
are familiar. Unfortunately, these tests and assumptions about the
site of injury may not apply to the sequelae experienced by the
survivor.17
It can be frustrating to the patient, family, and physician and
devastating in disability cases when a physician reports, “None
of the testing I ordered showed damage,” or, “All of the patient’s
tests are normal.” Unfortunately, although the physician is saying,
“The tests are normal,” the patient, family and courts often hear,
‘There is nothing wrong,” rather than that the wrong tests may
have been ordered.
For example, nerve conduction studies (NCS) test only the
largest nerve trunks, but do not test pain pathways, which usually
contribute a large component of the lightning injury survivor’s
complaint. Fatigue, weakness, and sensory disturbances may be
mediated by neural end-plate damage or sensory terminal
damage, neither of which is detected by NCS. Functional deficits
that may be readily apparent by history, talking with the family,
neuropsychological testing, or other functional testing are not
detected by anatomic tests, such as CT and MRI. Unfortunately,
testing for damage to finer nerves and end plates, using func-
tional MRI and other tests applicable to a survivor’s symptoms,
may not have been undertaken for technical, monetary, or other
reasons. This does not mean the symptoms are imagined, only
CHAPTER 5  Lightning-Related Injuries and Safety
that appropriate diagnostic testing is not available at this time.
Advancing knowledge may shed light on various new modalities
to test, such as hippocampal size.241
Limits to Reporting
Physicians may be more comfortable with or may be constrained
to use codes (e.g., DSM) for existing and known diagnoses. This
may lead to diagnoses of PTSD, adjustment disorder, and depres-
sion because they are secondary to the uncoded overall syn-
drome, which is more correctly a post–electric shock syndrome.
These diagnoses only describe a portion of what the patient may
be experiencing. It is not surprising that an electrical event should
give rise to a trauma response or to difficulty adjusting to new
limitations, brain injury, or chronic pain, but this is not the total
picture. Unfortunately, psychiatric or psychological diagnoses
may distract from recognition and treatment of underlying organic
damage.
RESEARCH METHODOLOGY PROBLEMS
Cooper92,95 highlights further features of what is not yet known
about lightning injury, documenting methodology difficulties.
Without knowledge of the basic physiology of the injury, only
general symptomatic aftercare can be rendered, instead of more
specific treatments and early interventions that might stop or
change the course of the injury cascade precipitated by the initial
injury. Therefore, medical treatment is frequently empirical and
based on symptomatology. Treatment of depressive symptoms is
particularly important and should not be delayed until more exact
pathophysiology is determined.
Bias in Research
Research on lightning injuries is difficult (Box 5-5). No public
health regulations require reporting, so cases are difficult to
collect and survivors difficult to locate in any systematic
manner.67,198,273
Although it may be convenient to target certain populations,
such as members of LSESSI, as study participants, people who
join support groups differ from those who do not. They represent
a subset of survivors who may have systematic biases developed
from the services and materials that LSESSI supplies to its
members.92,95,254 In addition, only limited research can be done
with this group because of ethical limitations on human research,
national dispersion, and lack of funding for research, among
other difficulties.
BOX 5-5  Research Problems
Human Research
Recruitment of cases
Study biases
Dispersion of participants
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, etc.
Requires specialized techniques
Bioengineering, collaboration
Expensive
113
 To separate lightning electrical effects from other etiologies,
it is necessary to obtain relatively recently injured patients (no
more than 6 to 12 months) with an otherwise uncomplicated
history. There should be no past history of alcohol or drug abuse,
head injury, psychiatric problems, or concurrent medical prob-
lems that cause neuropathic pain or psychiatric symptoms, and
no blast effect during the injury that would confound investiga-
tion of the traumatic effects of lightning. Unfortunately, this
narrows the available participant pool.
Experimental Vehicles
Because it is difficult to recruit volunteers, credible animal work
is a reasonable alternative.12,14,208,226,301 Cooper and colleagues107-109
have developed a reasonable rat model that demonstrates most
of the clinical signs seen in humans. Unfortunately, such research
is expensive, time-consuming, and sometimes requires large
numbers of animals to show significant differences. Most prob-
lematic is the delivery of a “standardized dose” of simulated
lightning that can reliably reproduce a specific (“standard”)
pattern of injury.
Equipment Requirements
Many hurdles must be overcome in research equipment design,
anesthetic choice, animal care, and shock timing and delivery.
Monitoring equipment must be electrically isolated from the
animal and shocking platform, or the connections may preferen-
MOUNTAIN MEDICINE
tially transmit the lightning shock to the equipment, not the
animal, clouding the experiment and destroying the equipment.
Some anesthetics are neuroprotective, and 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 either to target or to avoid the “vulnerable
period” must be done on a statistically predictive basis, because
direct sensing of the specific targeted cardiac cycle would result
in damage to the equipment.
PART 1
Survival Statistics
Box 5-6 lists factors concerning the unknown issues as to why
the vast majority of lightning casualties survive.67 Characteristics
of a lightning strike or possibly the mechanism by which the
current impinges on the individual may be different for lightning
fatalities. Timing of the lightning strike may be the important
factor, particularly if it hits during a more vulnerable portion of
the cardiac cycle. Although possible, it is unlikely that the physi-
cal characteristics of people differ sufficiently to cause a differ-
ence in mortality. A more likely explanation is that many strikes
may not meet thresholds (see IEC advances in next section) in
particular cases.
Remote and Psychological Symptoms
A further area of active research is the etiologic origin of symp-
toms not directly in the line of passage of current.20 This includes
industrial electrical injuries as well.278 Even when there is no
indication of current near the brain or evidence of blast/blunt
injury, patient histories and neuropsychological tests consistently
suggest an organic origin to the deficits.17
BOX 5-6  Why Do 70% to 90% of Lightning Strike
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)
114
BOX 5-7  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
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 and difficult to measure.
Some note that the neuropsychological constellation resem-
bles the psychological effects of other syndromes, such as trau-
matic brain injury and the response to autoimmune disorders. It
is possible that the symptom complex represents a “final common
pathway” of brain injury from many etiologies.17 Box 5-7 lists
other possible factors yet to be verified.
Andrews20,21 and Reisner330,331 have specifically developed
cogent theories of the psychological injury. To be credible, these
theories need to explain several facets, including the constellation
of symptoms, its organicity, symptoms developing over time with
some being time-lagged, and the specific underlying organicity
localizing the injury.
Both theories are similar. Although some current will pass
through the brain in any shock, it will often be minute. It is
probable that a chemical generated in the current pathway will
affect the brain; a likely substance is cortisol. The interaction
between cortisol as a cytotoxic, brain-derived neurotrophic factor
and recognition that the hippocampus is one of only two sites
in the brain capable of cellular regeneration are noted parts of
one theory.21 Insights from the theory of depression implicate the
hippocampus as a site of cell loss,51,116,310,352,361,362,382 which is sup-
ported by both PTSD and psychiatric depression research.310 The
same cell loss occurs in industrial electrical injury.241 Also, a
substance yet to be identified is released from vascular epithe-
lium with an electric shock, which can act at substantial distance
on other epithelia.308 The site in the hippocampus and limbic
systems creates a good localization for the symptoms. Reisner’s
theory331 is similar but implicates oxidative free radicals as a
mediating influence. Research in this area is supported by
advances in imaging technology provided by high-field MRI
scanning.
Technical Matters
The degree of lightning injury, or “dose,” varies considerably with
the mechanisms of injury (e.g., direct, splash, contact).16 Thresh-
olds are being quantified more accurately by the International
Electrotechnical Commission (IEC) for short-duration pulses.205
Other technical factors regarding interaction of a lightning stroke
with the body, such as the effect of multiple return strokes and
any “capacitive memory,” are poorly known. Although flashover
occurs, the amount and path of energy going through victims
versus around them and the duration of energy flow initially or
with return strokes are known only by implication.16 The degree
that flashover electricity can induce opposite charge, damage, or
arrhythmias inside the body is unknown. Although these factors
have been calculated based on engineering assumptions, actual
measurements remain to be done. Finite-element modeling may
offer the best alternative.
The IEC205 recently discussed extension of pulse safety in two
areas. It is now believed that with present knowledge, safety
standards can be extended to cover the safety of lightning pulse
widths from about 1 to10 milliseconds down to 1 microsecond.
This development is paralleled by extension of waveform fre-
quency standards up to approximately 150 kHz, which is relevant
to lightning circumstances and the cell membrane filter time
constant.151
Knowledge of conduction mechanisms at shorter pulse
widths and higher frequencies draws on tissue conduction dis-
persions, as well as known conduction and membrane excita-
tion properties.
Electroporation
In terms of the damaging influences of current on tissue, certain
matters remain to be investigated. Lee246 has corroborated elec-
troporation of muscle cell walls with high-voltage electrical injury
that generates high internal electric fields. Applicability of elec-
troporation to lightning injury has not been established.88,92,246
Sites of Injury in the Body
Microscopic studies are needed to examine actual fine loci of
injury within the body. For example, what might be the effect
on motor end plates and the neuromuscular junction? Does this
underlie the symptoms of muscular weakness and fatigue? It is
unknown if the findings of Koshima and associates233 are as
applicable to lightning injury as to high-voltage injury.
Predictability of Lightning and Forecasting
Researchers are able to describe the characteristics of lightning,
how it forms, and how it acts. Wide variability in atmospheric
conditions gives rise to equally intense lightning events, and it
must always be remembered that lightning is stochastic when its
parameters are quantified. Modeling of lightning behavior must
have this probabilistic nature in mind, particularly where protec-
tion is involved.139,154,324,325
Lightning Danger Warnings
In the United States, NWS is charged with providing severe-
weather warnings to minimize property and personal injury. One
of the difficulties in forecasting is the compromise between
absolute safety that results from issuing many warnings that may
later turn out to be “false” and lesser guarantees of safety with
fewer but more reliable warnings. People learn not to pay atten-
tion when too many warnings prove false. An additional com-
plication is that because of the small areas where thunderstorm
cells arise, it is impossible for regional forecasts to cover all of
them. Individuals should be aware of the general weather fore-
casts and incorporate their own knowledge of local weather
patterns, along with an eye and ear to the sky, when fast-
changing weather is predicted, to notice rapid development of
nearby storms that may contain dangerous lightning. Preplan-
ning, alertness, and knowing the lightning safety rules, such as
“When thunder roars, go indoors,” and “No place outside is safe
when thunderstorms are in the area,” can save lives.
LIGHTNING EXPOSURE AND SAFETY BEHAVIOR
Unfortunately, some risks have no halfway measures that will
significantly improve safety. Lightning is one of those. Currently,
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. Responsible outdoor behavior
involves always having an escape route to safety in mind. Avoid-
ance 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 life, 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 (summer afternoons) can minimize but
cannot 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 containers are used in many countries in indus-
trial, heavy construction and mining sites and are moved as
needed by truck or helicopter (Figure 5-53). Discarded containers
CHAPTER 5  Lightning-Related Injuries and Safety
Window with metal screen 2.0 X 0.25 meters
0.40 meters
Canopies
FIGURE 5-53  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.)
are sometimes adapted to become open stalls in public markets.
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 carries 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
purists about altering the environment for what may not be per-
ceived as a likely or major risk.
LIGHTNING SAFETY RESEARCH
There are 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 difficult to identify. Although the phenomenon of light-
ning has become better understood in the last two decades, many
features of how lightning results in fatalities and injuries remain
elusive. In addition, more examination is needed to determine if
there are differences in the injury pattern between developing
and developed countries.
The mechanisms of lightning injury have been categorized
more completely than ever before, and identifying this mixture
of mechanisms has made a difference in lightning safety advice.
Most importantly, the common perception of a direct strike is
now thought to represent only 5% or less of lightning injury.
However, the estimates of Cooper95 and others are based on
subjective experience of researchers studying large numbers of
cases, showing the need to better identify the ratio of mecha-
nisms causing lightning injury. Distribution of injuries between
the five types may be different in developing countries but has
not been investigated. It appears that fires originating in thatched
dwellings and other structures are quite common in developing
countries, so that confusion and paralysis of people inside may
hinder them from escaping in time; this is not an issue inside
substantial structures of the more developed world. The issue of
the upward leader with regard to human injury needs more
study. Postevent recognition of streamer shock (vs. EPR) needs
particular attention, although it is difficult to see how these will
be differentiated.
Roeder339 provides a set of questions and comments on
research needed to improve lightning safety. The requirements
can be divided into several main groups: safety of buildings and
vehicles, determining the range of safe distance from lightning,
and demographics.
Building and Vehicle Safety
Lightning safety recommendations now state that safety is
reached inside large, well-constructed buildings with plumbing
115
 and electrical wiring in the walls, or within fully enclosed, metal-
topped vehicles.* Although fatalities in these locations are rare
in developed countries, multiple injuries per incident continue
to occur in developing countries, where there may be no sub-
stantial buildings or metal vehicles for miles in any direction.
Small structures are always problematic, so recommendations
stress staying away from them, although it is possible to make
them safe in certain situations.229 A related question is the
degree of interruption of the lightning strike by metal meshwork
as opposed to the solid conductive sheeting that makes a
Faraday cage.
The amount of time people spend outdoors is a key factor.
People may now spend more of their time inside safe buildings
and vehicles than in the past. Although social data are extremely
difficult to quantify, knowing the answers may explain a portion
of the steady decrease in lightning fatality rates in developed
countries studied in recent years.189,198
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 a likely contributor to the higher lightning
fatally rate in such regions compared with more developed
countries.189
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
MOUNTAIN MEDICINE
compiled.112,194 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.122 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.202
How long a lead time to seek safety is needed for the general
public, at airports, sports events, and other locations? The lead
time includes identifying the safe places that are nearby and the
time 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
PART 1
lightning exposure in exchange for economic efficiency.
The role of cloud lightning in the warning process is also not
fully understood. Does an overhead flash without a cloud-to-
ground flash demand the same response? What are the safe
distances to anvil lightning? With development of total lightning
detection, it is becoming possible to address these questions in
a more systematic way.123
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
audibility of thunder is not well understood from the practical
viewpoint of lightning safety. The issues involved are the normal
distance that thunder can be heard, effect of nearby noise on
that distance, role of cloud lightning in producing thunder to its
use in warnings, transmission velocity of thunder, and relation-
ship of hearing thunder to the actual lightning threat.339
Demographics
Lightning fatality and injury rates are quite well known in devel-
oped countries. The global impact of lightning, however, is not
well investigated. 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.333
Global lightning impacts were first estimated by Holle and
López197 to be 24,000 deaths and 240,000 injuries annually 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. Another estimate is 6000 deaths and 60,000 injuries
per year globally.59 Local organizations examining lightning are
being established.
*References 43, 105, 117, 119, 120, 187, 201, 264, 292, 384.
116
Availability of safe versus unsafe buildings and vehicles is
important in understanding 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.339 Such information can 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 very low frequency (VLF) and low fre-
quency (LF) range that propagate along the earth are used to
detect and locate return strokes in cloud-to-ground flashes. Such
sensors can also locate distant lightning in the VLF range because
signals propagate thousands of kilometers between the Earth and
ionosphere.113
The U.S. National Lightning Detection Network 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 bench-
mark for cloud-to-ground lightning detection; typical distances
between its sensors are 300 to 350 km (180 to 210 miles). 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%.45,113,145 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 cloud-
to-ground flash are also located by the NLDN, and half of cloud
flashes contain pulses that are strong enough to be detected and
located.113
Direction finding and time-of-arrival methods have been com-
bined into an advanced method that allows global coverage to
detect lightning over extremely long distances.121 The Global
Lightning Dataset GLD360 achieves 70% cloud-to-ground flash
detection efficiency with a horizontal location accuracy of 2 to
5 km (1.2 to 3.1 miles). Several lightning detection satellites make
twice-daily or regional passes; the new GOES-R lightning sensor
scheduled for launch in 2016 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 mapped by regional very high
frequency (VHF) networks that use direction finding and/or time-
of-arrival techniques over line-of-sight distances.122,185,235-237,257
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 does the NLDN, because they use line-of-sight
detection in the VHF range. Some of the cloud flashes seen by
these networks are immense and have major implications for
lightning safety. One cloud flash in Texas was measured to have
a continuous horizontal channel measuring more than 300 km
(180 miles) in length and lasting 5.7 seconds.244
Continued deployment of 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 differ-
ing demands for lightning information.113
APPLICATIONS
The first operational U.S. lightning detection network was de­
veloped for early recognition of lightning-caused fires. Eventu-
ally, 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 distribu-
tion systems in lightning-prone areas. As a result, this was the
other early application of such wide-area networks.113 In these
situations, each flash or stroke is carefully identified as the cause,
for example, of a power-line fault on a transmission or distribu-
tion line. 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.113
A very broad array of applications of lightning detection data
has developed over the last three decades. There are more than
3000 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 catego-
ries: those of the direct threat from lightning, and lightning as an
indicator, substitute, or covariate.
Direct Threat from Lightning
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 shipping and navigation. However, linkage of
lightning network data with human casualties is only occasionally
made; such studies show a tendency in many recreational situa-
tions to involve weak storms with short lifetimes.183,184,202,214,250
Indicator Lightning
Climatologies of lightning have been developed over a variety
of regions and time periods.194 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 thunder-
storms and associated impacts are most likely. Lightning clima-
tologies have been found to be easier to compile than many
other data sets, such as radar reflectivity and satellite data, since
VLF and LF lightning detection is unaffected by terrain, and the
data sets are relatively compact for long periods and large areas.
In remote regions where conventional radar and surface
observations are not available, tracking thunderstorms and assess-
ing tropical and nontropical cyclone status are important chal-
lenges 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 long-
range lightning data has indicated presence of sporadic cloud-
to-ground lightning in the inner cores of tropical cyclones that
may be useful for assessing their intensity changes.
Meteorologists use lightning data in many other ways to indi-
cate 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; location of frontal boundaries; and when excessively
CHAPTER 5  Lightning-Related Injuries and Safety
high lightning rates are occurring in a thunderstorm that may
indicate significant weather of many types. Isolated versus orga-
nized thunderstorms can sometimes be assessed better with
lightning data than with radar and satellite information. Lightning
data can also be used to indicate location and timing of a devel-
oping low-pressure region over the oceans, as well as presence
of very cold air aloft. In addition, some winter storms have dis-
tinct bands of ice and snow that include lightning where the
heaviest precipitation is falling.
Substitute Lightning
In many situations, such as over oceans and less developed
countries, desired meteorologic data are not available to identify
situations that might 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. Similarly, meteorologic radar information is
lacking in mountainous areas of the United States below moun-
taintops because the radar beam is blocked, so lightning can be
used to identify thunderstorms in rugged terrain. Rainfall can be
estimated with lightning information in regions, times, or areas
where 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 Lightning
When radar, satellite, and surface data are available, real-time
lightning detection data can be used to identify trends that occur
simultaneously with, 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 assimilation of lightning network information into
numeric weather prediction models to help initialize them by
better locating convection.
There is 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
degrade from terrain effects. Changes of cloud-to-ground light-
ning polarity and rate changes, as well as ratios of cloud to
cloud-to-ground lightning, are topics that require large, accurate,
and complex data sets and statistical analyses over multiple
regions. They hold promise for many applications.
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117
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117.e7
PART 2

Cold and Heat

 CHAPTER 6 
Thermoregulation
NISHA CHARKOUDIAN AND LARRY I. CRAWSHAW
A warm body has long been recognized as one of the primary
conditions of human 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 operat­
ing 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 compli­
cated 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 rela­
tionships among the ambient thermal environment, thermal char­
acteristics of the body, and physiologic systems that govern
human thermoregulation. First, some overall concepts of tem­
perature regulation are reviewed, as well as a way to conceptual­
ize the system. Second, the range of normal body temperatures
is covered, along with the consequences of higher and lower
body temperatures. Third, methods and potential pitfalls of moni­
toring body temperature are outlined, after which the physical
factors that affect heat flow are discussed. Fourth, the neuronal
systems involved in processing thermal information (i.e., sensa­
tion, integration, and output) are reviewed, followed by a detailed
description of the effector organ responses involved in the main­
tenance of thermal homeostasis. Last, modifications of ther­
moregulatory responses, induced alterations of the regulated
temperature, and changes in the responsiveness as well as in the
capabilities of the thermoregulatory system are noted. In this
chapter, 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 maintain­
ing 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 physiologic (autonomic) pro­
cesses such as dilation of the skin blood vessels, sweating in the
heat, and shivering in the cold. Figure 6-1 provides an overview
of this process.38 Information about body temperature is inte­
grated by central nervous system (CNS) structures, which elicit
efferent neurogenic responses to correct any changes. Increases
in body temperature elicit efferent neurogenic cutaneous vaso­
dilation and sweating to increase heat dissipation. Conversely,
decreases in body temperature elicit cutaneous vasoconstric-
tion (decreased heat dissipation) and shivering (increased heat
generation).
Figure 6-2 emphasizes how these responses are controlled—
via negative feedback systems with a primary feed-forward input
from skin sensors that monitor ambient temperature.106 The feed-
forward input from the skin allows for the elicitation of thermo­
regulatory responses without an “error signal” from the primary
regulated variable, core body temperature.148 Thus, core tem­
perature can remain relatively constant under widely varying
environmental conditions. This is particularly helpful in cold
environments, where decreases in skin temperature can elicit
120
substantial vasoconstriction and shivering before dangerous core
hypothermia develops. In addition, without this feed-forward
input, when large thermal stresses are encountered, greater devi­
ations in core temperature would be necessary to elicit sufficient
restorative responses.
Figure 6-3 illustrates some of the concepts that relate to the
thermoregulatory system and are discussed in this chapter. Under
normal conditions, body temperature is relatively constant over
a range of ambient temperatures, as 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 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 compro­
mised, which leads to decreases in the ability to defend against
low temperatures (dashed line at “d”). This could indicate a
problem with metabolic stores, or high temperatures (dashed line
at “e”), which may indicate dehydration. 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 esti­
mate of the temperature of critical internal organs and are quite
stable across individuals. In a study that involved 700 observa­
tions of 148 healthy individuals,131 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 thermoregulatory system. At low environmental tempera­
tures, regional heterothermy that results from peripheral vaso­
constriction 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 tempera­
tures at various locations within the core. However, because of
decreased temperatures in the outer shell, a nude person resting
at 20° C will have a total heat content that is about 200 kilocalo­
ries (kcal) lower than when resting at 35° C.197 If the peripheral
vessels were suddenly dilated, an immediate drop in core tem­
perature of about 3.5° C (6.3° F) would result. Because of local
and systemic influences of temperature on skin blood flow, this
type of extensive vasodilation can happen in a wilderness
medicine setting if a hypothermic individual is rapidly rewarmed
using surface rewarming methods. In a hypothermic individual,
the discrepancy between core and shell temperatures could
be considerably greater and could result in a dangerous postdila­
tion drop in core temperature. Such an extensive vasodilation
would also result in a large drop in peripheral vascular resistance,
which would put the individual at risk for dangerous hypoten­
sion. Therefore, such methods should be used with caution
while carefully monitoring a patient’s vital signs. A method for

(−) ↑ Heat dissipation
↑ Internal temperature
Cutaneous vasodilation
↑ Skin temperature
Sweating
A of conditions can lead to core hyperthermia or hypothermia.
CNS
POAH
↓ Heat dissipation
↓ Internal temperature (−) Cutaneous vasoconstriction
↓ Skin temperature ↑ Heat generation
Shivering
B side effects of prescription drugs, or other factors. When inter­
FIGURE 6-1  Schematic overview of the integrative control of thermo-
regulation in humans. As shown at A, an increase in internal and/or
skin temperature is relayed by neural signals to the central nervous
system (CNS) nuclei involved in thermoregulation (primarily the preop-
tic area/anterior hypothalamus, POAH). This then elicits efferent 
neurogenic cutaneous vasodilation and sweating, which increases 
heat dissipation, minimizing further increases in body temperature. As
shown at B, a decrease in internal and/or skin temperature is sensed
by the CNS and results in increased cutaneous vasoconstriction
(decreased heat dissipation) and shivering (increased heat generation).
(From Charkoudian N: Skin blood flow in adult human thermoregula-
tion: How it works, when it does not, and why, Mayo Clin Proc 78:603-
612, 2003.)
Disturbance (Ta)
Sensor
Feed-forward
signal
Regulated
Controlled
Controller variable
system
(Effectors) (Tcore)
(Body mass)
Sensor
Feedback signal
FIGURE 6-2  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.)
estimation of the potential drop in core temperature after periph­
eral vessel dilation is given in Estimating Mean Body Tempera­
ture, later.
A different type of heterothermy that occurs during hyperther­
mia in some species is known as “selective brain cooling.” The
idea is that, during severe heat stress, brain temperature can be
maintained lower than the rest of body core temperature, thus
protecting the brain from potential neuronal damage from
excessively high temperatures. This phenomenon clearly exists
in mammals with a carotid rete, where countercurrent heat
exchange can cool the blood, which will then perfuse the brain.138
Although humans do not possess a carotid rete, alternative mech­
anisms have been proposed as a basis for selective brain cooling.
Existence of this phenomenon in humans has been vigorously
debated for decades.19,29,30,157,232 Recent, direct measurements of
jugular venous temperature and calculations of thermal gradients
in the areas perfusing the brain suggest that selective brain
cooling is not a physiologically relevant phenomenon in humans
during exercise or hyperthermic exposure,158 although it may
occur under certain, specialized “man-made” conditions, such as
CHAPTER 6  Thermoregulation
during surgery.14
Although an abnormal core temperature is often a signal that
“something is wrong,” it is not a very specific signal. A variety
Under some circumstances, the central neural mechanisms that
regulate body temperature may be defending an altered core
temperature for reasons described later in this chapter. Alterna­
tively, the thermal load posed by the environment or by heavy
exercise may be too great for the capacity of the thermoregula­
tory effectors to dissipate heat. This is generally referred to as
“uncompensable heat stress,” whereas heat exposure in which
body temperature can be regulated is referred to as “compen­
sable.” Finally, CNS control of body temperature could be
deranged as a result of substance abuse, extreme temperatures,
preting a particular core temperature, it is important to evaluate
all these alternatives. Accidents in the wilderness often involve
many aspects of thermal balance being compromised, and an
altered body temperature is 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. This effect is characterized by an exponential equa­
tion, and for ease of comparison between different sensitivities
to temperature change, the term Q10 is typically used. Q10
describes the factor by which a rate increases with a 10° C (18° F)
increase in temperature. For example, with a 10° C (18° F) increase
in tissue 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
equation197:
R 2 = R 1 × Q10 ( [ T2 − T1 ] 10 )
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. Thus, if fever
or strenuous exercise were to increase body temperature by 2° C
(3.6° F), basal metabolic rate would be increased by 22%.
°C °F
39 (102)
b
Core temperature
38 (100)
a
37 (98)
d e
36 (96) c
35 (95)
Ambient temperature
FIGURE 6-3  Stylized diagram representing body temperature at dif-
ferent ambient temperatures. The relatively flat portion of the three
traces a, b, and c represents the range of normothermia. Trace a rep-
resents 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 evi-
dence for how the system works, Eur J Appl Physiol 109:5, 2010.)
121
 Within the normal range of body temperatures, higher tem­
peratures 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 com­
plications in many wilderness medical situations and therefore
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.
Core hypothermia can also be dangerous to human survival
and recovery from injury. Core temperatures of 34° to 36° C (93.2°
to 96.9° F) disrupt many important physiologic functions, which,
taken together, may significantly affect patient outcome. Such
mild hypothermia impairs recovery from surgical procedures as
a result of factors that include 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.59,70,118,123 In most situations, it is important to
maintain the patient at normothermic levels.
Traumatic brain injury can be present in wilderness accidents,
and it may be accompanied by unregulated hyperthermia.
Heightened temperatures can exacerbate cerebral inflammation
and lead to increased neuronal damage.224 There is current inter­
est in invoking mild hypothermia to minimize damage to the CNS
COLD AND HEAT
after neurologic injury.162 However, when this approach is used,
care must be taken to deal with the side effects mentioned
previously.171
MONITORING TEMPERATURE OF THE
CORE AND OTHER SITES
The overall status of the thermoregulatory system is determined
PART 2
by measuring the core temperature. This can be done at a
number of sites with several types of instruments (i.e., thermom­
eters). In the following paragraphs, the relative merits of locations
and different types of thermometers are discussed.
MONITORING THE CORE TEMPERATURE
A history of clinical thermometry is available,130 as are good
overviews of the assessment of core temperature.12,36,245 Sites for
measuring body 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. What­
ever 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.
TYPES OF THERMOMETERS
The handheld electronic thermometer has replaced the mercury-
in-glass thermometer, and it has been widely used for many
years. Electronic thermometers can use thermistors or thermo­
couples as sensors, have the requisite degree of accuracy, and
are 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 have a range low enough to
122
monitor skin temperature in cold environments. A second elec­
tronic thermometer with a wide temperature range is important
for measuring skin temperature, as a backup for the standard
clinical thermometer, and for measuring the temperature of other
objects such as liquids. Alternate probes and spare batteries for
both instruments are essential.
Tympanic infrared (IR) radiometers are often used in hospital
settings. However, even in this relatively predictable environ­
ment, some controversy exists regarding their ability to assess
core temperature accurately.160,179 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 advan­
tage is that the reading takes only a few seconds,36 but questions
remain regarding the overall accuracy of the measurement dis­
played. 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, IR tympanic thermometry
provides an excellent estimate of the core temperature.203 In
clinical settings, the results are less consistent. In one study, IR
tympanic thermometry produced core temperatures that were
much more variable than rectal temperatures. Even after correct­
ing for the higher rectal values (0.5° C [0.9° F]), tympanic measure­
ments 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.170
In one instance, a child who arrived at an emergency depart­
ment (ED) presented with tachycardia and skin vasoconstriction.
Separate tympanic IR 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)182. Alternatively, in a hospital
setting with a trained operator and immobile patients, two brands
of IR tympanic thermometers produced readings that were closer
to pulmonary artery readings than those obtained from the axilla
or the rectum.178
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.12,130 Because these
measurements are compromised by the thermoregulatory vascu­
lar changes associated with heat conservation and heat dissipa­
tion and by changes in ambient temperature,95 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 repre­
sents 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 prox­
imity to other locations that have differing rates of metabolism
and perfusion. Nevertheless, because of the generally high
overall rates of tissue perfusion in mammals, deep core tem­
peratures rarely differ by more than 0.5° C (0.9° F). The tempera­
ture 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. When carefully measured in a
surgical or laboratory setting by trained personnel, esophageal
and tympanic temperatures are essentially the same as the tem­
perature of the pulmonary artery,178,193 whereas rectal tempera­
ture averages about 0.4° C (0.7° F) lower, and axillary and oral
temperatures are about 0.2° C (0.4° F) and 0.4° C (0.7° F) lower,
respectively.12,178
Although esophageal temperature is somewhat difficult to
obtain, this is the site that is most likely to reflect accurately the
temperature of the pulmonary artery. Measurement at this loca­
tion accurately follows changes in core temperature and is rea­
sonably 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 proce­
dure is routinely used in physiology experiments, it is somewhat
unpleasant for conscious patients, particularly those with a
strong gag reflex, and clearly inappropriate if airway problems
are present. 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,
many studies have indicated that tympanic temperature is affected
by ambient temperature and local facial cooling.193,223
In steady-state conditions, rectal temperature is a good index
of core temperature.248 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.178 There is a thermal gradient
along the rectum, so all measurements should be made at a
standard depth; 4 cm (1.6 inches) is recommended,12 although
in a careful study of different depths, sites less deep than 10 cm
(4 inches) showed some systematic differences.121 The higher
temperatures recorded in this region may be caused by a com­
bination of low perfusion rates, digestive reactions, and bacterial
activity, but there is not clear evidence of this.130 For assessing
core temperature during outdoor exercise in the heat, the
National Athletic Trainers’ Association recommends using only
rectal temperature.33 A subsequent study and review of the litera­
ture also concluded that “rectal temperature is the only suitable
and valid index for the monitoring of body temperature in a field
setting.”73
Oral (sublingual) temperature is an excellent index of core
temperature, provided that the mouth is kept closed. The sub­
lingual 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 tempera­
ture; these should be avoided during the period that immediately
precedes the measurement.12,130 The use of an electronic ther­
mometer with a rapidly responding sensor makes this measure­
ment considerably more accurate and rapid than when it is
performed with a mercury-in-glass thermometer.
Although axillary temperature can reflect core temperature, it
has a number of negative characteristics and should be used only
as a last resort. Axillary temperature is affected by local blood
flow as well as by thermal and nonthermal sweating.12 Changes
in core temperature are slow to affect the axillary temperature,
and there is high interpatient variability.178 However, this mea­
surement has proved to be particularly useful for assessing core
temperature in infants.12,130
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 tem­
perature and core temperature. Recently, the validity of such
estimates was evaluated for patients undergoing various proce­
dures, including cardiac surgery during extracorporeal circula­
tion; these studies included core temperatures as low as 18.5° C
(65.3° F).122 “Peripheral compartment temperatures were esti­
mated using fourth-order regression and integration over volume
from 18 intramuscular needle thermocouples, 9 skin tempera­
tures, and ‘deep’ hand and foot temperatures.”122 The authors
concluded that the estimation of MBT from Burton’s original
formula27 “is generally accurate and precise.”122 That formula is
as follows:
MBT = 0.64 ( Core temperature ) + 0.36 ( Mean skin temperature )
Ramanathan174 found that a 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
CHAPTER 6  Thermoregulation
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.49,85,142,151,197 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 equa­
tion. 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 con­
ductive 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 MBT will fall. Alternatively, if Htot
is greater than the net heat exchange, heat content of the body
will increase, and MBT 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 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 convec­
tion. Adequate insulation should be placed under patients who
are in contact with hot or cold substrates. The equation that
governs heat exchange by conduction follows:
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.143
The thermal conductivity of several substances is given in
Table 6-1. Note that water has 25 times the conductivity of air
TABLE 6-1  Thermal Characteristics of Select Substances
Conductivity Specific Volumetric
(cal • s−1• Heat (cal • Heat Capacity
Substance cm−1 • °C−1) g−1 • °C−1) (cal • L−1 • °C−1)
Air 0.000057 0.24 0.29
Water 0.0014 1.0 1000
Granite 0.007 0.2 540
Muscle tissue 0.0011 0.8 850
Fat tissue 0.00051 0.5 460
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.
123
 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 heat of various substances is
also given in Table 6-1. Water has particularly high specific heat,
as does muscle tissue, which consists mostly of water. However,
specific heats can be misleading, so volumetric heat capacities
are also listed in Table 6-1. 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 a person in the water, the consequence of
these properties is that skin temperature is almost always within
1° C of water temperature, and heat transfer to or from the envi­
ronment is greatly facilitated. In cool water during rest, skin
blood flow is minimized as a result of peripheral vasoconstric­
tion. 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 shiver­
ing at about 33° C (91° F).153
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
COLD AND HEAT
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 pro­
duced 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 predomi­
nates at air speeds of less than 0.2 m/sec (0.7 ft/sec), whereas
forced convection is more important at greater air speeds.142
PART 2
The relationships that define heat exchange as a result of
convection can be complicated. They depend on surface tem­
perature profiles, surface shape, flow dynamics, density, conduc­
tivity, and specific heat. Any factor that impedes the movement
of the boundary layer (i.e., the molecules immediately adjacent
to the body) greatly impairs convective heat transfer.
Brengelmann and Brown20 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 IR 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 radia­
tion. 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 IR (first-term)
radiation and solar (second-term) radiation is given by the fol­
lowing equation:
H r = σe sk e a ( Tsk 4 − Ta 4 ) + a(1 + r )s
where Hr is the radiative heat exchange; σ 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 kelvins [K]); Ta is the ambient temperature (given in K); a is
the absorptance; r is the reflectance; and s is the solar radiation.
124
For temperatures in the physiologic range and where (Tsk − Ta)
is less than 20° C (68.0° F), several authors have noted that IR
radiation heat exchange is about proportional to Tsk − Ta.18,197
Also, the spectrum of emitted radiation depends on the tempera­
ture of the object. At physiologic temperatures, the predominant
wavelengths of emitted radiation are longer (IR), whereas at
higher temperatures (e.g., 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 con­
sequences. The middle IR radiation that is emitted by mammals
is maximal, regardless of skin pigmentation or the color of cloth­
ing. 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 environ­
mental 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 can be a significant net loss of radia­
tion to the sky. Under the relatively thermoneutral conditions
noted earlier,20 radiant heat loss accounts for about 45% of the
total heat loss.
EVAPORATIVE HEAT EXCHANGE
When water changes state, a large amount of energy is either
absorbed or given off. Evaporation of 1 gram (0.035 oz) of water
at 35° C (95.0° F), which is the usual skin temperature of a person
who is sweating,197 requires the input of 0.58 kcal of thermal
energy. In the field the preferred cooling measure is to splash
water on the patient, coupled with air fanning.81 Heat absorbed
by the evaporation of 100 cc of water will lower body tempera­
ture by about 1° C (1.8° F). In a neutral thermal environment,
active thermoregulatory sweating does not occur, and evapora­
tion accounts for only 15% of the total heat loss. Of this, slightly
more than one-half is the result of evaporation from the respira­
tory tract, with the remainder coming from water that passively
diffuses through the skin and evaporates.20
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 patient’s
body is considerably colder than 43° C, water condenses in the
airways. For every gram (g) of liquid water that is formed, the
body heat content increases by 0.58 kcal; the formation of 100 g
of liquid will increase body temperature by about 1° C.
THERMOREGULATORY NETWORK
A regulatory system requires sensing the controlled variable,
comparing it with an ideal value, and producing an appropriate
output signal. The following sections outline the role of the
nervous system in maintenance of a stable body temperature.
PERIPHERAL THERMAL SENSORS
The entire outer surface of the body (i.e., the skin) is well sup­
plied with sensitive thermoreceptive structures. Because one
destination of the output of these thermoreceptors 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 the cutaneous thermoreceptors
demonstrate substantial dynamic sensitivity.9,88 Therefore, a
change in ambient temperature can be perceived as “cool” or
“warm” simply because of a change from a previous steady level
of temperature (e.g., moving from a warm room to a cooler
room), even if the absolute temperature is not objectively “cool.”9
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 pathways that synapse in the
reticular area.24 Although cortical thermal input is part of the
sensory information used to reconstruct the external thermal
 CHAPTER 6  Thermoregulation
40

°C
30

A
Shield Shield 1 sec

40

°C
30

Shield Shield
B
W C W C
Thermocouple

Cold spot Shield

Warm spot A B
Nose

FIGURE 6-4  Impulses from a recording that includes a single warm fiber and a single cold fiber. A, In this
recording, a shield was periodically placed in front of and then moved away from the skin site that was
innervated by the warm fiber. The discharge stops immediately when the skin is shielded from the radiation
source. B, In this recording, the shield was simultaneously placed in front of the skin site innervated by
both the warm fiber and the cold fiber. This caused excitation of the cold fiber and inhibition of the warm
fiber. (From Hensel H, Kenshalo DR: Warm receptors in the nasal region of cats, J Physiol [Lond] 204:99,
1969.)

environment, reticular input is more important for behavioral and
autonomic regulation of body temperature.55
The structure, location, and properties of peripheral thermo­
receptors are well documented. Thermal sensors are free nerve
endings and are categorized as warm or cold. Cold receptors are
found immediately beneath the epidermis, whereas warm recep­
tors are located slightly deeper in the dermis. The hallmark of
both types of receptors is their extremely high rate sensitivity
(Figure 6-4). 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 acti­
vate neuronal responses that are subjectively reported as “cold
pain” and “warm pain.”87
Over the past two decades, work with the use of cloning and
ion channel characterization has provided insight into molecular
mechanisms of central and peripheral temperature transduction.
A family of related temperature-activated transient receptor
potential (TRP) ion channels is highly sensitive to temperature.35
Although originally identified in the context of noxious heat
sensation, TRP channels have been found to be ubiquitous and
have multiple roles in cardiovascular, metabolic, volume regula­
tory, and many other integrative physiologic mechanisms.61,246
In terms of thermal sensation, the cloned receptors TRPV3
and TRPV4 respond over a range similar to that of the warm
receptors previously described,80 whereas TRPM8 responds simi­
larly to the cool receptors. TRPM8 also responds to menthol,
eucalyptol, and icillin.136,169 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 hot peppers.167 In human skin circulation, the TRPV
receptors appear to be involved in local thermal vasodilation
(below the pain threshold), because stimulation of these recep­
tors with local application of capsaicin shifts thermal responsive­
ness of the local cutaneous vasodilator response.214 However,
neurogenic vasodilation in response to whole-body heating does
not appear to be affected by acute or chronic local capsaicin
treatment.39 TRP channels are also involved in activation of
brown adipose tissue thermogenesis during cold exposure, and
as such have been proposed as a target for weight loss with
capsaicin or capsaicin derivatives.243 As examples of the ubiqui­
tous, integrative nature of TRP superfamily, TRPM2, TRPM4, and
TRPM5 respond to warm temperatures and are also involved in
insulin secretion226 and taste.220 However, they are not regarded
as warm receptors for thermal sensation, because sensory neurons
do not appear to express those subtypes. In addition to TRP
channels, some members of the TREK/TRAAK K(2P) potassium
channel subfamily also appear to be involved in warmth and
cold perception.7,125,155
Psychophysical and physiologic studies indicate that thermal
receptors are not uniformly distributed across the body surface
and that there are many more cold receptors.87 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 receptors that respond
to warmth.176,219 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 because of a high density of thermal
receptors, whereas by comparison the extremities have a lower
density of receptors and therefore poor sensitivity. Other regions
of the body are intermediate in sensitivity.217
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 restor­
ative 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 cooling the lower
leg.53 Another study evaluated regional trunk and appendage

125
 sensitivity to cooling by assessing the magnitude of the gasping
response that occurs at the onset of immersion.26 In this case, A B C mV
exposing various parts of the body to water at 15° C (59.0° F) 0
indicated that the upper torso had the greatest cold receptor
density or sensitivity (or both). The lower torso was somewhat 32° C –40
less sensitive, with the arms and legs exhibiting similar but con­
–80
siderably lower sensitivity.
0
CENTRAL THERMAL SENSORS 36° C –40
Many sites within the body are capable of eliciting generalized
–80
thermoregulatory responses. Such areas include the abdominal
viscera, spinal cord, hypothalamus, and lower portions of the 0
brainstem.16,85 The specific mechanisms by which heating or
cooling these areas elicits thermoregulatory responses are incom­ 39° C –40
pletely understood. Although some central nuclei contain neurons –80
that are clearly temperature sensitive,15,17 responses in other 400 ms
areas may result from modulation of synaptic connections rather
than from stimulation of neurons that change their firing rate FIGURE 6-5  Effects of temperature on the activity of three different
in response to temperature. Input from central, temperature- types of hypothalamic neurons. A, Low-slope temperature-insensitive
sensitive neurons is not rate sensitive; rather, it is a direct reflec­ neuron. B, Moderate-slope temperature-insensitive neuron. C, Warm-
tion of the absolute temperature.15,17 The area that has the highest sensitive neuron. The thermosensitivity in each case was 0.06 (A), 0.5
thermal sensitivity and has received the most experimental atten­ (B), and 1.1 impulses s−1• °C−1 (C). All three types of neurons displayed
tion is the preoptic area/anterior hypothalamus (POAH). Heating depolarizing prepotentials, and action potentials occurred when the
or cooling this portion of the brainstem elicits the entire array of prepotentials reached threshold. As exemplified in C, putative post-
autonomic and behavioral heat loss and heat gain responses, synaptic potentials (especially inhibitory ones) were often observed in
respectively.84 Neurons in this portion of the brain exhibit both all neuronal types. (From Griffin JD, Kaple ML, Chow AR, et al: Cellular
mechanisms for neuronal thermosensitivity in the rat hypothalamus,
warm sensitivity and cold sensitivity.15,16 Data from hypothalamic
J Physiol 492:231, 1996.)
slice preparations with the use of synaptic blockers indicate that
COLD AND HEAT

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.15,16,57
Figure 6-5 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
PART 2
stimuli, such as osmotic pressure, glucose concentration, and
steroid hormone concentration.205 Such neurons could form the
basis for the interactions between the homeostatic systems
described later in this chapter.
Figure 6-6 illustrates the response of a warm-sensitive POAH
neuron in a slice preparation. This cell is excited by increased

on hyperpolarizing (K+) conductances.79 Work involving the use temperature, low glucose, or increased osmotic pressure.17
of hypothalamic slices has also established that about one-half Because TRPV protein expression has been detected in the
of the thermosensitive neurons also respond to nonthermal POAH, it was proposed that the TRPV channels may underlie the

Glu Osm P
25

20
Imp/sec

15

10
5
0

42
Temp (° C)

37

32

0 5 10 15 20 25
Time (min)

FIGURE 6-6  Response of a warm-sensitive preoptic nucleus–anterior hypothalamic area neuron to changes
in temperature, glucose concentration, and osmotic pressure. Downward arrows indicate media changes.
(From Boulant JA, Silva NL: Neuronal sensitivities in preoptic tissue slices: Interactions among homeostatic
systems, Brain Res Bull 20:871, 1988.)

126
thermosensitivity found in POAH neurons,167 and that both TRPV1 anatomic, and imaging techniques have been used to extend our

and TRPV2 channels may be active within the physiologic range
of temperature.109,172 However, some evidence is contrary to the
proposal of TRPV1 as a thermosensor.181
CENTRAL NEURAL STRUCTURES RESPONSIBLE
FOR CONTROLLING THE LEVEL OF
BODY TEMPERATURE
As mentioned previously, the brain is capable of accurately
regulating body temperature under a wide range of conditions.
Although almost all portions of the CNS can potentially be
involved, the most critical neuroanatomic structures for thermo­
regulation include the spinal cord, brainstem, hypothalamus, and
septum. The preoptic area and anterior hypothalamus are par­
ticularly important for both integration and sensing of internal
temperature.15,17,84 Recent advances in neurophysiologic, neuro­
CHAPTER 6  Thermoregulation
understanding of the systems involved in regulation of body
temperature.139,140,244 In this context, the median preoptic nucleus,
medullary raphe region, and dorsomedial hypothalamus have
been identified as important areas for integration of thermo­
regulatory signals with cardiovascular, volume regulatory, and
other related physiologic systems.134,137,148 Other notable advances
include demonstration of the relative independence of popula­
tions of neurons that control separate effector systems107,135,247 and
elucidation of a pathway that conveys cold-sensitive afferent
(feed-forward) information to the hypothalamus.149
Figure 6-7 presents a schematic model for regulation of body
temperature, with credit to many others in the field besides the
authors listed. For ease of understanding, many aspects of the
system’s complexity have been simplified or modified. The mul­
tiple inputs to this system not shown include those mentioned
in the previous discussion of central thermoreceptors (e.g.,

Dorsomedial Cerebral cortex

hypothalamus Sensory integration and
Preoptic area/ localization of peripheral
anterior ac GABA thermal information
hypothalamus G +
L
+
U −
G Thalamocortical Learned behavioral
A
B
− − − relay responses—
A integrate cortical, limbic,
oc and brainstem information

Midbrain
Lateral Reward system activated
parabrachial + + when thermal deficit
nucleus GLU decreased

Postural reflexes
Rostral ventro– − Sprawl
medial medulla
G + G
L A Huddle
Rostral raphé U B +
A
pallidus To final autonomic
organization and
output
Collateral Sweat
fibers Vasodilation
ascending to
midbrain Increase metabolic
heat production
Vasoconstriction
Dorsal horn– To
spinal column + +
thalamus
Input from
cutaneous
temperature Cold
receptors Heat loss
skin Warm
skin Cold defense

+
Effector
output

0 0 0
35 37 39 35 37 39 35 37 39
Cold environment Core temperature (° C) Warm environment
Neutral environment
FIGURE 6-7  Simplified schematic diagram of the basic parts of the nervous system responsible for regulat-
ing internal body temperature. Details of how this system functions are given in the text. ac, Anterior
commissure; GLU, glutaminergic synapse; GABA, GABAergic synapse (GABA, γ-aminobutyric acid); 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.)

127
 glucose concentration, osmotic pressure) as well as factors
covered later in this chapter (e.g., time of day, hormone levels,
pyrogen titer, oxygen concentration of blood). In addition, ther­
moreceptors from many locations in the body provide input to
this system. The key sensing elements of Figure 6-7 involve the
peripheral warm and cold receptors and the central thermodetec­
tors, the latter depicted by solid cell bodies and bold axons.
Peripheral input originates in the skin and enters the CNS 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 infor­
mation. 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.149 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
on which they synapse. The systems that subserve heat loss and
cold defense appear to inhibit each other reciprocally 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 6-7, 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
COLD AND HEAT
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 6-7. The middle graph illustrates the situation for a person
with a body temperature of 37° C (98.6° F) in a thermoneutral
environment. At 37° C, 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
PART 2
cold defense or the heat loss system. The graph on the left illus­
trates 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 envi­
ronment; this situation is depicted in the right graph. 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 main­
tain 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 ther­
moregulatory system. Postural reflexes (e.g., huddling, sprawling)
and learned behavioral thermoregulatory responses are initiated
by cold and warm error signals. Although the mechanism is
not entirely 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 by cell bodies located in the ventral midbrain.96
EFFECTOR RESPONSES
VASCULAR ADJUSTMENTS
Cardiovascular responses to thermal stress are largely geared
toward changing blood flow to the skin surface, thereby increas­
ing or decreasing convective heat transfer to the skin and to the
external environment, as appropriate for the internal and external
thermal environments.20,37,38,101 In general terms, an important
function of the circulatory system is to maintain a relatively
homogeneous internal body temperature. Heat from metaboli­
128
cally active organs is convectively distributed to portions of the
body where less heat is produced. More frequently 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. Fat has about one-half the tissue conductivity of muscle
and typically has a much lower rate of blood perfusion. Never­
theless, shunting blood away from major portions of the body is
at least as important for determining overall conductivity as 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.60 Thus, directing blood away
from poorly insulated (and more highly conductive) regions
reduces heat loss and preserves core temperature.
The cutaneous microcirculation is the primary circulation
responsible for controlling heat transfer to the environment.37,38,101
Microcirculatory units contain capillaries, arterioles, venules,
metarterioles, and arteriovenous anastomoses (AVAs). The skin
has a compliant vascular bed, with the majority of cutaneous
blood volume contained in a plexus of veins just under the
surface. The slow linear velocity of flow in this venous plexus
allows for substantial heat transfer to occur between the skin and
environment, particularly when skin blood flow is elevated.186
The major systemic neural control of skin blood flow occurs
through two branches of the sympathetic nervous system: nor­
adrenergic vasoconstrictor nerves and a non-noradrenergic active
vasodilator system.37,101 The vasoconstrictor system exhibits tonic
activity and is responsible for most of the smaller, daily changes
in skin blood flow that occur during minor changes in environ­
ment or activity.194 This system is also responsible for the dramatic
decreases in skin blood flow that occur with cold exposure, when
skin blood flow can approach zero. Vasoconstrictor nerves
release norepinephrine, which interacts primarily on the vascular
smooth muscle with α1- and α2-adrenergic receptors to cause
vasoconstriction. Glabrous skin (i.e., palms, lips, soles) contains
numerous AVAs and is innervated only by sympathetic vasocon­
strictor fibers. Therefore, all the dramatic changes in skin blood
flow that can occur in these regions are controlled by changes
in vasoconstrictor neural activity.
Nonglabrous (i.e., hairy) skin is innervated by sympathetic
vasoconstrictor and vasodilator fibers and contains few AVAs.
In contrast to the vasoconstrictor system, the active vasodilator
system in human skin does not exhibit tonic activity and is only
activated during increases in internal temperature. The vasodila­
tor system operates through cholinergic nerve co-transmission.
Although several candidate vasodilators have been studied, the
specific vasodilator substance has not been identified; vasoactive
intestinal polypeptide is a likely candidate.8,235 Additionally, nitric
oxide has an important role in active vasodilation, contributing
about 30% to the total neurogenic vasodilation seen during
whole-body heat stress.111,112 Active vasodilation accounts for 80%
to 90% of the increases in skin blood flow during heat stress,
with about 10% to 20% caused by withdrawal of tonic activity
of vasoconstrictor nerves.101 Thermoregulatory vasodilation can
result in skin blood flow values up to 8 L/min and 60% of cardiac
output, making the skin circulation extremely relevant to systemic
hemodynamics, particularly during severe heat stress.37,186
Cutaneous vascular responses to temperature are affected by
excessive exposure to ultraviolet B (UVB) radiation. Moderate
sunburn impairs the vasoconstrictor response to cold; an associ­
ated uncontrolled increase in thermal conduction is still present
1 week after exposure, although the original erythema will have
disappeared.164
CENTRAL SIGNAL
Vascular changes are bioenergetically the least costly thermo­
regulatory 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, or the
“neutral zone” of human temperature regulation.194 In dogs,
manipulation of hypothalamic temperature in this range confirms
a high level of vasomotor activity between the thresholds for
the activation of panting and shivering.86 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.21,194
Although most peripheral arterioles are well supplied with
adrenergic receptors, thermoregulatory innervation is not homo­
geneously distributed. For example, the density of thermosensory
innervation in the lips, ears, and distal extremities is higher than
in other areas; immersing the feet in cold water thus leads to
marked vasoconstriction in the hands and forearms, but not in
the abdomen or upper arms.78
LOCAL MODULATION
In addition to systemic (whole-body) stimuli that elicit cutaneous
vasoconstriction and vasodilation through changes in whole-
body temperature, local temperature of the skin can substantially
change skin blood flow through local mechanisms that do not
require intact neural input.101 Local warming of the skin elicits
substantial, rapid vasodilation and can cause maximal vasodila­
tion when temperature is held at 42° to 44° C for 25 to 30
minutes. This local warming response occurs in two phases: an
initial peak that occurs within the first few minutes of heating
and that depends on local sensory innervation, and a slower,
prolonged phase that reaches a plateau at 25 to 30 minutes. The
plateau phase of vasodilation largely depends on nitric oxide
(40% to 70%, depending on the population studied).37,101
Local cooling can decrease superficial cutaneous blood flow
to almost zero.38,101 Although vascular beds on the skin surface
constrict in response to cooling, other vascular beds dilate when
cooled.66,67 The specific response to cold shown by cutaneous
vessels follows from the observed distribution and properties of
the α-adrenergic vascular receptors. Local temperature affects the
α2- and α1-adrenergic 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.46,67
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.62,67
The responsiveness of cutaneous blood vessels is diminished
in people with type 2 diabetes mellitus, both in terms of local
responses to temperature and responses to whole-body heat­
ing,208,209 resulting in impaired ability to thermoregulate in the
heat. The increased incidence of type 2 diabetes among the
general population may therefore presage a greater number of
patients exhibiting severe hyperthermia.38
EVAPORATIVE COOLING
At high workloads and at environmental temperatures approach­
ing 37° C (98.6° F), the only way to maintain thermal balance is
to augment evaporative cooling by activating the eccrine sweat
glands. This sympathetic, 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 sustainably produce as much as 1 to 2 L of sweat per hour.2
High rates of sweating occur on the forehead, neck, anterior and
posterior portions of the trunk, and dorsal surfaces of the hands
and forearms. Lower rates occur on the medial femoral regions,
lateral trunk areas, and palms and soles.151 Sweat is secreted in
these latter two areas in response to a combination of stimuli,
including both nonthermal (emotional, exercise) and thermal
inputs.20,187 Because sweating is cholinergically mediated, it can
be completely abolished by atropine. Sweat gland activity inter­
acts 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.78,128 Several
reviews discuss the many aspects of sweating disorders.44,128,213,229
CENTRAL SIGNAL
CHAPTER 6  Thermoregulation
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 each degree increase above thermoneutral values, internal
temperature is about 10 times as important as mean skin tem­
perature for eliciting an output to the sweat glands.144,146
LOCAL MODULATION
Local effects are also important for determining the output of
sweat glands. Sweat gland 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.145
Moderate sunburn disrupts evaporative cooling. This effect is
locally mediated and involves decreases in both responsiveness
and capacity of the sweat glands.163
METABOLIC ADJUSTMENTS
Heat is an inevitable byproduct of the inefficiencies of the body’s
metabolic reactions. When oxidizing foodstuffs to carbon dioxide
and water during production and transport of adenosine triphos­
phate (ATP) to the functional systems of the cells, about 75% of
the original chemical potential energy is given off as heat. With
the exception of chemical energy sources that are excreted or
used to perform physical work, the remaining 25% of the original
energy is also converted to heat when ATP is used in the numer­
ous metabolic reactions of the body.198 Mammals, compared with
poikilotherms such as reptiles or fish, use much more ATP to
maintain ionic and electrochemical balances of the cells,216 as
well as for other necessary functions. This leads to greatly
increased metabolic heat production (relative to poikilotherms),
which forms the basis of 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
continually 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 nonshiv­
ering responses. Shivering is muscular contraction for the spe­
cific purpose of producing heat, consisting of simultaneous
rhythmic excitation of agonistic and antagonistic skeletal muscles.
Under normal circumstances, carbohydrate oxidation provides
the major substrate for shivering. In glycogen-depleted individu­
als, shivering levels are maintained by the greatly increased
oxidation of lipid and protein reserves.83 Nonshivering heat pro­
duction (or nonshivering thermogenesis) is associated with the
presence of uncoupling protein 1 (UCP-1) in brown adipose
tissue and is under strong sympathetic neural regulation in
humans and other species.139,140 UCP-1 is a transmembrane
protein 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 energy released during substrate oxidation
is not conserved as ATP, heat is generated. Although brown
adipose tissue was previously believed to be of little importance
in adult humans, recent research has indicated the presence
and physiologic significance of active brown adipose tissue in
adults.56,139,140,189
Hormonal responses contribute importantly to increases in
metabolism with cold exposure. Evidence shows that both epi­
nephrine and thyroid hormones are released in humans exposed
to cold environments.69,211 Both these hormones augment overall
tissue metabolism. Circulating epinephrine and norepinephrine
are increased as part of the overall sympathoexcitatory response
to body cooling. These hormones interact with β-adrenergic
receptors on brown adipose tissue and in skeletal muscle to
increase mitochondrial uncoupling, thereby increasing nonshiv­
ering thermogenesis.233,234
129
 Thyroid hormone acts by both accelerating ATP turnover
and reducing efficiency of ATP synthesis, contributing about
30% of resting metabolic heat production.204 Thyroid hormone
levels are ultimately controlled by thyrotropin-releasing hor­
mone (TRH), which is synthesized and released in the paraven­
tricular nucleus of the hypothalamus (PVN). Cold exposure
increases biosynthesis, processing, and release of TRH through
α- and β-adrenergic mechanisms, and a subsequent increase in
thyroid hormone levels appears to increase thermogenesis in
part through binding to thyroid hormone receptors on brown
adipose tissue.65
Basal metabolic rate (BMR), when calculated on a weight-
specific basis, decreases with body size. This relationship holds
within as well as across species. BMR relates to size according
to the following equation.197
 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 documenta­
tion is available for this response, and most models of the ther­
moregulatory 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
COLD AND HEAT
act as a proportional controller, and that skin temperature
provides a feed-forward input to the system.84,100 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).240
Evidence indicates that humans have a control system similar
to that of medium-sized mammals such as dogs or wolves. In a
PART 2
summary of their data and of that collected previously, Hong and
Nadel92 noted that the central output for shivering is augmented
by an 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 suppres­
sion on the shivering response, possibly as a consequence of an
increased arousal response.92
LOCAL MODULATION
Although the central and local effects of decreased core tempera­
ture 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 with severe hypothermia (~30° C [86.0° F] core tempera­
ture), the shivering response is lost altogether.20 This decrement
likely involves impaired transmission of neural signals, because
the muscles themselves are quite responsive below this tempera­
ture. For example, in vitro studies show that limb muscles and
diaphragm muscles develop peak tensions that are not greatly
affected by temperatures as low as 25° C (77.1° F), and fatigue
resistance is considerably increased at 25° C.173,199 Likewise, alter­
ing the local skin and superficial muscle temperature of the
anterior thigh through a range of temperatures between 12° and
40° C (53.6° and 104.0° F) for 30 minutes had minimal effect on
subsequent isometric peak torque production during isometric
knee extensions to exhaustion.225 Additionally, time to fatigue
was longer at the coolest temperature.
BEHAVIORAL ADJUSTMENTS
In most wilderness situations, a variety of ambient temperatures
is available, and external insulation is easily adjusted. Under
130
these conditions (particularly in cold environments), the choice
of thermal microenvironment and clothing provides a much
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.52 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 autonomic augmentation of conduc­
tive, convective, evaporative, and radiative heat losses.
Cabanac28 found that internal body temperature determined
whether a particular surface temperature was perceived as pleas­
ant or unpleasant. When individuals 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 persons. An overall sensation of “ther­
mal 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; participants had no problem correctly iden­
tifying the actual peripheral temperature. This study also con­
firmed the intimate relationship between the thermoregulatory
network and the pleasure-pain system.165
CENTRAL SIGNAL
Compared with the knowledge about autonomic thermoregula­
tion, we know little about the neural mechanisms that underlie
behavioral thermoregulation. As noted in previous sections, the
POAH plays a key role in autonomic thermoregulation. It is also
important for behavioral thermoregulation, because local heating
and cooling of this area lead to the appropriate behavioral
response.31,190 Although animals with lesions of the POAH are
severely compromised in their ability to use autonomic thermo­
regulatory effectors, their ability behaviorally to thermoregulate
is relatively intact.32,191 These results indicate that the preoptic
area is not as crucial for behavioral thermoregulatory processes
as for autonomic processes. Alternatively, lesions of the lateral
hypothalamus, which is involved in various reward systems,
result in the loss of behavioral thermoregulation.192
Recent studies involving positron emission tomography (PET)
and functional magnetic resonance imaging (fMRI) have demon­
strated that temperature signals from the body surface reach the
insular cortex.50,93,161 However, insular activation correlates with
the discrimination between hot and cold rather than with thermal
pleasure, so this system is likely minimally involved with behav­
ioral thermoregulatory processes. Also, thermal pleasantness is
clearly important for behavioral thermoregulation. In other stud­
ies involving fMRI, 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.107,180
Because behavioral processes are usually activated by feed-
forward signals before body core temperature changes, signals
from the skin are clearly important. In a study involving persons
who were given the choice of moving between 8° C (46° F) and
46° C (115° F), behavior (i.e., moving between environments) was
the primary method of thermoregulation.196 Physiologic (auto­
nomic) responses occurred but were minimal and secondary to
choice of environment. Furthermore, skin temperature was the
primary driver of these behavioral choices, because core tem­
perature changes were minimal throughout the study.196 Although
feed-forward information from the skin appears to predominate
in this type of behavioral thermoregulation, severe deviations in
core temperature disrupt ability of feed-forward information to
contribute to appropriate behavioral responses. When this occurs,
the person no longer feels too hot or too cold, and the desire
to take corrective action is lost.
Regional differences exist in the contribution of the body
surface to thermal comfort.150 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 people
preferentially to 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 tem­
perature regulation probably originate with disruption of central
control mechanisms. Skeletal muscle function is fairly resistant to
impairment by thermal mechanisms, as described previously. If
this occurs, however, 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
many conditions that affect both the regulated temperature and
effectiveness of the thermoregulatory system.
NORMAL VARIATIONS IN REGULATED
TEMPERATURE AND ABILITY TO MAINTAIN
BODY TEMPERATURE
The same body temperature can represent a different set of
conditions 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 central thermoregulatory nuclei. Unlike the feed-forward
input received from peripheral temperature, the magnitude of
the error signal for increased heat dissipation is determined
simply by the increase in body temperature.218 A person who is
exercising heavily (or who has just exercised) in a neutral envi­
ronment will have an unusually high body temperature, whereas
a person who is sleeping or resting quietly will have a relatively
low body temperature. Core temperature increases at the onset
of exercise. The time course and magnitude of the temperature
increase during exercise depends on several factors, including
absolute exercise intensity (metabolic heat production), environ­
ment, body mass, and body surface area.98
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.3-5 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 early-
morning low was 36.4° C (97.6° F), and the mean late-afternoon
high was 36.9° C (98.4° F).153 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.3-5 The body’s biologic clock may directly
modulate the body temperature rhythm. The suprachiasmatic
nucleus in the hypothalamus is the main pacemaker for the cir­
cadian system of the body. The core molecular mechanisms of
the circadian clock consist of autoregulatory transcription and
translation loops by the clock genes and 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.147,227
Thermoregulatory responses to exercise are affected by the
circadian clock as well. At the daily low (5:00 AM), the perceived
exertion for a standardized task is the greatest, and thermoregula­
CHAPTER 6  Thermoregulation
tion 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 respon­
sive.230 Results of studies involving heat dissipation mechanisms
during passive heat exposure or exercise suggest that the thresh­
old for the onset of heat dissipation responses is shifted over the
circadian cycle.3-5,215 Sensitivity (responsiveness) of the sweating
signal with respect to increases in core temperature does not
appear to change over the course of the day;5,215 results regarding
cutaneous vasodilator sensitivity were less consistent, with some
studies showing changes3,4 while others did not.215 An excellent
overview of body temperature cycles is available.177
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.129 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. We are anecdotally aware of three individuals whose core
temperature is consistently 35.5° to 36.5° C (95.9° to 97.7° F).
These individuals state that occasionally they have felt ill with a
fever, but were told by a physician that their temperature of 37° C
(98.6° F) was normal. For these individuals, however, it was not
normal; a 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 age 2 years.177 Under thermoneutral
conditions, rectal temperatures of older adults are similar to those
of younger people, whereas oral and axillary temperatures are
slightly lower.105 A recent overview of circadian temperature and
aging is available.231
Of the major regulatory systems, temperature regulation is
unique in the extent to which the effector organs are shared with
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, as detailed by Cooper,48 include incon­
sistencies between chronologic age and physiologic viability and
the increased incidence of interfering disease states and cerebral
microinfarcts as aging progresses.
Thermoregulatory capacities of young people show a progres­
sive increase, but these are not fully developed until after puberty.
Effectors that are more important to infants than to adults include
certain behavioral responses (including 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 accompa­
nies cold stress.113
Sweating is present and effective in children, but the typical
high capacity for evaporative heat loss that is present in adults
is attained only following the changes that occur with puberty.64
Factors that affect loss of body heat during cold stress throughout
the adult years have been investigated with a multiple regression
analysis. Fitness, fatness, and age from the 20s to the early 50s
131
 were evaluated. Fitness had no effect, but fatness impaired heat
loss. Aging during this period was correlated with progressive
weakening of the vasoconstrictor response to cold.25
Individuals in their late 60s and beyond have a definite
decrease in thermoregulatory capacity. Sweating is lessened in
response to passive heating,97 vascular responses to heating and
cooling are significantly reduced,91,110,113 and a distinct shivering
tremor is rarely observed.113 In older adults, thermoregulatory
sympathetic nerve impulses to the skin are reduced by 60%,77
several mechanisms of cutaneous vasoconstriction and vasodila­
tion are impaired,91 and resting metabolic rate is lower than in
younger individuals.236
Young children and older adults are particularly vulnerable to
thermal extremes and should be given treatment priority when
possible. Both groups are susceptible to climatic heat injury. If
core temperatures exceed 40° C (104° F) and are accompanied by
an 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; if available, ice should be
placed around the groin, in the axillae, and around the neck.
Cool water should be sprayed on the skin and the individual
then fanned. Blood gas and electrolyte status should be deter­
mined and any appropriate treatment measures taken.34
Sex and Reproductive Hormone Status
Women have a number of physiologic and morphologic charac­
teristics that could theoretically produce differences in the regula­
tion of body temperature. These include smaller blood volume,
lower hemoglobin concentration, smaller heart, smaller lean
COLD AND HEAT
body mass, greater percentage of subcutaneous and total body
fat, greater surface area–to–mass ratio (due to smaller overall
body size), thinner extremities, and cyclic changes in sex hor­
mone levels. In general, however, historical studies that originally
suggested major differences in thermoregulation between men
and women were poorly controlled or unclear in data presenta­
tion.43 Most reports have shown that when age, thermal accli­
mation, body size, maximal aerobic capacity, cardiovascular
responses during exercise, and relative workload are matched,
PART 2
sex differences in thermoregulation are minimal.71 In particular,
a recent, well controlled comparison of thermoregulatory re­
sponses between men and women during exercise concluded
that female sex was associated with a slight impairment of ther­
moregulatory heat dissipation only at very high exercise intensi­
ties,72 and the impairment was not such that it would cause an
increase in dangerous levels of hyperthermia in women.
The menstrual cycle, oral contraceptives, menopause, and
pregnancy are all associated with important effects on the ther­
moregulatory system. Relative to the early follicular phase of the
menstrual cycle, core temperature is typically 0.3° C (0.5° F) lower
during the late follicular (preovulatory) phase, when estrogen is
elevated unopposed by progesterone, and 0.5° to 0.7° C (1.0° to
1.3° F) higher in the midluteal phase, when both progesterone
and estrogen are elevated.115,116,215 Thermoregulatory control
mechanisms are similarly shifted across the menstrual cycle, such
that heat dissipation responses, including cutaneous vasodilation
and sweating, are initiated at lower temperatures during the
preovulatory phase and higher temperatures during the midluteal
phase.40,116,215 These influences are also seen with the exogenous
hormones in oral contraceptives.40,42 Such data support the idea
that estrogen tends to promote peripheral vasodilation and a
lower body temperature, whereas progesterone tends to promote
increased body temperature.41,116
The effects of reproductive hormones on thermoregulation
in postmenopausal women undergoing hormone replacement
therapy are generally consistent with those just described in
younger women. Administered estrogen acts to lower the core
temperature at which heat loss effector mechanisms are activated
and results in a lowered core temperature.22,222 The addition of
exogenous progestins reverses these effects.22 Although less work
has been done on the thermoregulatory effects of testosterone,
epidemiologic studies indicate that lower testosterone concentra­
tion may be associated with a sensation of cold.76
During menopause, fluctuating hormone levels are thought to
contribute to hot flashes or “flushes,” which involve increases in
132
sweating, vasodilation, and heart rate.126,127 Heat and exercise may
be particularly stressful during and after these episodes. An
increase in body temperature caused by heat exposure or exer­
cise could also trigger a hot flash.117 The integrative mechanism
for the thermal responses appears to involve estrogen activating
central (POAH) warm-sensitive neurons, which then trigger heat
dissipation responses.205 Hot flashes may be associated with
activation of the insular cortex,68 as well as circulating serotonin
levels.133 Additionally, nitric oxide has been shown to contribute
to the peripheral vasodilator response.94
Pregnancy is of special concern to the physician in the wilder­
ness. This concern does not apply to well-hydrated women who
are exercising at submaximal levels, because the thermoregula­
tory 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 pro­
gressively lower levels so that, near term, the steady-state tem­
perature during exercise is about 1° C (1.8° F) lower than before
conception.124 This reduces thermal stress on the fetus, which is
typically 0.5° C (0.9° F) warmer than the mother.47,212
However, concern is warranted if hyperthermia develops in
pregnant women. Animal experiments and epidemiologic analy­
sis 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.124 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 exercis­
ing, 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 comfort­
able pace, and avoid swimming in warm water or immersing
themselves in hot tubs.212 A program of water aerobics for preg­
nant women was reported to decrease requests for analgesia
when these women gave birth, and it was not found to be det­
rimental to the health of the mother or the child.6
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 perturbation or physiologic/pathophysiologic state. In
such circumstances, altered body temperature may be beneficial
and should not necessarily be manipulated until the underlying
condition is improved.
FEVER
The association between illness and increased body temperature
has been recognized for thousands of years. Febrile body tem­
peratures for resting young adults include a morning temperature
of 37.3° C (99.2° F) or higher, which increases gradually to 37.8° C
(100.0° F) for early afternoon and evening. Such elevated tem­
perature needs to reflect a regulated increase to be considered
a true fever.
Pathogens that cause fevers 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 cytokines,131 including interleukin-1 (IL-1), interleukin-6,
and macrophage inflammatory protein-1. The thermoregulatory
“resetting” that results in a regulated increase in body tempera­
ture is initiated by activation of the complement cascade in the
liver, which then initiates afferent neural signaling to the hypo­
thalamus via a prostaglandin E2–dependent vagal mechanism.13,185
Aspirin and related drugs block fever by inhibiting prostaglandin
synthesis.13,185 In addition to causing fever, IL-1 and other cyto­
kines have many other effects, including decreased appetite,
hypoferremia, activation of B and T lymphocytes, and increased
slow-wave sleep.114
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 inter­
feron production are all augmented. The most important aspect
of fever may be to increase greatly the temperature of the periph­
eral tissues by selecting a warmer microclimate, adding insula­
tion, and making 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, the activation, pro­
liferation, 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 them­
selves, as well as for antigen-nonspecific defense systems, are
much lower, at about 1.5 to 5.36.184
The presence and beneficial effects of fever have been docu­
mented in a variety of cold-blooded and warm-blooded verte­
brates 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. In addition, for patients with limited fluid,
oxygen transport, or cardiopulmonary reserves, a febrile re­
sponse should be treated with antipyretics.110 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.54,200 In many cases, this fall is caused by a
decrease in the regulated temperature. In the case of high con­
centrations 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.54 Indeed,
mouse studies have shown that lowered body temperature coun­
teracts ethanol toxicity.132 In humans as well, a 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, individuals reported
a warm sensation that paralleled the increase in sweat rate.242 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 sen­
sation became more intense, although the discrimination of cold
was impaired after the ingestion of ethanol.241,242 However, lower
blood ethanol levels associated with moderate consumption in
humans have minimal and inconsistent effects on thermal balance
of the whole body.58,103
Excellent overviews of the effects of general anesthetics on
perioperative thermoregulation are available.201,202 Many of these
substances (e.g., halothane, fentanyl and nitrous oxide, enflu­
rane, 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 near normal. In the con­
ditions under which general anesthetics are normally adminis­
tered, 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 pressure. This difference
is associated with higher preoperative plasma norepinephrine
levels, which may intensify the vasoconstriction response.108
Cutaneous warming before and during anesthesia prevents the
development of hypothermia and decreases the incidence of
CHAPTER 6  Thermoregulation
infectious complications.118,201
SEVERE HYPOXIA AND ENDOTOXIN SHOCK
When inspired oxygen concentration falls to between 10% and
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.74,237 For
humans who are exercising in 28° C (82.4° F) water under eucap­
nic conditions, decreasing inspired oxygen to 12% lowers the
core temperature thresholds for vasoconstriction and shivering
and increases the rate of core cooling by 33%.104 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 regu­
lated temperature may involve differential sensitivities of central
neurons; hypoxia specifically increases activity of warm-sensitive
neurons in the POAH.221
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 tem­
perature for a severely compromised animal.183
ALTERED SYSTEM RESPONSIVENESS
AND CAPACITIES
A number of situations alter responsiveness of the thermoregula­
tory 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 initi­
ated is also lowered. The net consequence of these adjustments
is that a heat-acclimated and exercise-acclimated individual can
work at a given level with far less increase in core temperature.146
A regimen of exercise in humid heat appears to decrease resting
core temperature in acclimated individuals.168 Repeated acute
increases in both core and skin temperatures contribute to
various changes involved in heat acclimation.175 Physical training
also increases skin blood flow at any given increase in core
temperature.100 Although acclimation to warm conditions pro­
duces many changes in the cardiovascular system, basic barore­
flex responses are not altered.239
Heat acclimation may result in protective cellular adaptations.
Intracellular heat shock protein (HSP) 72 is likely involved in
the maintenance of cellular protein conformation and homeosta­
sis during hyperthermia, inflammation, and injury.141 Consistent
with this, a 10-day program of heat and exercise acclimation
increased HSP-72 levels in peripheral blood mononuclear
cells.238
Chronic cold exposure alters many thermoregulatory systems.
These effects can accrue to both evolutionary change and long-
term individual thermal acclimation. In many cases, resting meta­
bolic rate is increased after repeated cold exposure;24 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.89
On initial exposure of extremities to cold, substantial cutane­
ous vasoconstriction is observed. At some point, however, cold-
induced removal of the superficial α-receptor inhibition leads to
transient vasodilation of the fingers, which occurs in a cyclic
133
 pattern.1,159 This so-called cold-induced vasodilation warms the
extremities, protects against frostbite, decreases pain, and im­
proves manual dexterity during prolonged cold exposure.1,90 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.78 No differences appear to exist between men and women
in the cold-induced vasodilation response.228 Individual differ­
ences 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.78
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.166 Competition between
skin and muscle for blood flow during hyperthermic exercise is
another consideration. During exercise, cutaneous vasodilation
is elicited later, at a higher internal temperature than in resting
hyperthermia, resulting in lower skin blood flow for a given
COLD AND HEAT
internal temperature during exercise than at rest.99 The arterial
baroreflex is another nonthermal reflex that can alter skin blood
flow responses to thermal stimuli. Activation of the baroreflex
using lower-body negative pressure (LBNP) causes decreases
in skin blood flow in both normothermic and hyperthermic
individuals.102
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
PART 2
contraction of the muscles. High muscle temperature increases
efficiency of muscle contraction.10,11 However, an excessive rise
in body temperature impairs endurance performance and leads
to more rapid fatigue. Some controversy surrounds the concept
of a “critical core temperature” (~40° C [104° F]) at which fatigue
occurs to protect the brain from neuronal damage caused by high
internal temperatures.75 Support for this includes observations
that time to exhaustion during heavy exercise is affected by
the initial body temperature.75,152,154 In a heat acclimation study,
individuals exercised until exhaustion at 60% of their maximum
 2 for 9 to 12 consecutive days at 40° C (104° F).154 The time
VO
to exhaustion became progressively longer with acclimation, but
core temperature at exhaustion remained at about 40° C. When
body temperature was altered by water immersion before bicycle
ergometer exercise at 40° C, time to exhaustion became progres­
sively longer as initial body temperature was progressively
lowered. Again, body temperature at exhaustion remained at
approximately 40° C.75
Recent evidence suggests that the story may not be as “simple”
as one core temperature that causes fatigue at the central level.
In a field study, runners with rectal temperature above 40° C
performed similar to runners with rectal temperature of 40° C or
lower at the end of 8-km (4.8-mile) time trials.63 With high skin
temperatures, cardiovascular mechanisms, including redistribu­
134
tion of blood flow from the core to the periphery, and associated
decreases in stroke volume maximize cardiovascular strain in
high environmental temperatures. These mechanisms appear to
be as important as the core temperature itself (or more so) with
regard to development of fatigue. The integrative contributions
of various mechanisms of fatigue are detailed in a recent
review.156
For maintenance of exercise performance and body tempera­
ture in a warm environment, body water status is critical.45,195 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, main­
taining 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 sweat­
ing response, and hypovolemia reduces skin blood flow.45,195
During compensable heat stress, in which a steady-state core
temperature can be maintained, hyperhydration has no effect on
thermoregulation.119 During uncompensable exercise heat stress,
in which core temperature continues to rise, hyperhydration
slightly increases the time to exhaustion, but only by delaying
hypohydration; thermoregulation is not affected.120 It is important
to be alert to the possibility of dehydration in many atypical situ­
ations. For example, swimmers training in an outdoor pool with
a water temperature of 26° C (78.8° F) lost sufficient fluid (2.5%
of their body weight) in 3 hours to compromise thermoregulatory
responses.210
Exposure to hypoxia can alter thermoregulatory vascular
responses, in part because hypoxia itself is a vasodilator.207
During exposure to cold, augmented vasoconstriction appears to
defend core temperature such that the rate of body cooling is
unaffected.206 Paradoxically, in a hot environment, hypoxia may
reduce the cutaneous vasodilator response for a given level of
hyperthermia.188 This may be caused by the sympathoexcitatory
influence of hypoxia.82 However, regional differences in the influ­
ence of hypoxia on blood flow and vascular tone make mecha­
nistic interpretation challenging.
ALCOHOL, DRUGS, ANESTHETICS, AND TOXINS
Although moderate doses of anesthetics and toxins may elicit
adaptive changes in the regulated body temperature, elevated
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., amphet­
amines, 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.23,51
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Complete references used in this text are available
online at expertconsult.inkling.com.
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134.e5
 CHAPTER 7 
Accidental Hypothermia
DANIEL F. DANZL AND MARTIN R. HUECKER
Although used for medical purposes for millennia, cold modali-
ties 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.253 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.65,226 Frosty conditions have
decided many battles. Numerous casualties occur even in train-
ing. Most cold injuries currently encountered affect destitute
urban people and wilderness or sports enthusiasts, such as skiers,
hunters, sailors, climbers, and swimmers.6,278 The popularity of
Arctic and mountain expeditions increases the number of persons
at risk.3,145 Among those challenging the environment are climb-
ers of Mt Everest, Mt Hood, and Denali.122,212,236
EPIDEMIOLOGY
In most countries, deaths from primary hypothermia are consid-
ered violent and classified as accidental, homicidal, or suicidal.41
Deaths from secondary hypothermia are usually considered natu-
ral complications of systemic disorders, including trauma, carci-
noma, 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.81
Hypothermia occurs in various locations and in all sea-
sons.33,222,293,340 In a multicenter survey of 428 cases of civilian
accidental hypothermia, 69 occurred in Florida.62,319 Urban set-
tings account for the majority of cases in most industrialized
countries.62,279,309 An annual average of more than 1300 deaths is
attributed to primary hypothermia in the United States. About
one-half these fatalities are in patients older than 65, and 67%
are males.17
The reason for any year-to-year decline in fatalities is unknown.
Of note, the incidence of secondary hypothermia fatalities is
much greater, but there are no reliable histologic criteria to
confirm that hypothermia is the cause of death.
CLASSIFICATIONS
Accidental hypothermia is best defined as the unintentional
decrease of about 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 pre-
optic and anterior hypothalamic nuclei (Table 7-1). Classically,
hypothermia is defined as a core temperature below 35° C
(95° F).78 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.182,61
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 divi-
sions that reflect the etiology of hypothermia include immersion
versus nonimmersion and acute versus chronic heat loss.204,228
Various physiologic stressors and other factors can impair
thermoregulation.286 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 dehydra-
tion, sleep deprivation, and fatigue. These challenges increase
heat loss through evaporation, radiation, conduction, and con-
vection, and compensatory responses often fail.204 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.62,222,270,340
For safety, experimental investigations of induced hypother-
mia 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 hypo-
thermia. 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 differ-
ences 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.34,78,120,229
NORMAL PHYSIOLOGY OF
TEMPERATURE REGULATION
Warm-blooded animals maintain a precariously dynamic equilib-
rium between heat production and heat loss.152,153 The normal
diurnal variation in humans is only 1° C (1.8° F). Because physi-
ologic changes occurring in humans are modified by predispos-
ing or contributory factors, the normal responses to severe
temperature depression require significant extrapolation.208,237
Basal heat production usually averages 40 to 60 kilocalories
per square meter (kcal/m2) of body surface area per hour, which
approximates the heat from a 100-watt incandescent bulb. This
increases with shivering thermogenesis,220 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 7-1).
Table 7-2 lists the physiologic characteristics of the four zones
of hypothermia.
PATHOPHYSIOLOGY
NERVOUS SYSTEM
Numbing cold depresses the central nervous system (CNS),
producing impaired memory and judgment, slurred speech,
and decreased consciousness. During cold-weather expeditions,
leaders are prone to impaired judgment, risk-taking behavior,
and the attendant trauma. Temperature-dependent enzyme
systems in the brain do not function properly at cold tempera-
tures that are well tolerated by the kidneys. As a result, most
patients are comatose below 30° C (86° F), although some remain
amazingly alert.138
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 initially
afford cerebral protection because of the diminished cerebral
metabolic requirements for oxygen.104 The electroencephalogram
135
 TABLE 7-1  Fahrenheit-to-Celsius Conversion Scale
mercury drops. After cerebral cortical function becomes impaired,
lower brainstem functions are also deranged.
Fahrenheit† Celsius* Fahrenheit† Celsius* Cerebrovascular autoregulation is protectively intact until the
temperature drops below 25° C (77° F). Although vascular resis-
95 35.00 63 17.22 tance is increased, blood flow is disproportionately redistributed
94 34.44 62 16.67 to the brain. In canine studies, blood flow in the brain, muscle,
93 33.89 61 16.11 kidneys, and myocardium recovers quickly to control levels after
92 33.33 60 15.56
rewarming. Flow deficits persist in the pulmonary, digestive, and
endocrine systems for up to 2 hours after rewarming.
91 32.78 59 15.00
Chilling the peripheral nervous system increases muscle
90 32.22 58 14.44
tension and preshivering tone, eventually leading to shivering.
89 31.67 57 13.89 Shivering, which is also centrally controlled, is a more efficient
88 31.11 56 13.33 heat producer than are voluntary muscle contractions of the
87 30.56 55 12.78 extremities.
86 30.00 54 12.22
85 29.44 53 11.67
84 28.89 52 11.11 CARDIOVASCULAR SYSTEM
83 28.33 51 10.56 Many cardiovascular responses caused by or associated with
82 27.78 50 10.00 hypothermia are well described.184 Cold stress increases con-
81 27.22 49 9.44 sumption of myocardial oxygen. Autonomic nervous system
80 26.67 48 8.89 stimulation causes tachycardia and peripheral vasoconstriction,
79 26.11 47 8.33 both of which increase systemic blood pressure and cardiac
78 25.56 46 7.78 afterload.
77 25.00 45 7.22 As core temperature drops, there should be a fairly linear
76 24.44 44 6.67 decrease in pulse rate. After premonitory tachycardia, decre-
75 23.89 43 6.11 mental bradycardia produces a 50% decrease in heart rate at
74 23.33 42 5.56 28° C (82.4° F). Because this bradycardia is caused by decreased
73 22.78 41 5.00 spontaneous depolarization of pacemaker cells, it is refractory
to atropinization. If there is a “relative” tachycardia not consis-
COLD AND HEAT

72 22.22 40 4.44
tent with the degree of hypothermia, the clinician should
71 21.67 39 3.89
consider occult trauma with hypovolemia, drug ingestion, and
70 21.11 38 3.33
hypoglycemia.
69 20.56 37 2.78 During hypothermic bradycardia, unlike normothermia, sys-
68 20.00 36 2.22 tole is more prolonged than diastole. In addition, the conduction
67 19.44 35 1.67 system is more sensitive to cold than is the myocardium, so the
66 18.89 34 1.11 cardiac cycle is lengthened. Cold-induced changes in pH, oxygen,
65 18.33 33 0.56 electrolytes, and nutrients also alter electrical conduction.203
64 17.78 32 0.00 Hypothermia progressively decreases mean arterial pressure
PART 2

and the cardiac index. Cardiac output drops to about 45% of

* C = (F − 32) × 5/9
† F = 9/5 C + 32
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 typically 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
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.
Mild, steady hypothermia in patients with poikilothermic ther-
moregulatory disorders causes electrocardiographic (ECG) altera-
tions and conduction abnormalities.9,71 First the PR, then the QRS,
and most characteristically the QTc intervals are prolonged.

Cold exposure

Thermosensitive end-organs (cutaneous and others)

Blood temperature Lateral spinothalamic tract Direct reflex

vasoconstriction

Relevant hypothalamic nuclei

(preoptic and anterior)

Involuntary Endocrinologic Autonomic Extrapyramidal Adaptive

muscle contraction nervous system stimulation behavioral
(shivering) of voluntary responses
skeletal muscles

FIGURE 7-1  Physiology of cold exposure.

136
 CHAPTER 7  Accidental Hypothermia
TABLE 7-2  Characteristics of the Four Zones of Hypothermia

Core
Temperature
Stage °C °F Characteristics

Mild 37.6 99.7 ±1 Normal rectal temperature

37.0 98.6 ±1 Normal oral temperature
36.0 96.8 Increases in metabolic rate, blood pressure, and preshivering muscle tone
35.0 95.0 Urine temperature 34.8° C (94.6° F); maximal shivering thermogenesis
34.0 93.2 Development of amnesia, dysarthria, and poor judgment; maladaptive behavior; normal blood pressure;
maximal respiratory stimulation; tachycardia, then progressive bradycardia
33.30 91.4 Development of ataxia and apathy; linear depression of cerebral metabolism; tachypnea, then progressive
decrease in respiratory minute volume; cold diuresis
Moderate 32.0 89.6 Stupor; 25% decrease in oxygen consumption
31.0 87.8 Extinguished shivering thermogenesis
30.0 86.0 Development of atrial fibrillation and other arrhythmias; poikilothermia; cardiac output two-thirds normal;
insulin ineffective
29.0 84.2 Progressive decrease in level of consciousness, pulse, and respiration; pupils dilated; paradoxical undressing
Severe 28.0 82.4 Decreased ventricular fibrillation threshold; 50% decrease in oxygen consumption and pulse; hypoventilation
27.0 80.6 Loss of reflexes and voluntary motion
26.0 78.8 Major acid-base disturbances; no reflexes or response to pain
25.0 77.0 Cerebral blood flow one-third normal; loss of cerebrovascular autoregulation; cardiac output 45% of normal;
pulmonary edema may develop106,258,264
24.0 75.2 Significant hypotension and bradycardia
23.0 73.4 No corneal or oculocephalic reflexes; areflexia
22.0 71.6 Maximal risk of ventricular fibrillation; 75% decrease in oxygen consumption
Profound 20.0 68.0 Lowest temperature for mechanical resumption of cardiac electromechanical activity; pulse 20% of normal
19.0 66.2 Electroencephalographic silencing
18.0 64.4 Asystole
13.7 56.7 Lowest adult accidental hypothermia survival106
15.0 59.0 Lowest infant accidental hypothermia survival264
10.0 50.0 92% decrease in oxygen consumption
9.0 48.2 Lowest therapeutic hypothermia survival237

Clinically invisible increased preshivering muscle tone can
obscure the P waves; ST-segment and T-wave abnormalities are
inconsistent.9,326 Of note, standard surface ECG electrodes, when
attached to dry skin, will accurately reflect cardiac electrical activ-
ity. Needle electrodes are not necessary to detect weak ECG
signals.170
The J wave (Osborn wave or hypothermic hump; Figure 7-2),
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.108,177 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.350 J waves are usually upright in aVL,
aVF, and the left precordial leads.4,158,241
J waves may represent hypothermia-induced ion fluxes, result-
ing in delayed depolarization or early repolarization of the left
ventricle, or there may be an unidentified hypothalamic or neu-
rogenic factor. J waves are not pathognomonic of hypothermia
but occur also with CNS lesions, focal cardiac ischemia, and
sepsis.158 J waves may also be present in young, healthy persons.
When pronounced, J waveform abnormalities can simulate myo-
cardial infarction. Computer software that can successfully rec-
ognize and suggest the diagnosis of hypothermia is not widely
available (see Figure 7-2).180,213,234
The prehospital capability to differentiate between J waves
and injury current is particularly important in rural and wilderness
settings with long patient transport times.60 Thrombolysis is
unstudied in accidental hypothermia but would be expected to
exacerbate coagulopathies.105
Below 32.2° C (90° F), all types of atrial and ventricular arrhyth-
mias are encountered.45,77 The His-Purkinje system is more sensi-
tive 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 (movements)
that initiate ventricular fibrillation (VF).
In addition to causing bradycardia, widening the QRS complex,
and prolonging the QT interval, hypothermia increases the dura-
tion of action potentials (Figure 7-3).20 During rewarming, non-
uniform 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
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 exacer-
bate the effects of prolonged action potentials. Most conspicu-
ously, 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 spontane-
ously 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 repolar-
ization, 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 hibernat-
ing animals during rewarming.151 Animals with this capacity
seem to be protected by a shortened QT duration and a calcium
channel handling system that prevents intracellular calcium
overload.

137
COLD AND HEAT

A
64 ATRIAL FIBRILLATION Req MD:
229 NONSPECIFIC INTRAVENTRICULAR CONDUCTION DELAY Acct No:
PART 2

114 INFERIOR INJURY, PROBABLE EARLY ACUTE INFARCT Field2:

412 ST ELEVATION, PROBABLE ANTERIOR INJURY Field3:
426 LATERAL LEADS ARE ALSO INVOLVED Field4:
–AXIS– Standard 12 Lead Report
Abnormal ECG
68
104
-ABNORMAL ECG- Unconfirmed Study

aVR V1 V4

aVL V2 V5

aVF V3 V6

B 25 mm/sec 10 mm/mV F 60 ~ 0.5 - 150 Hz

FIGURE 7-2  The J or Osborn wave of hypothermia. Note that the obvious J waves are usually misinter-
preted by the computer as injury current or nonspecific interventricular conduction delay (A and B).

138

0 mV
−90 mV
37° 32° 27°
FIGURE 7-3  Example of the effects of temperature on action poten-
tials in cardiac cells.
Asystole and VF may both result from hypovolemia, tissue
hypoxia, therapeutic manipulations, acid-base fluxes, autonomic
dysfunction, and coronary vasoconstriction coupled with in-
creased blood viscosity. Other causes may include rough han-
dling 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.
Contributing to afterdrop is the simple temperature equilibration
between the warmer core and cooler periphery. Circulatory
changes account for another set of observations. The countercur-
rent cooling of blood that perfuses cold extremities results in
core temperature decline until the existing temperature gradient
is eliminated. In cold-water immersion, collapse after rescue may
also result from abrupt hypotension following 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.99,100 Hayward123 measured his own esophageal,
rectal, tympanic, and cardiac temperatures (via flotation tip cath-
eter) during rewarming after being cooled in 10° C (50° F) water.
On three different days, rewarming was achieved by 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
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 7-4). The largest core
A B
FIGURE 7-4  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.)
temperature afterdrops occur when participants are rewarmed
CHAPTER 7  Accidental Hypothermia
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 mecha-
nisms are responsible for afterdrop.100 Stimulating peripheral
blood flow can increase afterdrop. Major afterdrops are also
observed when frostbitten extremities are thawed before crystal-
loid volume resuscitation and thermal stabilization of the core
temperature.
RESPIRATORY SYSTEM
Any exposure to a large chill initially stimulates respiratory
drive, which is followed by progressive depression of respira-
tory minute volume as cellular metabolism is depressed.267 The
respiratory rate often falls to 5 to 10 breaths/min below 30° C
(86° F), and ultimately, brainstem neurocontrol of ventilation
fails. An important physiologic observation is that carbon diox-
ide (CO2) production drops 50% for each 8° C (14° F) fall in
temperature. In severe hypothermia, CO2 retention and respira-
tory acidosis reflect the aberrant responses to normothermic
respiratory stimuli.96
Other pathophysiologic factors contributing to ventilation-
perfusion mismatch include decreased ciliary motility, increased
quantity and viscosity of secretions, hypothermic acute respira-
tory distress syndrome, and noncardiogenic pulmonary edema.310
The thorax loses elasticity, and pulmonary compliance drops.
The respiratory “bellows” stiffen and fail because of a decline in
contractile efficiency of the intercostal muscles and diaphragm.
Box 7-1 lists pertinent, potentially protective or detrimental
factors that affect tissue oxygenation in endothermic humans.
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 diure-
sis, 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 effi-
ciently clear nitrogenous wastes.
The etiology of the cold diuresis is multifactorial.110 Suggested
mechanisms include inhibition of antidiuretic hormone (ADH)
release and decreased renal tubular function. Neither hydration
nor ADH infusions influence the diuretic response, which appears
BOX 7-1  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
139
 to be an attempt to compensate for initial relative central hyper-
volemia that is caused by vasoconstrictive overload of capaci-
tance 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 urine output 3.5 times, and the presence of
ethanol impressively doubles this diuresis.
COAGULATION
Coagulopathies often develop in hypothermic patients because
of effects on the enzymatic nature of the activated clotting
factors.88 In vivo, clotting prolongation 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.79
The reversible hemostatic defect created by hypothermia may
not be reflected by the reported “normal” prothrombin time (PT),
PTT,272 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.269 When rapid rewarming is difficult, concentrations of
0.01 to 1 nM of desmopressin may partially reverse hypothermia-
COLD AND HEAT
perature at which enzyme activity slows significantly is 34° C
(93.2° F).334 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 hypother-
mia, with a sequence similar to that seen in disseminated intra-
vascular coagulation (DIC). This produces a higher incidence of
thromboembolism during hypothermia. Causes include thrombo-
plastin release from cold tissue, simple circulatory collapse, and
release of catecholamines and steroids. Because levels of fibrin
split products can be normal, bleeding is not always considered
a hematologic manifestation of DIC.
Whole-blood viscosity increases with the hemoconcentration
seen after diuresis and the shift of fluid out of vascular com­
partments. Red blood cells (RBCs) simply stiffen and have
diminished cellular deformability when chilled.258 The elevated
viscosity of hypothermia is also exacerbated by cryoglobuline-
mia. Cryofibrinogen is a cold-precipitated fibrinogen occasion-
ally seen with carcinoma, sepsis, and collagen vascular diseases.
Blood viscosity is increased by the transient increases in platelet
and RBC counts seen with mild surface cooling. This explains
the increased coronary and cerebral thromboses that occur in
winter.204
PREDISPOSING FACTORS
The factors that predispose to hypothermia can be separated into
those that decrease heat production, increase heat loss, and

induced coagulopathy in vitro.351 impair thermoregulation.204 There is significant overlap between

Thrombocytopenia as a cause of bleeding becomes progres-
sively 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 neonates and
older adults.
PART 2
these groups (Box 7-2).
DECREASED HEAT PRODUCTION
Thermogenesis is decreased at both extremes of age.54 In older
adults, neuromuscular inefficiency and decreased physical activ-
ity impair shivering. Aging progressively diminishes homeostatic
and cold-adaptive capabilities. Although most older adults have

Coagulopathy in trauma patients is attributed to enzyme normal thermoregulation, they tend to develop conditions that
inhibition, platelet alteration, and fibrinolysis. The critical tem- impair heat conservation.265

BOX 7-2  Factors Predisposing to Hypothermia

Decreased Heat Production • Toxicologic effects Iatrogenic

Endocrinologic Failure • Metabolic failure • Emergency childbirth
• Hypopituitarism • Subarachnoid hemorrhage • Cold infusions
• Hypoadrenalism • Pharmacologic effects • Heatstroke treatment
• Hypothyroidism • Hypothalamic dysfunction Miscellaneous Associated Clinical States
• Lactic acidosis • Parkinson’s disease
• Multisystem trauma
• Diabetic and alcoholic ketoacidosis • Anorexia nervosa
• Recurrent hypothermia
• Cerebellar lesion
Insufficient Fuel • Episodic hypothermia
• Neoplasm
• Hypoglycemia • Shapiro syndrome
• Congenital intracranial anomalies
• Malnutrition • Infections: bacterial, viral, parasitic
• Multiple sclerosis
• Marasmus • Pancreatitis
• Hyperkalemic periodic paralysis
• Kwashiorkor • Carcinomatosis
Increased Heat Loss • Cardiopulmonary disease
• Extreme physical exertion
Environmental • Vascular insufficiency
Neuromuscular Physical Exertion
• Immersion • Uremia
• Age extremes • Paget’s disease
• Nonimmersion
• Impaired shivering • Giant cell arteritis
• Inactivity Induced Vasodilation
• Sarcoidosis
• Lack of adaptation • Pharmacologic effects • Shaken baby syndrome
• Toxicologic effects
Impaired Thermoregulation • Systemic lupus erythematosus
Peripheral Failure Erythrodermas • Wernicke-Korsakoff syndrome
• Neuropathies • Burns • Hodgkin’s disease
• Acute spinal cord transection • Psoriasis • Shock
• Diabetes • Ichthyosis • Sickle cell anemia
• Exfoliative dermatitis • Sudden infant death syndrome
Central or Neurologic Failure
• Cardiovascular accident
• Central nervous system (CNS) trauma

140
 Older adults are physiologically less adept at increasing heat
production and the respiratory quotient, which is the ratio of the
volume of CO2 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 adap-
tive behavior. Metabolic studies also demonstrate that in severely
hypothermic older adults, lipolysis occurs in preference to
glucose consumption.235,254
Neonates have a large surface area–to–mass ratio, a relatively
noninsulating subcutaneous tissue layer, and virtually no behav-
ioral 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” oxida-
tive brown adipose tissue.
No cause-and-effect relationship has been found between
hypothermia and the mortality rate of premature infants.282
Although the smaller infants in a neonatal intensive care unit are
at the greatest risk for hypothermia, mortality is related to hypo-
thermia 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 parents, perinatal
morbidity, and low socioeconomic status. In babies with more
chronically induced subacute hypothermia, lethargy, a weak cry,
and failure to thrive are common.314
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 intra-
cranial hemorrhage; hypothermia is also observed in shaken
baby syndrome.
Endocrinologic failure, including hypopituitarism, hypoadre-
nalism, and myxedema, frequently decreases heat production.
Interestingly, congenital adrenal hyperplasia with mineralocorti-
coid insufficiency is more common in cold climates, possibly
an adaptive response to prolonged exposure to cold tempera-
tures, because “normal” cold diuresis is reduced in these
patients.
Hypothyroidism is often occult, with no history of cold intol-
erance, dry skin, lassitude, or arthralgias. A thyroid scar or any
history of thyroid hormone replacement should be suggestive.
The degree of temperature depression correlates fairly directly
with mortality. About 80% of patients in myxedema coma,
which is several times more common in female patients, are
hypothermic.
The effects of insufficient nutrition extend from hypoglyce-
mia to marasmus to kwashiorkor. Kwashiorkor is less often
associated with hypothermia than is marasmus, because of the
insulating effect of hypoproteinemic edema. 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 clumsi-
ness 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
for hypothermia.155
INCREASED HEAT LOSS
Poorly acclimated and insulated individuals often have high dia-
phoretic, convective, and evaporative heat losses during expo-
sure to cold. Because the skin functions as a radiator, any
dermatologic malfunction increases heat loss. Such erythroder-
mas include psoriasis, exfoliative dermatitis, and toxic epidermal
necrolysis.
Burns and inappropriate burn treatment cause excessive
heat loss, as do other iatrogenic factors, including massive cold
intravenous (IV) infusions and overcooling heatstroke patients.
When CO2 is used for abdominal insufflation before laparos-
copy, warming the gas before administration helps prevent
CHAPTER 7  Accidental Hypothermia
hypothermia.
Many pharmacologic and toxicologic agents both increase
heat loss and impair thermoregulation.152,153,320 The most com-
mon is ethanol, which interacts with every putative thermo­
regulatory neurotransmitter. Although ingestion of ethanol
produces a feeling of warmth and perhaps visible flushing, it is
the major cause of urban hypothermia.62,222 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. Body
temperature is lowered both from cutaneous vasodilation with
radiative heat loss and from impaired shivering thermogenesis.
Chronic ethanol ingestion damages the mammillary bodies and
posterior hypothalamus, which modulates shivering thermogen-
esis.259 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 cloth-
ing in response to a cold stress.110
The neurophysiologic effects of ethanol are modified by dura-
tion and intensity of exercise, food consumption, and applied cold
stress.92 Aging increases sensitivity to the hypothermic actions of
ethanol. Chronic ingestion yields tolerance to its hypothermic
effects, and rebound hyperthermia may be seen during with-
drawal. Conditions associated with ethanol ingestion that adversely
affect heat balance include immobility and hypoglycemia.345
Inhibited hepatic gluconeogenesis coexists with malnutrition.
Hypothermic alcoholic ketoacidosis occurs.340 IV thiamine is diag-
nostic 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 consid-
ered as having central, peripheral, metabolic, and pharmacologic
or toxicologic effects.
Central Effects
Central conditions may directly affect hypothalamic function and
mediate vasodilation. Traumatic lesions include skull fractures,
especially basilar, and intracerebral hemorrhages, most often
chronic subdural hematomas. Pathologic lesions include neo-
plasms, congenital anomalies, and Parkinson’s disease. Patients
with Parkinson’s or Alzheimer’s disease, because of global neu-
rologic impairment, are particularly at behavioral risk. Finally,
cerebellar lesions also impede heat production because of inef-
ficient choreiform shivering.
Hypothermia can occur with Reye’s syndrome. In Hodgkin’s
disease, hypothermia is seen only in previously febrile patients
with advanced disease. This is a disease-associated functional
disorder of thermoregulation, similar to that seen in anorexia
nervosa. Centrally induced hypothermia is completely antago-
nized with thyrotropin-releasing hormone.
Peripheral Effects
Peripheral thermoregulation fails after acute spinal cord tran­
section. Patients are functionally poikilothermic as soon as
peripheral vasoconstriction is extinguished.219 Other peripheral
impediments to thermostability include neuropathies and diabe-
tes mellitus. Hypothermia is more common in older adult dia-
betic patients than in the general population, even after
excluding patients with diabetic metabolic emergencies. The
common denominator in 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.232
141
 Pharmacologic or Toxicologic Effects
Numerous medications and toxins in therapeutic or toxic doses
impair centrally mediated thermoregulation and vasoconstric-
tion.156,352 The usual offenders are barbiturates, benzodiazepines,
antimanic agents, and antidepressants. Reduced core temperature
may be a prodrome of lithium poisoning. Organophosphates,
narcotics, glutethimide, bromocriptine, erythromycin, clonidine,
fluphenazine, bethanechol, atropine, acetaminophen, and carbon
monoxide (CO) all cause hypothermia. Hypothermia after acute
CO poisoning is associated with increased mortality.
RECURRENT HYPOTHERMIA
Recurrent and episodic hypothermia are widely reported. The
recurrent variety is more common and is usually secondary to
ethanol abuse, with one person having survived 12 episodes.58
Severe, recurrent presentations are also caused by self-poisoning
and anorexia nervosa.
Persons with episodic hypothermia can be divided into two
groups, 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 epilepti-
COLD AND HEAT
cus. Since hypothermia does not result from experimental
sectioning of the corpus callosum, associated lesions, includ-
ing lipomas, probably cause thermoinstability. Spontaneous
periodic hypothermia may reflect a diencephalic autonomic
seizure disorder and can accompany paroxysmal hyper­
tension. Vasomotor and thermoregulatory mechanisms
are successfully treated with anticonvulsants. Florid psychiat-
ric symptoms often mask these intermittent hypothermic
episodes.
Group 2: This group consists of persons who remain cold for
PART 2
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.204 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, men­
ingitis, encephalitis, bacterial endocarditis, typhoid, miliary
tuberculosis, syphilis, brucellosis, and trypanosomiasis.192 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. Other causes include vascular insuf-
ficiency, giant cell arteritis, uremia, sickle cell anemia, Paget’s
disease, sarcoidosis, and sudden infant death syndrome. Magne-
sium sulfate infusion during preterm labor can produce hypo-
thermia with fetal and maternal bradycardia, and hypothyroidism
can be manifested as hypothermia after preeclampsia (see
Box 7-2).
TRAUMA
Hypothermia protects the brain from ischemia but can result in
arrhythmias, acidosis, and coagulopathies and extracts a high
metabolic cost during rewarming.95 Hypothermia hinders
protective physiologic responses to acute trauma and affects
pharmacologic and therapeutic maneuvers necessary to treat
injuries.15,26
142
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 that the most severely injured
patients are in hemorrhagic shock.126,225 One study assessed the
impact of hypothermia as an independent variable during resus-
citation from major trauma.95 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 dramati-
cally jeopardize thermostability. Hypothermia is often obscured
by obvious hemorrhaging and injuries. Liberalized indications for
Focused Assessment with Sonography for Trauma (FAST) ultra-
sound examinations can minimize unnecessary computed tomog-
raphy (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.111,112 Thermal insults are often added during a trauma
resuscitation. The patient is completely exposed for examination,
and resuscitative procedures cause further heat loss.287
When stratifying patients with the anatomic ISS, hypothermic
patients may have a higher mortality rate than similarly injured
patients who remain normothermic. Caution is advised when
using trauma revised injury severity score (TRISS) methodology.
It is less valid during hypothermia because the physiologic com-
ponents overestimate injury severity. To illustrate this point, some
component of hypotension is normal for a given degree of
hypothermia.300
Various adverse physiologic events accompany hypothermia
with trauma.201,202 Decreased skin and core temperatures without
compensatory shivering thermogenesis occur 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).32 The
cascade of enzymatic reactions is impaired and plasma fibrino-
lytic 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). Postinjury life-threatening coagulopathy in the seriously
injured patient who requires massive transfusion is predicted by
persistent hypothermia and progressive metabolic acidosis.55,89
The appropriate target core temperature for a hypothermic
patient with an isolated severe head injury is unclear. The target
temperature could help balance neuroprotection against the
adverse hematologic and physiologic consequences of hypother-
mia18,210 (see Cerebral Resuscitation, later.)
PRESENTATION
The patient’s history may suggest hypothermia.32 Diagnosis is
simple when exposure is obvious, as with avalanche victims.
Subtle presentations, however, predominate in urban settings.
Patients 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 accident (CVA, stroke),
and psychiatric emergencies (Box 7-3).
During the head, eye, ear, nose, and throat examination,
abnormal findings can include decreased corneal reflexes, mydri-
asis, strabismus, flushing, erythropsia, facial edema, rhinorrhea,
and epistaxis. Mild hypothermia usually does not depress pupil-
lary light reflexes.
 CHAPTER 7  Accidental Hypothermia
BOX 7-3  Signs of Hypothermia

Head, Eye, Ear, Nose, Throat • Gastric dilation in neonates or in adults • Suicide
• Mydriasis with myxedema • Organic brain syndrome
• Decreased corneal reflexes • Vomiting • Anorexia nervosa
• Extraocular muscle abnormalities Genitourinary • Depression
• Erythropsia • Apathy
• Anuria
• Flushing • Irritability
• Polyuria
• Facial edema • Oliguria Musculoskeletal
• Epistaxis • Testicular torsion • Increased muscle tone
• Rhinorrhea • Shivering
• Strabismus Neurologic
• Rigidity or pseudo–rigor mortis
• Depressed level of consciousness
Cardiovascular • Paravertebral spasm
• Ataxia
• Initial tachycardia • Opisthotonos
• Dysarthria
• Subsequent tachycardia • Compartment syndrome
• Amnesia
• Arrhythmias • Anesthesia Dermatologic
• Decreased heart tones • Areflexia • Erythema
• Hepatojugular reflux • Poor suck reflex • Pallor
• Jugular venous distention • Hypoesthesia • Cyanosis
• Hypotension • Antinociception • Icterus
• Peripheral vasoconstriction • Initial hyperreflexia • Scleral edema
Respiratory • Hyporeflexia • Ecchymosis
• Initial tachypnea • Central pontine myelinolysis • Edema
• Adventitious sounds Psychiatric • Pernio
• Bronchorrhea • Frostnip
• Impaired judgment
• Progressive hypoventilation • Frostbite
• Perseveration
• Apnea • Panniculitis
• Mood changes
• Cold urticaria
Gastrointestinal • Peculiar “flat” affect
• Necrosis
• Ileus • Altered mental status
• Gangrene
• Constipation • Paradoxical undressing
• Abdominal distention or rigidity • Neuroses
• Poor rectal tone • Psychoses

Cardiovascular findings after initial tachycardia include brady-
arrhythmias and hypotension. Heart sounds may be muffled and
distant. Tachypnea, an early respiratory finding, is usually fol-
lowed by progressive hypoventilation with bronchorrhea and
adventitious sounds. Because the gastrointestinal (GI) 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. Urine output ranges from
initial polyuria resulting from cold diuresis to anuria. The inci-
dence 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 CVA. 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, as with 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 con-
traction 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.204 Spinal cord and
other CNS lesions may be obscured by depressive neurologic
changes that normally accompany hypothermia.
Psychiatric presentations and suicide attempts associated with
hypothermia often are initially misdiagnosed. Preexisting psychi-
atric disorders can blossom in the cold, even if they were stabi-
lized in temperate climates.29 Mental status alterations include
anxiety, impaired judgment, perseveration, neurosis, and psycho-
sis.145 Leaders of expeditions can become moody, apathetic,
uncooperative, and risk taking. Older adult patients often with-
draw in confusion, become silent, and display lassitude and poor
judgment. A peculiar or 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.167 The clothing is removed in
a preterminal effort to address impending thermoregulatory col-
lapse, and many persons are mistakenly identified as sexual
assault victims. This phenomenon is also seen in hypothermic
children. Undressing may result from Alzheimer’s disease before
the patient wanders into the cold.165
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 syn-
dromes often develop because of associated conditions causing
prolonged compression and immobility, in addition to com­
partment hypertension seen during reperfusion of frostbitten
extremities.
Dermatologic presentations of hypothermia include erythema,
pallor, edema, and scleral edema. Cold urticaria, frostnip, frost-
bite, and gangrene should also cause the clinician to consider
this diagnosis. Pernio is also observed with chronic myelomono-
cytic leukemia.
LABORATORY EVALUATION
ACID-BASE BALANCE
The strategy for achieving and maintaining acid-base balance in
hypothermia differs from that of normothermia.68,121,141,162 After
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

143
 mainly by direct respiratory depression. In addition, as body
temperature decreases, solubility of CO2 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.129
Nevertheless, reliable clinical prediction of the acid-base status
in accidental hypothermia is not possible. In one series of 135
patients, 30% were acidotic and 25% alkalotic.222
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. Despite flow changes in a canine model of moder-
ate 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 greatly 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 initial 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 7.42.339 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, Rahn264 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 7-5).268
COLD AND HEAT
Relative alkalinity of tissues makes physiologic sense. Intracel-
lular electrochemical neutrality ensures optimal function of
enzyme systems and transport proteins at all temperatures and
allows excretion of the neutral intracellular waste product
urea.13
Depressed metabolism and CO2 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,
PART 2
the peptide-linked histidine-imidazole buffering system.
One homeostatic approach to maintain a steady pH is to keep
the bicarbonate content constant. This is achievable only if total
blood CO2 content does not change. Because CO2 solubility
increases with temperature depression, alveolar ventilation must
increase to compensate by lowering the PaCO2. Active ectotherms
8.0
lood
ected b
corr
n
7.7 ic” u
t o t herm
“Ec
“Endothermic” corrected blood
7.4
pH
er
7.1
al wat
N eutr
6.8
0 cardiac toxicity. An important caveat is that the well-known
40 37 30 20 10 0 diagnostic ECG changes are often obscured by hypothermia, and
Temperature (° C)
FIGURE 7-5  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 pro-
gressively diminishes if the arterial blood gases are temperature cor-
rected. 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.
144
exhibit this respiratory adaptation and do not depress their respi-
ratory minute volume when cold. This response, termed the
ectothermic, or alpha-stat, strategy, allows them to maintain total
bicarbonate and CO2 content while increasing pH. 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.
Induced hypothermia, which clearly differs from accidental
hypothermia, might benefit from the alpha-stat approach, with
improved neurologic outcome and myocardial function.69,162,179,268
On the other hand, various animal models suggest that the
pH-stat strategy may be preferable.76 Accidental hypothermia in
a human should not be considered a protective form of hiberna-
tion. The ectothermic (alpha-stat) approach appears to ensure
adequate alveolar ventilation and acid-base balance at any tem-
perature when the uncorrected pH is 7.42 and the uncorrected
PaCO2 is 40 mm Hg.132,162,273
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, or myxedematous; or has
secondary hypothermia.192 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 elec-
trolyte values.120 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
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
GI 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 physio-
logically 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 (ADH)
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 GI function.
When hyperkalemia is identified, the physician should search
for other causes of metabolic acidosis, crush injury or rhabdo-
myolysis, renal failure, postsubmersion hemolysis, or hypoaldo-
steronism. Temperature depression can increase hyperkalemic
VF can occur with serum potassium levels of less than 7 mEq/L.
Hypothermia has no consistent effect on magnesium or
calcium levels. Severe hypophosphatemia can occur during treat-
ment 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. Cre-
atine kinase (CK) levels over 200,000 international units (IU) are
observed, and rhabdomyolysis is often present.58

FIGURE 7-6  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.
Inhibition of cellular membrane transport decreases glucose
utilization. In addition, insulin release and activity are greatly
reduced below 30° C (86° F). Because target cells are insulin
resistant, hyperglycemia is frequently seen initially. Markedly
elevated glucose levels often correlate with hyperamylasemia and
increased cortisol secretion.340
Acute hypothermia initially elevates the serum glucose level
through catecholamine-induced glycogenolysis. Chronic expo-
sure after exhaustion and glycogen depletion leads to hypogly-
cemia.305 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.
Ongoing fluid shifts render the BUN a poor reflection of circula-
tory volume status.97
The relationship between primary accidental hypothermia and
hyperamylasemia appears to correlate with the severity of tem-
perature depression, but preexisting or hypothermia-induced
pancreatitis is present in up to 50% of patients. The abdominal
examination is frequently unreliable. Therefore, lipase levels
should be measured, except in minor cases.51 Ischemic pancre-
atitis is attributable to microcirculatory collapse in hypothermia.
Decreased pancreatic blood flow activates many proteolytic
enzymes.
TREATMENT
Four decisive factors should be considered when assessing non-
perfusing, severely hypothermic patients at the site. Rescuers
should reconsider the decision to resuscitate if there is evidence
of asphyxia or lethal injuries. A rigid thorax precludes closed-
chest 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. Bedside echocardiography is an ideal tool
to assess cardiac activity.28,229
The combination of cold and exhaustion is a common cause
of hypothermia in the field.142,223,224 The individual’s cold tolerance
depends on temperature, wind, clothing worn, and wetness. It
does not take an extremely cold temperature to produce hypo-
thermia after energy depletion. As mental function decreases, the
hypothermic patient cannot respond to the rising threat. Judg-
ment is impaired, and the patient seldom takes necessary precau-
tions to prevent further disaster.24
Field presentation of patients who are awake covers a wide
spectrum. Some persons are obtunded but conscious. Patients
CHAPTER 7  Accidental Hypothermia
may or may not be shivering and often have a distant gaze and
slurred speech.98
The type of power available in the transport vehicle deter-
mines the options for active rewarming. These include forced-air
warming devices, heated IV fluids, and resistive and combustive
heat.99,101,106
Comatose patients require careful handling because they are
extremely likely to develop VF and asystole with rough handling
(Figure 7-6). Gurneys should be carried or rolled slowly to avoid
jostling, and “code 3, full lights and sirens” transport should be
avoided if patients are perfusing spontaneously.
It is often impossible for rescuers to separate primary from
secondary hypothermia when an unwitnessed cardiac arrest
patient is found in a frigid environment. Patients with cold, stiff,
and cyanotic primary hypothermia and fixed and dilated pupils
have been “reanimated.” A succinct summary of prehospital care
of the hypothermic patient is rescue, examine, insulate, and
transport.
The initial rescuer and first responder often encounter obsta-
cles to preventing further heat loss.224,335 In certain imposing
geographic settings, treatment protocols are helpful to standard-
ize 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.78,274 Aeromedical transport is often ideal in
these circumstances.347 In difficult environments, proper proto-
cols with rehearsal and critique of mass casualty plans in the
cold are very important.
The history obtained at the scene helps determine optimal
treatment. The pertinent medical history regarding prior cardio-
pulmonary, endocrinologic, and neurologic conditions is par­
ticularly helpful. The circumstances of discovery, duration of
exposure, associated injuries or frostbite, and obvious predispos-
ing conditions should be recorded. No prognostic neurologic
scale (e.g., Glasgow Coma Scale score) is valid during hypother-
mia, but trends are often useful.
Accurate field measurement of core temperature is diffi-
cult.306 The International Commission for Mountain Emergency
Medicine recommends tympanic or esophageal field measure-
ments, although these have significant limitations. Never insert
an esophageal probe unless the patient is already tracheally
intubated.62,274
Prolonged field treatment should be avoided whenever pos-
sible, although the rescuer must attempt to prevent further heat
loss (Box 7-4). The rescuer should anticipate the presence of an
irritable myocardium, hypovolemia, and a large temperature gra-
dient between the periphery and the core.353
The crux of the prehospital quandary surrounds the safety of
providing prehospital heat. On the one hand, the original “meta-
bolic icebox” concept223,224 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.
145
 BOX 7-4  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.
The rescuer should stabilize injuries, protect the spine, splint
fractures, and cover open wounds. Rescuer safety concerns typi-
COLD AND HEAT
cally include unstable snow or ice and falling rocks.263
Passive external rewarming with dry insulating materials
minimizes conductive, convective, evaporative, and radiant heat
losses. Remove any wet clothing from awake patients, and insu-
late them with sleeping bags, insulated pads, plastic “bubble
wrap,” metallized or regular blankets, or even newspaper. One
device has a nylon shell and a polyester-pile liner to wick mois-
ture. In a survey of common field rewarming methods used by
mountain rescue teams, the most common techniques included
PART 2
chemical pads, sleeping bags, body-to-body contact, and hot-
water bottles.118
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 caf-
feinated drinks. A significant diuresis is usually associated with
the cooling process, so the patient’s fluid balance must be reas-
sessed. Once mildly hypothermic patients are well hydrated, they
can be walked out to safety.
Handle severely hypothermic patients gently, immobilizing
them to prevent exertion. Although exercise can rewarm a person
more rapidly than shivering, it also greatly increases afterdrop.97,100
Patients must be kept in a horizontal position whenever possible
to minimize orthostatic hypotension. Vigorously massaging cold
extremities is also contraindicated, because skin rubbing, as with
ethanol, suppresses shivering thermogenesis and increases cuta-
neous vasodilation.
Field management of the comatose patient first involves ven-
tilation 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 cardiac conduction. The single greatest
factor in maintaining perfusion during severe hypothermia is
oxygenation.98 At altitude, a portable hyperbaric chamber may
prove useful.42
During a storm, prolonged field rewarming may be the only
viable option until meteorologic conditions become more favor-
able for land or, preferably, aeromedical evacuation.347 Many
prehospital medications freeze in solution. If this occurs, their
pharmacologic activity after thawing is indeterminate (see Appen-
dix at the end of this book).
The rescuer should administer an IV fluid challenge with 250
to 500 mL of heated (37° to 41° C [98.6° to 105.8° F]) 5% dextrose
in normal saline solution. Empirical 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. Con-
146
cerns regarding these agents before warming include precipita-
tion of acute withdrawal, seizures, and markedly increased
oxygen utilization.
Most patients are volume depleted. Nevertheless, iatrogenic
volume overload should be avoided, because myocardial con-
tractility 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 commer-
cially available.
Intravenous 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 battery or from a DC converter plugged into an
AC outlet.
Some warmers run on 12 volts from any vehicle or portable
battery. The current drain can be 4 amperes, and the insulation
case may lose 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.257 Another option is an in-line battery-powered, dispos-
able, lightweight fluid-warming device.
Peripheral vessels may be difficult to locate, and IV lines are
difficult 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.
The methods selected to stabilize core temperature should be
tailored to the severity of hypothermia and the field circum-
stances.313 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 water-
proof insulation suffices for mild chronic hypothermia. The addi-
tion of a vapor barrier will reduce evaporative heat loss.127,128
Other common equipment types include duvets and plastic
bubble wrap.159
In a series of patients requiring cardiopulmonary bypass
(CPB), hypothermia was maintained during transport.332 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 gentle
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 per-
sonnel comfort is important to maximize performance, and it is
unlikely that heating the interior above 25° C (77° F) will acceler-
ate 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.82 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 heating147 and might be a viable option in some transport
situations.
Inhalation therapy is safe for active rewarming of patients with
profound hypothermia in the field.120 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 can occur while using inhalation rewarming
devices in volunteers, illustrating the importance of proper
instruction for the rescuer.302 Under certain conditions, the impact
of field inhalation therapy on the rate of rewarming may not be
significant.106 In shivering, mildly cold patients the thermal advan- convective warming is more efficient than resistive heating.147 The

CHAPTER 7  Accidental Hypothermia

tage is minimal.74,218
One rewarming device weighs 3 kg (6.6 lb), 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 active
humidifiers.195,196
Commercially available lightweight, portable, noninvasive
core-rewarming systems that deliver heated humidified air or
oxygen at 42° to 44° C (107.6° to 111.2° F) are available. Some
systems consist of a heating chamber connected by a corrugated
hose to a one-way flow valve and an oronasal mask. The tem-
perature 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 patient 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,120 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.335
A hydraulic sarong or vest, in which heated water is circulated
via a hand pump, is another option.118 Immersion rewarming is
dangerous in the field because monitoring and resuscitation
capabilities are limited.
Charcoal heaters can deliver 100 watts for 8 hours. The char-
coal “vest” burns a briquette and has a favorable heat-to-weight
ratio, unlike most rewarming devices.52 Battery polarity is critical
to prevent CO exposure.302 The battery must be inserted correctly
to avoid a CO exhaust hazard. Do not use in an aircraft. These
devices can circulate hot air within a blanket or sleeping bag and
provide a comfortable, warm, and dry environment for transport-
ing patients.
Another option is a modified forced-air warming system for
field use.75,101 It covers the patient’s trunk and thighs and can
adapt to various transport vehicle power sources. Experimentally,
U.S. Army has a commercially available Hypothermia Prevention
Management Kit. A heat-reflective shell and blanket with chemi-
cal heat packs provide 6 hours of heat.
PREHOSPITAL LIFE SUPPORT
The Wilderness Medical Society has published evidence-based
guidelines providing consensus suggestions for evaluation and
treatment of hypothermic patients. The key factors to guide treat-
ment are the level of consciousness, intensity of shivering, and
cardiovascular stability.353 An altered mental status or lack of
shivering after minimal cold exposure should suggest secondary
hypothermia. The value of characterizing the five stages of the
“Swiss” hypothermia grading system is limited by the high vari-
ability of physiologic responses during hypothermia.78,353
A patent airway and the presence of respirations must be
established (Figure 7-7). The patient may appear apneic if
the respiratory minute ventilation is significantly depressed. A
common error in tracheally intubated patients is excessive ven-
tilation, 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 patient 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.
The palpation of peripheral pulses is often difficult in vaso-
constricted and bradycardic patients.252 Apparent cardiovascular
collapse may actually reflect cardiac output that can meet minimal
metabolic demands. The rescuer should auscultate and palpate
for at least 1 minute to find pulses if a cardiac monitor or portable
ultrasound is unavailable. Iatrogenic VF can easily result from
chest compressions that are not indicated.
When a cardiac monitor is available, use maximal amplifica-
tion to search for QRS complexes. If the patient is in VF, the
rescuer should attempt defibrillation initially with 2 watt sec/kg
and up to 200 watt sec. The energy requirement for defibrillation
does not increase in hypothermia. If the patient does not respond,
generally defer further attempts, and assume that the patient must

Rescue/examine

Yes Responsive

No

Respirations

Yes No
Heated humidified
Assume cardiac output ventilation

Insulate
Electrical Cardiac monitor
IV
D5 NS complexes
Heated humidified Nonperfusing rhythm
Cardiac monitor oxygen
Central pulse No (PEA) Chest compression
Gentle evacuation
Yes

Hospital assessment

FIGURE 7-7  Prehospital life support. IV D5 NS, Intravenous 5% dextrose in normal saline; PEA, pulseless
electrical activity.

147
 be rewarmed at least past 30° C (86° F) before further attempts.7 TABLE 7-3  Core Temperature Measurements
Effective CPR in deep accidental hypothermia is demonstrated in
many cases. One patient fully recovered with extracorporeal Type Advantages Considerations
rewarming after 130 minutes of CPR and 38 defibrillation
attempts.242 Rectal Convenient Insert 15 cm (6 inches)
Do not perform defibrillation if organized, narrow electrical Continuous Lags during transition from
complexes are seen on the monitor.187 Most monitors and defibril- monitoring cooling to rewarming
lators are not tested for operation at temperatures below 15.5° C Falsely elevated with peritoneal
(59.9° F). Standard monitor leads do not always stick well to cold
lavage
skin, so benzoin may be useful. If this fails, needle electrodes
Falsely low if probe is in cold
may be necessary. Another option is to puncture the Gelfoam
conventional monitor pad with a small-gauge injection needle.336 feces or when lower
Unresponsive patients should be carefully assessed for a extremities are frozen
central pulse before assuming they have pulseless electrical activ- Esophageal Convenient Insert 24 cm (9.5 inches) below
ity (PEA). The lowest temperature at which mechanical reestab- Continuous larynx
lishment of cardiac activity has been successful is 20° C (68° F),64 monitoring Tracheal misplacement
and defibrillation attempts rarely succeed below 30° C (86° F). If Aspiration
resuscitation in the field is unsuccessful, rewarming and CPR Falsely elevated with heated
should be continued during transport to the ED.251 inhalation
Tympanic Approximates Probe: tympanic membrane
MANAGEMENT IN THE EMERGENCY hypothalamic perforation; canal hemorrhage
DEPARTMENT temperature Infrared: unreliable; cerumen
via internal effect
The history obtained from a hypothermic patient is often unreli- carotid artery
able, so it is prudent to confirm hypothermia and monitor with Bladder Convenient Unreliable
continuous core temperature measurements. Diagnostic errors in Continuous Falsely elevated with peritoneal
the ED usually result from incomplete monitoring of vital signs. monitoring lavage
Doppler ultrasound may be necessary to locate a pulse and Falsely low with cold diuresis
should be supported by continuous ECG monitoring. The physi-
COLD AND HEAT

cian should also address the requirements for resuscitation and

initiate advanced life support when necessary (Box 7-5).295
Temperature Measurement
Few emergency departments have a hypothermia protocol.107
Most have adequate equipment for accurate core temperature
measurement.166,238 Rectal measurements are most practical clini-
cally for mild cases but may not reflect cardiac or brain tempera-
tures. An indwelling thermistor probe placed to a depth of 15 cm
PART 2
mometers that are in contact with the tympanic membrane. These
are usually impractical except in anesthetized patients. External
auditory canal thermometers that measure infrared emission from
the tympanic membrane are available. These are actually “epi-
tympanic” thermometers.355 Infrared external auditory canal
thermometers are not very sensitive. Tympanic thermometers are

(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 7-3).341
Esophageal temperature measurements are far preferable in
severe cases when airway protection is provided with endotra-
cheal intubation. Esophageal temperature approximates cardiac
temperature. Because the upper third of the esophagus is near
the trachea, the probe may read falsely high during heated inha-
lation therapy if the probe is positioned too proximally. The
probe does not have markings but should be placed 24 cm (9.5
inches) below the larynx into the lower third of the esophagus.
The greatest discordance between rectal and esophageal tem-
peratures is noted during the transition phase between cooling
and rewarming.
Tympanic temperature theoretically approximates hypotha-
lamic temperature and can be accurately measured with ther-
BOX 7-5  Resuscitation Requirements
Thermal Stabilization
• Conduction
• Convection
• Radiation
• Evaporation
• Respiration
Maintenance of Tissue Oxygenation
• Adequate circulation
• Adequate ventilation
Identification of Primary vs. Secondary Hypothermia
Rewarming Options
• Passive external rewarming
• Active external rewarming
• Active core rewarming
inaccurate if the canal is full of cerumen or snow, or is not
adequately sealed.85
Although bladder temperature measurement devices can be
incorporated into the urinary drainage catheter, the readings
are frequently unreliable. Measurements are falsely elevated with
heated peritoneal lavage and, more often, low as a result of
cold-induced diuresis and crystalloid resuscitation.
Initial Stabilization
After core temperature measurement, all clothing should be
gently removed or cut off with minimal patient manipulation.251
Immediately insulate the patient with dry blankets. Apply a
cardiac monitor, and insert IV catheters as needed. Arterial cath-
eter insertion may help in managing select, profoundly hypother-
mic 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.50 Central venous catheters should not be
inserted into the right atrium, because this could precipitate
arrhythmias. 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.172 In one study of hypothermic patients on CPB,
the finger probes were inaccurate.46 The probe may be 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 individuals. There is less failure with
forehead pulse oximetry compared to fingertip readings.205
In theory, combining pulse oximetry with near-infrared spec-
troscopy could provide tissue perfusion information during hypo-
thermic vasoconstriction. More practically, an accurate core and
peripheral muscle temperature would prove just as useful. The
value of end-tidal CO2 measurements to assess adequacy of tissue
perfusion and tracheal tube placement is established at normal
temperatures. Most of these devices, however, measure only the

148
CO2 content of dehumidified air and thus cannot be used during
airway rewarming.
Laboratory evaluations, except in some patients with 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.61
The indications for radiography should be liberalized from
normothermia. Radiologic evaluation of poorly responsive pa-
tients must include cervical and other spine images to detect
occult trauma. Chest radiographs may predict lung collapse
during rewarming when cardiomegaly and redistribution of vas-
cularity are already present. Abdominal imaging should be ob-
tained 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 vascu-
lar occlusion, and colonic dilation is often present in conjunction
with myxedema coma. The use of FAST may be helpful.58
Nasogastric tube insertion should be performed after endotra-
cheal intubation in moderate or severe hypothermia, because
gastric dilation and poor GI 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 hypo­
thermia usually requires only modest amounts of crystalloids. In
more severe cases, volume shifts and elevated blood viscosity
from hemoconcentration, lowered temperature, increased vascu-
lar 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 rewarm-
ing. Hemodilution is usually not a problem and is seen only
during massive crystalloid resuscitation of actively hemorrhaging
patients.31,58
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 dif-
ficult. Because hypothermia results in natriuresis, saline depletion
may be present. Further causes of sodium losses include prior
diuretic therapy and GI losses. Preexisting total body sodium
excess is seen with congestive heart failure, cirrhosis, and
nephrosis. In these patients, serum sodium and osmolality values
are often normal. Rarely, serum sodium level is low because of
free water excess. Other causes include myxedema, panhypopi-
tuitarism, and inappropriate ADH 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. Theo-
retically, Ringer’s lactate solution should be avoided because a
cold liver cannot metabolize lactate. In severe cases, some clini-
cians favor a mixture of crystalloids and colloids.
The patient should be monitored for standard clinical signs
of fluid overload, including rales, jugular venous distention,
hepatojugular reflux, and S3 cardiac gallop. Persistent cardiovas-
cular instability often reflects inadequate intravascular volume.
As mentioned, a properly placed central venous pressure cath-
eter, such as a femoral line that does not enter and irritate the
right atrium, has a role. Pulmonary wedge pressure measure-
ments 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
CHAPTER 7  Accidental Hypothermia
BOX 7-6  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
increased. In neonates, adequate fluid resuscitation greatly de-
creases 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. The
fluxing relationship between active vascular capacity and circulat-
ing fluid volume depends not only on the mechanism of cooling
but also on the method of rewarming.353
Hypothermic patients, particularly those with frostbite, are at
high risk for extremity compartment syndromes and rhabdomy-
olysis. Pelvic fracture belt slings should be considered only
to temporarily stabilize coexistent exsanguinating major pelvic
fractures.
REWARMING OPTIONS
Hypothermia is an extremely heterogeneous condition, and
definitive evidence-based treatment guidelines do not exist.
Therefore, rigid treatment protocols are ill advised.274,280,356 A
versatile approach to rewarming can be developed after careful
consideration of the observations from animal experiments,
human experiments on mild hypothermia, and various clinical
reports (Box 7-6).113,114,260 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 7-7).
PASSIVE EXTERNAL REWARMING
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
BOX 7-7  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 7-2)
149
 techniques deliver heat directly to the skin. Examples include
2.0 forced-air rewarming, immersion, arteriovenous anastomosis
Mild (AVA) rewarming, plumbed garments, hot-water bottles, heating
Moderate
pads and blankets, and radiant heat sources.69,328
1.5 Severe
During rewarming of hypothermic patients, there are meta-
bolic pH and inflammatory interleukin fluxes.216,321 Cytokine pro-
duction may be activated by accidental hypothermia.2
°C

1.0
ACTIVE EXTERNAL REWARMING
0.5 The interpretation of survival rates with AER is affected by various
risk factors and patient selection criteria.296 Some experimental
and clinical reports link AER with peripheral vasodilation, hypo-
tension, and core temperature afterdrop, but previously healthy,
0 young, and acutely hypothermic patients are usually safe
1 2 3 4 5 6 7 8 candidates for AER.31 Heat application confined to the thorax
may mitigate many of the physiologic concerns pertaining to
-IV

R
R

BE -

G -

VA CR
TU R

VA CR
AS

C
PE

AE

AC GE
E
AC
the depressed cardiovascular and metabolic systems, which are
R

-E
LA A
LA A
AC

-M

R
unable to meet accelerated peripheral demands.318 Combining
R
AC

T.

truncal AER with active core rewarming may further avert many
N

BC
P
T/

potential side effects.74

ET

Treatment modalities
FIGURE 7-8  First-hour rewarming rates from a large multicenter
survey. ACR, Active core rewarming; AER, active external rewarming;
ECR, extracorporeal rewarming; ETT, endotracheal tube; GBC, gastric-
bladder-colon; IV, intravenous; NT, nasotracheal tube; P, peritoneal;
PER, passive external rewarming. (Data from Danzl DF, Pozos RS,
Auerbach PS, et al: Multicenter hypothermia survey, Ann Emerg Med
COLD AND HEAT
Forced-Air Surface Rewarming
Forced-air surface warming systems efficiently transfer heat.11,99,176
Hot air is circulated through a blanket. The air exits apertures
on the patient side of the cover, permitting the convective trans-
fer of heat.215 In one study that rewarmed accidental hypothermia
patients in the ED, rewarming shock and core temperature after-
drop were not noted299 with the use of heated inhalation and

16:1042, 1987.)
to minimize the normal mechanisms of heat loss. When the wind
is blocked, less heat escapes through radiation, convection, and
conduction. Conditions with higher ambient humidity slightly
limit respiratory heat loss.
Aluminized body covers also reduce heat loss.83 Nevertheless,
PART 2
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.115
A study of full-body forced-air warming compared a com-
mercially available convective blanket with simple air delivery
beneath bedsheets.163 Directed 38° C (100.4° F) warm air under
the sheets warmed standardized thermal bodies containing water

endogenous thermogenesis must generate an acceptable rate of
rewarming for PER to be effective.239 Humans are functionally
poikilothermic below 30° C (86° F), and metabolic heat produc-
tion 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 gly-
cogen is depleted before or during cooling.
Older adult patients in whom mild hypothermia develops
gradually are less acceptable candidates for PER. When rewarm-
ing times are markedly prolonged (more than 12 hours), com-
plications tend to increase.
Patients who are centrally hypovolemic, glycogen depleted,
and without normal cardiovascular responses should be stabi-
lized 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])
hours far exceeded 0.5° C (0.9° F) per hour, with no increase in
mortality rate (Figure 7-8).62
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).185 Rapid identification of any impediment to normal
thermoregulation, such as cardiovascular instability or endocri-
nologic insufficiency, is essential.186 Intrinsic thermogenesis may
also be insufficient after traumatic spinal cord transection or
pharmacologically induced peripheral vasodilation. Some patient
populations generally require active rewarming.66 For example,
aggressive rewarming of infants minimizes energy expenditure
and decreases mortality. In these circumstances, vigorous moni-
toring for respiratory, hematologic, metabolic, and infectious
complications is essential.329
When active rewarming is needed, heat can be delivered
externally or to the core. Active external rewarming (AER)
very efficiently. Commercially available convective air rewarming
devices are also effective. Another option is conductive warming
with a warm-water–filled heat exchange blanket.
The use of forced-air surface warming systems is most practi-
cal in the ED.174,189 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.118 In particular, avoid
resistance-heat electric blankets on which a patient lies, because
vasoconstricted capillaries are compressed and burns occur
easily.
Another AER option is a thermoregulatory system that circu-
lates warm water through energy transfer pads placed on the
chest and lower limbs.48 The core temperature measured via
probe is fed back to the control module.
Immersion
Immersion in a 40° C (104° F) circulating bath presents difficulties
in monitoring, resuscitation, treatment of injuries, and mainte-
nance of extremity vasoconstriction to prevent core temperature
afterdrop. In normothermic men with coronary artery disease,
the cardiovascular stress and arrhythmogenic response to immer-
sion in a hot tub are mild, less than those induced by exercise.
In contrast, placing the hands and feet in warm water theoreti-
cally opens arteriovenous shunts and accelerates rewarming in
acute hypothermia. Scandinavian palmar heat packs may capital-
ize on this physiology.
Arteriovenous Anastomosis Rewarming
The original description of this noninvasive AER technique is by
Vangaard.324 Exogenous heat is provided by immersion of the
distal extremities (hands, forearms, feet, calves) in 44° to 45° C
(111.2° to 113° F) water. The heat opens arteriovenous anasto-
moses (AVAs). These structures are 1 mm (0.04 inch) below the
epidermal surface in the digits.16,220 Countercurrent heat loss is

150
minimized because the superficial veins are not close to the arte-
rial 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.296
A permutation of AVA rewarming is negative-pressure rewarm-
ing. Under hypothermic conditions, the AVAs remain closed
during peripheral vasoconstriction. In combination with localized
heat application, application of subatmospheric pressure theoreti-
cally 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. After a vacuum pressure of −40 mm Hg is
created, heat is applied over the dilated AVAs. The thermal load
can be provided by an exothermic chemical reaction or a heated
perfusion blanket.
The clinical efficacy of AVA rewarming in accidental hypo-
thermia is unclear.39,56 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,109 but another study compar-
ing negative-pressure rewarming with forced-air warming failed
to replicate these results.308
Active Core Rewarming
Various techniques that can effectively deliver heat to the core
include heated inhalation, heated infusion, diathermy, lavage
(gastric, colonic, mediastinal, thoracic, peritoneal), and extracor-
poreal rewarming. Figure 7-8 lists average first-hour rewarming
rates reported with some of these techniques in one multicenter
study. Although hemodynamic instability impacts the rewarming
strategy, noninvasive techniques often succeed unless significant
comorbidities exist.269,323
Airway Rewarming
The effectiveness of the respiratory tract as a heat exchanger
varies with technique and ambient conditions.218 Dry air has low
thermal conductivity, and complete humidification coupled with
an inhalant temperature of 40° to 45° C (104° to 113° F) is
required.267 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.27
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 by
mask and 1.22° C (2.2° F) per hour by ETT.222 In a multicenter
survey,62 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. The
decremental efficiency at higher temperatures slows the rate
(10 kcal/hr) in mild cases.62
Thermal countercurrent exchange in the cerebrovascular bed
of humans67 affects the efficiency and influence of heated-mask
ventilation during hypothermia. Known as the rete mirabile, this
system could preferentially rewarm the brainstem. Heated inhala-
tion by face mask continuous positive airway pressure (CPAP)
may correct the ventilation-perfusion mismatch.40 Heated humidi-
fied oxygen by 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 vaporiza-
tion of water in the lungs is slightly lower than 540 kcal/g H2O.
This is multiplied by the liters per minute (L/min) 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.58
Heated humidified inhalation ensures adequate oxygenation,
stimulates pulmonary cilia, and reduces the amount and viscosity
of cold-induced bronchorrhea. Although preexisting premature
CHAPTER 7  Accidental Hypothermia
100
O2 (% saturation)
50 NORMAL
T 37° C
pH 7.40
0
0 50 100
PO2 (mm Hg)
FIGURE 7-9  Oxyhemoglobin dissociation curve at 37° C (98.6° F). At
colder temperatures, the curve shifts to the left.
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 experi-
mentally the core temperature continues to rise.56
There are numerous oxygenation considerations in hypother-
mia (see Box 7-1). The “functional” value of hemoglobin at 28° C
(82.4° F) is 4.2 g/10 g in patients on CPB. The oxyhemoglobin
dissociation curve also shifts to the left (Figure 7-9). This impairs
release of oxygen from hemoglobin into the tissues. Although
some patients can self-adjust their respiratory minute volume
(RMV) for current CO2 production, this may not be possible if
there are additional toxins or metabolic depressants.58
Most humidifiers are manufactured in accordance with Inter-
national Standards Organization (ISO) regulations. The humidifier
will not exceed 41° C (105.8° F) close to the patient outlet with
a 6-foot (180-cm) tubing length.331 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 by ETT 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
outside the patient circuit.331 Label all modified equipment to
avoid routine use. A volume ventilator with a heated cascade
humidifier can also deliver CPAP or positive end-expiratory pres-
sure (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.58
In stable patients, circumventing the 41° C ceiling may not be
worth the effort because the clinical benefit is modest.162
Heat and moisture exchangers function as artificial nares by
trapping exhaled moisture and then returning it. The exchangers
provide inadequate humidification to treat accidental hypother-
mia. With prolonged use, ETT occlusion and atelectasis are both
problems.49
Airway rewarming is indicated in the ED when core tempera-
ture is lower than 32.2° C (90° F) on arrival. Although airway
rewarming provides less heat than 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 temperature
after resuscitation was 31.2° C (88.2° F) in those with refractory
151
 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 Warm
volume resuscitations.26,291 One liter of fluid at 42° C (107.6° F) saline
provides 14 kcal to a 70-kg (154-lb) 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 15 min
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.119,277
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,
calcium-free crystalloid. Portable and other commercial fluid
warmers heat cold crystalloid and blood through a heat exchanger
at flow rates of up to 500 mL/min.
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 tem-
perature significantly different from that of circulating blood may Drainage
produce myocardial thermal gradients. In one study, heated IV
fluid, up to 550 mL/min, was administered through the internal
COLD AND HEAT

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 FIGURE 7-10  Gastric lavage.
hemolysis.90,288
Using amino acid infusions may accelerate energy metabo-
lism.285 Fever is common in patients receiving hyperalimentation. with warm fluids. Disadvantages include the small surface area
In patients recovering from elective surgery, however, amino available for heat exchange and the large amount of fluid escap-
acids have no significant thermogenic effect.133 The results might ing into the duodenum.38 Regurgitation is common, and the
differ in energy-depleted patients with chronically induced acci- technique must be terminated during CPR. Esophageal and
PART 2

dental hypothermia.
In summary, IV 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.148 A mathematic model indicates that infu-
sion heating devices are essential in trauma patients with high
fluid requirements.26
HEATED LAVAGE
Gastrointestinal Lavage
Heat transfer from irrigation fluids is usually limited by the avail-
able surface area. The irrigant should not exceed 45° C (113° F).
Direct GI 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 by gravity drain-
age 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 antici-
pation of dilutional electrolyte disturbances.
To avoid these limitations, a double-lumen esophageal tube
is available, as are other modified tubes. Patients should be tra-
cheally intubated before gastric lavage. Because of the proximity
of an irritable heart, overly vigorous placement of a large gastric
tube is not 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.62
Commercially available kits designed for gastric decontamina-
tion are convenient (Figure 7-10). 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.191 After 15 minutes the solution is aspirated and replaced
bladder heat exchange are also very limited.336,337 Aesthetic obsta-
cles aside, heat transfer through colonic irrigation is negligible.
Mediastinal Lavage
Mediastinal irrigation and direct myocardial lavage are alterna-
tives in patients lacking spontaneous perfusion. A standard left
thoracotomy is performed while CPR is continued. Opening the
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.36
The physician may attempt internal defibrillation after myo-
cardial temperature reaches 26° to 28° C (78.8° to 82.4° F). Unless
a perfusing rhythm is achieved, lavage and all available heating
techniques are 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 contin-
ued rewarming via thoracic irrigation.
A median sternotomy also allows ventricular decompression
and direct defibrillation.190 One potential disadvantage of both
these techniques is that open cardiac massage of a cold, rigid,
and contracted heart may not generate flow.5,57 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 initi-
ate all other available rewarming modalities.
Thoracic Lavage
Irrigation of the hemithoraces is a valuable rewarming
adjunct.37,171,317 An important semantic issue is that closed thoracic
lavage via two thoracostomy tubes differs from open mediastinal
and direct myocardial lavage. With the latter, closed-chest CPR
is not possible. Two large-bore thoracostomy tubes (36 French
[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

152

Saline
Heat exchanger
Fluid
Air
warmer eliminator
Water seal
chest drain
A
FIGURE 7-11  Thoracic lavage. A, Cycle. B, Cross section. AA, ascending aorta; RB, right bronchus;
SVC, superior vena cava; T6, sixth thoracic vertebra.
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 7-11A).169
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.260 Ideally, connect into the tubing with stan-
dard 0.19-inch internal-diameter suction connection tubing and
a sterilized plastic graduated two-way connector, because this
facilitates adaptation to any size of chest tube (Figure 7-11A).
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 7-11B).
Fluid can be infused into the anterior higher chest tube (affer-
ent limb) and suctioned or gravity drained out the lower posterior
tube (efferent limb) into a water-seal chest drain.117 Infusion
inferoposteriorly with suction anteriorly can increase dwell
times.148 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 tube left in place
to allow residual drainage.
Closed sterile thoracic lavage is a natural choice in the ED
during potentially salvageable cardiac arrest resuscitations.346
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
Warmed
CHAPTER 7  Accidental Hypothermia
saline
Rib
2
AA S 3
V
C
RB Lung
4
T6
Midclavicular 5
line
6
Saline out
Postaxillary
line B
Autotransfusion
bag
massage of a rigid, contracted heart may not be possible in severe
cases before bypass, which is a problem with mediastinal
irrigation.5,57,61
Various complications should be considered. Left-sided tho-
racostomy 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 cardiovas-
cular effects.157,256
Peritoneal Lavage
Heated peritoneal lavage is a technique available in most facilities
(Figure 7-12). Heat is conducted intraperitoneally via isotonic
dialysate delivered at 40° to 45° C (104° to 113° F).327
Before lavage is initiated, imaging should be obtained because
subsequent films may reveal 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 pene-
trates the peritoneum, and a guidewire is introduced. Entry into
the peritoneum is usually recognizable by a distinct “pop.” Dis-
posable kits are available. 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 supplementa-
tion can be used. Isotonic dialysate is heated to 40° to 45° C (104°
153
 14F catheter

Peritoneum

Fascia of
linea alba

Wire

FIGURE 7-13  Peritoneal lavage. A 14F catheter is of a caliber that can

infuse fluids rapidly.

Umbilicus Catheter 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 cath-
COLD AND HEAT

eter, as found in cavity drainage kits (Figure 7-13). The catheter

can be placed with the Seldinger technique. The higher drainage
capability greatly 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 unavail-
able. In addition, direct hepatic rewarming reactivates detoxi­
PART 2

B fication and conversion enzymes. Peritoneal dialysis worsens

preexisting hypokalemia. Vigilant electrolyte monitoring is essen-
tial 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 effec-
tive as partial cardiac bypass in resuscitating severely hypother-
mic dogs.341 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
8F catheter inadequate visceral perfusion during CPR.
Peritoneal lavage is invasive and should not be routinely used
in treating stable, mildly hypothermic patients. This technique is
indicated in combination with all available rewarming techniques
in cardiac arrest patients.

C loop catheter has a temperature control element at the tip.
FIGURE 7-12  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.
ENDOVASCULAR WARMING
Another active rewarming option is endovascular warming with
commercially available temperature control devices. They are
used in EDs for therapeutic cooling of resuscitated comatose
cardiac arrest patients.344
Less invasive and technically easier than extracorporeal
rewarming, endovascular systems that involve femoral vein cath-
eterization may prove to be a promising alternative. The closed-
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).181
EXTRACORPOREAL BLOOD REWARMING
Table 7-4 summarizes the techniques for extracorporeal blood
rewarming.

154

TABLE 7-4  Techniques for Extracorporeal
Blood Rewarming
Technique Comments
Cardiopulmonary Full circulatory support
bypass 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)
Continuous Percutaneous Seldinger technique to insert
arteriovenous catheters
warming 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
Venovenous Circuit not complex
rewarming 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
Hemodialysis 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
Modified from Danzl DF: Hypothermia, Semin Resp Crit Care Med 23:57, 2002.
Hemodialysis
Standard hemodialysis is widely available, practical, portable, and
efficient and should be strongly considered in perfusing patients
with significant electrolyte abnormalities, renal failure, or intoxi-
cation with a dialyzable substance.140,233,247 Two-way flow cathe-
ters allow the option of cannulation of a single vessel.183,307 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 place-
ment is a major advantage. Hemodialysis via two separate single-
lumen catheters placed in the femoral vein can achieve continuous
blood flow at 450 to 500 mL/min.130,131 In-line hemodialysis also
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.111,125,298,315
The circuit is not complex and is more efficient than many
other nonbypass modalities. There is no oxygenator, and be-
cause the method does not provide full circulatory support,
volume infusion is the only option to augment inadequate car-
diac output. Although the use of CAVR is limited by profound
hypotension, high-flow venovenous rewarming may prove to be
an alternative.150
In another variation of the extracorporeal venovenous circuit,
CHAPTER 7  Accidental Hypothermia
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 subcla-
vian 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
The CAVR technique involves the use of percutaneously inserted
femoral arterial and contralateral femoral venous catheters.93,94
This technique requires a blood pressure of at least 60 mm Hg.
The Seldinger technique is used to insert 8.5F catheters. Heparin-
bonded tubing circuits obviate the need for systemic anticoagula-
tion. CAVR has principally been performed on traumatized
patients (Figure 7-14).
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. 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.230
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 (88 lb). Coagulation begins to appear in the hepa-
rinized circuits at around 3 hours.
Cardiopulmonary Bypass
Partial or complete CPB or extracorporeal membrane oxy­
genation (ECMO) should be considered in unstable, severely
hypothermic patients.14,33,211,270,348 Favorable considerations in-
clude absence of severe head injury or asphyxia.292 Some cen-
ters initiate CPB or ECMO only if the presenting arterial pH is
above 6.5, serum potassium is below 10 mmol/L, and core tem-
perature is above 10° to 12° C (50° to 54° F).135,332
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).91
A major advantage of CPB is preservation of oxygenated flow
if mechanical cardiac activity is lost during rewarming.73,144 CPB
is three to four times faster at rewarming than other active core
Water
outlet
Cold
blood
inflow Femoral
artery
Femoral
vein
Warm blood
outflow
Water
inlet
(40° C)
Filter
FIGURE 7-14  Schematic of continuous arteriovenous rewarming.
155
 Oxygenator
and
vortex pump
Portable Heat
bypass exchanger
machine
FIGURE 7-15  Femoral-femoral bypass.
COLD AND HEAT
rewarming (ACR) techniques, and it reduces the high blood
viscosity associated with severe cases. CPB should also be con-
sidered 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.154
Various extracorporeal rewarming techniques can be lifesav-
ing in select profound cases of hypothermia.122 A 65-year-old
woman survived sequela free after 520 minutes of cardiac arrest
PART 2
treated with CPR and CPB.221 Complete recovery was also
reported in three severely hypothermic tourists after prolonged
periods of cardiac arrest and CPR.5 In a review of 17 cases, there
were 13 survivors.297,332 In another series rewarming 32 patients
with CPB, 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, mechanical pump, membrane or bubble oxy-
genator, and heat exchanger (Figure 7-15). 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. Consider use of 32F venous and 28F arterial
cannulae with the open surgical technique, and 21F venous and
19F arterial cannulae if inserted percutaneously.8 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.19
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 one review,
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.297 Con-
sider the use of vasodilator therapy with IV nitroglycerin to
facilitate perfusion.199,200 Initiate bypass flow rates at about 2 L/
min and gradually increase 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.207
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
156
Arterial line
16-20F
Venous line
16-30F
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) gradients21or 10° C (18° F) gradients.22 Neuromonitoring
during rewarming is advised. In severe cases, evoked cerebral
responses before EEG regeneration could help assess the recov-
ering brain.284
A variety of techniques decrease the need for IV anticoagula-
tion with heparin, which previously limited clinical applicabil-
ity.168 Heparin-coated perfusion equipment can be considered
without systemic heparinization in patients with hypothermic
cardiac arrest and intracranial trauma. The use of nonthrombo-
genic pumps, coupled with enhanced physiologic fibrinolysis
seen in the first hour of CPB, should be considered. ECMO
requires lower levels of anticoagulation in addition to the pos-
sibility of prolonged extracorporeal-assisted resuscitation; these
factors may explain the published mortality reduction compared
with CPB.33
Complications with the standard technique include vessel
damage, air embolism, hemolysis, DIC, and pulmonary edema
(Box 7-8). ECMO appears to decrease the incidence of severe
pulmonary edema in some patients.33 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
BOX 7-8  Extracorporeal Rewarming: Complications
and Contraindications
Complications
• Vascular injury
• Air embolism
• Pulmonary edema
• Coagulopathies (hemolysis, disseminated intravascular
coagulation)
• Frostbite tissue damage
• Extremity compartment syndromes
Contraindications
• Futile resuscitations
• Lack of venous return
• Intravascular clots or slush
• Complete heparinization would be hazardous*
• Cardiopulmonary resuscitation is contraindicated (see Box 7-9)
*Unless with athrombogenic tubing or adequate physiologic fibrinolysis.

BOX 7-9  Contraindications to Initiating
Cardiopulmonary Resuscitation in Accidental
Hypothermia
• 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.
Data from Zafren K, Giesbrecht GG, Danzl DF, et al. Wilderness Medical Society
practice guidelines for the out-of-hospital evaluation and treatment of
accidental hypothermia. 2014 update. Wilderness & Environmental Medicine
2014;25:425–445.
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
perfused patients. The value of the maintenance of some degree
of mild hypothermia after hypothermic cardiac arrest and extra-
corporeal 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.271
In hypothermic cardiac arrest, rewarming should be attempted
via CPB and hemodialysis when CPR is not contraindicated (Box
7-9), unless frozen intravascular contents prevent flow. 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.21,329,347
Yes
Yes
Cardiac monitor
Core temperature
Below 32.2° C
(90° F)
Above 32.2° C
(90° F)
PER
ACR and truncal AER
FIGURE 7-16  Emergency department algorithm. ACR, Active core rewarming; AER, active external rewarm-
ing; CPB, cardiopulmonary bypass; PEA, pulseless electrical activity; PER, passive external rewarming.
Diathermy
CHAPTER 7  Accidental Hypothermia
Diathermy, the transmission of heat by conversion of energy,
is a potential rewarming adjunct in accidental hypothermia.197
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. Contraindica-
tions include frostbite, burns, significant edema, and all types of
metallic implants and pacemakers.
Under ideal conditions in a laboratory study, radio-wave fre-
quency (13.56 MHz) electromagnetic regional heating of hypo-
thermic dogs after immersion does not damage tissue at 4 to 6
watts/kg and rapidly elevates core temperature.342 In one study,
16 piglets were rewarmed with microwave irradiation “until they
squealed and suckled.”357 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.160
Both ultrasonic and low-frequency microwave diathermy can
deliver large quantities of heat below the skin. Potential compli-
cations 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.
CARDIOPULMONARY RESUSCITATION
Basic and advanced life support recommendations in hypother-
mia continue to evolve* (Figure 7-16). Cardiac output generated
with closed-chest compressions maintains viability in select
*References 187, 227, 242, 248, 295, 353.
Responsive
No
Respirations
No
Tracheal intubation and
heated humidified oxygen
Cardiac monitor
Electrical complexes Arrest rhythm
Central pulse Attempt
defibrillation
Yes No
(PEA)
All ACR and CPB
157
 patients with hypothermia.303 The optimal rate and technique
remain unclear. Definitive prehospital determination of cardiac
activity requires a cardiac monitor or portable ultrasound, because
misdiagnosis of cardiac arrest is a hazard. Peripheral pulses are
difficult to palpate when extreme bradycardia is present with
peripheral vasoconstriction.124,249,343
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.116,245 The role of acid-base fluxes is not clear. Mild
alkalosis appears somewhat protective against VF during con-
trolled, induced hypothermia.179
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 7-1). Eventually, regional cerebral oxygen saturation
monitoring may help differentiate shockable VF and ventricular
tachycardia (VT).1
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. CO2 production also
COLD AND HEAT
drops by one-half with an 8° C (14.4° F) fall in the temperature.
During induced hypothermia, carbogen (1% to 5% CO2 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 intuba-
tion reflected coincidental episodes and a mis-citation regarding
a series of hypothermic overdoses.87,188 In a multicenter survey,
endotracheal intubation was performed on 117 patients by mul-
PART 2
tiple operators in various settings.62 No induced arrhythmias were
recognized, which is consistent with several reports.186,222 Poten-
tial 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.103 Ciliary activity is
depressed in hypothermia, frothy sputum produces chest conges-
tion, and bronchorrhea resembles pulmonary edema. Fiberoptic
or blind nasotracheal intubation may be preferable to cricothy-
roidotomy when cold-induced trismus or potential cervical spine
trauma is present. Oral rather than nasal intubation is advisable
in patients with coagulopathy, to avoid 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 neu-
romuscular blockade. Drug metabolism is also prolonged with
vecuronium and atracurium. As a result, neuromuscular blockade
should be avoided.162 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. Antegrade flow occurs without
left ventricular compression in a normothermic canine model.240
Closed-chest compressions increase intrathoracic pressure.206
When thoracic inlet venous valves are competent, the resultant
pressure gradient between arterial and venous compartments
generates supradiaphragmatic antegrade flow.
The “cardiac pump” model is predicated on closure of the
mitral valve and opening of the aortic valve during chest com-
pression. This allows a forward stroke volume. During release of
compression, transmitral flow can fill the left ventricle. Optimal
cardiac output is thus generated by achieving the maximal
158
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 momen-
tum) compressions. Compression of a cold, stiff chest wall may
be equivalent to low impulse.57
In hypothermia, the role of a “thoracic pump” with the heart
as a passive conduit is an attractive hypothesis. The phasic altera-
tions in intrathoracic pressure generated by compressions are
equally applied to all 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 hypother-
mia. 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 CPB is
an option.36,37,38
Chest wall elasticity is also decreased with cold, as is pulmo-
nary compliance. If the abdominal muscles are not kneadable,
the clinician should 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 compart-
ment pressure gradients.
Despite these potential physiologic explanations, a large
number of neurologically intact survivors are reported after pro-
longed closed-chest compressions. The explanation lies in mea-
suring intrathoracic pressures during hypothermic closed-chest
compressions.23
Perfusion enhancement maneuvers remain largely unstudied
in hypothermia. Ancillary abdominal binding might favorably
inhibit paradoxical diaphragmatic motion.57,240 Simultaneous com-
pression 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 intraaortic balloon
is another option.
Mechanical thoracic compression devices should be consid-
ered during prolonged resuscitations with limited availability of
personnel. In addition, an automatic mechanical chest compres-
sion device may serve as a bridge while establishing the capabil-
ity for CPB.343
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 normother-
mic closed-chest compressions. Blood flow to these areas did
not decrease with time, unlike in the normothermic group. Hypo-
thermic 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.209
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 CPR62 (see Box 7-9).
Cardiac output is the product of heart rate and stroke volume;
therefore, the optimal closed-chest compression rate should be
the fastest rate allowing optimal ventricular filling. Many patients
have recovered neurologically with slow compression rates. One
recovered after 220 minutes at half the normal compression
rate.243 A patient at 16.9° C (62.4° F) recovered neurologically after
307 minutes of intermittent CPR. At 3-month follow-up, she
showed a good physical and neurologic recovery.23 The optimal
rate probably has a direct linear relationship with the degree of
hypothermia.
Tissue decomposition, apparent rigor mortis, dependent livid-
ity, and fixed, dilated pupils are not reliable criteria for withhold-
ing CPR. In addition, intermittent flow may provide adequate
support during evacuation. CPR should not be withheld only
because continuous chest compressions cannot be ensured.44,78
Intermittent flow may be preferable to no flow. The lowest tem-
perature documented in an infant survivor of accidental hypo-
thermia 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).102,237,244 One patient recov-
ered after 6.5 hours of closed-chest compressions.193 In Saskatch-
ewan in 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.102
CEREBRAL RESUSCITATION
The ability to reestablish cerebral blow flow (CBF) with CPR and
improve neurologic outcome is inversely proportional to the
duration of cardiac arrest. Significant delay can greatly elevate
the cerebral perfusion pressure (CPP) required to establish
CBF.18
It appears that thermal stabilization rather than aggressive field
rewarming should be the focus, except for severely hypothermic
patients or those in cardiac arrest. Mild hypothermia may be
therapeutic and improve neurologic outcome after global cere-
bral ischemia. Hypothermia decreases glutamate release, meta-
bolic demand, free radical formation, and release of inflammatory
cytokines.
In the prehospital setting, addressing disproportionate hypo-
tension, hypoperfusion, and hypoxia is paramount. Once the
airway is secured, elevating the head 5 to 10 degrees can attenu-
ate intracerebral hypertension induced by global cerebral isch-
emia. Normally, CBF is independent of CPP over a range of
pressures. After cerebral autoregulation is extinguished, CBF pas-
sively depends on the arterial blood pressure. When venous
access is difficult, medications may be administered intratrache-
ally or via the intraosseous route. Of interest, large internal
jugular catheters may partially obstruct cerebral venous outflow.353
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
PEEP 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 hyperven-
tilation except in the rare case of a cranially traumatized hypo-
thermic patient 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.210
Postischemic hyperglycemia is potentially detrimental, because
glucose levels over 250 mg/dL are associated with lactate genera-
tion and exacerbation of metabolic acidosis.
Cerebral resuscitation strategies in hypothermia reflect com-
plex neurophysiology. 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. CBF 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, cel-
lular depolarization, and acidosis. Even when cold, neurons are
more susceptible to hypoxic insult than are glial or endothelial
cells.139
When reperfusion is reestablished, the initial transient hyper-
emic 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 charac-
terized 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.47
The decrease in CBF decreases mitochondrial ATP generation.
Ionic gradients collapse across the neuronal membrane, as a
result of failure of the sodium-potassium (Na-K) pump. Sodium
influx results in depolarization, which causes axonal release of
the excitatory neurotransmitter glutamate. Glutamate is the ulti-
mate trigger of neuronal injury caused by N-methyl-D-aspartate
receptor activation, because it allows cellular calcium influx.
Second messengers in the cascade are signals during ischemia
CHAPTER 7  Accidental Hypothermia
from trigger events that activate other second messengers or
perpetrators of damage. Intracellular overload of calcium inhibits
mitochondrial respiration. In addition, nitric oxide synthase gen-
erates NO and ROS, both of which damage DNA and increase
cytokine levels. In the field, emphasis should be placed on avoid-
ance of factors known to exacerbate adverse neuronal responses
to cerebral ischemia: disproportionate hypotension, hypoperfu-
sion, hyperglycemia, hypoxia, and hyperoxia.
RESUSCITATION PHARMACOLOGY
The pharmacologic effects of medications are temperature depen-
dent; the lower the temperature, the greater 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.182 Medications are not
given orally because of decreased GI 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 tem-
perature depression, the possibility of hypovolemia, hypoglyce-
mia, 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.186
If intraarterial pressure is not consistent with the degree of
hypothermia, judicious use of inotropic agents may be neces-
sary.246 Dopamine can be a successful adjunctive treatment.281
Dopamine reverses cardiovascular depression under hypothermic
conditions, equivalent to up to 5° C (9° F) rewarming. Shock
requiring vasoactive drugs is a risk factor for mortality.37
In severe cases, the target mean arterial pressure is about
60 mm Hg. Epinephrine and vasoconstrictors should probably
be avoided.175,178 Balancing the need for flow versus pressure,
one might suggest therapy with labetalol, IV nitroglycerin, and 2
to 4 mcg/kg of dopamine.354
Epinephrine is not recommended for hypothermic cardiac
arrest below 30° C (86° F). In porcine models, there is no evi-
dence that repeated or high-dose epinephrine during hypother-
mic CPR improves outcome.175,178 In the same model, a single
0.4-unit/kg dose of vasopressin below 30° C (86° F) improved
defibrillation success.283
There is conflicting evidence regarding cardiovascular func-
tion after rewarming. In some studies, there is complete reversal
of cold-induced changes, whereas in another, the physiologic
response to norepinephrine is paradoxical.338
Patients with profound hypothermia after ethanol ingestion
have been resuscitated with low-dose dopamine support. In
frostbite victims, however, the use of catecholamines may jeop-
ardize the extremities.199,200 Catecholamines also exacerbate pre-
existing 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),43 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.30 Low-dose dopa-
mine (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.
THYROID
The most dramatic Rip Van Winkle–type rude awakening from
hypothermic myxedema coma was Dr. Richard Asher’s patient
in the 1950s. He was successfully metabolically aroused from a
159
 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.204
Myxedema coma is usually precipitated in older adult patients
with chronic hypothyroidism who are stressed by trauma, infec-
tion, anesthesia, or medication ingestion. Typical nonspecific
laboratory abnormalities include hyponatremia, anemia, and liver
function tests and lipid elevations. If myxedema coma is sus-
pected, thyroid function studies, including serum thyroxine (T4)
by radioimmunoassay, triiodothyronine (T3) resin uptake, and
thyroid-stimulating hormone level, should be obtained and serum
cortisol level measured.
Considering the previous discussion, administer 250 to
500 mcg of levothyroxine (T4) intravenously over several minutes,
without waiting for confirmatory laboratory results. Daily injec-
tions 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 IV 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 the T4 is eventually con-
COLD AND HEAT
verted by the peripheral tissues into T3.
CORTICOSTEROIDS
Acute cold stress and many coexisting disease processes stimu-
late 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 secre-
PART 2
tion may also be a neurogenic or an emotional response in the
conscious person to an unpleasant environment.
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 insuffi-
ciency, because ACTH levels return to normal after rewarming.
Serum cortisol levels are usually 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 physi-
cal 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 over-
doses and in spinal shock and appears to have activity at the
µ-opioid receptor sites.58
RESUSCITATION COMPLICATIONS
ATRIAL ARRHYTHMIAS
All atrial arrhythmias, including atrial fibrillation (AF), should have
a slow ventricular response during temperature depression. AF is
typically noted below 32° C (89.6° F). AF usually converts sponta-
neously during rewarming, and digitalization or other pharmaco-
logic intervention is not warranted. Electrophysiologic studies
show that the interval prolongation present on His bundle elec-
trocardiography is unresponsive to atropine. Mesenteric emboli-
zation and embolic stroke are potential hazards when the rhythm
converts back to sinus rhythm. Hypothermia renders the negative
inotropic effects of calcium channel blockers redundant.58
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.
160
VENTRICULAR ARRHYTHMIAS
Preexisting chronic ventricular ectopy may be suppressed in a
cold heart. Ectopy developing during rewarming is problematic.
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
(nine cases) and benign.266 Ventricular extrasystoles developed
in 10 patients, but none experienced VT or VF during rewarming.
The terminal rhythm in the eight patients who died while being
monitored was asystole and not VF. The energetics of the fibril-
lating hypothermic ventricle suggest that asystole may consume
less energy and may be more protective.
Pharmacologic options are limited because hypothermia
induces complex physiologic changes that result in abnormal
responses.349 Drug metabolism and excretion are both progres-
sively decreased. In normothermia, class IA ventricular antiar-
rhythmics have negative inotropic and indirect anticholinergic
effects and moderately decrease conduction velocity (Box 7-10).
Procainamide increases the incidence of VF during hypothermia.
Quinidine has been useful during induced profound hypother-
mia, preventing VF during cardiac manipulation at 25° to 30° C
(77° to 86° F). The efficacy and safety of disopyramide are
unknown.
The role of the class IB agent lidocaine for prophylaxis or
treatment is unresolved. In animal studies, lidocaine and pro-
pranolol have minimal hemodynamic effects in hypothermia. If
normothermic effects persist 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 is effective in several
animal studies and ineffective in others.80,304 It is not commercially
available. This class of agents seems most ideal pharmacologi-
cally 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 7-11). Two cases of
chemical ventricular defibrillation after infusion of bretylium
(10 mg/kg) in accidental hypothermia are reported.58,173
BOX 7-10  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

BOX 7-11  Antiarrhythmic Characteristics
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
In a study to evaluate the effects of bretylium administered
after induction of hypothermia, only 1 of 11 dogs given bretylium
(mean, 40.5 mg/kg) before five invasive maneuvers developed
VF.231 No dog, including control animals, fibrillated during endo-
tracheal intubation. Of note in discussions regarding prophylaxis,
3 of the 11 dogs converted to VF during the drug infusion.
Because catecholamine levels increase during cooling, the dem-
onstrated protection appears to result from alteration of electro-
physiologic properties of the cardiac tissues.
Amiodarone is another class III drug that possesses direct
antifibrillatory activity.164 In a canine model of severe hypother-
mic VF, neither bretylium nor amiodarone improved resuscita-
tion.304 The safety of the class III antiarrhythmic agent D-sotalol
is problematic.20 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 intravenously can spontaneously defibrillate most
patients on CPB at 30° C (86° F) with induced hypothermia.
Emergency transvenous intracardiac pacing of bradyarrhyth-
mias is extremely risky with cold hearts because it frequently
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.136 In a canine model, TCP restored and maintained
hemodynamic stability and rewarmed hypothermic animals twice
as rapidly as it did the controls.72
In summary, there are no commercially available ventricu-
lar antiarrhythmics proven safe and effective in accidental
hypothermia.
SEPSIS
In hypothermia, the classic signs of infection, including erythema
and fever, are absent.192 Rigors and shakes resemble shivering.
The initial history, physical examination, and laboratory data are
often unreliable, so repeated evaluations and comprehensive
culturing are mandatory. 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 com-
mon causative organisms include gram-negative bacteria, gram-
positive cocci, oral anaerobes, and Enterobacteriaceae.192
The core endotoxin components of gram-negative bacteria
normally signal macrophages. At a normal or elevated tempera-
ture, active cytokine triggers include tumor necrosis factor,
interleukin-1, and interleukin-6. Bone marrow release and circu-
lation of neutrophils are compromised for up to 12 hours. In
addition, human and porcine neutrophils are susceptible to hypo-
thermia. In vitro, neutrophil migration and bacterial phagocytosis
are reduced at 29° C (84.2° F). Neutrophilic extermination of
various bacteria, including Staphylococcus aureus and Streptococ-
cus faecalis, is also impaired.
Acquired neutrophil dysfunction occurs. In addition, hypo-
thermia is associated with decreased neutrophil levels in near-
drowned 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 patient’s
age and the clinical series reported.192,340 In one large group of
infants, more than half were septic. Although there were no reli-
CHAPTER 7  Accidental Hypothermia
able 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 Haemophi-
lus and Enterobacteriaceae.
Lung infections are reported in many hypothermic infants.
Evaluation of the gastric aspirate is a diagnostic predictor of
sepsis in the majority of infected infants. In several studies, sepsis
is found in a large percentage of hypothermic infants, and empiri-
cal broad-spectrum antibiotics are warranted.
In adults, the incidence of infection ranges from less than 1%
to more than 40%, depending on patient selection criteria.61
Serious soft tissue or pulmonary infections may be common.192
Occult bacteremia is uncommon, as is meningitis.340 In other
studies of hypothermic older adult patients admitted to hospitals,
most have had evidence of probable or definite infections.63
In summary, unlike children and older adults, most previously
healthy young adults do not need empirical antibiotic prophy-
laxis. 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 choos-
ing 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 pathog-
nomonic finding at autopsy.194,261,262 Establishing hypothermia as
the primary cause of death requires an adequate history of expo-
sure and the absence of other lethal findings at necropsy.149
Unnatural deaths in nursing home patients, for example, may be
significantly underreported for these reasons.53
Macroscopic skin changes can suggest the diagnosis. Hyper-
emia of the dorsa of the hands and knees is often found. Non-
pathognomonic pancreatic findings include fat necrosis, aseptic
pancreatitis, and hemorrhage. Pulmonary changes consist of
intraalveolar, interstitial, and intrabronchial hemorrhages.
An eye that has been directly exposed to the environment can
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
CO2 content vary inversely with temperature, with values signifi-
cantly higher in the winter. An elevated vitreous glucose in a
nondiabetic patient should suggest hypothermia.
The total urinary catecholamine, particularly epinephrine,
content was high in one group of casualties known to be hypo-
thermic. Erosions of the gastric mucosa, termed Wischnewsky
spots, are also frequently found.316 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.261
PREVENTION
To function optimally “as the water stiffens” requires an under-
standing of the principles of heat conservation and loss. Well-
trained and educated urban adults can participate in prolonged
Arctic maneuvers safely.289,290,311
To maintain core temperature in the narrow band necessary
for peak functioning in cold environments, appropriate adaptive
behavioral responses are essential.137 Autonomic and endocrino-
logic mechanisms are only supplemental.
Studies of human cold adaptation reach highly variable con-
clusions. 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.
161
 Excellent physical conditioning with adequate rest and nutri-
tion is paramount. 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 them-
selves, including long-distance skiers, should switch garments
depending on current exertional heat production.139 Dehydration
must be avoided, and 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. 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 The
U.S. Army mnemonic COLD, in reference to insulation with cloth-
ing, means clean, open during exercise to avoid sweating, loose
layers to retain heat, and dry to limit conductive heat losses.
Prevention of urban accidental hypothermia requires continu-
ous 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.
OUTCOMES
Partially in reaction to the dramatic reports of reanimations, the
historical standard of care has been that “no one is dead until
they are warm and dead.” Clearly, some victims are indeed “cold
and dead,” and it would be useful to identify them safely.10,275
Survival is difficult to predict because human physiologic
responses to temperature depression vary so widely.214,217,255,333
The type and severity of the underlying or precipitating disease
process are two determinants.325 Age extremes, although not
statistically correlated with survival, are often associated with
severe illnesses. In a multicenter survey, however, there were no
significant age differences in mortality.62
Gender, trauma, infection, and toxin ingestions affected sur-
vival differently in multiple, uncontrolled clinical studies.134,279
There were no clinically significant differences in male versus
female profiles in the multicenter survey.62 From a large hypo-
thermia database, a hypothermia outcome score could enable
multiple observers at different sites to assess treatment modalities
and outcome predictors.271 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.59,161
Reporting unusual cases to a hypothermia registry could stimulate
advances in treatment.143,221
In a multiple regression analysis of 234 cases in Swiss clinics,198
the most common 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.292 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 inde-
pendent risk factor.255
In a study of CPB survivors, 15 of the 32 patients are
long-term survivors.332 Their neuropsychological functioning after
prolonged prehospital circulatory arrest is encouraging. These
patients were not asphyxiated before becoming hypothermic. A
literature review on the outcomes of 68 patients resuscitated with
CPB notes the survival rate was 60%, and the coldest survivor
was 15° C (59° F).330 In a series of 26 patients given extracorporeal
rewarming, those with nonasphyxiated deep accidental hypo-
thermia had a reasonable prognosis.86
A valid triage marker of death is needed because vital organ
damage is difficult to predict.249,250 In one retrospective analysis
of primarily avalanche burial victims, extreme hyperkalemia
was noted on initial examination, and resuscitation proved
fruitless.276 A serum potassium below 7 mmol/L may be a valu-
able indicator for survival.25 In the Mt Hood tragedy, the non­
survivors were also hyperkalemic (serum potassium level
>10 mmol/L).122 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.34,73 In
both these reports, asphyxia and compression injury may have
been contributory. Do not attempt resuscitation if an avalanche
victim is buried longer than 35 minutes with a snow-obstructed
airway.353 Other indicators of a grave prognosis include a core
temperature below 12° C (53.6° F), arterial pH below 6.5, or evi-
dence of intravascular thrombosis (direct visualization; fibrino-
gen <50 mg/dL).
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 CHAPTER 8 
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 8-1).
Immersion in cold water is a hazard for anyone who partici-
pates in recreational, commercial, or military activities in the
oceans, lakes, and streams of all but the tropical regions of the

162
 ing 1489 people died in the water, despite the arrival of a rescue

CHAPTER 8  Immersion into Cold Water

BOX 8-1  The Official Canadian Temperature
vessel within 2 hours. Almost all these people were wearing “life
Conversion Chart preservers,” yet their causes of death were officially listed as
“drowning.”119 However, their deaths were more likely caused by
10° C (50° F)
Americans shiver uncontrollably.
immersion hypothermia. Survivors reported hearing victims’
Canadians plant gardens. screams for periods long enough (>1 hour) to indicate that the
0° C (32° F) individuals in the water survived for a time sufficient to result in
American water freezes. severe hypothermia.102,110
Canadian water gets thicker.
−18° C (0° F) RECREATIONAL ACTIVITIES AND COLD WATER
New York City landlords finally turn on the heat.
Canadians have the last cookout of the season. A Canadian Red Cross Report stated that, from 1991 to 2000,
−51° C (−60° F) there were 5900 water-related deaths in Canada. Of recreational
Mt St. Helens freezes. boating drownings, 283 (21%) occurred in “extremely cold”
Canadian Girl Guides sell cookies door to door. water, which means colder than 10° C (50° F). Of the 14% of all
−114° C (−173° F) boating drownings in which the victims were wearing personal
Ethyl alcohol freezes. flotation devices (PFDs), most of these occurred in cold water,
Canadians get frustrated when they can’t thaw the keg. and death resulted from hypothermia. Also, 232 snowmobilers
−273° C (−460° F) drowned after breaking through the ice, and 218 individuals died
Absolute zero; all American atomic motion stops. after falling through the ice during other activities. Case Studies
Canadians start saying, “Cold, eh?” 8-1 to 8-4 illustrate problems that might occur with immersion
−295° C (−500° F)
hypothermia during recreational boating, hiking, snowmobiling
Hell freezes over.
A U.S. hockey team beats Canada in the Olympic gold medal
and other activities.
game.
COMMERCIAL ACTIVITIES ON COLD WATER
Numerous examples exist of maritime occupational accidents. In
1982 the offshore mobile oil-drilling platform Ocean Ranger col-
world. Recreational aquatic activities include swimming, fishing, lapsed in mountainous seas near Newfoundland, Canada; the
sailing, power boating, ocean kayaking, white-water rafting, water temperature was −1° C (30.2° F) (Video 8-1). Eighty-four
canoeing, ocean surfing, windsurfing, waterskiing, diving, hunt- workers were plunged into the water, and, despite the presence
ing, and using personal watercraft. In addition, winter activities of a rescue vessel, all of them died. Immersion hypothermia was
such as driving on icy roads and snowmobiling can involve cold- a significant factor in these deaths, although the inability of the
water exposure as a result of accidental entry into lakes and workers to combat rough seas and to maintain airway freeboard
streams.1 Commercial activities that involve water include fishing, (i.e., the distance between the water surface and the mouth) were
shipping, offshore oil drilling, and diving. Military operations also major problems.127
over cold water include U.S. Coast Guard (Figure 8-1), Navy, and
Marine Corps missions. U.S. Army, Air Force, and Marine Corps
forces may encounter cold-water exposure during winter opera-
tions 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 individual 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 immer-
sion 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
(59° F). Table 8-1 shows the variation in water temperature
throughout the year at various sites in North America.180 Figure
8-2 shows typical worldwide sea surface temperatures for Novem-
ber, with data from 2015.126 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 A
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 7 discusses land-based
hypothermia; Chapter 69 provides a more complete discussion
of drowning; and Chapter 71 discusses diving injuries.

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 remain-
B
FIGURE 8-1  A, Canadian Coast Guard rescue boat in rough seas.
B, U.S. Coast Guard helicopter rescue in rough seas. (A courtesy
Canadian Coast Guard; B courtesy of Gordon Giesbrecht and Alan
Steinman).

163
 PART 2 COLD AND HEAT

164
TABLE 8-1  Mean Water Temperatures in °C (°F)*

Site January February March April May June July August September October November December

Kodiak, Alaska 0 (32) 0 (32) 2 (35.6) 4 (39.2) 7 (44.6) 9 (48.2) 12 (53.6) 12 (53.6) 10 (50) 7 (44.6) 4 (39.2) 2 (35.6)
Victoria, British 7 (44.6) 7 (44.6) 7 (44.6) 9 (48.2) 10 (50) 11 (51.8) 11 (51.8) 11 (51.8) 11 (51.8) 10 (50) 9 (48.2) 8 (46.4)
Columbia
Astoria, Oregon 4 (39.2) 5 (41) 7 (44.6) 10 (50) 13 (55.4) 16 (60.8) 19 (66.2) 21 (69.8) 17 (62.6) 13 (55.4) 9 (48.2) 5 (41)
San Francisco 11 (51.8) 11 (51.8) 12 (53.6) 12 (53.6) 12 (53.6) 12 (53.6) 13 (55.4) 13 (55.4) 12 (53.6) 12 (53.6) 11 (51.8) 11 (51.8)
San Diego 14 (57.2) 14 (57.2) 15 (59) 16 (60.8) 17 (62.6) 18 (64.4) 20 (68) 20 (68) 20 (68) 18 (64.4) 16 (60.8) 15 (59)
Mobile, Alabama 10 (50) 10 (50) 14 (57.2) 21 (69.8) 23 (73.4 28 (82.4) 29 (84.2) 29 (84.2) 27 (80.6) 23 (73.4) 19 (66.2) 14 (57.2)
Miami, Florida 21 (69.8) 21 (69.8) 23 (73.4) 25 (77) 27 (80.6) 29 (84.2) 30 (86) 30 (86) 29 (84.2) 27 (80.6) 25 (77) 23 (73.4)
Norfolk, Virginia 17 (62.6) 16 (60.8) 15 (59) 18 (64.4) 20 (68) 24 (75.2) 26 (78.8) 26 (78.8) 25 (77) 25 (77) 21 (69.8) 21 (69.8)
Cape May, New 3 (37.4) 3 (37.4) 5 (41) 10 (50) 14 (57.2) 19 (66.2) 23 (73.4) 23 4 (39.2) 21 (69.8) 17 (62.6) 11 (51.8) 6 (42.8)
Jersey
Traverse City, 2 (35.6) 1 (33.8) 1 (33.8) 1 (33.8) 1 (33.8) 3 (37.4) 5 (41) 10 (50) 10 (50) 6 (42.8) 5 (41) 4 (39.2)
Michigan
Puerto Rico 26 (78.8) 26 (78.8) 26 (78.8) 26 (78.8) 26 (78.8) 27 (80.6) 27 (80.6) 27 (80.6) 28 (82.4) 27 (80.6) 27 (80.6) 26 (78.8)
Honolulu, Hawaii 24 (75.2) 24 (75.2) 24 (75.2) 24 (75.2) 25 (77) 25 (77) 26 (78.8) 26 (78.8) 27 (80.6) 26 (78.8) 25 (77) 25 (77)
*Temperatures of <25° C (77° F) are noted in red.
 CHAPTER 8  Immersion into Cold Water
FIGURE 8-2  Worldwide sea surface temperatures for November 2015. (From the National Center for
Environmental Prediction, Space Science and Engineering Center, University of Wisconsin–Madison.
www7320.nrlssc.navy.mil/GLBhycom1-12/navo/globalsst_nowcast_anim30d.gif.)

Case Study 8-1  LONG-TERM IMMERSION IN Case Study 8-2  PANIC IN ICE WATER
MODERATELY COLD WATER
In February 1990, four teenage boys broke through the ice on
On February 28, 2009, four friends who were all former or Convict Lake in California. After one boy escaped and sum-
current football players in their mid-20s set out on a fishing trip moned help, a series of adults—including two lay and three
in a 6.3-m (21-foot) boat into the Gulf of Mexico west of Tampa professional rescuers—approached and also broke through the
Bay, Florida. According to the survivor’s account,148 their boat ice. It was not until a properly equipped rescue team arrived
capsized in a storm before they could return to shore, and the “that a safe rescue attempt could be made … on one lone adult.
four men were thrown into the 18° C (65° F) water. Weather In just fifteen minutes, three boys and four of their five adult
conditions were 4.3-m (14-foot) seas and winds of 15 to 18 m/ rescuers were dead.”48 Despite the common belief at the time,
sec (30 to 35 knots). None of the men was wearing a PFD at the victims did not perish as a result of hypothermia but rather
the time of the capsizing. One of the survivors dove under the from cold- and panic-induced incapacitation and drowning.
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 hypo-
thermia as a result of the combination of a low level of body-fat Case Study 8-3  “SKATING” ON THIN ICE
insulation, cold-water temperature, effect of the wind on their In the winter of 1997-1998, four people died when their snow-
wet clothing, and strenuous work to remain on the boat or to mobile broke through the thin ice of Lake Scugog, near
get out of the water. Two victims died after about 13 hours, a Toronto, Ontario, Canada. The deaths occurred, ironically,
third died after 25.5 hours, and the lone survivor was rescued during Snowmobile Safety Week in North America. The Cana-
after 43 hours by the U.S. Coast Guard. The first casualty was dian Safety Council reported that, in 1997, 101 people were
the lightest (≈98 kg [216 lb]) and wore only swimming trunks killed in snowmobile mishaps, the majority of them by drown-
and a keyhole PFD; he had discarded his T-shirt, wind pants, ing and hypothermia after crashing through ice on frozen rivers
and jacket to try to dive under the boat for supplies. The and lakes.1
second casualty, who died at about the same time, was the
heaviest (≈120 kg [265 lb]), but had spent far more time
immersed in the water than had the others. The third casualty
survived another 12 hours, but 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 strug-
gled 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 insula-
tion (sweatpants, sweatshirt, water-resistant and fleece-lined
hooded coat, skullcap, and gloves). He had a core temperature
of 31.9° C (89.5° F) after 43 hours at sea (Figure 8-3). This case
is referenced throughout this chapter. FIGURE 8-3  U.S. Coast Guard vessel approaching a survivor who is
sitting on top of an overturned boat. (Courtesy U.S. Coast Guard.)

165
 Case Study 8-4  PROBLEMS WITH COLD-WATER
RESCUE
During winter 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 (2- to 3.3-foot) waves and
30 km/hr (18.7 mile/hr) 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 core
temperature (Tco) in the hospital 44 minutes after rescue was
23.4° C (74.1° F); subsequent resuscitation efforts were unsuc-
cessful. The remaining seven survivors were resuscitated from
Tco as low as 25° C (77° F). This case illustrates the rapidity of
onset of immersion hypothermia in lean subjects and the poten-
tially serious consequences of cardiovascular instability, circum-
rescue 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 Study 8-5  DANGERS OF FISHING IN
COLD WATER
COLD AND HEAT
In December 2004, the fishing vessel Northern Edge capsized
near Nantucket, Massachusetts, in 4° C (39.2° F) water and 3- to
4-m (9.8- to 13.1-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 pas-
sengers and crew, capsized in the turbulent waters of the Til-
PART 2
lamook 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 the
crewmen to don survival suits.
Fishing vessel mishaps are a common cause of immersion
hypothermia. Case Studies 8-5 and 8-6 illustrate the problems
that face the commercial fishing industry (Figure 8-4).
Another commercial maritime disaster involving mass casual-
ties from immersion hypothermia and drowning was the capsiz-
ing and sinking of the collier Marine Electric off the coast of
Virginia in the early-morning hours of February 12, 1983 (Video
8-2) (www.uscg.mil/history/docs/casrep/1983marineelectric.pdf).
The vessel began taking on water in gale-force winds and seas
up to 11 m (35 feet) in height. Before the crew of 34 could
Case Study 8-6  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 cap-
sizing 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, mortality rate for fisher-
men was 179 per 100,000 workers; this is 16 times higher than
the averaged rates for firefighters and police officers.
166
abandon ship, the vessel capsized, throwing most of the men
into the 4° C (39° F) water (air temperature was −1.7° C [29° F]).
Only three of the crew survived despite the presence of PFDs;
as in the Ocean Ranger case, the crewmembers were incapaci-
tated by the cold water and unable to maintain airway freeboard
in the heavy seas.
The Marine Electric disaster had one beneficial outcome.
Despite the loss of 31 lives in this case, the disaster resulted in
establishment of the now-famous U.S. Coast Guard (USCG)
Rescue Swimmer program. USCG helicopters were on scene
within about 2.5 hours of the Marine Electric’s capsizing, but
without rescue swimmers, they could not recover possible sur-
vivors from the water because of the high seas and cold-water–
induced incapacitation of the crew. USCG Rescue Swimmers have
saved thousands of lives since their creation after this disaster.
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, pro-
vided many examples of accidental immersion in cold water.
Molnar124 reviewed several hundred of these cases, including 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 hypo-
thermia 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 USCG 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 the crewmen were wearing dry suits with
insulation as well as PFDs, but they were without insulated
headgear. They left the boat to swim toward 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 set-
tings 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 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
Motor vehicle submersions account for approximately 10% of
all drownings, including approximately 400 fatalities in North

FIGURE 8-4  Fishing and merchant vessels in distress in rough seas. (Courtesy U.S. Coast Guard.)
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 ice 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 restriction of alcohol use),
hypothermia is not easy to prevent. Hypothermia is now more
widely recognized than in the past, but the prevention of immer-
sion hypothermia is still a difficult and often expensive proposi-
tion. 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 (Video 8-3).
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 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 72% of respondents
thought that, under these conditions, a victim would experience
life-threatening hypothermia in less than 10 minutes. As dis-
cussed later, most adults can survive for 1 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
CHAPTER 8  Immersion into Cold Water
problems for both primary victims and 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 core temperature (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 hypother-
mia is provided in Chapter 7. This 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 cold-
water immersion can be divided into four phases: (1) initial
immersion and the cold shock response, (2) short-term immer-
sion 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 origi-
nate from or are influenced by a variety of pathophysiologic
mechanisms. Deaths have occurred during all four phases of
immersion.
PHASE 1: THE COLD SHOCK RESPONSE
(0 TO 2 MINUTES)
The cold shock response occurs during the first 1 to 2 minutes
of cold-water immersion and depends on the extent and rate of
skin cooling. The responses are generally those that affect the
167
 respiratory system, heart, and the body’s metabolism (Figure
8-5).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. Sub-
sequent 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 hyperven-
tilation 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 (Videos 8-4 and 8-5).
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 isch-
emia and arrhythmias, including ventricular fibrillation (VF).
Sudden death can occur either immediately or within minutes
after immersion as a result of syncope or convulsions, which can
lead to drowning, vagal cardiac arrest, or VF in susceptible
individuals.23,44,103,118,167
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 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 8-6
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.

RAPID SKIN COOLING

STIMULATION OF
PERIPHERAL RECEPTORS
COLD AND HEAT

GASP REFLEX AND PERIPHERAL TACHYCARDIA

HYPERVENTILATION VASOCONSTRICTION

↑ Filling
INABILITY ↑ HYPERTENSION pressure
HYPOCAPNIA TO HOLD (arterial and
BREATH venous pressure)

↑ Cardiac
PART 2

output
Respiratory Inspiratory
alkalosis shift
↑ WORK OF
HEART
Ventricular Vessel
fibrillation rupture

↓ Coronary
blood flow
↓ Serum and
↓ Cerebral body fluid Dyspnea
blood flow Ca2+
Myocardial
ischemia
Cerebrovascular
Tetanic spasms accident
Convulsions
↑ Ventricular
irritability
Panic
Cerebral
hypoxia
Arrhythmias/
Swim
ventricular
failure
fibrillation

Disorientation
INHALATION Stimulation
Loss of
OF WATER of nasal and
consciousness
glottal receptors

Drowning Vagal arrest

FIGURE 8-5  Possible cold shock responses. (From Edmonds C, Lowry C, Pennefather J: Cold and hypo-
thermia. In Diving and subaquatic medicine, Oxford, UK, 1992, Butterworth-Heinemann.)

168
 CHAPTER 8  Immersion into Cold Water
70 Non-staged

Ventilation volume (liters • min–1)

60

50

40

30

20 Staged
10

0
FIGURE 8-7  Swim failure test of a woman not wearing a personal flota-
tion device (PFD) and a man wearing a PFD swimming in cold (14° C
50 [57.2° F]) water. The man experienced difficulty early on as a result of
Respiratory frequency (breaths • min–1)

gasping and uncontrolled breathing (i.e., cold shock response) and

45 Non-staged likely would have drowned if he was not wearing a PFD. (Courtesy
Gordon G. Giesbrecht.)
40

35 respiratory effects are under control, immediate action should be

taken. If self-rescue is not possible, actions to minimize heat loss
30 should be initiated by remaining as still as possible in the heat
escape lessening position (HELP), in which the arms are pressed
25 against the chest while the legs are pressed together, or by hud-
dling with other survivors (Figure 8-8).86 Drawstrings should be
20 tightened in clothing to decrease the flow of cold water within
Staged clothing layers (see Videos 8-4 and 8-5).
15
–20 0 30 60 90 120 150 180 PHASE 3: ONSET OF HYPOTHERMIA (IMMERSION
Immersion time (s) FOR LONGER THAN 30 MINUTES)
FIGURE 8-6  Respiratory responses (minute ventilation and respiratory Most cold-water deaths likely result from drowning during the
rates) to sudden and graded immersion into cold water. Error bars = first two phases of cold-water immersion, as discussed previ-
standard deviation. (From Hayward JS, French CD: Hyperventilation ously. In general, true hypothermia usually only becomes a
response to cold water immersion: Reduction by staged entry, Aviat significant contributor to death if immersion lasts more than 30
Space Environ Med 60:1163, 1989.) to 60 minutes. A survey indicates that even medical practitioners
greatly underestimate the time required for a person to become
hypothermic in cold water.47 In fact, 72% of respondents
believed that a properly clothed adult would become hypother-
PHASE 2: COLD INCAPACITATION mic after less than 10 minutes in ice water (0° C [32° F]) (Figure
(5 TO 15 MINUTES) 8-9). An individual who survives the immediate and short-term
phases of cold-water immersion faces the possible onset of
For persons who survive the cold shock response, significant hypothermia, because continuous heat loss from the body even-
cooling of muscle and nerve fibers—especially in the extremities— tually decreases Tco. Many predictive models to determine the
continues, with most of the effect occurring during the first 15 Tco response to cooling are based on the relationships among
minutes of immersion. This cooling has a direct deleterious effect body composition, thermoregulatory response (i.e., shivering
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,40,51,133,134,191 and swim failure (Figure 8-7).
It has been shown that this effect is primarily the result of periph-
eral 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
best to avoid cold-water exposure completely. If cold-water
immersion occurs, it is best quickly to determine and 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 FIGURE 8-8  Group huddle techniques for decreasing the cooling rates
when cold shock responses predominate. However, after of survivors in cold water. (Courtesy Gordon G. Giesbrecht.)

169
 BOX 8-2  The 1-10-1 Principle BOX 8-3  Controversy Box: Time to Hypothermia

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 personal flotation device, 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.
thermogenesis), clothing and insulation, water temperature, and
sea conditions90,163,197,202,207 (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 another hour or
more 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 8-2).
COLD AND HEAT
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.
rescue periods, despite the survivor being recovered in an appar-
ently 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 col-
lapse to describe these events. Deaths have occurred within
minutes before rescue, while climbing out of the water, while
being hoisted onto a helicopter, within a few minutes of entering
CAUSE OF DEATH IN COLD (NO FLOTATION)
100.0

The relative contributions of the first three phases to death in 90.0

cold water of varying temperatures are estimated schematically Relative contribution to death (%)
in Figure 8-10. In colder water, if no flotation is worn (A), death 80.0
occurs as a result of cold shock or cold incapacitation. Only if 70.0
flotation is worn (B) will a victim survive long enough to die as
a result of hypothermia (Box 8-3). 60.0 Cold
incapacitation
50.0 Cold shock
PHASE 4: CIRCUM-RESCUE COLLAPSE
40.0 Hypothermia
PART 2

Anecdotal cases of fatalities among immersion hypothermia

victims have been noted during the immediate pre- and post- 30.0
20.0
10.0
0.0
60 0 5 10 15 20
A Water temperature (° C)
Question 1: Time to become hypothermic
50 Question 2: Time to life-threatening cooling CAUSE OF DEATH (WITH FLOTATION)

100.0
Percent of responses

40
90.0
Relative contribution to death (%)

80.0
30
70.0
60.0 Cold
20 incapacitation
50.0
Cold shock
40.0 Hypothermia
10
30.0
20.0
0 10.0
16–30 31–60 >60
10

5
5

0.0
–1
0–
6–

Time periods (min)

11

0 5 10 15 20
FIGURE 8-9  Estimates of 661 respondents regarding how long it B Water temperature (° C)
would take to become hypothermic (yellow bars) and to die of hypo-
thermia (purple bars) in ice water when wearing winter clothing. (From FIGURE 8-10  Estimation of the relative contributions of cold shock,
Giesbrecht G, Pretorius T: Survey of public knowledge and responses cold incapacitation, and hypothermia to death in water at different
to educational slogans regarding cold water immersion, Wilderness temperatures. A, Estimation if no flotation is available. B, Estimation if
Med Newslett 19:261, 2008.) flotation is available.

170
 CHAPTER 8  Immersion into Cold Water
Heart rate (min–1)
200 72 102

160

BP (mm Hg)
120
80
40
0

(FALL IN CVPα 12 mm Hg)

CVP (mm Hg)

20

0
20
Lift Re-immersion

Time (s)

FIGURE 8-11  Heart rate and blood pressure responses during the vertical removal of a test volunteer from
cold water. (From Golden FS, Hervey GR, Tipton MJ: Circum-rescue collapse: collapse, sometimes fatal,
associated with rescue of immersion victims, J R Navy Med Serv 77:139, 1991.)

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 8-11); and (3) factors
that potentiate the risk of VF (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,
even after cold-water immersion has ended.2,13,20,57,75,141,147,194 After-
drop of as much as 5° to 6° C (9° to 10.8° F) has been observed
in humans6,43,161 (Figure 8-12). This afterdrop has long been

37.5

37
Temperature (° C)

36.5

36
Injection
period

35.5
Baseline Exit Transfer
Immersion Chamber rewarming
35
0 50 100 150 200
Time from cold water exit (min)

FIGURE 8-12  Core temperature response of a nonshivering volunteer (whose response was inhibited with
meperidine [in five aliquots during injection period]) during spontaneous warming (red), inhalation warming
(blue), and forced-air warming (green). Warming took place in a chamber at −20° C (−4° F). Only forced-air
warming reversed the afterdrop. Temperature remained low for several hours, even with inhalation warming.
(From Giesbrecht G, Wilkerson J: Hypothermia, frostbite and other cold injuries, ed 2, Seattle, Wash, 2006,
The Mountaineers Books.)

171
 proposed to be the major cause of post-rescue death, because
further cooling of the heart might result in a temperature at which
VF or cardiac arrest could occur.13
Golden and colleagues73 discount the importance of this phe-
nomenon and propose the collapse of arterial pressure as the
cause of death during rescue. They correctly note that afterdrop
occurring 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
VF. They also propose that removal from cold water results in a
precipitous fall in blood pressure, inadequate coronary blood
flow, and myocardial ischemia, which may precipitate VF. 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 barore-
ceptor reflexes. However, this mechanism cannot fully account
for all the other 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) caused a fivefold decrease in the electrical threshold for
VF.25 Also, an increase in the rate of myocardial cooling may
COLD AND HEAT
likely stimulate fibrillation. On the basis of the large afterdrop
values described previously, it is plausible that continued Tco
cooling in significantly hypothermic patients could result in VF,
caused primarily by spontaneous fibrillation of the cold myocar-
dium or secondary to a cold-induced increase in sensitivity to
other fibrillation stimuli.
Death may occur within minutes to hours after rescue. A
rescued victim may be severely compromised with cold alkaline
or acidic blood returning from the extremities, a heart that is
PART 2
extremely prone to failure, a decrease in or a loss of conscious-
ness, or low blood volume (hypovolemia). Sudden redistribution
Patient’s ability to
Core rewarm without
Classifications temperature external heat source
Normal Above 35° C
(95° F)
Mild 35-32° C
(95–90° F)
Moderate 32-28° C
(90–82° F)
Severe Below 28° C
(82° F)
Below 25° C
(77° F)
Bold text shows the major thresholds between stages of hypothermia.
FIGURE 8-13  Classification of levels of hypothermia on the basis of core temperature and clinical
presentation.
172
of blood to the extremities (especially the lower extremities) may
cause collapse as a result of decreased blood pressure and car-
diovascular instability, sudden return of metabolic byproducts to
the irritable heart, or continued decrease in temperature (after-
drop) of an irritable heart. The Tco will continue to drop, and the
heart will 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 core temperature 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 classifica-
tions are used here (Figure 8-13). 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 VF or asys-
tole. Death from hypothermia is generally a result of cardiore-
spiratory 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 exog-
enous variables that affect cooling rate (e.g., clothing, water
Clinical presentation
Cold sensation;
shivering
Good Physical Mental
impairment impairment
• Fine • Complex
motor • Simple
• Gross
motor
Limited Below 30° C (86° F)
shivering stops;
loss of consciousness
Unable Rigidity
Vital signs reduced or absent
Severe risk of mechanically
stimulated (rough handling)
ventricular fibrillation (VF)
Unable Spontaneous ventricular
fibrillation (VF);
cardiac arrest
temperature, sea state, flotation, behavior), preclude exact pre-

CHAPTER 8  Immersion into Cold Water

dictions of survival time. However, sufficient experimental data 0.07
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 0.06
survivor is trying to combat rough seas, this level of dysfunc-
tion may potentiate drowning. At a Tco of 30° C (86° F), uncon-
sciousness is probable. Even if a survivor is wearing a 0.05
self-righting PFD that has been designed to maintain airway

Cooling rate (° C min–1)

freeboard in an unconscious person, drowning is probable at
this Tco in any sea state where water can enter the unconscious
survivor’s mouth and nose. In one study on survivors wearing 0.04
a type I PFD in a wave tank, even 15-cm (6-inch) waves were
capable of covering a person’s nose and mouth in the absence
of evasive action to maintain airway freeboard, something an 0.03
unconscious survivor would be unable to do. At a Tco of less
than 25° C (77° F), VF or asystole often occur spontaneously.29
Of these three core temperatures, 30° C (86° F) is the most prac-
0.02
tical for defining the limits of survival in cold water (see Sur-
vival Modeling, p. 185).18,29,158,159,163
The rate of body Tco cooling during cold-water immersion
depends on the following variables: water temperature and sea 0.01
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.
0 5 10 15 20 25
Water temperature (° C)
WATER TEMPERATURE AND SEA STATE
Water temperature and sea state are critically important to the FIGURE 8-14  Relationship between water temperature and mean
intensity of the cold shock response, the onset of physical and rectal temperature cooling rate in lightly clothed, nonexercising males
mental impairment, and the rate of Tco cooling. Figure 8-14 and females during immersion in seawater. Error bars = standard devia-
graphically illustrates the inverse linear relationship between tion. (From Hayward JS: The physiology of immersion hypothermia. In
water temperature and Tco cooling rate.82 Water conducts heat Pozos RS, Wittmers LE, editors: The nature and treatment of hypother-
mia, Minneapolis, 1983, University of Minnesota Press.)
away from the body approximately 25 times as fast as does air
at the same temperature.125

THERMAL PROTECTION
Many studies over the past few decades have evaluated the
relationships of different types of protective clothing with heat TABLE 8-2  Mean Linear Cooling Rates for Lean Men
loss and cooling rates.* Almost all these have been conducted in Dressed in Various Types of Garments in Calm Water
calm water or in laboratory settings. As illustrated by the cooling at 10° C (50° F)
rate data in Tables 8-2 and 8-3, such studies have generally
shown that, in calm water, intact “dry” and insulated garments Cooling Rate Given as
provide better protection than do “wet” insulated garments, and Type of Protective Clothing °C/hr ±SD (°F/hr ±SD)
that well-insulated garments provide significantly better protec-
tion than do poorly insulated garments. Figure 8-15 shows Control (equivalent to ordinary street 3.2 ±1.1 (5.8 ±2.0)
various types of cold-water protective garments. clothes)
Although calm-water studies have value in that they compare
the relative degree of protection afforded by different types of “Wet” Design
protective clothing, many immersion accidents occur in rough Thermal float coat (loose-fitted, 1.6 ±0.6 (2.9 ±1.1)
water.143,168,169 In this environment, a survivor’s cooling rate may 5.4-mm [0.21-inch] closed-cell
be affected by swimming to maintain airway freeboard, passive foam-insulated jacket)
body movements caused by waves, flushing of cold water Short wet suit (custom-fitted, 3.2-mm 1.2 ±0.4 (2.2 ±0.7)
through “wet” suits, and leakage of cold water into “dry” suits. [0.13-inch] closed-cell foam that
For example, individuals in a wave tank demonstrate higher covers the arms, the trunk, and the
energy expenditure and faster cooling rates than do those in upper thighs)
calm water.81 Several experimental studies have demonstrated Insulated coveralls (loose-fitted, 1 ±0.4 (1.8 ±0.7)
significantly faster cooling rates for human volunteers wearing 3.2-mm [0.13-inch] closed-cell foam
“wet” protective garments in rough or turbulent water142,158,203 that covers the extremities and the
than for persons in calm water. Even “dry” suits have shown trunk)
degradation of protection in rough water. In a study of dry Full wet suit (custom-fitted, 4.8-mm 0.7 ±0.3 (1.3 ±0.5)
immersion suits in 16° C (60.8° F) water, Ducharme and Brooks31 [0.19-inch] closed-cell foam that
found that wave heights of up to 70 cm (28 inches) resulted in covers the extremities and the trunk)
a 14% decrease in total suit insulation and an average 45%
decrease in thermal resistance at the head and trunk regions of “Dry” Design
the suits. Immersion suit (loose-fitted, 4.8-mm 0.5 ±0.3 (0.9 ±0.5)
[0.19-inch] closed-cell foam with
sealed openings)

From Steinman AM, Hayward JS, Nemiroff MJ, et al: Immersion hypothermia:
Comparative protection of anti-exposure garments in calm versus rough seas,
*References 5, 35, 83, 89, 98, 99, 109, 132, 150, 158, 159, 166, 170, 172, Aviat Space Environ Med 58:550, 1987.
173, 175, 198, 203. SD, Standard deviation.

173
 TABLE 8-3  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)
Ratios as Compared
with Control
Mean Cooling Rate
Clothing Type Given as °C/hr (°F/hr) Direct Inverse

Dry, closed-cell foam insulation (4.8-mm [0.19-inch] thick) 0.31 (0.56) 0.14 7.35
Wet, closed-cell foam insulation (4.8-mm [0.19-inch] thick) 0.54 (0.97) 0.23 4.26
Dry and uninsulated (watertight shell over lightweight clothing) 1.07 (1.93) 0.47 2.15
Control (lightweight clothing alone) 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.

Figure 8-16 shows a comparison of cooling rates for lean
males dressed in the various types of protective clothing shown
in Figure 8-15 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 almost doubled in rough seas
compared with those seen in calm seas. This was primarily
COLD AND HEAT
PART 2
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 than that seen in calm water.
The “dry” suit, which did not leak, showed no significant differ-
ence between calm and rough seas.
Estimated survival times in rough seas, on the basis of experi-
mental data, were published for thin males wearing different

A B C D

E F G
FIGURE 8-15  Antiexposure garments. A, Float coat. B, Aviation coveralls with personal flotation device.
C, Boat-crew coveralls or snowmobile suit. D, Short wet suit worn as an undergarment. E, Full wet suit with
personal flotation device. F, Insulated dry suit. G, Immersion suit. The garments in A, B, and C are loose-
fitting, closed-cell, foam-insulated wet suits. The garments in D and E are tight-fitting, closed-cell, foam-
insulated wet suits. The garments in F and G are closed-cell, foam-insulated dry suits.

174
 CHAPTER 8  Immersion into Cold Water
12
Flight suit
11
Float coat
10
Death from
Shorty wet suit 9 hypothermia
8 highly probable

Survival time (hr)

Aviation coveralls

Boat crew coveralls 7

Wet suit
Calm
Dry suit
Rough
Survival suit
0 1 2 3
Cooling rate (° C/hr)
FIGURE 8-16  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: Immer-
sion hypothermia: Comparative protection of anti-exposure garments
in calm vs rough seas, Aviat Space Environ Med 58:550, 1987.)
types of protective clothing in 6° C (42.8° F) water.159 Table 8-4
shows these times for three different levels of survival. Underly-
ing 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 uncon-
sciousness occurs at a rectal temperature of 30° C (86° F).
4. Self-righting flotation maintains airway freeboard when survi-
vors are unconscious.
When comparing these estimated survival times with those of
Figure 8-17 (i.e., calm-water survival times), the reader must
recall that Figure 8-17 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 light-
weight 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 8-17
and Table 8-4. We must emphasize that the estimates in Table
8-4 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 range average 25% to 30%
body fat, the estimates of “time to unconsciousness” and “time
6 rs
ole
5 co s
ow ler
Sl c oo
4 ge
era lers
3 Av t coo
Fa s
2 Death from hypothermia
4 highly improbable
1
0
0 5 10 15 20 25
Water temperature (° C)
FIGURE 8-17  Predicted calm-water survival time (defined as the time
required to cool to 30° C [86° F]) in lightly clothed, nonexercising
persons in cold water. The graph shows a line for the average expec-
tancy 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 adults and teenagers
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, par-
ticularly 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 M16120.6, 1995.)
to cardiac arrest” must be considered conservative for a broader
spectrum of adults.
A recent video production called Cold Water Boot Camp
(Video 8-6) tested various flotation ensembles, including closed-
cell and inflatable PFDs, heavy dry suits, and lighter extended-
wear (paddling) dry suits. Figure 8-18 schematically shows that
Tco and survival time decrease as the amount of thermoprotection
and flotation decreases (Box 8-4).

TABLE 8-4  Estimated Survival Times for Lean Persons (Mean Body Fat = 11.1%) Wearing Various Types of Protective
Clothing in Rough Seas
Estimated Survival Time (hr) (95% CI)
Time to Incapacity (hr) Time to Unconsciousness Time to Cardiac Arrest
Clothing Type (T = 34° C [93.2° F]) (hr) (T = 30° C [86° F]) (hr) (T = 25° C [77° F])

Control (lightweight clothing) 0.4-1.3 0.8-2.6 1.3-4.3

Torn, non–foam-insulated, dry coveralls (50.8 mm 0.9-2.7 1.6-5.2 2.5-8.4
[2-inch] tear in left shoulder)
Closed-cell foam-insulated, wet coveralls (3.2-mm 1-2.9 1.9-6 3-9.9
[0.13-inch]–thick insulation in loose-fitted coveralls)
Closed-cell foam-insulated, custom-fitted wet suit 1.6-4.7 3.1-9.9 4.9-16.2
(4.8-mm [0.19-inch]–thick insulation; tight-fitted)
Intact, non-foam–insulated, dry coveralls (watertight 2.9-8.8 5.7-18.2 9.1-30
shell over thick, fiberfill, insulated underwear)

From Steinman AM, Kubilis P: Survival at sea, report no CG-D-26-86, US Coast Guard. 1986, National Technical Information Service.
CI, Confidence interval; T, temperature.

175

Flotation
High thermal protection
Core temperature
The advantage of body fat as an insulator against cold is
discussed earlier. With the use of an extrapolation of a linear
cooling rate to 30° C (86° F), Figure 8-17 shows predicted calm-
water survival times of lightly clothed, nonexercising individuals
in cold water. The graph shows a line for the average survival
expectancy. A broad zone indicates the large amount of indi-

Flotation
Moderate thermal protection
Flotation
No thermal protection
No flotation
No thermal protection
Time
FIGURE 8-18  Schematic estimation of core temperature and survival
times with varying flotation devices and thermal protective clothing.
vidual variability associated with different body sizes, builds, and
degrees of fatness. The zone would include approximately 95%
of the variation expected for adults and teenagers under the
conditions specified. For the zone in which death from hypo-
thermia 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. Again, importantly, Figure 8-17 dis-
cusses only calm-water survival times. Because rough-water con-
ditions decrease survival times, as discussed later, Figure 8-17
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

BOX 8-4  Controversy Box: Flotation Clothing Impedes
Because of the difference in thermal conductivity between air
Escape from Submersed Vehicles and water (as discussed previously), heat loss from body surfaces
immersed in cold water is much greater than from body surfaces
In many winter road jurisdictions, workers are mandated to wear
exposed to cold air, even considering the effect of windchill.
thermoprotective flotation jackets or overalls. Some workers resist
Thus, immersed victims should attempt to get as much of their
COLD AND HEAT

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, PFDs might impede
exit and are not recommended for vehicle use in any situation.59
PART 2
bodies out of the water as possible (Figure 8-20) (see Cold-Water
Survival, later).
HEAD IMMERSION
Exposure of the dorsal head to cold water may increase a survi-
vor’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,
BODY MORPHOLOGY (SIZE AND COMPOSITION)
Children cool faster than adults because children have a greater
surface area–to–mass ratio. The rate of heat loss 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 larger adults, and tall, lanky individuals cool
faster than short, stout individuals. Body composition is also 2.0
important. Subcutaneous fat is a very efficient insulator against
heat loss, and cooling rate is inversely related to skinfold thick-
ness. For example, persons in the 10th percentile for skinfold
thickness and mass wearing light clothing in 5° C (41° F) water 1.5
have nine times the core cooling rate of those in the 90th per-
Fall in Tre ° C

centile for skinfold thickness and mass.132 Figure 8-19 shows the
linear relationship between change in Tco and mean skinfold
thickness.101 Shivering, which is a primary defense against Tco
1.0
cooling, also varies with skinfold thickness. At a given skin tem-
perature, the shivering response is less in persons with greater
amounts of subcutaneous fat.108 In moderately cold water tem-
peratures (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 individu- 0.5
als because of greater shivering thermogenesis in the low-fat
group. 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 0.05 0.10 0.15 0.20 0.25
Tco cooling rate is fairly linear after Tco begins to decline. This Reciprocal of mean skinfold thickness mm–1
has been shown to be true for mildly hypothermic experimental
participants. The only data that exist for severely hypothermic FIGURE 8-19  Relationship between subcutaneous fat thickness in 10
humans are those from the infamous Dachau concentration camp men and the decline in rectal temperature during 30-minute immer-
atrocities, in which conscious victims were inhumanely cooled sions in stirred water at 15° C (59° F). Skinfold thickness is given as a
to death in ice water.2 Because these unfortunate victims were mean of readings at the biceps, the abdomen, and subscapular and
emaciated and ill, these data do not apply to healthy, cold-water subcostal sites. Tre, Rectal temperature. (From Keatinge WR: Survival
immersion volunteers and should be considered atrocious. in cold water, ed 2, Oxford, 1969, Blackwell Scientific Publications.)

176
 insulated, there was no Tco cooling with the head out of the

CHAPTER 8  Immersion into Cold Water

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 signifi-
cantly increased the rate of Tco cooling to 5.0° C/hr (9° F/hr)
(Figure 8-31).
These results did not confirm the supposition of proportion-
ately greater heat loss from the head. The measured heat loss

FIGURE 8-20  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.)

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
through the head either through convection (heat loss from the
blood that perfuses the scalp) or conduction (direct heat loss
through bone and soft tissue).206 One hypothesis predicts sub-
stantial heat loss through the head because of abundant scalp
vascularity and because the scalp vasculature does not vasocon-
strict in response to cold as do superficial blood vessels in other
body areas.45 Alternatively, heat loss from the back of the head FIGURE 8-21  Effectiveness of various types of personal flotation
might be minimal, because dorsal head and neck immersion devices for keeping the head and the upper chest out of the water.
would only involve an additional 3% to 5% of the body surface Top left, Type I jacket; top right, type 3 jacket; bottom left, typical
area.107 In addition, conductive heat loss directly through the keyhole inflatable jacket; bottom right, waist-mounted inflatable
scalp and skull is likely to be minimal.206 device. (Courtesy Gordon G. Giesbrecht.)
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. Alexander2
reported the data regarding head cooling from studies carried
out on prisoners of war in Dachau during World War II. 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 regard-
ing 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 evaluated the effects of dorsal
head and neck immersion among human volunteers immersed
in 10° C (50° F) water on Tco cooling rates and mental perfor-
mance. Dorsal head and neck immersion (with the body insu-
lated) 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 signifi-
cant correlations between diminished cognitive performance and
decreasing Tco. The time required to complete correctly 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). Figures 8-21 to
8-30 demonstrates the effects of different PFDs on the position
of the head in water.
Giesbrecht and co-workers46 repeated the head-cooling study
with participants immersed in 12° C (53.6° F) water whose shiver- FIGURE 8-22  Lead investigator testing head cooling during a submer-
ing thermogenesis had been inhibited with intravenous me­ sion study to assess the relative contributions of the head and body
peridine to model severe hypothermia.67 When the body was to core-temperature decline in cold water.

177

COLD AND HEAT
FIGURE 8-23  Lead investigator assessing participant in dorsal head
and body immersion study in cold water.
PART 2
FIGURE 8-25  Cognitive function testing in a participant wearing a
prototype inflatable personal flotation device in a study to assess the
relative contributions of the dorsal head and the body to core-
temperature decline and cognitive function in cold-water immersion.
178
FIGURE 8-24  Participant testing prototype inflatable personal flota-
tion device in a study to assess the relative contributions of the dorsal
head and the body to core-temperature decline and cognitive function
in cold-water immersion.
FIGURE 8-26  Dorsal head–only immersion in a study to assess the
relative contributions of the dorsal head and the body to core-
temperature decline and cognitive function in cold-water immersion.
The participant is wearing a full-body dry suit so that only his dorsal
head is exposed to the cold water. Core temperature from the esopha-
geal site, skin temperatures, oxygen consumption, and carbon dioxide
production are being measured.
FIGURE 8-27  Participant adopting the heat escape lessening position
(HELP) while wearing a prototype inflatable personal flotation device
in a study to assess the relative contributions of the dorsal head and
the body to core-temperature decline and cognitive function in cold-
water immersion.
 been determined, but the implications are clear for manufacturers

CHAPTER 8  Immersion into Cold Water

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 practical (Box 8-5).

FIGURE 8-28  Investigator testing the flotation posture of a prototype

inflatable personal flotation device in an “unconscious” survivor.

FIGURE 8-30  Participant rewarming in a circulating warm-water bath

in a study to assess the relative contributions of the dorsal head and
the body to core-temperature decline and cognitive function in cold-
water immersion.

38.0
Esophageal temperature (° C)

37.5
†
37.0 †

36.5
*
36.0
*
35.5
35.0 **
FIGURE 8-29  Participant emerging from cooling tank after a dorsal
head, full-body immersion in a study to assess the relative contribu- 34.5
tions of the dorsal head and the body to core-temperature decline in 34.0
cold water. Note the peripheral vasodilation. Participant’s core tem-
perature was 34° C (93.2° F). 33.5
–20 –10 0 10 20 30
Time (min)
from the head in both head-immersed conditions was only about Body insulated, head out
60 kilojoules (kJ) compared with 18 kJ to 33 kJ in the two
Body insulated, dorsal head in
head-out conditions. By contrast, total body heat loss in the
body-exposed configurations was about 1100 kJ and 1260 kJ, Body exposed, head out
respectively, for head-out and back-of-the-head-in conditions. Body exposed, dorsal head in
Thus, the head accounted for only about 3% and 5% of the total
body heat loss, respectively, in the body-exposed conditions. The FIGURE 8-31  Core-temperature response to immersion in 12° C
majority of the difference in heat loss in the body-immersed (54° F) water with the head out or the dorsum immersed in body-
conditions came from immersion of the anterior thorax rather insulated and body-exposed conditions; shivering was inhibited with
than from the dorsal head and neck. Nevertheless, it is important meperidine to mimic a severely hypothermic, nonshivering victim. Error
to recognize that, although no significant increase occurred in bars = standard deviation. (From Giesbrecht G, Lockhart T, Bristow G,
heat loss through the head, there was a disproportionate increase et al: Thermal effects of dorsal head immersion in cold water on non-
in Tco cooling. The mechanisms for this disparity have not yet shivering humans, J Appl Physiol 99:1958, 2005.)

179

BOX 8-5  Controversy Box: You Lose Most of Your
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 core temperature.
Thus, head contact with cold water should be minimized whenever
possible by changes in posture and maximum practical insulation.
BEHAVIOR AND POSTURE OF THE BODY
IN COLD WATER
Behavioral variables also affect Tco cooling rate. Hayward and
colleagues85 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. 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
COLD AND HEAT
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 drownproof-
ing 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 (see Figure 8-8). 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 colleagues145 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.
EXERCISE
Normally, the advice is not to exercise while awaiting rescue in
cold water. 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.
Færevik and colleagues39 studied participants wearing neoprene
survival dry suits in a wave tank with water temperature of 0° C

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
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 8-32. In
PART 2
(32° F) and air temperature of −5° C (23° F). When they 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 8-33). Thus, if
enough insulation is worn, the heat of exercise can be contained
within the insulation, which attenuates the drop in Tco.
SHIVERING

normothermic circumstances, heat produced locally in peripheral Shivering is a thermoregulatory function during which involun-
muscles is transferred to the core by venous return. By contrast, tary muscle contraction increases heat production in an effort to
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 exces-
sive movement in the water (e.g., swimming, performing the
37.8 * 100.0

37.6 99.7

37.4 99.4
Metabolic Heat Production
Temperature (° C)

Temperature (° F)
37.2 99.0

37.0 98.6
↑ Local ↑ Local ↑ Body
heat production blood flow movements 36.8 98.2
in periphery to periphery 36.6 97.8

36.4 97.5

↑ Convective ↑ Convective heat ↑ Convective 36.2 97.2

heat transfer loss (blood flow) and conductive
36.0 96.8
(blood flow) to periphery heat loss
to core and environment to environment 0 30 60 90 120 150 180 210 240 270 300 330 360
Time (min)

A, No exercise
Heat gain Heat loss
B, Intermittent leg exercise

Balance depends on FIGURE 8-33  Rectal temperature for six volunteers during immersion
• Medium (water or air) in 0° C (32° F) water and −5° C (23° F) air. A, No exercise, and B, inter-
• Temperature gradients mittent leg exercise for 5 minutes every 20 minutes (mean ± standard
(within tissue and at surface) deviation). Asterisk (*) indicates significantly higher rectal temperature
• Type and level of activity in condition B compared with condition A from 40 to 180 minutes.
• Insulation Error bars = standard deviation. (From Faierevik H, Reinertsen RE,
FIGURE 8-32  Factors that influence total thermal balance during Giesbrecht GG: Leg exercise and core cooling in an insulated immer-
increases in metabolic heat production (i.e., voluntary exercise and sion suit under severe environmental conditions, Aviat Space Environ
involuntary shivering). Med 81:1, 2010.)

180
prevent or minimize Tco cooling. Shivering intensity increases as when Tco ≤30° C [86° F]). The power of shivering is especially

CHAPTER 8  Immersion into Cold Water

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 8-32).
Figure 8-34 illustrates how shivering heat production can main-
tain Tco in cold air and how it can arrest the fall in Tco in both
cool and colder water. In colder water, the combination of shiv-
ering thermogenesis and body insulation (as a result of peripheral
vasoconstriction) may result in maintenance of a steady-state Tco,
although below normothermic levels. At even lower water tem-
peratures, Tco will continue to decrease. This decrease accelerates
when shivering thermogenesis eventually stops as a result of
hypothermia-induced thermoregulatory impairment (this occurs
important during consideration of the clinical classification of
hypothermia and rewarming therapies, because this valuable heat
source is an efficient mechanism for rewarming the core during
postimmersion recovery and resuscitation (see Rescue [Self-
Initiated or Assisted] and Medical Management, later).
NONTHERMAL FACTORS
Underwater divers often experience “symptomless” or “unde-
tected” 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 Sund-
berg117 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

10° C Air exposure (2 hr)

37.5 15° C Water immersion (3 hr)
37
37
Tes (° C)

36.5

Tes (° C)
36.5 Warm bath
36
36
Cold air 35.5
35.5 Immersion
0 20 40 60 80 100 120 140 35
1000 0 50 100 150 200 250
800 1400
VO2 (mL/min)

VO2 (mL/min)

1200
600 1000
800
400 600
200 400
.

200
0 0
0 20 40 60 80 100 120 140 0 50 100 150 200 250
A Time (min) B Time (min)

28° C Water immersion 8° C Water immersion

38 37.5
37.5 37
Tes (° C)

Tes (° C)

37 36.5
36
36.5
35.5 Immersion
36
0 20 40 60 80 100 120 140 35
0 20 40 60 80 100 120 140
Immersion
2500 Exercise Rest 2000

2000 1500
VO2 (mL/min)
VO2 (mL/min)

1500
1000
1000
500
.
.

500

0 0
0 20 40 60 80 100 120 140 0 20 40 60 80 100 120 140
C Time (min) D Time (min)

FIGURE 8-34  Effectiveness of shivering heat production for preventing the onset of hypothermia during
exposure to A, 10° C (50° F) air; B, 28° C (82° F) water; C, 15° C (59° F) water; and D, 8° C (46° F) water. Tes,
Esophageal temperature.

181
 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 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 to 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 condi-
tions.38,83,100 Under hypothermic conditions, where vasocon-
striction 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 immer-
COLD AND HEAT
sion 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
PART 2
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 gluconeogen-
esis,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 cogni-
tive alteration may be functionally related to the reduced
shivering response.
6. Cold-induced diuresis is increased. Alcohol inhibition of anti­
diuretic 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 approximately 8 mL/
min). For longer immersions (>1 hour), alcohol potentiates
the development of dehydration and hypovolemia.
For most humans, high doses of alcohol (i.e., blood level
>200 mg/dL) have an anesthetic effect. Major impairment of
mental, motor, and involuntary function (including thermoregula-
tion) occurs. Alcoholic persons who “pass out” in cold locations
(i.e., “urban hypothermia”) rapidly and passively become hypo-
thermic.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,
182
including ability to control the cold shock response; ability to
swim and maintain airway freeboard; 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, dye, smoke, 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 potenti-
ates the risk of drowning. This response and the resulting inca-
pacitation have been suspected as the primary causes of drowning
after short-term (<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 cerebrovas-
cular accident (stroke) in persons with arterial disease or hyper-
tension.165 In addition, reflex gasping and hyperventilation165,174
significantly shorten the duration of breath holding.84,88,165 Figure
8-35 illustrates this phenomenon. Loss of breath-holding capacity
can have severe consequences for survivors attempting under-
water 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 white-water river.88,144,169
110
Second submersion
100 (after habituation
and hyperventilation)
90
80
Breath-hold duration (sec)
70
Pre-submersion mean
60
50
40
30
First submersion
20
10
0
0 5 10 15 20 25 30 35
Water temperature (° C)
FIGURE 8-35  Effect of water temperature on maximum breath-hold
duration in young, physically fit participants (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 fol-
lowed 2 minutes of acclimatization to the water. The last 10 seconds
of the acclimatization was accompanied by 10 seconds of hyperventila-
tion. Error bars = standard deviation. (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.)
 Respiratory difficulties induced by the cold shock reflexes
make breathing while swimming extremely difficult. Golden and
Hardcastle70 have demonstrated “swim stroke/respiration asyn-
chrony” that leads to water inhalation and swimming failure.
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 cold water’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. All
these factors combined may incapacitate even physically fit
and capable swimmers. Keating and colleagues104 observed
sudden incapacitation in two experimental volunteers (both
good swimmers) who were immersed in 4.7° C (40.5° F) water.
One inhaled water because of respiratory difficulty and fatigue
after swimming for 7.5 minutes and had to be pulled from the
water. The second volunteer lasted only 1.5 minutes 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 swim-
ming failures and unexpected submersions has led the USCG 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 8-6),
and habituation to cold immersion. Tipton and colleagues171
demonstrated that habituating participants 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% reduc-
tion in respiratory rate during the 30- to 180-second interval
after immersion in 10° C (50° F) water. Tidal volume and heart
rate response demonstrated similar declines in habituated indi-
viduals. 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 person’s skin significantly decreases cardiorespiratory reflex
responses to sudden immersion.118,172,173,175 Tipton and Golden172
demonstrated that individuals 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,
compared with controls with neither torso 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. Tipton and colleagues173 also demonstrated that
even loose-fitting and poorly insulated clothing can attenuate
the magnitude of the cold shock response compared with immer-
sion in swimming trunks only. When volunteers were immersed
in 10° C (50° F) water wearing either conventional clothing
or conventional clothing plus windproof/showerproof foul-
weather clothing, cardiopulmonary and thermal responses were
significantly less than those in individuals 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.
ABILITY TO SWIM AND MAINTAIN
AIRWAY FREEBOARD
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 apti-
tude to combat the effects of wave action.155,169 Although a PFD
assists with maintenance of airway freeboard, any combination
of flotation posture and sea state in which water can enter the
nose or mouth can lead to aspiration and possible drowning. If
waves are present, it is usually necessary for a survivor to actively
CHAPTER 8  Immersion into Cold Water
combat a potential loss of airway freeboard through effective
swimming motion, something an unconscious survivor cannot do
or a survivor at night cannot do if waves are not visible.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 these environments, the survivor may
still have to cope with the effects of cold wind, spray, and waves
(Figure 8-36; see also Figure 8-20).
BEHAVIOR OF THE SURVIVOR IN THE WATER
Survivor location has a significant effect on Tco cooling rate and
survival time. The USCG and other rescue organizations recom-
mend 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 recom-
mendation derives from the higher thermal conductivity of water
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 convec-
tive heat loss, and spray and periodic wetting from breaking
waves result in conductive heat loss.162,164 Steinman and Kubilis159
confirmed these observations. The cooling rates of thin male
volunteers 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-foot) break-
ing 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/hr (17.40 to 20.50 miles/hr)
wind, and occasional breaking waves while sitting atop an
overturned boat (see Figure 8-36).
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 8-37. 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
survived the heavy seas, high winds, and 18° C (65° F) water.
He survived for 43 hours, primarily by exiting the water and
sitting atop the capsized boat (see Figure 8-20). The other three
men spent much more time immersed and wore less insulation;
thus they cooled faster and perished (see Survival Modeling,
later).
Survivors should attempt to lift 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 recom-
mendation. 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 believe erroneously 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 misunder-
standing. This has occasionally led survivors to abandon a posi-
tion 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.
183
 A B
COLD AND HEAT

C
FIGURE 8-36  Testing protective clothing in rough seas: A, atop an overturned boat; B, in a one-person
life raft; C, free swimming with only a personal flotation device. (Courtesy Alan Steinman)
PART 2

Environment

Water

5.82 3.28 2.87 2.81 1.71 0.85

Raft

3.41 1.13 0.81 0.63 0.61

Boat

2.51 0.95 0.69 1.10

FS NX BC AC WS NI
FIGURE 8-37  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-minute 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 miles/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-minute 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-D-26-86, Springfield, Va, 1986, National Technical
Information Service.)

184

Accidental cold-water immersion
Don’t panic,
breathing under control
PFD on
Rescue possible Rescue unlikely
STAY Estimated time
to swim to safety
>45 min <45 min
STAY Consider
SWIMMING
Decide early
Commit to decision
FIGURE 8-38  Algorithm for making the decision to stay or swim when immersed in cold water. PFD, Per-
sonal flotation device.
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 espe-
cially 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
Tco. Ducharme and Lounsbury32 specifically evaluated this issue
by comparing the cooling rates and swimming distances for both
novice and expert swimmers in a swimming plume. Experimental
participants, 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 compared with holding still. The novice swimmers
traversed about 800 m (2625 feet) and the expert swimmers
about 1400 m (4593 feet) during their swim. Thus, swimming
may well have allowed the participants 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 participants 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 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
CHAPTER 8  Immersion into Cold Water
No PFD
Something buoyant Nothing to
to hold on to hold on to
STAY No choice
but to swim
protective clothing. There is no uniformly correct answer to the
question, “Should I swim for it?” Each survival situation must be
evaluated individually (Figure 8-38 and Box 8-6).
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
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 Tikui-
sis162,163 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. The model was developed on the basis of
experimental data about cooling with different types of flotation
devices and thermal protective clothing (Figure 8-39),158,159 shiver-
ing control and capacity,38 body composition (Figure 8-40), 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
USCG started using a new decision tool: the Probability of Sur-
vival Decision Aid (PSDA), which was developed by Xu and
BOX 8-6  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
personal flotation device, 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 8-38).
185
 first and third fatalities (13.5 and 25.7 hours, respectively) were
36 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,
30 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
24 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
ST (hr)

18 dove under the surface and drowned. Therefore, it is likely that

gh some other factors also contributed significantly to his death.
Hi

m
Because this victim spent so much more time immersed in the

w
iu

Lo
water than did the others, he may have ingested significant

ed
12

M
6

36
0
0 5 10 15 20
30
A Tw (° C)

24
36

ST (hr)
18
COLD AND HEAT

30

12
24
ST (hr)

18 6
h
Hig
12 0
PART 2

m 0 5 10 15 20
diu
Me
A Tw (° C)
6
Low
36
0
–10 –5 0 5 10
30
B Ta (° C)

FIGURE 8-39  Prediction of survival time (ST) for an average individual 24

under varying degrees of clothing protection (see Figure 8-15). A, For
immersion in rough seas versus water temperature, low = nude, flight
ST (hr)

suit, float coat, aviation coveralls, boat-crew coverall, or torn coverall);

18
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 miles/hr) under wet condi-
tions versus air temperature, low = nude, flight suit, or aviation coverall;
medium = float coat, boat-crew coverall, short wet suit, full wet suit, 12
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.) 6

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 8-41 shows predicted survival times for
victims in varying water temperatures. Presently, the PSDA pre-
dicts 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
0
–10 5 0 5 10
B Ta (° C)
FIGURE 8-40  Predicted survival time (ST) for individuals wearing boat-
crew coveralls (see Figure 8-15) 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.)

186
 CHAPTER 8  Immersion into Cold Water
100

0C
Number of survivors 80 5C
10C
15C
60

40

20

A
0
0 5 10 15 20 25 30 35
Immersion time (hr)

FIGURE 8-41  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, US Army
Research Institute of Environmental Medicine.)

amounts of seawater; this was described and would be consistent B

with some of his actions and symptoms. The lone survivor lasted
FIGURE 8-42  Dye marker (A) and smoke flare (B) signals. (Courtesy
longer than predicted with a Tco of approximately 32° C (89.6° F)
Gordon G. Giesbrecht.)
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 shiver-
ing many hours before rescue. This long-lasting and high-intensity
shivering heat production would have a significant effect in
attenuating the drop in Tco. Predictive modeling has many inher-
ent complications, but the PSDA results indicate the value of
modeling as well as of providing some insight into the ther­
mophysiology and pathophysiology present during this epic
struggle.

SIGNALS A
Effective signals can greatly increase the chance of survival by
bringing rescue and shortening the duration required to survive.
Figures 8-42 and 8-43 show various types of signals, including
dye, smoke, group formations, streamers, and flares. One inher-
ent signal can be the clothing that is worn. It is a great advantage
to wear colorful PFDs or other colorful clothing. For example,
USCG rescue personnel found Nick Schuyler after 43 hours of
immersion in the Gulf of Mexico because of his bright-orange
jacket (see Figure 8-20).

PHYSIOLOGIC RESPONSES TO B
COLD-WATER SUBMERSION WITH
THE HEAD UNDER WATER
Drowning is covered in detail in Chapter 69. However, a brief
discussion is included here to provide a more complete descrip-
tion 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., cold-water drowning). The most
important factors in these unusual cases are low water tempera-
ture and subsequent brain cooling. This principle has been used
in clinical practice for years. For example, cardiopulmonary
bypass used to cool neurosurgical patients to a Tco of approxi-
mately 9° C (48.2° F) made it possible to arrest brain blood flow C
for at least 55 minutes, with full neurologic recovery.135 The full
explanation for these recoveries relates to both (1) the mecha- FIGURE 8-43  Differences in visibility in water based on suit color (A)
nisms for and amounts of brain and body cooling and (2) the and whether a group is stationary in a star formation (B) or kicking the
mechanisms for the protective effect of this cooling. legs (C). (Courtesy Gordon G. Giesbrecht.)

187
 MECHANISMS FOR BRAIN AND BODY COOLING
Children have an advantage in cold-water submersion incidents, 160
because their greater surface area–to–mass ratio allows for faster 140
conductive cooling, which provides cerebral protection on the
basis of decreased cerebral metabolic requirements of oxygen 120

Survival time (min)

(CMRO2). The mammalian dive reflex, which initiates intense
bradycardia and shunts blood flow to important core organs such 100
as the heart and brain, has also been implicated. A third factor 80
that has recently been explored is the possibility that cold-water
ventilation may result in rapid and extensive cooling during 60
submersion.
The effectiveness of the human dive reflex, especially the 40
breath-hold response, is controversial. Nemiroff,129,130 who 20
reported one of the largest series of successful resuscitations of
submersion victims, believes the dive reflex plays an important 0
role, particularly in children and infants and especially in neo- 7 17 27 37
nates. Hayward and colleagues88 believe that the enhanced
success of resuscitation associated with cold-water submersion is Core temperature (° C)
more a result of hypothermia than of the dive reflex.138
It is important to note that the protective effect of cooling FIGURE 8-44  Schematic presentation of survival time at different core
and brain temperatures. Red, Prediction based on a temperature coef-
depends on the Tco at cessation of oxygen delivery and the sub-
ficient (Q10) of 2. Blue, Prediction based on a Q10 of 3. Green, Predic-
sequent rate and extent of the decrease of Tco. Because Tco is tion based on the Q10 effect plus other factors, such as changes in
likely to be near normal at the onset of an accidental submersion, neurotransmitter release (i.e., glutamate and dopamine). Actual sur-
rapid cooling after the onset of ischemia is important for survival. vival times from both neurosurgical and accidental hypothermia cases
Conduction alone probably cannot account for the rapid decrease fall outside of the range predicted based on Q10 alone; thus some
in Tco that occurs during cold-water submersion incidents. Conn other factors must also contribute to survival.
and colleagues22 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. Tco
COLD AND HEAT

decreased by 11° C (19.8° F) after 4 minutes in the completely

submersed dogs, 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 compared with
only surface conduction in the control dogs. The general conclu-
sion that brain cooling is accelerated considerably by respiration
of cold water has been proposed by others54,68,74 and mathemati-
cally predicted by Xu and colleagues.206 Although breath holding
PART 2
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.14,15,64,123,146,204
Submersion likely promotes cerebral death as tissue ischemia
depletes high-energy phosphates and leads to membrane depo-
larization. This stimulates release into the extracellular space of
excitatory neurotransmitters such as glutamate and dopamine,
which mediate postsynaptic depolarization and cause calcium

may occur during submersion, a physiologic break point occurs, entry into the cell. Calcium influx mediates production of oxygen
at which time involuntary breathing movements predominate.4 and hydroxyl free radicals (which may be involved in reperfusion
This factor, when coupled with unconsciousness, could reason- injury) and release of free fatty acids, which results in eicosanoid
ably be expected to result in the respiration of water, at least
under certain circumstances. Experimental and anecdotal evi-
dence 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 breath-
ing water in and out just before escaping the cockpit.12 Whether
or not this occurred has not been confirmed. Start of anoxia and expected time
Myocardial to cerebral injury and/or death
infarction
MECHANISMS FOR THE PROTECTIVE EFFECT 40
Core temperature (° C)

Imm
OF BRAIN COOLING 35 ersio Hypothermia-
n hy
Hypothermia provides an advantage during anoxic periods, such poth induced
30 erm
ia cardiac arrest
as cold-water submersion, because of what is known as the
“metabolic icebox.” Whole-body or focal hypothermia has long 25
been used to extend biologic survival time during surgery under 20
ischemic conditions. Cerebral protection under hypothermic con- Submersion hy
pothermia — CW
ditions has commonly been attributed to decreased CMRO2, 15 ND
according to the temperature coefficient (Q10) principle. Although
10
the Q10 of the whole body is about 2, the Q10 of the brain Neurosurgery
increases from approximately 3 between 27° and 37° C (80.6° and Start of
5 cooling
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 0
insult for 5 minutes at 37° C (98.6° F), cooling to 27° C (80.6° F) –30 0 30 60 90 120 150 180 210 240 270 300
or to 17° C (62.6° F) would provide 15 and 72 minutes of protec-
Time (min)
tion, respectively, based solely on the decreased CMRO2 (Figure
8-44). Although long survival times at brain temperatures less FIGURE 8-45  Schematic representation of theoretical times to cere-
than 20° C (68° F) may be predicted on the basis of increasing bral injury or death after the sudden onset of anoxia. Examples include
Q10 and diminishing CMRO2, some additional mechanisms may anoxia induced by myocardial infarction at normal core temperatures,
be required to explain intact survival after prolonged submersion, hypothermia-induced cardiac arrest during immersion hypothermia,
when reported core temperatures are often above 30° C (86° F). ischemia-induced cardiac arrest after cold-water drowning (CWND),
These factors are schematically shown in Figure 8-45. Since the and electrically induced arrest after protective cooling for neurosur-
early 1990s, several studies that have been directed mainly gery. Note that the times shown here are representational; actual
toward the protection of the brain during or after cerebral survival times may vary.

188
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 sup-
pression 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 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 mecha-
nisms 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 disad-
vantage depends on whether there is cessation of oxygen deliv-
ery, and, if so, what Tco is when anoxia occurs and how much
the Tco subsequently declines. These factors are schematically
illustrated in Figure 8-45. If oxygen delivery is not compromised
(i.e., during immersion hypothermia), Tco cooling will eventually
lead to death from cardiac arrest. However, if oxygen delivery is
compromised (i.e., during submersion hypothermia and cold-
water drowning), Tco and brain cooling will prolong survival
compared with a condition in which Tco cooling does not occur
(i.e., myocardial infarction). These factors are important to under-
standing 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 faster.
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. In ice-cold water,
loss of arm control and 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 8-46 and can be
seen in Cold Water Boating (Video 8-7). It is initiated by putting
the arms up on the ice and pulling 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, 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
CHAPTER 8  Immersion into Cold Water
Hold on
Kick your feet to get horizontal
Kick and pull
Slide along: DO NOT STAND
FIGURE 8-46  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.
www.wildernessmedicinenewsletter.com.)
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 reason-
ably close (i.e., <30 minutes 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 neces-
sary, 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 exit the cold water unaided
might not yet be very hypothermic, physical incapacitation will
become 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 sur-
vival 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 vari-
ability): 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 (see Box 8-2).
Swimming should be minimized, because it causes the body
to lose heat much faster than 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 ini-
tially 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
189
 conserve as much body heat as possible. Remain as still as pos-
sible. 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.

ASSISTED RESCUE OF A VICTIM WHO HAS A

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 B
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.
Assess the Situation
1. Assess the victim’s physical and emotional condition.
COLD AND HEAT

2. Assess the ice and water conditions (e.g., ice thickness, water
current). C
3. Assess the equipment that you have that might be useful in
a rescue. FIGURE 8-47  Professional rescue of a volunteer from ice water. A
4. Assess the rescue skills that are possessed by you and by rescue sling is placed around the victim’s chest (A), and the rescuer
those who are with you. 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
Follow the Rescue Sequence Gordon G. Giesbrecht.)
The rescue sequence progresses from lowest-risk actions to
PART 2

highest-risk actions. Low-risk actions should be taken first. Pro-

gression to higher-risk actions is dictated by training level and
available equipment.
1. Shore-assisted rescues involve talking, throwing, and reach-
ing; 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. 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 8-47).
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 untrained bystanders apply
the acronym STOP to their actions: stop, think, observe, and plan.
Stop the urge to rush up to help the victim, 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. Lastly, 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 to 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 near 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 the body and under the arms, to put an arm
through the loop and bend the elbow around the rope, or simply
to hold on to the loop.
Reach
It may be possible to reach a victim with some implement, such
as a tree branch, ladder, or any object 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 object. 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 the 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 the person can
survive; emphasize that help is on the way.
RESCUE BY TRAINED PERSONNEL
This discussion is 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

190
professional rescuer should follow the policies and procedures

CHAPTER 8  Immersion into Cold Water

BOX 8-7  Controversy Box: A Hypothermic Patient
of their local jurisdictions.
Trained personnel should first use the lower-risk techniques Presents an Emergency That Must Be Dealt  
described earlier. If these do not work, personnel should imple- with Quickly
ment the higher-risk techniques described by many ice-rescue
training institutions.48 Briefly, trained rescuers must not go on the Although severe hypothermia is a critical condition, rescue and
ice unless they are wearing a thermal protective dry suit and treatment do not necessitate rapid and reckless actions. Rescuers
and medical providers should take the time required to safely
PFD. The rescuers should also be secured by a safety rope that
remove the victim from the cold stress and then do as much as
is operated by a trained colleague. possible to be gentle and to keep the patient horizontal. The
Platform-assisted rescues involve working from or with a flota- patient’s core has been cooling gradually for a long time (i.e.,
tion platform, such as an inflatable boat or another buoyant hours or even days), and a delay of a few minutes to get
device. These techniques involve pushing or being transported organized for treatment will not make the patient’s condition
on the buoyant platform. The first choice is to push the platform worse. However, rushing may result in patient jostling that induces
toward the victim and to use it as a reaching device. Alternatively, ventricular fibrillation and cardiac arrest.
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 cannot recover the patient horizontally, they should place the
be used to ensure that a panicking victim does not pose a threat victim in a supine posture as soon as possible after removal from
to the rescuer. After the victim is securely contacted, the victim cold water (Box 8-7).157
and the rescuer can be pulled toward shore by the attendants Hoist extractions can be done from a helicopter (Figure 8-49)
on shore (see Figure 8-47). or boat. Two slings can be used to keep the patient close to
horizontal compared to a single sling (Figure 8-50).
RESCUE FROM OPEN WATER
Retrieval of a victim from cold-water immersion must be per-
formed with caution. Sudden reduction of the “hydrostatic
squeeze” applied to tissues below the water’s surface may poten-
tiate 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 hypother-
mic 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 FIGURE 8-49  U.S. Coast Guard helicopter hoist rescue with a rescue
and aboard the rescue vehicle3,73,157 (Figure 8-48). If rescuers swimmer and a victim. (Courtesy Gordon G. Giesbrecht.)

A B

C D
FIGURE 8-48  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
FIGURE 8-50  Comparison between single (A) and double (B) sling
methods for hoisting to a helicopter or boat. The double sling method
places the patient in a more horizontal position. (Courtesy Garrick
Kozier.)

191
 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 the person has been
rescued as a result of the physiologic processes described earlier
as “afterdrop.” To diminish this effect, the patient’s physical activ-
ity 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 helicop-
ter).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 VF.87
Experiments on moderately hypothermic volunteers with esopha-
geal 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 stim-
ulation of the cold myocardium is another suspected cause of
death after rescue.110,192
Several extraction techniques are presented in Figure 8-48 and
Videos 8-7 and 8-8. The technique depends on the number of
rescuers, the design of the boat platform and the resultant free-
board, and the equipment on hand. Victims can be pulled by
their clothing or PFDs; placed into single or double rescue slings,
COLD AND HEAT
rescue nets, or even hoists; and extracted either headfirst or
horizontally. It is easier to be gentle and to keep the victim hori-
zontal 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
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.
PART 2
MEDICAL MANAGEMENT
This section describes prehospital management of hypothermia
with specific reference to immersion pathophysiology. Chapter 7
describes the hospital management of both accidental immersion
and land-based hypothermia. Prehospital management of hypo-
thermia 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.208 Medical personnel must exercise
good clinical judgment to balance all these factors to select
appropriate therapeutic modalities (Box 8-8).
The primary goals of prehospital management of victims of
accidental immersion hypothermia are prevention of cardiopul-
monary arrest; prevention of continued Tco decline; moderate,
safe core rewarming, if practicable; and transportation to a site
BOX 8-8  Controversy Box: Prehospital Warming Is
Dangerous and Should Be Avoided
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 core temperature 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.
192
BOX 8-9  Controversy Box: Afterdrop Is an Artifact
and Is Unimportant
Rescuers and emergency medical personnel should be aware that
core temperature will continue to drop after an individual has
been removed from the cold stress (see Figure 8-12). 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 should
remain horizontal, and the arms and legs should not be rubbed or
massaged in an effort to warm the patient.
of definitive medical care.33,79,105,112,152,157 Aggressive rewarming in
the field has been contraindicated in the past, because the means
to 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 too aggressive. Figure
8-51 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
next may be appropriate (Box 8-9).
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 not to focus solely on trauma injuries. Several
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 the signs and
symptoms (see Figure 8-13). Generally, if mentally alert and
shivering vigorously, the patient can be considered mildly hypo-
thermic. If shivering is waxing and waning or absent, or if con-
sciousness is diminished or absent, the patient 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 detect;3,156 therefore, rescuers should take
60 seconds to assess these vital signs.3 If neither the pulse nor
breathing is detectable, rescuers should commence cardiopulmo-
nary resuscitation (CPR) in accordance with normal basic life
support (BLS) protocols.3,156 Figure 8-52 is a field algorithm for
assessment and treatment of a cold patient by search/emergency
personnel.152,208
Cardiac rhythm should be carefully monitored. Percutaneous
electrodes may be required to overcome interference from muscle
fasciculations or shivering. Endotracheal intubation and adminis-
tration 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 available,
oxygen may supplement ventilation. Mouth-to-mouth or mouth-
to-mask ventilation has the added advantage of providing a small
amount of carbon dioxide (CO2) for the patient’s inspired gases.
This may be useful for prevention of hypocapnia caused by rela-
tive hyperventilation in a severely hypothermic patient whose
metabolic CO2 production is diminished.28 This is important
because hypocapnia may decrease the threshold for VF.
Hypothermic patients with any detectable pulse or respiration
do not require the chest compressions of CPR, although severe
 CHAPTER 8  Immersion into Cold Water
Power Heat level/ Treatment
source Heat source aggressive effectiveness
Prehospital Hospital Hypothermia Frostbite
Fire XX XXX
Chemical pack – √
Non-
electric IV fluid √ –
Low-to-moderate
Warm sweet drink heat √ –
Inhalation warming – –
Nonaggressive
Warm water bottles √ √
Warm body √ √
Charcoal HeatPac √√ √
Electric blanket Electric blanket √ √
Water blanket Water blanket √ √
Electric Forced air Forced air √
√√
120 VAC warming warming
Warm shower XX –
Warm bath Warm bath High XXX –
Lavage heat √√√ –
CAVR √√√ –
Aggressive
Fem-fem √√√ –
Bypass √√√√ –

√, Effectiveness –, Not effective or applicable X, Harmful

FIGURE 8-51  Heat sources that could be used for hypothermia rewarming classified by location, heat level
or aggressiveness, and treatment effectiveness for hypothermia and frostbite. Drinks should only be given
to a patient who is alert and unlikely to choke (i.e., mild hypothermia). Inhalation warming will reduce
respiratory water loss but will add little heat to the body core. CAVR, Continuous arteriovenous
rewarming.

bradycardia and bradypnea may be present.3,156 This differs from
normothermic CPR protocols, when 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 VF from mechanical stimulation
of the irritable myocardium29 (Box 8-10).
If a victim of cold-water immersion is found floating face-
down, drowning should be suspected and managed accordingly
(see Chapter 69). In this case, correction of anoxia is paramount,
and consideration of hypothermia is of secondary importance.3,130
Normal advanced cardiac life support (ACLS) protocols should
not be routinely applied to severely hypothermic patients in
BOX 8-10  Controversy Box: Cardiopulmonary
Resuscitation (CPR) Should Be Started Rapidly if a
Pulse Cannot Be Found Quickly
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 8-52).152
cardiac arrest, because management beyond BLS differs from that
used for normothermic patients.3,29 Defibrillation and pharmaco-
logic interventions are usually ineffective for myocardial tempera-
tures of less than 30° C (86° F).3,7,29 Furthermore, repeated
defibrillatory shocks may damage the myocardium.3,156 Defibril-
lation 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 ACLS pro-
tocols may be used.3 All intravenous (IV) fluids should be warmed
before administration. However, it may be necessary to extend
the recommended interval for IV medications because of the
patient’s reduced metabolic rate.
For the unconscious hypothermic patient who is not in car-
diopulmonary arrest, endotracheal or nasotracheal intubation
should be performed gently. The insertion of pacemaker wires
and central venous catheters has been suspected of precipitat-
ing VF, but prior ventilation with 100% oxygen has been associ-
ated with a decreased risk for VF.27,28 Rescuers should not
withhold endotracheal intubation, if indicated, for fear of pre-
cipitating VF.3
If the patient does not require immediate life support interven-
tion, a thorough and systematic examination must be performed
as quickly as possible before the initiation of treatment for hypo-
thermia. Because severely hypothermic patients may have a
greatly 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 (CNS), 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 CNS signs. Rescuers should evaluate the level of

193
 INSULATION, STABILIZATION, AND REWARMING
After removal 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
1. From outside ring to centre: assess Consciousness, (i.e., 1° to 2° C/hr [1.8° to 3.6° F/hr]). Strategies for moderate
Movement, Shivering, Alertness
2. Assess whether normal function, or impaired or no function
rewarming in the field vary with the equipment available, training
3. Treat according to appropriate result-quadrant 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
1. Handle gently 4. lnsulate/ cooling is an obvious first requirement. The main goals for rescue
2. Keep horizontal vapour barrier
1. Reduce heat 3. Increase heat
3. No standing/ 5. Heat applied to personnel are to maintain or improve cardiorespiratory stability
loss (e.g., add production
dry clothing) (e.g., exercise)
walking for at upper trunk and to minimize Tco afterdrop, which can depress cardiac tem-
least 30 min. 6. High-calorie perature and potentiate VF.
2. Provide
food/drink
high-calorie
7. Monitor until
food or drink
improvement Packaging
(at least 30 min.)
8. Evacuate if no
The purpose of packaging a patient in the field or during pre-
improvement hospital transport is to minimize all sources of heat loss: evapora-
tion, conduction, convection, and radiation. Rescuers should
maintain the patient in a horizontal position to prevent hypoten-
sion, and movement of the patient must be kept to a minimum.
Clothing should be cut away if it is wet but only 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 8-53). This protection
must include the head and neck. Incorporation of a windproof
and waterproof layer or vapor barrier assists in prevention of
convective and evaporative heat loss. This is particularly impor-
COLD AND HEAT

tant for patients who require helicopter evacuation, because

1. Treat as Moderate Hypothermia, and 1. Handle gently 6. Heat applied to downwash from helicopter rotor blades can reach wind speeds
a) IF no obvious vital signs, 2. Keep horizontal upper trunk
THEN 60-second breathing / 3. No standing/walking 7. Volume
pulse check 4. No drink or food replacement
5. Insulate/ with warm
b) IF no breathing / pulse,
vapour barrier intravenous fluid
THEN Start CPR
8. Evacuate carefully
2. Evacuate carefully ASAP
FIGURE 8-52  Algorithm for field assessment and treatment of a cold
patient. (Copyright 2016 Baby It’s Cold Outside; PDF can be down-
loaded from www.BICOrescue.com.)
PART 2

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. Esopha-
geal temperature at the level of the atria is the most clinically Tarp or Pad
useful Tco obtainable, because this site most closely parallels Plastic
cardiac temperature.56,87 However, most rescue personnel are not Plastic Apply Heat
or Foil
Sleeping Bag or Blanket

equipped to measure esophageal temperature. Rectal tempera- 4

ture is not easily obtained, as rescuers often show reluctance to
obtain a recording from this site in the field, and incorrect ther- 2 3
mometer placement may cause an erroneous reading. If neither
esophageal nor rectal temperature is taken, oral or axillary tem-
perature is of limited value; neither will accurately reflect Tco in 1
a victim of immersion hypothermia. Facial cooling affects oral
temperature, and cold skin temperature affects axillary record-
ings. However, the patient’s Tco will not be lower than that 9
indicated by an oral or axillary recording. Thus, rescuers can use
even superficial temperatures in a limited way to monitor the 5
patient’s status, although this is not ideal.
Hemorrhage should be controlled in the usual manner. Anti-
6 8 7
shock 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. Because hypo-
thermia itself can cause hypotension without massive fluid losses, FIGURE 8-53  Instructions for hypothermia wrap (The Burrito) for a
antishock trousers should be used only if required for temporary cold patient. (Copyright 2016 Baby It’s Cold Outside; PDF can be
stabilization of a suspected pelvic fracture.29 downloaded from www.BICOrescue.com.)

194

FIGURE 8-54  Patient is exposed to strong rotor wash when being
hoisted to U.S. Coast Guard helicopter. (Courtesy Art Allen.)
in excess of 160 km/hr (100 miles/hr), thereby potentiating sig-
nificant heat loss from windchill (Figure 8-54). 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 clothing cannot be changed (e.g., 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 Tco >32° C [89.6° F]) are usually capable of rewarm-
ing themselves without difficulty. Heat production from shivering
can reach levels that are five to six times that of the resting meta-
bolic rate.38 Shivering is thus a highly effective means of rewarm-
ing, particularly if rescuers insulate the patient’s body and head
with vapor-barrier garments to minimize evaporative heat loss.56
Vigorous shivering has been shown to produce 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 trans-
portation for definitive care. However, rescuers should be aware
that prolonged periods of shivering consume the patient’s endog-
enous energy reserves. Thus, rescuers should administer oral
glucose-containing fluids to conscious patients who have ade-
quate cough and gag reflexes. Attention to energy reserves in
unconscious and severely hypothermic patients is also important.
Warmed IV glucose solutions are useful for these patients as part
of definitive resuscitative and rewarming protocols, as described
later.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 inha-
lation 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 rewarm the hypothermic patient com-
pletely, heated and humidified ventilation helps to insulate the
airway from further evaporative heat loss. However, some
studies have shown that inhalation rewarming reduces meta-
bolic heat production provided by shivering.54 In experimental
volunteers 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 mucocili-
ary 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
CHAPTER 8  Immersion into Cold Water
inhalation warming as an adjunct to overall rewarming
strategies.3,27,29,33,49,157,195
Warmed Intravenous Fluids
Administration of warmed IV fluids (40-42° C [104-108° F]) 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 IV fluids
(at room temperature or colder) be administered. Plastic IV fluid
bags can be easily carried inside of a rescuer’s clothing (prefer-
ably next to the skin) to keep the fluids warm and to supply
some perfusion pressure.
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 8-12). 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.
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
his 1823 text Narrative of a Journey to the Shores of the Polar Sea
in the Years 1819, 20, 21, describes this technique for resuscita-
tion of an expedition member who was recovered from ice-filled
water.41 When wrapped together in a blanket or sleeping bag, a
rescuer can transfer body heat to a hypothermic patient. However,
experimental studies on human volunteers have failed to dem-
onstrate a rewarming advantage with this technique for shivering
individuals. When volunteers were cooled to an average Tco of
34.6° C (94.3° F), body-to-body rewarming proved no better than
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. The following theoretical 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 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, non-
shivering adult produces only about 100 kcal/hr).62
2. External heat from body-to-body contact will inhibit the
hypothermic victim’s endogenous heat production through
shivering.56
3. Once body-to-body rewarming is initiated, transport of the
patient and heat donor will be difficult, if not impossible.
However, for severely hypothermic and nonshivering victims
or for victims whose shivering thermogenesis is inhibited by
alcohol, medications, age, or other factors, body-to-body rewarm-
ing 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 hypother-
mic patients has been a traditional method of field rewarming.
195

FIGURE 8-55  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
important areas for heat transfer (surrounding or near the heart) to a
cold patient.
Particularly when applied to the patient’s thorax, including
axillae, chest, and upper back, (areas with high potential for
conductive heat transfer),85 hot-water bottles, chemical and char-
COLD AND HEAT
coal heat packs (Figure 8-55), heating pads, and other warmed
objects have been used to attempt to stabilize the patient’s Tco.
If a patient is shivering vigorously, Tco will warm at a similar rate
as with external heat.21,56,80,113,160 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 sig-
nificant rewarming advantage for hypothermic individuals when
PART 2
shivering was pharmacologically inhibited.92
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 carbon
monoxide hazard within an enclosed space.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 AVAs and increases superficial
venous return via the rete. Warmed venous blood thus reaches
the core without excessive countercurrent heat loss to cold arter-
ies (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 Experimental studies have confirmed
the efficacy of this technique.188 Mildly hypothermic participants
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 after-
drop than with shivering alone (0.4° C [0.7° F] vs. 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]) than 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 locations 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
196
observed in the experimental volunteers, even when their
extremities were immersed in 45° C (113° F) water, although some
complained of initial discomfort at this temperature. Rescuers
opting to use AVA rewarming should consider starting with a
water temperature of 42° C (108° F) and gradually raise the tem-
perature to 44° C (111° F).188
Another concern with AVA rewarming involves potential car-
diovascular instability. Hypotension may result from an increase
in peripheral blood flow in a hypovolemic patient. If the patient
is required to be in a semiupright position to receive AVA
rewarming, orthostatic hypotension could potentially add to car-
diovascular instability. No experimental data support these
potential cardiovascular problems, but studies of AVA rewarming
have been performed only on mildly hypothermic individuals.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 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 mildly,
moderately, and severely hypothermic subjects. In mildly hypo-
thermic experimental patients, FAW was associated with a 30%
smaller afterdrop compared with shivering alone. Furthermore,
during the initial 35 minutes of rewarming, shivering patients
experienced net heat loss of 30 to 50 W, 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
(in conjunction with warmed IV fluids and inhalation warming)
achieved a rewarming rate of 2.4° C/hr (4.3° F/hr), which was
almost twice that of patients treated only with warmed IV fluids
and inhalation warming (1.4° C/hr [2.5° F/hr]).153
In another series of human experiments, a FAW device
designed for field use was associated with a significantly higher
Tco rewarming rate (5.8° C/hr [10.4° F/hr]) than with shivering
alone (3.4° C/hr [6.1° F/hr]), but it showed no advantage over
shivering with regard to decreasing afterdrop.35 When shivering
was inhibited with meperidine in volunteers,57 FAW was associ-
ated with a 50% decrease in afterdrop and a 600% increase in
rewarming rate compared with spontaneous rewarming alone.67
A different prototype FAW device that used a collapsible rigid
patient cover and that was evaluated experimentally on non-
shivering volunteers was associated with a smaller afterdrop
and faster rewarming rate than with spontaneous rewarming
alone.60
In summary, FAW has shown significant promise as both a
field and a hospital treatment modality. It is a safe, noninvasive
technique that can both decrease afterdrop and increase the Tco
warming rate of immersion hypothermic patients. Figure 8-56
schematically illustrates Tco responses to various rewarming meth-
odologies 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 knowl-
edge 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 hypo-
thermic patients are best managed in hospitals equipped to
handle potential complications and 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.
During transport to a site for definitive medical care, emer-
gency medical personnel should frequently monitor the patient’s
Tco and other vital signs. In addition, they should attach an
 REWARMING

Shivering
Start or
40 cooling High moderate
Core temperature (° C)

heat heat High

Invasive heat
35 Shivering heat
End
cooling Moderate
30 heat
Nonshivering
25 End
cooling No
heat FIGURE 8-57  Norwegian ice breaker.
20
Time

FIGURE 8-56  Effectiveness of various rewarming techniques under

shivering and nonshivering hypothermic conditions. The dashed line
indicates the approximate core temperature at which shivering is spon-
taneously abolished.
electrocardiography monitor and continue administration of
warmed IV fluids, heated and humidified air or oxygen, and other
rewarming efforts discussed previously. Rescuers should maintain
the hypothermic patient in a horizontal posture and 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 immer-
sion hypothermia patients requires understanding the physiologic
events that occur during cooling and recovery. With such under-
standing, medical personnel can better prepare for and manage
this potentially difficult environmental exposure. When prehos-
pital 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 8-57).
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Complete references used in this text are available
online at expertconsult.inkling.com.
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CHAPTER 9 
Frostbite
LUANNE FREER, CHARLES HANDFORD, AND CHRISTOPHER H.E. IMRAY
Frostbite is a true freezing injury, and depending on the severity,
ice crystals will tend to form in deep and superficial tissues.
The degree of injury is a complex interaction of many factors,
including environmental (e.g., temperature, windchill, length of
exposure, altitude) and individual (e.g., genetics, comorbidities,
medications/drugs, clothing, skin products, previous frostbite
injury).
This chapter reviews current understanding of the history,
epidemiology, physiology, pathophysiology, and classification of
frostbite, as well as risk factors, clinical presentation, field and
hospital evaluation, treatment, prevention, and consultation strat-
egies. Although the principles of prevention and treatment trans-
fer from urban to wilderness settings, the time to definitive
treatment of frostbite is often prolonged, and resources are
almost always limited in the wilderness setting. Therefore, wher-
ever possible, we incorporate special considerations for wilder-
ness management. Hypothermia and nonfreezing cold-induced
injuries are discussed in Chapters 7 and 10.
CHAPTER 9  Frostbite
HISTORY OF FROSTBITE
A 5000-year-old pre-Columbian mummy discovered in the
Chilean mountains is widely recognized as the earliest docu-
mented evidence of human frostbite.151 In 218 BC, Hannibal lost
almost half his army of 46,000 to cold injuries in only 15 days
when crossing the Pyrenean Alps. Dr. James Thatcher wrote in
1778 that 10% of George Washington’s colonial army had been
left to perish in the winter cold during his campaign against the
British soldiers.164
Although frostbite was a known consequence of military
campaigns in the cold for thousands of years, the first authorita-
tive report of mass casualties was by Baron Larrey, surgeon-in-
chief of Napoleon’s army during the invasion of Russia in the
winter of 1812-1813.105 Larrey introduced the concept of friction
massage with ice or snow, avoidance of heat during thawing,
and the idea that cold injuries were similar to burn injuries.
These concepts are better understood against the background as
197
 viewed by Larrey; soldiers with cold injuries rapidly rewarmed
their extremities over roaring fires (65° to 75° C [149° to 167° F])
after long marches, only to renew the trek and refreeze their
extremities the next day. Larrey recognized that warming was
good, but cautioned against the use of excessive heat and ulti-
mately recognized the freeze-thaw-freeze cycle. Napoleon left
France with 250,000 men and returned 6 months later with only
350 effective soldiers. The remainder were casualties to cold or
starvation.105
During both world wars and the Korean conflict, at least 1
million cases of frostbite occurred.142,181,198 High-altitude frostbite,
first described in 1943, was recognized from the treatment of
aviators in World War II, when gunners of aircraft flying between
7620 and 10,668 m (25,000 and 35,000 feet) fired machine guns
through open ports, removing their bulky mittens and jackets to
improve the dexterity that they thought was crucial to saving
their lives.198
Until the 1950s, treatment of cold injuries basically followed
Larrey’s guidelines. In 1956, experimental laboratory work
encouraged Meryman, the U.S. Public Health Service district
medical officer in Tanana, Alaska, to try rapid rewarming at
37.8° C (100° F) on a patient with frostbite and hypothermia.25,131
This was the genesis and has become the cornerstone of the
method currently used in Alaska and popularized by Mills.130,131
EPIDEMIOLOGY
No comprehensive statistical data are available on the incidence
of frostbite, but it is much more prevalent during military cam-
COLD AND HEAT
paigns and is a known hazard for mountain climbers and polar
explorers. The typical frostbite patient is either working or rec-
reating in cold and/or high-altitude environments, is homeless,
or is accidentally trapped outdoors in the winter.98,101,146 The
patient is typically 30 to 49 years old, and in more than half of
urban cases, is intoxicated.
CIVILIAN
PART 2
In the nonadventurer U.S. civilian population, Mills129-131 had col-
lected 500 cases in Alaska by 1963, Cook County Hospital in
Chicago recorded 843 cases from 1962 to 1972, and Detroit
Receiving Hospital reported on 154 patients treated between 1982
and 1985.17,74,102 The incidence of frostbite in Finland calculated
in a 9-year retrospective query of hospital admissions was 2.5
cases per 100,000 inhabitants.87
MILITARY AND OCCUPATIONAL
The mean annual incidence of frostbite in the Finnish military
was reported as 1.8 episodes per 1000 persons, with the head,
hands, and feet most often affected.107 In a more recent study of
almost 6000 Finnish military recruits, 44% reported at least one
episode of frostbite during their lifetime, and the annual inci-
dence was 2.2%; the head, hands, and feet were the sites most
frequently afflicted.47 Among refugees navigating a high-altitude
military line of control during December 1988 to March 2003,
2564 cases of frostbite were treated at local hospitals in Muzaf-
farabad, Azad Kashmir.92
MOUNTAINEERING
A 10-year retrospective review of medical records of the British
Antarctic Survey revealed that the incidence of frostbite was
approximately 65.6 cases per 1000 persons per year.28 During a
10-year period in the Karakorum Mountains, 1500 cases of frost-
bite were treated at tertiary care medical facilities; all victims were
males age 17 to 43 years. The incidence is unknown because the
total number of potential exposures was unrecorded.71 In a
questionnaire-based study of 637 mountaineers, the mean inci-
dence of frostbite was 366 cases per 1000 persons per year,70
and of 2219 south-side Mt Everest climbers in 7 years (2001–
2007), the base camp medical clinic at Mt Everest saw 35 cases
of frostbite (and estimates at least a comparable number of
patients not brought for treatment at the facility).56
198
ANATOMY AND PHYSIOLOGY
Physiologically, humans are tropical animals, better suited to
losing heat than retaining it. When naked and at rest, a per-
son’s neutral environmental temperature is 28° C (82.4° F). With
an environmental drop of 8° C (14.4° F) to 20° C (68° F), the
metabolic rate must double to avoid lowering of body
temperature.
The rate at which heat is lost by radiation is a function of
the temperature of the cutaneous surface, which in turn is pri-
marily a function of the rate of blood flow through the skin.
Heat is poorly conducted from warmer internal tissue to the
cutaneous surface because adipose tissue is a good heat
insulator.
As a result, cutaneous circulation is key to development of
frostbite. Because of its role in thermoregulation, normal blood
flow of skin far exceeds its nutritional obligation. The skin holds
a complex system of capillary loops that empty into a large,
subcapillary venous plexus containing the majority of the cutane-
ous blood volume. Under normothermic conditions, 80% of an
extremity’s blood volume is in the veins of skin and muscle. Skin
blood volume depends in part on tone in resistance and capaci-
tance blood vessels, and tone in turn depends largely on ambient
and body temperatures. Under basal conditions, a 70-kg (154.3-
lb) person has total cutaneous blood flow of 200 to 500 milliliters
per minute (mL/min). With external heating to maintain skin
temperature at 41° C (105.8° F), this may increase to 7000 to
8000 mL/min, whereas cooling the skin to 14° C (57.2° F) may
diminish it to 20 to 50 mL/min.
Blood flow through apical structures, such as the nose, ears,
hands, and feet, is most variable because of richly innervated
arteriovenous connections. Blood flow to hand skin can be
increased from a basal rate of 3 to 10 mL/min/100 grams (g) of
tissue to a maximum of 180 mL/min/100 g of tissue. This cutane-
ous vascular tone is controlled by both direct local and reflex
effects. Indirect heating (warming a distant part of the body)
results in reflex-mediated cutaneous vasodilation, whereas direct
warming results in vasodilation dominated by local effects. When
both types (central and peripheral) of heating or cooling are
present, their effects are additive.
Cutaneous vessels are controlled by sympathetic adrenergic
vasoconstrictor fibers, and vascular smooth muscles have both
α-adrenergic and β-adrenergic receptors. Vasodilation in the
hands and feet is passive, so maximal reflex vasodilation occurs
after sympathectomy.
When the hand or foot is cooled to 15° C (59° F), maximal
vasoconstriction and minimal blood flow occur. If cooling
continues to 10° C (50° F), vasoconstriction is interrupted by
periods of vasodilation and an associated increase in blood and
heat flow. This cold-induced vasodilation (CIVD), or “hunting
response,” recurs in 5- to 10-minute cycles and provides some
protection from the cold. There is considerable individual varia-
tion in the amount of CIVD, and it is believed this might explain
some of the variation in susceptibility to frostbite. Prolonged
repeated exposure to cold increases CIVD and offers a degree
of acclimatization. Inuit, Sami, and Nordic fishermen have a
strong CIVD response and very short intervals between dilations,
which may contribute to maintenance of hand function in the
cold environment.66
Normal skin maturation and tissue function rely on mainte-
nance of permeability and integrity of all tissue membranes. A
steady-state relationship of prostaglandins, particularly pros­
taglandin E2 (PGE2, vasodilator) and PGF2α (vasoconstrictor),
is crucial for normal skin function. Imbalance may disrupt
cell membrane equilibrium. This relationship is controlled
through PGE2–9-ketoreductase and nicotinamide adenine dinu-
cleotide phosphate (NADPH). Low concentrations of PGE2–9-
ketoreductase found in normal skin emphasize an active biologic
presence.
It is not difficult to imagine why frostbite tends to affect tissues
that are acral (e.g., fingers, toes, ears, nose) and that receive
diminished blood supply as a result of vasoconstriction, thereby
conserving heat for the core. The nose and corneas may be dif-
ficult to protect from cold wind and are particularly vulnerable;
face coverings such as a balaclava and goggles should be con-
sidered in extreme conditions. In addition, men who jog, ski, or
otherwise exercise in the cold may be prone to penile frostbite,
especially if fast speeds create a headwind. Clothing becomes
moist with sweat in the groin, and the tip of the penis is vulner-
able, especially if unprotected by a wind-resistant or windproof
outer layer.56,76
PATHOPHYSIOLOGY OF FROSTBITE
The pathophysiology of frostbite has been categorized in several
different ways, illustrating the numbers of variables that affect
the extent and depth of tissue damage. Frostbite may be divided
into four pathologic phases: prefreeze, freeze-thaw, vascular
stasis, and late ischemic. Overlap occurs among these phases.
The changes during each phase vary with rapidity of freezing
and duration and extent of injury.
Some believe that it is conceptually more clear to divide
pathologic changes occurring in frostbite into two categories:
those resulting from direct cellular injury and those from indirect
cellular effects, or progressive dermal ischemia,138 a similar patho-
physiology described in thermal burn patients.119,120,163
DIRECT CELLULAR INJURY
Regardless of the classification scheme, researchers agree that the
changes caused by direct injury include the following211,212:
• Extracellular ice formation
• Intracellular ice formation
• Cell dehydration and shrinkage
• Abnormal intracellular electrolyte concentrations
• Thermal shock
• Denaturation of lipid-protein complexes
Cells subjected to a slow rate of cooling (over hours) develop
ice crystals extracellularly in the cellular interspaces. Rapid
cooling (over seconds to minutes) produces intracellular ice
crystals, which are more lethal to the cell and less favorable for
cell survival. In a clinical cold injury, the slower rate of freezing
does not produce intracellular crystals;124,125 however, the extra-
cellular ice formed is not innocuous. It draws water across the
cell membrane, contributing to intracellular dehydration. The
theory of cellular dehydration was originally proposed by Moran
in 1929 and subsequently supported by Meryman’s study of
“ice-crystal nucleation.”124,125,127,136 Cellular dehydration produces
modification of protein structure because of high electrolyte
concentrations, alteration of membrane lipids, alteration of cel-
lular pH, and imbalance of chemical activity.116,118,128 This phe-
nomenon subsequently permits a marked and toxic increase of
electrolytes within the cell, leading to partial shrinkage and col-
lapse of its vital cell membrane. These events are incompatible
with cell survival.
Not all the water within a cell is freezable. A small amount
of unfrozen water, “bound water,” constitutes up to 10% of the
total water content and is held tightly in the protein complex
within the cell. Regardless of how rapid or marked the cold
injury, this bound water remains liquid. At temperatures below
−20° C (−4° F), approximately 90% of available water is frozen.208
Although the theory of ice crystal disruption of cell structure is
attractive, it has yet to be conclusively proven.
“Thermal shock” is the phenomenon of sudden and profound
temperature change in a biologic system. Precipitous chilling has
been theorized to be incompatible with life, but the severity of
this phenomenon is debatable. Another poorly understood
concept is the manner in which subzero temperatures produce
denaturation of lipid-protein complexes. One proposed theory
hypothesizes detachment of lipids and lipid protein from cell
membranes as a consequence of the solvent action of a toxic
electrolyte concentration within a cell.42,110 No direct evidence
supports an alteration of enzyme activity during freezing, but
DNA synthesis is inhibited.85 On the other hand, there is indirect
evidence of ox liver catalase inactivation caused by denaturation
and structural alteration of lactic acid dehydrogenase after freez-
ing and thawing.112,179
CHAPTER 9  Frostbite
INDIRECT CELLULAR DAMAGE/PROGRESSIVE
DERMAL ISCHEMIA
Indirect cellular damage secondary to progressive microvascular
insults is more severe than the direct cellular effect. This is sup-
ported by the observation that skin tissue subjected to a standard
freeze-thaw injury, which consistently produced necrosis in vivo,
survived as a full-thickness skin graft when transplanted to an
uninjured recipient site.197 Conversely, uninjured full-thickness
skin did not survive when transferred to a recipient area pre-
treated with the same freezing injury. Thus, direct skin injury is
reversible. The progressive nature of injury is probably secondary
to microvascular changes.
Approximately 60% of skin capillary circulation ceases in the
temperature range of 3° to 11° C (37.4° to 51.8° F), while 35%
and 40% of blood flow ceases in arterioles and venules, respec-
tively.161 Capillary patency is initially restored in thawed tissue,
but blood flow declines 3 to 5 minutes later. Three nearly simul-
taneous phenomena occur after thawing: momentary and initial
vasoconstriction of arterioles and venules, resumption of capillary
circulation and blood flow, and showers of emboli coursing
through microvessels.212 Ultimately, there is progressive tissue
loss caused by progressive thrombosis and hypoxia. This is
similar to the tissue loss seen in the distal dying random flap and
the no-reflow phenomenon. For both these, in addition to the
effect of arachidonic acid metabolites, oxygen free radicals have
been shown to be detrimental and contribute to tissue loss. It
has been proposed that this may be the case with frostbite
injury.24
Emerging concepts, perhaps including the deleterious role of
protein kinase C in mitochondrial dysfunction during reperfusion
injury and the role of nitric oxide production and activation, will
no doubt be incorporated into our understanding of frostbite
injury as scientific understanding evolves.
Considerable evidence indicates that the primary alteration
caused by cold injury is to vascular endothelium.210 At 72 hours
after a freeze-thaw injury, vascular endothelium is lost in capillary
walls, accompanied by significant fibrin deposition. The endo-
thelium may be totally destroyed, and fibrin may saturate the
arteriole walls.134,210,212 Ultrastructural derangement of endothelial
cells after the thaw period has been observed by electron micros-
copy in capillaries of the hamster cheek pouch following subzero
temperatures.156 The endothelial injury was confirmed by dem-
onstrating fluid extravasation from vessels almost immediately
after thawing.212 As in other forms of trauma, vascular endothelial
cells swell and protrude inward into the lumen until they lyse.
Venules appear more sensitive to cold injury than do other
vascular structures, partly because of lower flow rates. Arterioles,
with a rate of flow almost twice that of venules, are less damaged
by freezing and develop stasis later than do venules. Capillaries
manifest the fewest direct effects of cold injury, but their flow is
quickly arrested as a result of their position between arterioles
and venules. Generalized stasis and cessation of flow are noted
at the point of injury within 20 minutes after freeze and thaw.
“White thrombi” (blood cells and fibrin) appear after platelet
thrombi as blood flow progressively slows. Sludging and stasis
result in thrombosis. Microangiography after cold injury shows
that although spasm of the arterioles and venules exists, it is not
marked enough to completely account for the decreased flow of
progressive microvascular collapse.4 In the 1950s, Kulka99,100
observed that vascular thrombosis after cold injury advanced
from the capillary level to that of the large vessels and ultimately
resulted in ischemic death of progressively larger areas. Viable
dermal cells may be observed histologically in cold-injured
tissues for up to 8 days or until occlusion of local vessels occurs.
This emphasizes that vascular insufficiency plays a major role,
and that direct injury to cellular structures and mechanisms may
be reversible. It also suggests other mechanisms, such as reperfu-
sion injury.
Because Cohnheim had shown changes in cold injury to be
similar to changes seen in other inflammatory states, Robson and
Heggers163 postulated that the progressive ischemia seen in frost-
bite might be caused by the same inflammatory mediators
responsible for progressive dermal ischemia in the burn wound.
199
 They evaluated blister fluid from patients with hand frostbite,
measuring levels of PGE2, PGF2α, and thromboxane B2 (TXB2).
Levels of the vasoconstricting, platelet-aggregating, and leukocyte-
sticking prostanoids (PGF2α and thromboxane A2 [TXA2]) were
greatly elevated. The investigators postulated that massive edema
after cold injury was caused either by leakage of proteins from
release of these prostanoids or by leukocyte sludging in the
capillaries and increased hydrostatic pressure. Studies have con-
firmed the similarity between cold injury and the burn wound.24
Severe endothelial damage was observed by researchers
studying a minimal cold-injury model in the hairless mouse.18 In
addition, the sequence of endothelial damage, vascular dilation,
vascular incompetence, and erythrocyte extravasation was con-
firmed. This led to speculation that arachidonic acid metabolites,
which may originate from severely damaged endothelial cells,
are important in progressive tissue loss. Significantly absent from
in vivo and microscopic observations were vascular spasm,
thrombosis, and fibrin deposition, all of which had previously
been implicated as pathophysiologic mechanisms. A rabbit ear
model demonstrated increased tissue survival after blockade of
the arachidonic acid cascade at all levels.157 The most marked
tissue salvage resulted when specific TXA2 inhibitors were
used. This has now been shown to be effective in clinical
situations.74
Reports in the 1940s documenting the histopathology of frost-
bite injury to the skin were not comprehensive. Historically,
studies by several investigators have been limited to skin biopsies
without documentation of location, exposure time, temperature,
or time elapsed since the injury.174
COLD AND HEAT
As early as 1991, Manson and co-workers111 proposed that
frostbite is characterized by acute tissue injury induced by freez-
ing and thawing. Initial complete ischemia is followed by reper-
fusion and later by tissue necrosis. The authors suggested that
the vascular events supported the hypothesis that free radical–
mediated reperfusion injury at thawing might contribute to tissue
necrosis after frostbite in a manner similar to that seen after
normothermic ischemia. Supporting evidence included electron
micrographs showing the appearance of severe endothelial cell
injury, beginning during freezing and extending through early
reperfusion. Later, neutrophil adhesion, erythrocyte aggregation,
and microvascular stasis were seen.
DEFINITIONS AND CLASSIFICATIONS
Classically, frostbite has been described by its clinical presenta-
tion, but this can be difficult to predict in the field and before
rewarming.97,131 Mills136,139 favors the use of two simple classifica-
tions: mild (without tissue loss) and severe (with tissue loss).
Historically, and following the classification of thermal burn
injury, frostbite has been divided into “degrees” of injury based
on acute physical findings after freezing and rewarming.
Frostnip is superficial and associated with intense vasocon-
striction. It is characterized by discomfort in the involved parts
(Figure 9-1; see also Figure 9-8). Symptoms usually resolve spon-
taneously within 30 minutes, and no tissue is lost. There is some
question whether this qualifies to be called an injury, because
neither frozen extracellular water nor progressive tissue loss is
routinely demonstrated.

More recently, experimental studies have been able to docu-
ment the histopathology of skin changes under controlled condi-
tions. In 1988, Schoning and Hamlet176,177 used a Hanford
miniature swine model for frostbite injury (−75° C [−103° F] expo-
sure for up to 20 minutes) to note progressive epithelial damage.
Early changes included vacuolization of keratinocytes; loss of
intercellular attachments and pyknosis occurred over 1 week or
more. This subsequently progressed to advanced cellular degen-
eration and formation of microabscesses at the dermoepidermal
PART 2
First-degree frostbite injury shows numbness and erythema.
There may initially be a firm, white or yellowish plaque in the
area of injury. There is no tissue loss, although edema is common
(Figure 9-2). Second-degree injury results in superficial skin vesic-
ulation (Figure 9-3). Clear or milky fluid is present in the blisters,
surrounded by erythema and edema. Third-degree injury shows
deeper blisters, characterized by purple, blood-containing fluid
(Figure 9-4). This indicates that the injury has extended into the
reticular dermis and beneath the dermal vascular plexus. Fourth-

junction. Later changes included epithelial necrosis and regenera- degree injury is completely through the dermis and involves rela-
tion, either separately or together within the same tissue. Such tively avascular subcuticular tissues (Figure 9-5). This tends to
histopathologic data favor the current standard of conservative
management of frostbite injury with delayed surgery.
However, Marzella and associates114 used a New Zealand
white rabbit ear model of frostbite injury and proposed that the
skin necrosis induced by frostbite injury was merely a reflection
of damage to the target cell—the endothelial cell. After submer-
sion of a shaved rabbit ear in 60% ethyl alcohol at −21° C (−5.8° F)
for 60 seconds, the entire microvasculature demonstrated endo-
thelial damage within 1 hour; erythrocyte extravasation occurred
within 6 hours. These early vascular changes in the rabbit ear
model are in contradistinction to the timing of vascular changes
in the Hanford miniature swine model; Schoning and Hamlet177
performed biopsies on animals exposed to frostbite injury (−75° C
[−103° F] for up to 20 minutes) and evaluated the specimens for
vascular inflammation, medial degeneration, and thrombosis. The
earliest change documented both grossly and microscopically
was hyperemia. Within 6 to 24 hours, leukocyte migration and
vasculitis were noted. However, the most severe vascular changes
of thrombosis and medial degeneration were not observed until
1 to 2 weeks after the injury.
Whether or not changes in the epidermis are primary or sec-
ondary to damage of underlying endothelial cells, it is clear that
these tissues have potential, although limited, capacity for regen-
eration. Human experience clearly suggests that robust local
tissue inflammation and coagulation stimulate microvascular
thrombosis and progressive cell death.138 A perfect representative
animal model for frostbite has yet to be found. A wide range of
animal models has been used to create and assess the condition.
Developing a consistent, reproducible, and appropriate model
would facilitate frostbite research.186 In recent years, both swine
and mouse models have been proposed to address this, aiming
to be inexpensive and easily reproducible.9,10,167 Although promis-
ing, their true value will be known when proven during further
trials. FIGURE 9-1  Frostnipped nose. (Courtesy Tim Glasset.)

200

FIGURE 9-2  Nordic skier with first-degree frostbite (central pallor
having cleared after rewarming) of the abdominal skin. This skier
reported having skied for 90 minutes in −23.3° C (−10° F) temperature,
unaware that his shirt, underneath a parka, had come untucked from
his trousers. (Courtesy Luanne Freer, MD.)
FIGURE 9-3  Climber with second-degree frostbite of the fifth finger
sustained after only several seconds’ exposure to −45.6° C (−50° F)
windchill when gloves were briefly removed to handle placement of a
carabiner to the fixed rope. Clear bullae developed after rewarming.
(Courtesy Luanne Freer, MD.)
FIGURE 9-4  Climber with second-, third-, and fourth-degree frostbite
of the hand. Note fingers 1 to 4 with hemorrhagic bullae over the areas
of third-degree injury, clear bullae over the dorsum of the hand with
second-degree injury, and deeply violaceous and unblistered fourth-
degree injury of the distal phalanx of the fifth finger. (Courtesy Luanne
Freer, MD.)
cause mummification, with muscle and bone involvement (Figure
9-6). Less severe bone injury in children may affect the growth
plate and result in developmental digital deformities.21,27
Cauchy and colleagues31 proposed a different classification of
frostbite injury for the hand and foot based on the risk for ampu-
tation of the affected part. An early prognosis prediction for
frostbite patients may be delayed by the lack of useful clinical
guidelines; this new classification scheme is intended to help
resolve such issues (Tables 9-1 to 9-3). The four severity levels
proposed provide earlier prediction of the final outcome of frost-
bite injury by using a technetium-99m (99mTc) bone scan in
conjunction with the clinical findings on presentation. The prob-
ability of bone amputation for the hand and foot could also be
correlated to the extent of frostbite injury seen at the initial pre-
CHAPTER 9  Frostbite
sentation and early 99mTc bone scanning. In a review of 70 cases
of severe frostbite injury, the probability of bone amputation was
1% for involvement of the distal phalanx, 31% when involvement
included the middle phalanx, 67% when involvement included
the proximal phalanx, and 98% and 100%, respectively, when
involvement included the metacarpal/metatarsal and carpal/tarsal
bones (see Table 9-3). Grade 1 lesions do not require hospitaliza-
tion or bone scans. Grade 2 lesions may require brief hospitaliza-
tion and bone scans. Rapid rewarming and treatment with
antibiotics and oral vasodilators appear to be sufficient for
healing. Grade 3 lesions are connected with a significant risk for
amputation and require rapid rewarming, antibiotics, aspirin, and
intravenous (IV) vasodilators. Grade 4 lesions have high risk for
amputation and complications such as thrombosis, sepsis, and
other systemic problems (see Table 9-3). Cauchy’s clinical/99mTc-
based classification scheme appears particularly useful in its
ability to predict at a very early stage the outcome of a frostbite
injury.31
CONTRIBUTING FACTORS
TEMPERATURE AND WINDCHILL
Air alone is a poor thermal conductor, and cold air alone is not
nearly as dangerous a freezing factor as a combination of wind
and cold.208 Wind velocity in combination with temperature
establishes the windchill index. For example, an ambient tem-
perature of −6.7° C (−19.9° F) with a 72-km/hr (45-mph) wind has
the same cooling effect as a temperature of −40° C (−40° F) with
a 3.2-km/hr (2-mph) breeze (Figure 9-7).198,200,203 Thus, it is impor-
tant to think in terms of heat loss, not cold gain. Frostbite occurs
when the body is unable to conserve heat or protect against
heat loss.
FIGURE 9-5  Climber with fourth-degree or severe frostbite injury just
hours after rewarming. Note absence of any blistering. Fingers are
insensate, and capillary refill is absent. (Courtesy Luanne Freer, MD.)
FIGURE 9-6  Photographs of 8-week follow-up of hand pictured in
Figure 9-5, showing complete mummification and autoamputation of
remaining digits. (Courtesy Luanne Freer, MD.)
201
 TABLE 9-1  Proposed Classification for Severity of Frostbite Injuries of the Extremities

Grade 1 Grade 2 Grade 3 Grade 4

Extent of initial lesion at day
0 after rapid rewarming
Bone scanning at day 2
Blisters at day 2
Prognosis at day 2
Sequelae
From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ
Med 12:248, 2001.
Absence of Initial lesion on distal Initial lesion on intermediary Initial lesion on carpal/tarsal
initial lesion phalanx (and) proximal phalanx
Useless Hypofixation of radiotracer Absence of radiotracer Absence of radiotracer uptake
uptake area area on the carpal/tarsal
Absence of Clear blisters Hemorrhagic blisters on the Hemorrhagic blisters over
blisters digit carpal/tarsal
No amputation Tissue amputation Bone amputation of the Bone amputation of the limb
digit ±systemic involvement ±sepsis
No sequelae Fingernail sequelae Functional sequelae Functional sequelae

TABLE 9-2  Management of Frostbite Injuries of the Extremities

On day 0, treatment consists of rapid rewarming for 2 hours in 38° C (100.4° F) water bath, with intravenous infusion of 400 mg chlorohydrate
of buflomedil and 250 mg aspirin. Subsequent treatment depends on the extent of the initial lesion, as follows:

Grade 1*: Absence of Grade 2: Initial Lesion over Grade 3: Initial Lesion over Grade 4: Initial Lesion over
Initial Lesion Distal Phalanx Intermediary (and) Proximal Phalanx Carpal/Tarsal

No hospitalization Hospitalization 2 days Hospitalization 8 days Hospitalization intensive care unit

COLD AND HEAT

Oral treatment for 1 week Possibly a bone scan at day 2 Bone scan at day 2 Bone scan at day 2
(aspirin, vasodilator)
— Oral treatment for 3 weeks IV administration for 8 days (aspirin, IV administration for 8 days (aspirin,
(aspirin, vasodilators), dressing vasodilators), dressing vasodilators), dressing
— — Bone scan near day 8 Possibly antibiotics
— — Bone amputation near day 30 Early bone amputation near day 3 if
sepsis
Recovery Recovery with moderate Bone amputation of digit with Bone amputation of limbs with
sequelae functional sequelae systemic involvement
PART 2

From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ
Med 12:248, 2001.
IV, Intravenous.
*See Figure 9-2.

TABLE 9-3  Probability of Amputation Based on the

Extent of the Initial Lesion
Probability of
Extent (Level of Bone Amputation
Involvement) (95% CI)

Hand 5 (carpal/tarsal) 100—

4 (metacarpal/metatarsal) 100—
3 (proximal phalanx) 83 (66;100)
2 (intermediary phalanx) 39 (25;52)
1 (distal phalanx) 1 (00;03)
Foot 5 (carpal/tarsal) 100—
4 (metacarpal/metatarsal) 98 (93;100)
3 (proximal phalanx) 60 (45;74)
2 (intermediary phalanx) 23 (10;35)
1 (distal phalanx) 0—
Hand and foot 5 (carpal/tarsal) 100—
4 (metacarpal/metatarsal) 98 (95;100) FIGURE 9-7  Jet stream on Mt Everest, premonsoon. Caudwell Xtreme
3 (proximal phalanx) 67 (55;79) Everest Expedition. (Courtesy Christopher H.E. Imray, MD.)
2 (intermediary phalanx) 31 (22;41)
1 (distal phalanx) 1 (00;02)

From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases

of severe frostbite lesions: A proposed new classification scheme, Wilderness
Environ Med 12:248, 2001.
CI, Confidence interval.

202
CONDUCTION

CHAPTER 9  Frostbite
The type and duration of cold contact are the two most important
factors in determining the extent of frostbite injury.198,200,203 Touch-
ing cold wood or fabric is not nearly as dangerous as direct
contact with metal, particularly by wet or even damp hands.60
This is a result of differences in thermal conductivity between
the materials..
Deep, loose snow, which traditionally has been thought to
insulate from the cold, may actually contribute to frostbite. Tem-
perature measured beneath deep snow is frequently much lower
than that on the surface. Washburn203 recounts one expedition
to Denali, Alaska, when members of his party found it extremely
difficult to keep their feet warm, despite a clear, sunny, −16° C
(3.2° F) day with little wind. One member inadvertently dropped
a thermometer in the snow and noted that it registered −25.6° C
(−14.1° F). Feet must be dressed for the temperature at their level
of their immersion in the snow, not for surface temperature A
protection.203

ALTITUDE
Ambient temperature drops by approximately 1.0° C (1.8° F) for
every 150 m (492 feet) of altitude gain. Many serious cases of
frostbite originate at high altitude, but it is difficult to sort out
the independent risk generated by hypobaria/hypoxia versus
cold exposure. Hashmi and colleagues71 reported 1500 cases
of high-altitude frostbite and observed a “very steep upward
curve” beyond a height of 5182 m (17,000 feet) above sea level.
CIVD has been shown to be diminished in non-native visitors
to high altitude.61 Some important sequelae of high-altitude
acclimatization—erythrocytosis and high-altitude dehydration—
result in hyperviscosity that may make frostbite more likely.
Garvey and associates59 demonstrated that erythremia in the
setting of a hypobaric environment provoked procoagulability in
a rhesus monkey model. B
Recent evidence using a real-time video-imaging technique
FIGURE 9-8  Sublingual microcirculatory flow at sea level (A) and
compared sublingual microcirculation at sea level and altitude.113
4900 m (16,076 feet) (B). There is a significant reduction in microcircu-
The study showed significant reduction in microcirculatory flow latory flow index at high altitude (4900 m) when compared with base-
index (MFI) at high altitude (4900 m [16,076 feet]) compared with line in small (<25 µm) and medium (26 to 50 µm) blood vessels.
sea level in small (<25 µm) and medium (26 to 50 µm) blood Caudwell Xtreme Everest Expedition. (From Martin DS, Ince C,
vessels (Figure 9-8). Larger vessels were not studied because of Goedhart P, et al: Abnormal blood flow in the sublingual microcircula-
the relative paucity of their representation in the vascular bed tion at high altitude, Eur J Appl Physiol 106:473, 2009.)
studied. The results showed further reduction in MFI within small
and medium vessels at extreme altitude (6400 m [20,997 feet]).
The very marked slowing of blood flow in the microcirculation other fabric between ice packs and bare skin to prevent this
at high altitude is easily appreciated. “Stagnant” hypoxia may complication.
occur in tissues as a result of reduced microcirculatory blood
flow and consequent failure of oxygen mass transfer. Further-
more, disparity between oxygen supply and demand at the
CLOTHING
microvascular level could lead to heterogeneous tissue oxygen- The degree of inadequacy of protective clothing varies with
ation and cellular hypoxia.83 These preliminary data are the first conditions and may contribute to insufficient conservation of
evidence demonstrating clear reduction in microcirculatory blood body heat.40 Tight-fitting clothing may produce constriction,
flow at altitude and may in part explain the apparent increased which hinders blood circulation and lessens the benefit of
incidence of frostbite at extreme altitude, because a reduction in
flow will be associated with reduction in heat transfer. Further
studies to assess the potential reversibility with supplemental
oxygen are indicated.
Hypoxic neurologic dysfunction is a feature among nonsurvi-
vors at extreme altitude; failure to adequately protect extremities
may contribute to the high incidence of frostbite at extreme
altitude.51 Inadequate fluid intake and poor nutrition are possible
risk factors.133,154

COOLANTS
Not all victims of frostbite are exposed to cold environments.
Case reports cite toxic dermatologic effects of propane, butane,
chloroethane, and liquid oxygen56,103,185,193,197 application to the
skin, either intentionally but exceeding time exposure for cryo-
therapy, or accidentally (Figure 9-9), as in the case of severe
frostbite requiring skin grafting in a child improperly using a
toilet air freshener containing propane and butane.103 FIGURE 9-9  Sherpa climber on day 4 of treatment for second-degree
Careless use of ice to cool a soft tissue injury can result in frostbite from propane leak in backpack on Mt Everest. (Courtesy
frostbite,64 so patients should be instructed to place a towel or Luanne Freer, MD.)

203
 A B
FIGURE 9-10  Early frostbite at 7950 m (26,083 feet) hours after summiting Mt Everest. Five pairs of socks
were being worn. The patient was advised to self-evacuate without rewarming frostbitten feet. Caudwell
Xtreme Everest Expedition. (Courtesy Christopher H.E. Imray, MD.)
heat-retaining air insulation. Wet clothing transmits heat from the
body into the environment, because water is a thermal conductor
superior to air by a factor of about 25.97 Clothing that transmits
moisture away from the body may be protective if an outer,
wind-resistant layer decreases heat loss. However, this wind-
resistant layer must retain the same transmission capabilities;
COLD AND HEAT
otherwise, clothing will still become moist. Clothes that decrease
the amount of surface area may decrease frostbite risk. Mittens
are more protective than gloves, because gloves have a greater
surface area and prevent air from circulating between fingers.
Poorly fitted boots notoriously generate frostbite injuries, even
when worn with excess socks (Figures 9-10 and 9-11).
Although up to 40% of total body heat loss can occur through
exposed head and neck areas,3 a study has refuted the widely
held belief that the head loses proportionally more heat than the
PART 2
FIGURE 9-11  Climber on South Col, Mt Everest (7950 m [26,083 feet])
with excess socks in hand, about to descend. Caudwell Xtreme Everest
Expedition. (Courtesy Christopher H.E. Imray, MD.)
204
rest of the body. In fact, any uncovered part of the body loses
heat in proportion to the body surface area exposed; appropriate
protection is important for all exposed skin.153
SKIN WETNESS/UNWASHED SKIN
Development of frostbite does not depend only on ambient
temperature and duration of exposure. Windchill, humidity, and
wetness predispose to frostbite. Skin wetting adds an increment
of heat transfer through evaporation and causes wet skin to cool
faster than dry skin.135 More important, water in the stratum
corneum can terminate supercooling by triggering water crystal-
lization not only in this layer but also in underlying tissue. Skin
wetness is therefore conducive to frostbite because it allows
crystallization to terminate supercooling after approximately one-
half the exposure time required by dry skin. This substantiates
the following clinical observation:
It has been found that supercooling displays itself in greater degree in
skin that remains unwashed. Washing the skin encourages freezing,
whereas rubbing the skin with spirit and anointing it with oil discourages
it. The capacity to supercool greatly would seem to be connected with
relative dryness of the horny layers of the skin. It is well known that
Arctic explorers leave their skin unwashed.107
ALTERED MENTAL STATUS (ALCOHOL, DRUGS,
MENTAL ILLNESS)
Putting on clothes in response to cold is not a reflex but requires
a conscious decision. When the ability to decide or to act is
impaired, there is risk for cold-induced injury; not surprisingly,
alcohol has been implicated in up to 53% of nonmilitary frostbite
cases.192 Once the injury had occurred, alcohol intake probably
did not significantly alter the course of events. Barillo and associ-
ates13 experimentally demonstrated increased mortality and a
detrimental effect of ethanol on tissue perfusion associated with
severe murine frostbite. Alcohol consumption promotes periph-
eral vascular dilation and increases heat loss, making an exposed
part more susceptible to frostbite.162
In one series of 20 urban frostbite patients, all had overt
or covert psychiatric disease.148 This prompted a retrospective
review that suggested between 61% and 65% of urban frostbite
patients have psychiatric disease, and some centers now advo-
cate psychiatric screening in all patients with of urban frostbite
injury.
FATIGUE
During World War II and the Korean conflict, clinical studies
indicated that cold injuries occurred with higher frequency
among soldiers in retreat.142,207 Fatigue and apathy increase the
incidence of cold injury. When warfare is proceeding toward
defeat, or in conditions of starvation, soldiers often become indif-
ferent to personal hygiene and clothing, and the frequency of
frostbite increases.95 Overexertion increases heat loss. A large
amount of body heat can be expended by panting, and perspira-
tion further compounds the problem of chilling. Both panting
and sweating consume energy, which compounds the fatigue
factor.
TOBACCO SMOKING
Impaired local circulation is a primary contributor to frostbite.
Cigarette smoking causes vasoconstriction, decreased cutaneous
blood flow, and tissue loss in random skin flaps.106 Reus and
colleagues160 documented that smoking induced arteriolar vaso-
constriction and decreased blood flow in a nude subject. Although
red blood cell velocity increased, the net effect was decreased
blood flow in cutaneous microcirculation during and immediately
after smoking. Curiously, habitual heavy smokers show higher
scores on the Resistance Index of Frostbite (RIF), which corre-
lates with lower risk for frostbite.36 Empirically, one could con-
clude that smoking, which induces vasoconstriction, should place
one at increased risk for frostbite, and research supports this.37,47,71
COMORBIDITIES
Drugs known to have vasoactive properties may predispose to
or worsen frostbite injury. Disease states that alter tissue perfu-
sion, such as diabetes, atherosclerosis, arteritis, and Raynaud’s
disease, predispose to frostbite (Figure 9-12).41,100
PREVIOUS FROSTBITE INJURY
An individual who has experienced prior cold injury is placed in
a high-risk category during subsequent cold exposure.129,207 For
undefined reasons, cold injury sensitizes an individual, so that
subsequent cold exposure, even of a lesser degree, produces
more rapid tissue damage.96 Cold-induced neuropathy may play
an important role in the long-term presence of cold sensitivity
after local cold injury. An alteration in somatosensory function
was found, and this was more pronounced in lower-limb
injuries.8
IMMOBILITY
Military studies emphasize that long periods of immobility con-
tribute to the extent of cold injury.96,97 Motion produces body
heat and improves circulation, especially in endangered limbs.
FIGURE 9-12  A 54-year-old man had an acute primary episode of
Raynaud’s disease after surfing for 80 minutes in water that was 21° C
(69.8° F). The distinctive asymmetric pallor of the terminal phalanges
of the fourth digit on the right hand persisted for 40 minutes. A sharp
demarcation between the second and third phalangeal joints was
evident, but no other symptoms were apparent. The pallor spontane-
ously resolved without cyanosis or redness of the affected area.
Medical evaluation subsequently revealed no disorder known to cause
secondary Raynaud’s phenomenon. (From Bluto MJ, Norman DA:
Acute episode of Raynaud’s disease, N Engl J Med 347:992, 2002.)
GENETIC PREDISPOSITION
CHAPTER 9  Frostbite
The deletion genotype (DD) for the angiotensin I–converting
enzyme (ACE) has been associated with increased vascular reac-
tivity in vivo and in vitro.23,75 Kamikomaki88 proposed that a case
of frostbite in a climber with ACE DD allele was caused by
genetic propensity for vasoconstriction.
Civilian clinical studies are inadequate for statistical evalua-
tion of factors such as race and previous climatic environmental
exposure.96,119,121 In a recent study, African Americans were
found to have difficulty generating increased metabolic rate
(measured by oxygen consumption [ VO  2 ] and rectal tempera-
ture) after acute cold exposure, and researchers suggest this
group may be at greater risk for cold injury.49 Military studies
suggest that women and blacks may be more susceptible to
cold injury.37,61 One author postulates that blacks are three to six
times more susceptible to frostbite than are whites because
blacks tend to initiate shivering at lower core temperatures and
tend to have long, thin fingers and toes, as well as thin arms
and legs, which do not conserve heat as efficiently as do their
white counterparts. In testing, black fingers cool faster when
immersed in cold water and reach a lower temperature before
the hunting response ensues.61 Individuals with type O blood
and from warmer climatic regions in the United States tend to
be more susceptible.61,207
An increased incidence of frostbite was reported in almost
6000 military recruits with cold-provoked white finger syndrome
and in those with hand/arm vibration.47,141
A low RIF, determined in a simple laboratory test, may be
indicative of increased risk for cold injuries during operations in
the field.36
CLINICAL PRESENTATION
In most patients, the initial clinical observation is coldness of the
injured part, and more than 75% complain of numbness. The
involved extremity feels clumsy or “absent” because of ischemia
following intense vasoconstriction. When numbness is present
initially, it is frequently followed by extreme pain (76% of
patients) during rewarming. Throbbing pain begins 2 to 3 days
after rewarming and continues for a variable period, even after
dead tissue becomes demarcated (22 to 45 days). After about 1
week, the patient usually notices a residual tingling sensation, a
result of ischemic neuritis, which explains why this sensation
tends to persist longer than other symptoms. Severity of the injury
usually defines the extent of neuropathologic damage. Because
different injuries are influenced by so many environmental and
individual factors, symptoms may vary greatly. In patients without
tissue loss, symptoms usually subside within 1 month, whereas
in those with tissue loss, disablement may exceed 6 months. In
all cases, symptoms are intensified by a warm environment.
Other sensory deficits include spontaneous burning and electric
current–like sensations. The burning sensation, which is fre-
quently early in presentation, subsides within 2 to 3 weeks and
is usually not present in patients with tissue loss. In those without
tissue loss, the burning sensation may resume on wearing shoes
or increasing activity. The electric current–like shock is almost
universal (97%) in patients with tissue loss. It usually begins 2
days after injury, lasts for about 6 weeks, and is particularly
unpleasant at night. All frostbite patients experience some degree
of sensory loss for at least 4 years after injury and perhaps
indefinitely.
The clinical appearance of frostbite depends on how quickly
the injured patient presents to care, and it is important to note
that this appearance may initially be deceiving.17,142 In the past,
patients in the Alps who arrived by helicopter within minutes of
their injury presented quite differently than did Himalayan climb-
ers, who had almost completely rewarmed during self-descent
and were fortunate if they were able to arrive at definitive care
even several days after injury.46 Fortunately, helicopter evacua-
tion is being used more widely in the regions with taller moun-
tains. Regardless of venue, only a few patients arrive with tissue
still frozen. At first, the extremity appears yellowish white or
mottled blue. It may be insensate and may appear frozen solid,
regardless of the depth of the injury. With rapid rewarming, there
205

A spontaneous rewarming. Anticipate that frostbitten areas will rewarm
B All constrictive and wet clothing should be replaced by dry, loose
COLD AND HEAT
FIGURE 9-13  Photo of climber 24 hours (A) and approximately 2
weeks after (B) deep frostbite injury to fingers, showing eschar forma-
tion. (Courtesy Luanne Freer, MD.)
is almost immediate hyperemia, even in some patients with the
most severe injuries. Sensation returns after thawing and persists
until blebs appear. At this point, an effort should be made to
PART 2
assess the severity of the injury.
After the extremity is rewarmed, edema appears within 3
hours and lasts 5 days or longer, depending on the severity of
the case. Vesicles or bullae appear 6 to 24 hours after rapid
rewarming. Clear bullae confer a better prognosis than hemor-
rhagic bullae, which indicate deeper injury. During the first 9 to
15 days, severely frostbitten skin forms a black, hard, and usually
dry eschar, whether or not vesicles are present (Figure 9-13).
Mummification forms an apparent line of demarcation in 22 to
45 days.142
FIELD TREATMENT
78
In 1957, Hurley stated, “Tissue cells can be affected by freez-
ing in three different ways: (1) a certain number of cells are
killed; (2) a certain number remain unaffected; and (3) a large
number are injured but may recover and survive under the
right circumstances.” Clearly, the major treatment effort must be
to salvage as many cells in the third group as possible. Frost-
bite treatment is directed separately at the prethaw and post-
thaw intervals.
SELF-RESCUE IN THE FREEZING ENVIRONMENT
The International Commission for Alpine Rescue (ICAR) gives
specific recommendations for self-rescue to persons working,
recreating, or otherwise exposed to a cold environment (Box
9-1). These guidelines advise seeking shelter from cold and wind,
drinking warm fluids, removing wet clothing, taking ibuprofen,
and attempting self-rewarming for 10 minutes. If at high altitude,
supplemental oxygen is advised, and if sensation does not return,
the patient is advised to discontinue any further exposure and
seek treatment.187 Although these guidelines may seem common
sense to most, climbers appreciate these guidelines for safety and
self-rescue when in an exposed, potentially dangerous, and
remote setting.
206
TREATMENT IN THE PREHOSPITAL
FREEZING ENVIRONMENT
The Alaska State guidelines for field treatment and transport of
patients with frostbite recommend the following:
If transport time will be short (1 to 2 hours at most), the risks posed
by improper rewarming or refreezing outweigh the risks of delaying
treatment for deep frostbite.
If transport will be prolonged (more than 1 to 2 hours), frostbite
will often thaw spontaneously. It is more important to prevent hypo-
thermia than to rewarm frostbite rapidly in warm water. This does not
mean that a frostbitten extremity should be kept in the cold to prevent
as a consequence of keeping the patient warm and protect them from
refreezing at all costs.1
The Joint Commission of Health and Human Services, emer-
gency medical services, and public health departments for Alaska
have published further guidelines for prehospital and bush clinic
care of frostbite. These guidelines are widely regarded as state-
of-the-art recommendations (Box 9-2). If a patient is referred
from a nearby location, no attempt at field rewarming is indi-
cated. Vigorous rubbing is ineffective and potentially harmful.
The extremity should not be intentionally rewarmed during trans-
port and should be protected against slow, partial rewarming by
keeping the patient away from intense campfires and car heaters.
wraps or garments. The extremity is padded and splinted for
protection, and oral ibuprofen, 400 mg twice daily, may be initi-
ated (ibuprofen may be more beneficial than aspirin because
aspirin may block more of the inflammatory cascade than is
helpful). Although a correlation exists between the length of time
tissue is frozen and the amount of time required to thaw that
tissue, no direct correlation exists between the length of time
tissue is frozen and subsequent tissue damage. Still, “rapid”
transport of frostbite patients (within 2 hours) is appropriate, and
one should not purposefully keep tissues below freezing tem-
peratures (unless there is risk of refreezing injury).123 If immediate
transport is not feasible, rapid rewarming should be instituted
(goal is to see blush of rewarming and/or 15 minutes immersed
in rewarming fluid) and the patient transported with protective,
dry, and nonadherent dressings to prevent refreezing. Appropri-
ate adequate analgesia should be administered; an IV or intra-
muscular (IM) opiate may be required. Blisters should be left
intact. Patients with long transport times are at greater risk for
(refreezing) recurrent injury. All efforts should be made to
BOX 9-1  Guidelines from ICAR for Self-Treatment of
Potential Frostbite
Emergency Treatment
In the Open with Possible Onset of Frostbite
• Move out of the wind; consider turning back; drink fluids (warm
if possible).
• Remove boots, but consider possible problems with
replacement if swelling occurs.
• Remove socks/gloves if wet. Exchange for dry clothing.
• Warm by placing foot/hand in companion’s armpit/groin for 10
minutes only.
• Replace boots.
• Give one dose of aspirin or ibuprofen to improve circulation (if
available and not contraindicated).
• Do not rub the affected part because this may cause tissue
damage.
• Do not apply direct heat.
If there is sensation, the patient can continue to walk.
If there is no sensation, the patient should go to the nearest warm
shelter (hut/base camp) and seek medical treatment.
At high altitude, give oxygen if available.
Modified from Syme D (for ICAR Medical Commission): Position paper: On-site
treatment of frostbite for mountaineers. High Alt Med Biol 3:297, 2002.
ICAR, International Commission on Alpine Rescue.
 CHAPTER 9  Frostbite
BOX 9-2  Alaska State Guidelines for Prehospital
Treatment of Frostbite
First Responder/Emergency Medical Technician—I, II, III/
Paramedic/Small Bush Clinic
Evaluation and Treatment
A. Anticipate, assess, and treat the patient for hypothermia, if
present.
B. Assess the frostbitten area carefully because the loss of
sensation may cause the patient to be unaware of soft tissue
injuries in that area.
C. Obtain a complete set of vital signs and the patient’s
temperature. A
D. Remove jewelry and clothing, if present, from the affected
area.
E. Obtain a patient history, including the date of the patient’s last
tetanus immunization.
F. If there is frostbite distal to a fracture, attempt to align the
limb unless there is resistance. Splint the fracture in a manner
that does not compromise distal circulation.
G. Determine whether rewarming the frostbitten tissue can be
accomplished in a medical facility. If it can, transport the
patient while protecting the tissue from further injury from cold
or impacts.
H. If the decision is made to rewarm frostbitten tissue in the field,
you should prepare a warm water bath in a container large
enough to accommodate the frostbitten tissues without
them touching the sides or bottom of the container. The
temperature of the water bath should be 99° to 102° F (37°
to 39° C).
• Generally, patients with frostbite do not require opiates
for pain relief; they occasionally need nonopiate pain B
medication or anxiolytics. If possible, consult a physician
regarding the administration of oral analgesics, such as FIGURE 9-14  A, Day 2 after exposure: field rewarming of frostbite
acetaminophen, ibuprofen, or aspirin. Aspirin or ibuprofen injury to Mt Everest summiteer at 6400 m (20,997 feet); B, Day 3:
may help improve outcomes by blocking the arachidonic field treatment of frostbite injury at 5300 m (17,388 feet). (Courtesy
acid pathway. Christopher H.E. Imray, MD.)
• Immersion injury or frostbite with other associated injuries
may produce significant edema and high pain levels. These
patients may need opiate pain medications for initial
treatment. In this case, advanced life support personnel prevent refreezing, because this creates a much worse outcome
should administer morphine or other analgesics in than does delayed thawing (Figures 9-14 to 9-16). A patient who
accordance with physician-signed standing orders or online must walk through snow should do so before thawing frostbitten
medical control. feet (see Figure 9-10). During transport, the extremities should
I. A source of additional warm water must be available. be elevated and tobacco smoking prohibited.130
J. Water should be maintained at approximately at 99° to 102° F The Wilderness Medical Society convened a panel of experts
(37° to 39° C) and gently circulated around the frostbitten in 2011 and 2014 to review recent literature and ICAR and Alaska
tissue until the distal tip of the frostbitten part becomes State guidelines in order to apply evidence grades based on the
flushed.
quality of supporting evidence and to balance the benefits and
K. Pain after rewarming usually indicates that viable tissue has
been successfully rewarmed.
risks for each modality according to methodology stipulated by
L. After rewarming, let the frostbitten tissues dry in the warm air. the American College of Chest Physicians.122,123 Their guidance is
Do not towel dry. in line with that of the Alaska guidelines. The review is a useful
M. After thawing, tissues that were deeply frostbitten may evidence-based reference for persons who do not routinely
develop blisters or appear cyanotic. Blisters should not be manage frostbite injuries.
broken and must be protected from injury.
N. Pad between affected digits and bandage affected tissues
loosely with a soft, sterile dressing. Avoid putting undue DEFINITIVE TREATMENT
pressure on the affected parts.
O. Rewarmed extremities should be kept at a level above the
(IMMEDIATE TREATMENT)
heart, if possible. Once in the emergency department (ED), if tissues are still
P. Protect the rewarmed area from refreezing and other trauma frozen, rapid rewarming should be started immediately. Any
during transport. A frame around the frostbitten area should associated traumatic injuries or medical conditions should be
be constructed to prevent blankets from pressing directly on identified. Systemic hypothermia should be corrected to a core
the injured area. temperature of at least 34° C (93.2° F) before frostbite manage-
Q. Do not allow an individual who has frostbitten feet to walk ment is attempted. Fluid resuscitation is usually not a problem
except when the life of the patient or rescuer is in danger. with isolated frostbite injuries, although one case of rhabdomy-
Once frostbitten feet are rewarmed, the patient becomes
olysis and acute renal failure has been reported.165 One must
nonambulatory.
remember that prolonged strenuous exercise or altitude exposure
From Department of Health and Social Services, Division of Public Health increases the risk for dehydration, so it is advised to encourage
Section of Community Health and EMS: State of Alaska Cold Injuries oral intake or IV fluids.
Guidelines, 2003 version rev 2005. http://www.chems.alaska.gov. Treatment is directed at the specific pathophysiologic effects
of the frostbite injury, either blocking direct cellular damage or
preventing progressive microvascular thrombosis and tissue loss.
Direct cellular damage is treated by rapid thawing of all degrees
of frostbite with immersion in gently circulating water warmed

207

A or clear blisters, which represent more superficial injury, are
COLD AND HEAT
B the arachidonic acid cascade but has the additional benefit of
FIGURE 9-15  A, Six weeks after injury: third toe is showing signs of
recovery. B, Ten weeks after injury: primary closure was achieved with
full-thickness skin cover to optimize the functional result. (Courtesy
Christopher H.E. Imray, MD.)
PART 2
to 37° to 39° C (98.6° to 102.2° F). 123,137
Adherence to this narrow
temperature range (as long as it is easy to monitor in the hospital)
is important, because rewarming at lower temperatures is less
beneficial for tissue survival, and rewarming at higher tempera-
tures may worsen the injury by producing a burn wound.57,74,132
Frozen extremities should be rewarmed until the involved skin
becomes pliable and erythematous at the most distal parts of the
frostbite injury. This usually takes less than 30 minutes. Active
motion during rewarming is helpful, but massage may compound
the injury. Extreme pain may be experienced during thawing,
and unless otherwise contraindicated, parenteral analgesics are
administered. Rapid return of skin warmth and sensation with
the presence of an erythematous color is a favorable sign,
whereas the persistence of cold, anesthetic, and pale skin is
unfavorable.
FIGURE 9-16  Integrated vascular/orthotic assessment in a specialized
clinic after surgery (in preparation for a further high-altitude expedi-
tion). (Courtesy Christopher H.E. Imray, MD.)
208
Rapid rewarming reverses the direct injury of ice crystal forma-
tion in the tissue. However, it does not prevent the progressive
phase of the injury. McCauley and associates119,120 have designed
a protocol based on the pathophysiology of progressive dermal
ischemia that has been quite successful in minimizing production
of local and systemic thromboxane by injured tissues. All patients
except those with the most minor frostbite injury should be
admitted to the hospital. Patients with minor injuries should be
admitted if, after rapid rewarming, a warm environment cannot
be ensured for the patient. No patient should ever be discharged
into subfreezing weather. Even with a warm car waiting, the
patient should be allowed to leave only with proper clothing,
such as stocking cap and wool mittens and socks.
Because the majority of frostbite injuries necessitate admission
to the hospital, a discussion of the protocol is warranted. White
debrided to prevent further contact of PGF2α or TXA2 with the
damaged underlying tissues. Unlike the clear blisters, hemor-
rhagic blisters reflect structural damage to the subdermal plexus.
It may be worthwhile to aspirate the thromboxane-containing
fluid out of these blisters, but debridement may promote desic-
cation of the deep dermis and allow conversion to a full-thickness
injury. It has been argued that hemorrhagic blisters should be
left intact; however, we tend to favor drainage. A specific throm-
boxane inhibitor, such as Aloe vera gel, is placed on the wounds,
and dressings should accommodate expected increasing edema.73
Aspirin was originally recommended to be given systemically to
block production of PGF2α and TXA2. The correct dose of aspirin
to block PGF2α is difficult to determine, however, so it has been
replaced by ibuprofen. Aspirin may still have a useful antiplatelet
action if ibuprofen is not available. Ibuprofen not only inhibits
fibrinolysis. Oxygen should be used to achieve normoxia in a
hypoxic patient and is used for frostbite injuries occurring at
extreme altitude.
EVALUATION AND TREATMENT
IN THE HOSPITAL
OVERALL STRATEGY
Frostbite is a thermal injury affecting the vasculature, microvas-
culature, and tissues of the extremities and, as such, shares many
clinical features with both vascular injuries and burn wounds.
This section discusses the aspects of definitive patient care,
including complete patient assessment, specific evaluation of the
frostbite injury regarding perfusion and tissue viability, and
optimal medical management, including proper selection of can-
didates for endoluminal treatments such as catheter-directed
thrombolysis or iloprost infusion. Early and late reconstructive
surgery, ablative surgery, rehabilitation, and frostbite prevention
strategies are also discussed.
INITIAL ASSESSMENT OF FROSTBITE AND
OTHER INJURIES
A rapid and detailed clinical assessment of the patient on arrival
in the ED is mandatory. The standard approach of assessing the
airway, breathing, and circulation takes precedence over assess-
ment of the frostbite injury. History and examination may reveal
coexisting problems, and although the frostbite injuries may
be visually distressing and severe, there may be more serious
injuries or medical conditions that require treatment first. Particu-
lar attention needs to be paid to hypothermia, limb fractures, the
peripheral circulation, and coexisting trauma. Medical conditions,
such as poor glycemic control and alcohol/drug use, must be
considered.
Principles
Hurley78 stated in 1957 that frostbite results in three zones of
tissue injury: dead tissue, normal living tissue, and an interface
zone. If we develop this concept further, immediately after the
index frostbite injury, the size of the interface zone is maximal
and potentially salvageable. Weeks after injury, the interface zone
will be negligible; as a result, the interface zone has a “dynamic”
component.56,78 The aim of early evaluation of the frostbite injury
is to try to determine the exact extent of the three zones so that
a subsequent multifaceted management plan may be directed to
optimize tissue salvage in the dynamic interface zone.
The initial injury, patient’s response, ambient temperature, and
time from initial cold injury to presentation at the hospital all
contribute to the extent of the intermediate, potentially salvage-
able interface zone. The patient who is transferred from the
mountainside directly to the ED by helicopter will have a rela-
tively large, potentially salvageable interface zone compared with
a patient who has undergone a much more lengthy evacuation
from a remote climbing region.
PATIENT CARE
Specialist Nursing Care
Almost all urban patients with significant frostbite should be
admitted to the hospital. Alcohol intoxication, psychiatric illness,
and homelessness are common features of the urban frostbite
patient, so immediate discharge is rarely prudent.
Overall goals of hospital treatment include keeping the patient
calm, well nourished, suitably hydrated, and pain free. Wound
care must be meticulous to avoid further trauma. Injured extremi-
ties should be elevated above heart level to attempt to minimize
edema. Physiotherapy is important, and the patient should be
encouraged to mobilize as soon as possible.206 Extremities should
be treated with clean dressings and twice-daily whirlpool baths
with an antiseptic such as chlorhexidine or povidone-iodine.
Topical Aloe vera gel should be applied every 6 to 8 hours
through resolution of blisters. This encourages the eschar created
by the blisters to separate from underlying healthy tissue.
Although patients may be housed anywhere that these objectives
can be achieved, vascular surgery or plastic surgery/burns wards
(with multidisciplinary input) tend to be most appropriate for
more severe injuries.
Frostbite blisters have been shown to contain high concentra-
tions of the vasoconstricting metabolites of arachidonic acid,
PGF2α and TXB2, which are known to mediate dermal ischemia
in burns and pedicle flaps. It is suggested that these may play a
role in the pathogenesis of frostbite.163 Debate continues about
management of such blisters and the risk versus benefit of poten-
tial introduction of infection. Current thinking is that clear/cloudy
blisters should be drained by needle aspiration (especially if the
bullae restrict movement), and that hemorrhagic (presumably
deeper) blisters should be left alone.123 In general, our view is
to support aspiration of all blisters. Optimally, large-blister
aspiration/deroofing will be carried out in a controlled environ-
ment using sterile procedures and anesthetics as needed.
TECHNIQUES TO EVALUATE TISSUE PERFUSION
Over the years, several diagnostic tests have been used to attempt
to predict severity and prognosis of frostbite injury. These include
plain radiographs, infrared thermography, angiography,65 triple-
phase bone scanning,33 laser Doppler, digital plethysmography,158
and magnetic resonance imaging/magnetic resonance angiogra-
phy (MRI/MRA). The most promising approaches seem to be
triple-phase bone scanning15,33 and MRI/MRA.14 Early diagnostic
digital subtraction angiography (before administration of tissue
plasminogen activator) is an essential first-line investigation for
the patient presenting acutely with severe frostbite injury without
significant comorbidities, where thrombolysis is an available
treatment modality and option.178
Duplex Ultrasonography
Duplex ultrasonography uses B-mode, pulsed-wave Doppler
ultrasonography to visualize blood flow within vessels and color
flow Doppler imaging to visualize the structure and hemodynam-
ics within vessels. In modern vascular units, there is a move
toward using duplex ultrasound examination as the first-line
investigative examination, reserving angiograms for situations in
which a therapeutic intervention is required. Ease of access,
CHAPTER 9  Frostbite
FIGURE 9-17  Vascular imaging at 7950 m (26,083 feet) using a
portable battery-powered SonoSite MicroMaxx duplex ultrasound
machine. Caudwell Xtreme Everest Expedition. (Courtesy Christopher
H.E. Imray, MD.)
portability, and the ability to make repeat examinations give the
technique certain advantages over other imaging modalities.
Many remote research stations and even large expeditions may
have portable ultrasound machines. Duplex imaging has been
used in the field at altitudes as high as 7950 m (26,083 feet)
(Figure 9-17). Ultrasound has been used to determine the need
for sympathetic blockade after frostbite.158
Magnetic Resonance Angiography
The MRI/MRA investigation has a theoretical advantage over
99m
Tc bone scanning because it allows direct visualization of
vessels (both patent and occluded), as well as imaging of sur-
rounding tissues. Some suggest that it shows a more clear-cut
line of demarcation of ischemic tissue.14 The other advantage of
MRA over angiography is that it is noninvasive. However, there
are relatively few accounts of its use in frostbite evaluation in
the literature.14,159
Technetium-99m Scanning
The first description of 99mTc scanning for assessment of bone
viability in patients with frostbite injuries was in 1976.109 The
degree of accretion of the 99mTc was found to depend on integrity
of the vascular supply. It was successfully used to distinguish
viable from nonviable bone. However, Miller and Chasmar126
found that very early 99mTc bone scanning in frostbitten patients
was not as accurate an indicator of the ultimate extent of tissue
loss as scanning at 5 days after injury. They also noted that
lesions appeared to fluctuate in extent over a 3-week period.
Cauchy and colleagues30,31 recognized that existing frostbite
classifications were based on retrospective diagnoses and were
not useful for predicting the extent of final tissue loss and prog-
nosis for frostbite patients. The 3- to 6-week waiting period
often necessary to determine severity of the lesion and resultant
need for amputation often caused considerable distress for
patients. The authors suggested a new classification system that
begins at day 0 (just after rewarming) and is based mainly on
the topography of the lesion and on early bone scan results.
This appears to be a very useful classification for the physician
and patient, in that it allows accurate determination at a very
early stage of the likely extent of subsequent tissue loss (see
Tables 9-1 to 9-3).
An interesting insight into some of the possible mechanisms
involved in certain frostbite injuries was described by Salimi
and co-workers,171 who designed an experimental model to
study pathogenesis and treatment of frostbite. Using 99mTc radio-
nuclide imaging, they monitored evolution and extent of tissue
damage relative to temperature, rate of freezing, and controlled
209
 rewarming. Characteristic serial changes were demonstrated on
sequential scans. Initial nonperfusion was followed by perfusion
and finally again by nonperfusion; this occurred in all areas
where necrosis subsequently developed. Reappearance of non-
perfusion corresponded to vascular injury. Vessel thrombosis was
found on pathology examination and may be related to reperfu-
sion injury.
These clinically relevant observations gave evidence to support
the concept of temporal “perfusion flux” in blood flow to a
frostbitten extremity. Initial reduction is often followed by a
temporary hyperperfusion phase before the final infarction phase
(probably secondary to endothelial dysfunction and thrombin
accumulation). Consequently, measurement of tissue perfusion
at a single time point may not be as accurate in predicting
outcome as originally believed.
Additional supporting evidence for perfusion flux in frostbite
comes from Cauchy and associates,30,33 who performed a more
detailed analysis of two-phase 99mTc bone scans. Sensitivity of
the technique was enhanced by performing a second scan more
than 5 days after rewarming. Comparative analysis of the two
scans demonstrated that some of the lesions continued to evolve A
between day 2 and day 8. Based on this finding, the authors
suggested that the outcome of lesions could still be modified
during this period. However, in the event of severe sepsis, the
results of the first bone scan can be used as an indication for
emergency amputation.31
Although the large retrospective study of Cauchy and col-
leagues30 using two-phase bone scintigraphy suggested that
nonuptake (or low uptake) in frostbite lesions had a strong cor-
COLD AND HEAT

relation with the subsequent need for amputation, another pro-

spective study has questioned some aspects of the technique.15
This latter study compared 22 controls with 20 patients with
frostbite. Serial scintigraphy using 99mTc was performed in some
patients. In line with the perfusion flux concept, the study sug-
gests that scintigraphy results are somewhat more variable than B
previously suggested, and that moderate to severe frostbite
lesions can be classified as having infarcted, ischemic, or hiber- FIGURE 9-18  Frostbitten left hand of a climber (A) taken 36 hours
nating (viable) tissue, similar to the classification employed when after injury, while climbing in Antarctica (B) Note the discoloration and
blister formation, iodine warming towels, and aseptic techniques used
PART 2

using myocardial scintigraphy. Absence of uptake of 99mTc, even

after the initial 10 days in this study, did not necessarily indicate
infarction and the need for amputation, because many such
lesions retain potential for vasodilation and recovery.
Triple-phase bone scanning (using 99mTc) has now become
more widely used in specialty units, often within the first few
days of presentation. This technique assesses tissue viability in
an effort to allow early debridement of soft tissue and early
coverage of ischemic bony structures.67
There are few prospective data on the efficacy of 99mTc scan-
ning in predicting the outcome of frostbite injuries. However, it
remains a very useful way of assessing potential tissue loss79
(Figures 9-18 to 9-21).
MEDICAL MANAGEMENT
Table 9-4 summarizes the drugs used in the management of
frostbite.
Tetanus Prophylaxis
Frostbite should be considered a high-risk injury. Tetanus pro-
phylaxis status should be completed in all patients according to
currently accepted guidelines.38
Heparin
Heparin is a naturally occurring anticoagulant that prevents for-
mation of clots and extension of existing clots within blood
vessels. Although true thrombi are not present in dilated,
erythrocyte-filled vessels immediately after thawing, they form
over the next few days. Heparin has been suggested as a possible
treatment for frostbite.180 Lange and Loewe104 demonstrated its
usefulness in experimental frostbite. Subsequent investigations
have been unable to substantiate these findings, and there is no
evidence that heparin alters the natural history of frostbite.21
Deep vein thrombosis (DVT) prophylaxis is indicated in any rela-
tively immobile frostbite patient.
in tented field hospital. A digital image was reviewed within 6 hours
by Dr. Imray in the United Kingdom, and management advice was
given over the Internet. (Courtesy Christopher H.E. Imray, MD. From
Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities:
Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)
Indications and Recommendations for Antibiotics
Clinicians have long been aware of the potential for infectious
complications in frostbite.147 The metabolic requirements of
infected and healing tissue are increased over those of normal
tissue. Consequently, should the marginally perfused interface
zone become infected, the resulting tissue loss is likely to be
increased. Although scant published evidence exists on their use
for frostbite, antibiotics are widely used.
When the skin is edematous, penicillin is administered pro-
phylactically because edema inhibits the skin’s inherent antistrep-
tococcal properties.138 If there are clinical signs of infection,
antibiotic use is absolutely indicated.
Wound cultures should be taken from infected tissue to guide
therapy. While awaiting identification of species and sensitivities,
practitioners should be aware that the common causative organ-
isms include Staphylococcus aureus, β-hemolytic streptococci,
gram-negative rods, and anaerobes. Empiric use of antibiotics to
cover these likely organisms should be considered pending
culture results. Although no evidence exists for their prophylactic
use, antibiotics should be considered if a large area of infarcted
tissue or significant edema is present, or if the patient is immune
compromised.
In a 12-year retrospective study, factors found to correlate
significantly with amputation after frostbite were duration of
exposure, lack of proper attire, remote geographic location, pres-
ence of wound infection, and delay in seeking treatment. Pro-
phylactic systemic antibiotics did not decrease the incidence of
wound infection.195

210
 CHAPTER 9  Frostbite
L R
A

B
FIGURE 9-19  Condition of hands of patient in Figure 9-18 on patient’s
arrival in the United Kingdom, 5 days after initial injury. (Courtesy L Marker R
Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al:
FIGURE 9-20  Technetium-99m bone scans performed on arrival of
Cold damage to the extremities: Frostbite and non-freezing cold inju-
patient in Figures 9-18 and 9-19 in the United Kingdom. The scans
ries, Postgrad Med J 85:481, 2009.)
show minimal perfusion to the terminal phalanges in the left hand,
suggesting that amputation of the distal phalanges is likely to be
necessary. (Courtesy Christopher H.E. Imray, MD. From Imray C,
Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite
Topical Aloe vera and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)
Experimental evidence from the frostbite rabbit ear model has
suggested a clearly defined role for thromboxane as a mediator
of progressive dermal ischemia in frostbite injuries. Rapid rewarm- without significant tissue loss. Increased tissue survival was dem-
ing helps preserve tissue by limiting the amount of direct cellular onstrated experimentally with preservation of the dermal micro-
injury. Selective management of blisters helps protect the sub- circulation by using antiprostaglandin agents and thromboxane
dermal plexus, and topical application of Aloe vera (e.g., Der- inhibitors.
maide Aloe cream or gel) combats the local vasoconstrictive
effects of thromboxane (Figure 9-22). Vasodilators
Animal studies suggest thromboxane appears to be a mediator The equation determining fluid flow within a tube was first
of progressive dermal ischemia in frostbite. In a rabbit ear frost- described in the 1840s by the French physician and physiologist
bite model, Heggers and associates74 compared the effect of (1) Jean Poiseuille. He demonstrated that flow was related to perfu-
the antiprostanoids (methylprednisolone), (2) aspirin combined sion pressure, radius, length, and viscosity. In a frostbite patient,
with Aloe vera, (3) methimazole, and (4) a control group that each of these parameters (other than length) can be optimized
received no therapy.119 Methimazole treatment gave 34.3% tissue using appropriate medical interventions.
survival; Aloe vera, 28.2% survival; aspirin, 22.5% survival; and
methylprednisolone, 17.5% survival. In a human study of 154
patients with frostbite, there was significant improvement in
outcome and reduction in amputation rates of treated patients
compared with controls (p <0.001). It was concluded that morbid-
ity of progressive dermal ischemia in frostbite may be decreased
by therapeutic use of inhibitors of the arachidonic acid cascade.
Aloe vera is the topical agent most often used.
Antiprostaglandin Agents
Nonsteroidal antiinflammatory drugs (NSAIDs), such as ibupro-
fen, act as a necessary adjuvant to rewarming because they
inhibit inflammatory reactions and pain by decreasing prostaglan-
din synthesis.74 Oral ibuprofen decreases systemic levels of
thromboxane. Ibuprofen (400 mg) may be given by mouth and
should be continued at a dose of 12 mg/kg body weight/day
(maximum, 2400 mg/day). This should ideally be commenced in
the field. FIGURE 9-21  Hands of patient in Figures 9-18 to 9-20 after 5 days of
McCauley and co-workers121 treated 38 patients with frostbite intravenous iloprost. (Courtesy Christopher H.E. Imray, MD. From
in a protocol designed to decrease production of thromboxane Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities:
locally and prostaglandins systemically. All patients recovered Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)

211
 TABLE 9-4  Frostbite Management: Drugs, Doses, and Modes of Action and Rationale*

Intervention Dose Action

Aspirin 75-250 mg orally once daily Antiplatelet agent, improve rheology

Ibuprofen 400 mg bid or tid orally Antiprostaglandin effect
Aloe vera gel or cream With dressing changes every 6 hr Topical antiprostaglandin effect
Oxygen 2 L/min above 4000 m (13,123 ft) or when Improve tissue oxygenation
SpO2 is below 90%
Hyperbaric oxygen therapy 2-2.5 atm 1-2 hr daily Improve tissue oxygenation; improve rheology
Iloprost 2-10 mg/hr IV titrated against side effects Vasodilator; improve rheology
Nitroglycerin 100 mcg IA single dose Vasodilator
Papaverine 300 mg over 1 hr IA Vasodilator
Reserpine 0.1 to 0.25 mg once daily Vasodilator
Buflomedil 400 mg IV or 300 mg bid orally Vasodilator; improve rheology
Pentoxifylline 400 mg tid orally for 2-6 weeks Vasodilator; improve rheology
10% Dextran 40 20-mL bolus, 20 mL/hr IV Improve rheology
t-PA 1 mg/hr IA or IV Thrombolytic agent
LMW heparin Prophylactic dosage subcutaneously DVT prevention; anticoagulant
Therapeutic dosage subcutaneously Maintain patency of recently thrombolysed vessels
Tetanus prophylaxis

bid, Twice daily; DVT, deep vein thrombosis; IA, intraarterially; IV, intravenously; LMW, low-molecular-weight; SpO2, oxygen saturation as measured by pulse oximetry;
tid, three times daily; t-PA, tissue plasminogen activator.
*This table is intended to be used as a potential frostbite formulary reference, not as a protocol for treatment. See text for further discussion.

Iloprost.  Prostaglandin E1 (PGE1) is a vasoactive drug that 47 frostbite patients who were rapidly rewarmed, received
COLD AND HEAT

dilates arterioles and venules, reduces capillary permeability,
suppresses platelet aggregation, and activates fibrinolysis. Its
intraarterial use has been effective in treating ischemic peripheral
vascular disease.
The potentially beneficial effect in treating frostbite injuries
with intraarterial PGE1 was first assessed in an animal model.209
PGE1 reduced the magnitude of frostbite injury when the injured
limb was slowly rewarmed. The data suggested a possible
role for the use of PGE1 in frostbite patients who have not under-
PART 2
250 mg of aspirin and 400 mg of IV buflomedil, and who were
then randomized to receive 250 mg of aspirin per day, plus
buflomedil, iloprost, or recombinant tissue plasminogen activator
with iloprost. The iloprost group had the lowest overall amputa-
tion rate. Although the ideal dose is undetermined, these encour-
aging data offer hope to frostbite victims.
Iloprost is best given as an IV infusion through a peripheral
or central line in a monitored vascular or general surgical unit.
The diluted iloprost should be delivered by an accurate rate

gone rapid rewarming. Since the first description of its use in
patients,68 PGE1 has been used with some success in frostbite
injuries.79,197
Further experimental evidence implicates an inflammatory
process in the underlying mechanism of tissue injury. It has been
postulated that progressive ischemic necrosis is secondary to
excessive TXA2 production, which upsets the normal balance
between prostacyclin (prostaglandin I2) and TXA2.144
Cauchy and co-workers29 showed a promising decrease in the
digit amputation rate with the use of IV iloprost in severe frostbite
injuries. The clinicians compared results of a controlled trial of
FIGURE 9-22  Aloe vera cream being applied at the Everest Base
Camp Medical Clinic. Note the care being taken to apply nonconcen-
tric dressings to allow for edema formation. (Courtesy Suzanne Boyle,
MD.)
delivery system, such as a syringe driver. The infusion is started
at a rate of 2 mg/hr and incrementally increased up to 10 mg/
hr, titrated against the side effects of facial flushing, headache,
nausea, and flulike symptoms. The infusion is usually run for 5
to 8 days for 6 hours a day.79,81 A practical guide and stepwise
algorithm was recently produced to aid clinicians (Figure 9-23).69
Reserpine.  Reserpine is a powerful vasodilator that acts by
inhibiting uptake of norepinephrine into storage vesicles.150 For
frostbite, it is used intraarterially. The first description in the
treatment of frostbite was by Snider and colleagues.183 An animal
study suggested that a regional “medical sympathectomy” may
be beneficial in reducing tissue loss after frostbite, especially
when rapid rewarming cannot be performed.182
Pentoxifylline.  Pentoxifylline, a methylxanthine-derived
phosphodiesterase inhibitor, has been widely used to treat inter-
mittent claudication, arterial disease, and peripheral vascular
disease and has yielded some promising results in human frost-
bite trials.72 It increases blood flow to the affected extremity,
increases red cell deformability, decreases platelet hyperactivity,
helps normalize the prostacyclin/TXA2 ratio, and has been shown
to enhance tissue survival. Pentoxifylline is also presumed to
lower pathologically increased levels of fibrinogen and may
protect against vascular endothelial damage. The drug’s efficacy
has been demonstrated in animal studies and approaches the
effectiveness of Aloe vera. The combination of pentoxifylline and
Aloe vera appears to be synergistic.128 A similar synergy of aspirin
and pentoxifylline was demonstrated in an animal study.155 Hayes
and co-workers72 have proposed a treatment using pentoxifylline
in conjunction with the traditional therapy of rewarming, soaks,
pain management, and blister debridement. They recommend
pentoxifylline in the controlled-release form of one 400-mg tablet
three times daily with meals, continued for 2 to 6 weeks. A
controlled study of pentoxifylline in the management of frostbite
has yet to be performed.
Buflomedil.  Buflomedil hydrochloride is a vasoactive drug
that may have a number of effects, including inhibition of

212
 CHAPTER 9  Frostbite
Iloprost
administration

Syringe driver Infusion

(preferred method) pump

100 mcg of iloprost with 100 mcg of iloprost with

50 mL of normal saline or 500 mL normal saline or
5% dextrose 5% dextrose

Days 1–3 Days 1–3

• Start at 1 ml/hr and • Start at 10 mL/hr and
titrate upwards by titrate upward by
1 mL/hr every 10 mL/hr every
30 mins–1 hr 30 mins-hr
Side Effects
• Check BP and P Headache • Check BP and P
30 minutes after Hypotension 30 minutes after
starting infusion. Flushing starting infusion
• If intolerable side Palpitations • If intolerable side
effects reduce rate effects reduce rate
by 1 mL/hr until side by 1 mL/hr until side
effects tolerable effects tolerable

Days 4–6
No need to
titrate upwards
Start at
optimum rate

Contraindications
Unstable angina; <6 months after myocardial infarction;
cardiac failure; severe arrhythmias; within 3 months of
cerebrovascular events; conditions that increase risk
of bleeding

FIGURE 9-23  Algorithm for the administration of intravenous iloprost for in-hospital thrombolysis of severe
frostbite injury. (From Handford C, Buxton P, Russell K, et al. Frostbite: a practical approach to hospital
management. Extrem Physiol Med 3:7, 2014.)

α-receptors, inhibition of platelet aggregation, improved erythro-
cyte deformability, nonspecific and weak calcium antagonistic
effects, and oxygen-sparing activity.35,115,117 A case series of 20
patients reported that early administration of IV buflomedil
appeared to reduce the risk for subsequent amputation.54
However, buflomedil has not been shown to reduce microcircu-
latory damage from acute, experimentally induced freeze injury.45
Although buflomedil does not have U.S. Food and Drug Admin-
istration (FDA) approval, it has been used extensively in France
to treat frostbite, with considerable beneficial effect.31
Blood Viscosity: Low-Molecular-Weight Dextran
It has been observed that shortly after thawing, cold-injured
vessels become dilated and filled with clumps of erythrocytes.
These clumps can be easily dislodged by gentle manipulation
and do not represent true thrombosis. Although the mechanism
that leads to erythrocyte clumping is not completely understood,
it may reflect cold-induced increase in blood viscosity. This sug-
gests that use of low-molecular-weight (LMW) dextran may be
beneficial for early treatment of frostbite. Although no controlled
clinical trial of LMW dextran has been reported, experimental
evidence supports its use. Weatherly-White and colleagues204
demonstrated that LMW dextran, 1 g/kg/day, protected against
tissue loss in the rabbit ear model. This led to the suggestion
that the use of 1 L of IV 6% dextran on the day of injury, fol-
lowed by 500 mL on each of 5 successive days, might be of
benefit.164 The extent of tissue necrosis was also found to be
significantly less than in controls, when hemodilution with
dextran was combined with water bath rewarming.
With our present understanding of the etiology of frostbite
and introduction of newer interventions (e.g., iloprost, t-PA),
there appear to be fewer cases when LMW dextran may have
benefit.
ENDOVASCULAR INTERVENTIONS
Thrombolysis with Tissue Plasminogen Activator
In 1963, Fogarty and co-workers52 reported treating acute occlu-
sion of a peripheral vessel with an embolectomy catheter tech-
nique. More recently, catheter-directed thrombolysis has been
used to clear distal arteries and the microvasculature using a
thrombolytic agent such as tissue plasminogen activator (t-PA).
Found in vascular endothelial cells, t-PA has fibrinolytic action and
plays an important role in the dynamic balance between clot for-
mation and lysis. Plasminogen and t-PA bind to the fibrin surface
of the thrombus, resulting in production of plasmin and subse-
quent dissolution of the thrombus. t-PA has been used extensively
in coronary, cerebrovascular, and peripheral arterial disease.143

213
 A small retrospective study reported successful use of catheter-
directed intraarterial t-PA to reduce amputation rates in frostbite.22
Among the six patients who received t-PA within 24 hours of
injury, 6 of 59 (10%) affected fingers or toes were amputated,
compared with 97 of 234 (41%) of those who did not receive
t-PA. It was postulated that rapid clearance of the microvascula-
ture improves tissue salvage. The protocol in this study employed
a 2- to 4-mg bolus of t-PA after the catheter was secured and
total maximum dose of 1 mg/hr run continuously while simulta-
neous heparin was given at 500 units/hr through the access
sheath and continued for 72 to 96 hours. When there was evi-
dence of digital flow by angiography, t-PA was discontinued. The
clinicians noted that there was limited benefit for administration
of t-PA when treatment was started more than 24 hours after the A
initial injury.
Twomey and associates191 reported another series using
0.15-mg/kg IV t-PA bolus, followed by 0.15-mg/kg/hr infusion
over the next 6 hours, to a total dose of 100 mg.191 Heparin was
started after completion of the t-PA infusion, and the partial
thromboplastin time was adjusted to twice that of normal control.
Warfarin was initiated 3 to 5 days after t-PA and continued for
4 weeks in this study, which found decreased amputation rates
similar to those in the study by Bruen and colleagues.22 Both
these studies demonstrated excellent and similar amputation rates
when using t-PA. However, Johnson et al.84 retrospectively
reviewed their experience with t-PA and found less promising
results (compared to Twomey et al.191),with 43 out of 73 at-risk
digits (by 99mTc triple-phase bone scintiscan) requiring amputa-
tion, representing an amputation rate of 59%. B
COLD AND HEAT

Successful use of the combination of intraarterial (IA) t-PA

FIGURE 9-24  Early appearance of hands. (From Sheridan RL, Gold-
(previous series were IV) and vasodilators infused coaxially has stein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with
recently been described in various studies.29,44,170,178 After proper hypothermia and frostbite, N Engl J Med 361:2654, 2009.)
rewarming, the patient undergoes an arteriogram to assess perfu-
sion and document vascular flow cutoff if present. A recent case
report study describes successful use of a combination of endo-
luminal approaches in a patient with frostbite affecting both
hands. Upper-extremity and hand angiography performed within
16 hours of the frostbite injury demonstrated thrombotic occlu-
PART 2

sive disease and vasospasm. Bilateral brachial artery catheters

were placed and a papaverine infusion initiated, followed by IA
t-PA thrombolysis.170 In a second case report, a 16-year-old boy
was treated for hypothermia and concomitant frostbite of the
right foot and both hands.178 The patient was rewarmed and then
treated with selective angiography and an IA vasodilator (nitro-
glycerin), followed by IA t-PA thrombolysis, which resulted in
salvage of the limbs, but loss of the right great toe (Figures 9-24
to 9-27). A proposed screening and treatment tool was included A
in the case report (Box 9-3).
Currently, IV administration of t-PA for frostbite injury is more
common; however, the previous case reports warrant future
comparison between IA and IV delivery. The variable response
to thrombolytic therapy has been reported.39
Current Strategy for Imaging and Thrombolysis in Acute
Phase of Frostbite
The role of thrombolytic therapy in the treatment of frostbite is
evolving rapidly. The aim of t-PA treatment is to attempt to clear
the microvascular thrombosis. However, there are both risks and
benefits to t-PA therapy, and an appropriate balance needs to be
struck.
The Patient.  t-PA should be considered for patients with a B
“significant” deep frostbite injury presenting to an appropriately
equipped unit within 24 hours of the injury. A significant frostbite FIGURE 9-25  Initial angiographic images of the hands of the patient
injury will vary from individual to individual, dominant versus in Figure 9-24. After the infusion of vasodilators, diagnostic angio-
nondominant hand, occupation, hands versus feet, and existing graphic images of the hands show relatively preserved perfusion of the
comorbidities. The injury will usually extend proximal to the thumbs and ring fingers, but abrupt termination of the proper digital
proximal interphalangeal joints. Experienced clinicians familiar arteries of each of the remaining fingers at the midphalangeal level.
with the techniques need to evaluate each injury to determine (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009:
whether intervention with t-PA is justified. A 16-year-old boy with hypothermia and frostbite, N Engl J Med
361:2654, 2009.)
Tissue Plasminogen Activator in the Field.  If a frostbite
patient is being cared for in a remote area, transfer to a facility
with t-PA administration and monitoring capabilities should be
considered if the patient will arrive in the specialist unit within
the first 24 hours after the injury. Use of t-PA in the field setting

214

A causes elevation of intracellular cyclic adenosine monophosphate
B amputation rate was observed in the buflomedil group, at
FIGURE 9-26  Repeat images of the hands of the patient in Figures
9-24 and 9-25 after 24 hours of intraarterial catheter-directed throm-
bolytic therapy with tissue plasminogen activator show greatly
improved perfusion at all levels. (From Sheridan RL, Goldstein MA,
Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia
and frostbite, N Engl J Med 361:2654, 2009.)
FIGURE 9-27  Appearance of right hand of the patient in Figures 9-24
to 9-26 at approximately 30 days. (From Sheridan RL, Goldstein MA,
Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia
and frostbite, N Engl J Med 361:2654, 2009.)
is not recommended because it may not be possible to detect
and treat bleeding complications.
The Hospital Unit.  The hospital unit needs intensive care
monitoring capabilities, and clinicians should be familiar with
IA angiography and t-PA. A review of absolute and relative
contraindications of t-PA should be undertaken. The Massachu-
setts General Hospital group has proposed a screening and treat-
ment tool for thrombolytic management of frostbite, including a
protocol (see Box 9-3).178
Choice of Imaging in the Patient Presenting within 24
Hours of Injury.  Angiography or 99mTc scanning should be
used to evaluate the initial injury and monitor progress after t-PA
administration per local protocol and resources. Angiography is
an invasive procedure that allows both diagnostic and therapeutic
measures to be carried out, unlike 99mTc scanning, which is only
diagnostic. Logical practice dictates that angiography be used to
monitor IA t-PA and 99mTc scanning used to monitor IV admin-
istration of t-PA. No evidence demonstrates superiority of one
imaging modality over the other.
Choice of Imaging in the Patient Presenting after 24
Hours of Injury.  In patients with delayed presentation (>24
hours from time of injury), 99mTc or MRA can be used to predict
CHAPTER 9  Frostbite
at a very early stage the likely levels of tissue viability and ampu-
tation when t-PA would not be considered.30,31,33
Papaverine
Papaverine is a powerful topical and intravascular vasodilator
that is used clinically as a smooth muscle relaxant in microvas-
cular surgery and that has been used to treat cerebral vaso-
spasm.89 The exact mechanism of action remains to be determined.
It appears that inhibition of the enzyme phosphodiesterase
levels. Papaverine might improve outcomes in early frostbite.
When used in conjunction with IA t-PA in older patients, papav-
erine appears to cause a less pronounced decrease in systemic
blood pressure than IA nitroglycerin in older adults.43
Iloprost versus Tissue Plasminogen Activator
Groechenig68 first reported his experiences with iloprost in 1994.
Despite the promising results of no amputations after iloprost
infusion, focus shifted away from iloprost toward t-PA. Cauchy
et al.29 published a randomized controlled trial to compare ilo-
prost and t-PA; 47 patients were included (407 at-risk digits),
each randomized into three arms: buflomedil, iloprost, or iloprost
and IV t-PA. All other treatments were the same. The highest
39.9%. No amputations were observed in the iloprost group,
whereas those treated with iloprost/IV t-PA had an amputation
rate of 3.1%.
Iloprost has some advantages compared with t-PA. Radiologic
intervention is not needed during its administration, which can
be carried out on a vascular or general surgery ward. In contrast,
with t-PA, it is advisable to be in an intensive care unit. Iloprost
is also safe to use in patients with is a history of trauma, as well
as for a delayed presentation, because there is some evidence
for its effectiveness 24 hours after injury. We have used it as late
as 5 days after injury; however, the longer the delay, the less
effective iloprost is likely to be.
Experts may prefer iloprost to t-PA because of its comparative
safety, ease of administration, and efficacy. However, iloprost is
not approved for use in frostbite in the United States. Either
treatment should be commenced as rapidly as possible. Figures
9-28 and 9-29 provide algorithms for the administration of recom-
binant t-PA (rt-PA)and iloprost and rt-PA and heparin, respec-
tively, for severe frostbite (see also Figure 9-23).69
BOX 9-3  Proposed Screening and Treatment Tool for
Use of Thrombolysis in Frostbite Patients
Treatment Screen (Four “Yes” Answers Required to Proceed
to Angiography)
Are the patient’s gas exchange and hemodynamics stable?
Is flow absent after rewarming (no capillary refill or Doppler
signals)?
Was the cold exposure time less than 24 hr?
Is the warm ischemia time less than 24 hr?
Treatment Protocol
Perform angiography with intraarterial vasodilators.
If there is still no flow after angiography with vasodilators, infuse
tissue plasminogen activator (t-PA) with systemic heparinization,
with priority to the hands—other sites receive a systemic dose.
Repeat angiography every 24 hr.
Indications for Stopping the Infusion of t-PA
When restored flow has been confirmed by angiography or clinical
examination
If a major bleeding complication occurs
After 72 hr of treatment
Postlysis Anticoagulation
One month of subcutaneous low-molecular-weight heparin at a
prophylactic dose
From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A
16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.
215
 Hospital
management

Time from initial

Grade 1
injury

< 24 hrs > or < 24 hrs

• Conservative
management
• No further Grade 3/4 Grade 3/4 Grade 3/4
investigations
• Discharge
• Follow up as Angiography Technetium99
outpatient bone scan

Thrombolysis with tPA as

Iloprost infusion
per hospital protocol
See Fig. 9-23
See Fig. 9-23

If expertise not available

COLD AND HEAT

or no higher level care for

monitoring thrombolysis,
transfer to tertiary hospital
or use iloprost

The evidence for management of Grade 2 frostbite is unclear. Admission is

likely to be necessary; however the decision to use further intervention should be
made on a case by case basis. Consider telemedicine consult.
PART 2

FIGURE 9-28  Algorithm for the use of recombinant tissue plasminogen activator (rt-PA, rTPA) and iloprost
in the management of frostbite injuries. (From Handford C, Buxton P, Russell K, et al: Frostbite: A practical
approach to hospital management. Extrem Physiol Med 3:7, 2014.)

ADJUNCTIVE TREATMENTS
Sympathectomy
Cutaneous vessels are controlled by sympathetic adrenergic vaso-
constrictor fibers, and vascular smooth muscles have both
α-adrenergic and β-adrenergic receptors. Because vasodilation of
extremities is passive, maximal reflex vasodilation occurs after
sympathectomy.
The use of sympathectomy (open or minimally invasive
surgery) has yielded mixed results. Surgical sympathectomy per-
formed within the first few hours of injury increases edema
formation and leads to increased tissue destruction. However, if
performed 24 to 48 hours after thawing, sympathectomy is
believed to hasten resolution of edema and decrease tissue loss.
Surgical sympathectomy may have a role in preventing certain
long-term sequelae of frostbite, such as pain (often caused by
vasospasm), paresthesias, and hyperhidrosis.188
In a study of 66 patients with frostbite, 15 patients with acute,
bilaterally equal, severe injuries were treated with immediate IA
reserpine in one limb and ipsilateral surgical sympathectomy.
Efficacy of therapy was assessed by comparison of the sympa-
thectomized limb with the contralateral untreated limb. There
was no conservation of tissue, resolution of edema, pain reduc-
tion, or improved function in sympathectomized limbs compared
with those treated with IA reserpine. One patient demarcated
more rapidly, and another patient appeared to be protected from
recurrent injury. Sympathectomy was not effective therapy for
acute frostbite, even when achieved early with IA reserpine. Late
protection against subsequent cold injury appears to be the only
benefit of surgical sympathectomy for frostbite.19
Because surgical sympathectomy is irreversible, great caution
should be exercised when considering its use, particularly with
the advent of alternative IV vasodilators. Many would argue there
is now no role for its use in the early management of frostbite.
However, some interest in a potential role for more selective
chemical sympathectomy remains.34,145
Hyperbaric Oxygen Therapy
Evaluating the effectiveness of use of hyperbaric oxygen therapy
(HBOT) in the management of frostbite is difficult. Although
several animal studies have demonstrated no benefit,138 two
recent human studies have yielded excellent results.50,199 Multiple
mechanisms of action are proposed, but the major changes are
postulated to occur in the microcirculation. HBOT reportedly
increases erythrocyte flexibility, decreases edema formation in
postischemic tissues, and is bacteriostatic. Such actions may
counteract vascular congestion, platelet aggregation, and infiltra-
tion of leukocytes seen in the microcirculation of frostbite
patients. Finderle and Cankar50 report successful HBOT of a
patient at 2.5 atm for 90 minutes daily for 28 sessions in a multi­
place chamber, without significant tissue loss; this treatment
started 12 days after injury. HBOT may also act as an antioxidant.
A series of case reports suggests significant beneficial effects from
HBOT.11,53,140,199,201
Cauchy and colleagues32 have recently suggested a novel use
for hyperbaric oxygenation. Most high-altitude expeditions have

216
 CHAPTER 9  Frostbite
Intraarterial thrombolysis with rTPA AND concurrent heparin infusion
via a single puncture dual-port sheath

rTPA – Alteplase Heparin

(Via end port of catheter) (Via side port of introduced sheath)

Step 1 • Use 1 mL of 5000 units/mL concentration

• Use 50 mg vials of rTPA into 50 mL syringe and top up to 50 mL
• Comes as 2 vials – 1 with powder, 1 with with normal saline
the solvent
• Mix the 2 together with spiked connector
provided. See diagram in leaflet
• Run continuously at 5 mL/hr =
• 1 mg/ml (50 mg in 50 mL)
500 units/hr
• Not necessary to monitor APTTR on this
dose
Step 2
• Take 4x 60 mL syringes with Luer lock ends
• Put 6 mL of 1 mg/mL solution into each
• Once rTPA stopped introducer sheath is
syringe (discard the rest)
left in situ with heparin infusion still
• Fill the remainder of syringes of 60 mL with
running through it – leave for 4 hours
normal saline (i.e., add 54 mL to each)

Final concentration of 0.1 mg/mL for the

infusion • Stop heparin and leave sheath in situ for
2 hr

• Label each syringe with patient details,

drug details, date/time of creation • Remove sheath and apply firm direct
• Keep solution refrigerated; can be kept pressure to puncture site with gauze
for maximum of 24 hr for 20 min
• If bleeding occurs after pressure, then
apply further pressure for 20 min
• If further bleeding, contact
• 30 mL bolus over 15 min (3 mg) followed vascular surgeon consultant and continue
by constant infusion of 10 mL/hr (1 mg) with application of pressure to puncture site
• Check radiologist’s notes prior to
commencing this for any adjustments
• When rTPA is stopped (usually at check
angiogram) the catheter is removed,
leaving the sheath in situ (see Heparin arm
[at right] for further instructions)

Monitoring during rTPA infusion

• Pulse/BP every 30 min
• No intramuscular injections during rTPA
• Vascular consultant/radiologist to decide duration of rTPA infusion
• If concerns regarding complications, contact on-call team immediately
• Do not discontinue rTPA infusion for more than 10 min (thrombus can form very quickly on catheters)

FIGURE 9-29  Algorithm for the intraarterial administration of rt-PA (rTPA) and heparin for in-hospital
thrombolysis of severe frostbite injury. (From Handford C, Buxton P, Russell K, et al: Frostbite: A practical
approach to hospital management. Extrem Physiol Med 3:7, 2014.)

access to a portable hyperbaric chamber to replicate low-altitude
conditions in acute mountain sickness when true descent is not
possible. The authors note that altitude itself exaggerates cold-
induced vasospasm and hypothesize that placing a frostbite
patient in a field hyperbaric chamber may dampen this response
and improve tissue perfusion. Although there is no evidence for
HBOT at altitude for frostbite, it warrants further investigation
because of its simplicity and likely availability during high-
altitude expeditions.
The role of HBOT in all stages of frostbite therapy warrants
further investigation because it is a relatively safe and inexpen-
sive treatment.90,202
Epidural Spinal Cord Stimulation
An anecdotal case series that described epidural spinal cord
stimulation versus conventional treatment reported good thera-
peutic effects in four young patients with frostbite of the lower
limbs. The authors state the mechanism of action is unknown,

217
 A conservative approach remains reasonable. In one of the
largest number of frostbite patients (847) treated simultaneously
(2-week period), during the Indo-Pakistan conflict in 1971, a
combination of LMW dextran, an antiinflammatory agent (oxy-
phenbutazone), and a vasodilator (isoxsuprine) was used for the
third-degree and fourth-degree injuries, improving limb salvage
compared with historical controls.12 A conservative approach
remains reasonable.

FIGURE 9-30  Axial fasciotomies on the dorsum of the left hand. (Cour-
tesy Christopher H.E. Imray, MD.)
but the treatment is reported to have resulted in rapid recovery,
reduced pain, and more peripheral level of amputation.7
SURGICAL TREATMENT
COLD AND HEAT
AMPUTATION
Surgery should usually be delayed unless there is evidence of
overwhelming sepsis.5 Because there is rarely a reason for rushing
to operate, a suitably experienced multidisciplinary surgical team
familiar with performing a range of amputations should under-
take the procedure(s). Careful preoperative planning involving
the relevant medical, surgical, physiotherapy, and occupational
therapy teams should take place.79,80 The level and type of tissue
excised during the amputation will be determined by the specific
injury or injuries.
Following amputation, primary skin cover is usually preferred.
The temptation to preserve bone length by accepting closure by
secondary intention or skin grafting needs to be balanced against
the problems associated with a dysfunctional, neuropathic, and
weight-bearing stump. Split grafts inserted directly onto bone
tend to ulcerate as a result of shear forces on insensate grafted
skin as soon as the patient mobilizes and becomes weight
bearing, so a delayed revision then becomes necessary. Inap-
propriate attempts at preserving long bone length restrict use of

The conventional teaching is that early surgical intervention has
no role in the acute care of frostbite. However, early surgical
intervention in the form of fasciotomy is required for compart-
ment syndrome in the immediate post-thaw scenario or for
ischemia from a constricting eschar or subeschar infection.62
Decompressing escharotomy incisions are rarely necessary to
increase distal circulation. If such escharotomies are necessary to
decompress digits and facilitate joint motion, incisions along the
transaxial line may be the most appropriate.121 However, many
PART 2
modern “intelligent” prosthetic limbs; preoperative consultation
with the rehabilitation/prosthetic team is strongly advised.
The patellar tendon–bearing orthosis technique was originally
designed to support body weight for treatment of the below-knee
segment that is structurally inadequate or causes severe pain.168,189
The technique allows unloading of the leg at the below-knee
level while retaining full knee movement. It is beneficial in

plastic and vascular surgeons would consider using transaxial

with axial incisions on the trunk and axial fasciotomy incisions
on the limbs (Figure 9-30). It is important that incisions avoid
injury to underlying structures.
Occasionally, early amputation is indicated if liquefaction,
moist gangrene, or overwhelming infection and sepsis develop.5
There is rarely any urgency to surgically intervene, so amputation
should be undertaken by a surgeon with appropriate experience,
usually 4 to 8 weeks after the injury. In the vast majority of
patients, it is a failure to delay surgery when it is the major source
of avoidable morbidity. The functional end result of any surgery
needs to be considered. Ideally, when major limb loss is foreseen,
early involvement of a multidisciplinary rehabilitation team will
result in better long-term function.80
Surgical intervention is normally reserved for late treatment
of frostbite. This is most often necessary if frostbite is severe or A
treatment has been delayed. Aggressive therapeutic measures can
often prevent or reduce progressive injury and gangrene. If gan-
grene ensues, amputation or debridement with resurfacing may
be necessary (Figure 9-31).
Surgery should be accomplished only after the area is well
demarcated, which generally requires 4 to 8 weeks. Historically,
aggressive early debridement and attempted salvage have been
thought to jeopardize recovering tissue and add to tissue loss.
Gottlieb and associates63 and Greenwald and colleagues67 have
taken a much more aggressive approach to coverage of severe
frostbite injury. Using 99mTc phosphate bone scans, they identify
nonperfused tissue by 10 days after injury and surgically remove
necrotic tissue. The remaining nonvascularized and nonviable,
yet non-necrotic and noninfected, tissue is salvaged by early
coverage with well-vascularized tissue. Theoretically, if nonvas-
cularized tissue has not undergone autolysis and is not infected,
it should behave like a composite graft. Preliminary reports are
promising, because with better imaging, more accurate prediction B
of viable tissue is possible. Anecdotal reports suggest that there
may be increased risk for infection when complex reconstruc- FIGURE 9-31  Bilateral below-knee amputation for frostbite in a home-
tions are undertaken at an early stage.81 less patient. (Courtesy Christopher H.E. Imray, MD.)

218
treatment of plantar neuropathic ulcers of the feet, allowing the

CHAPTER 9  Frostbite
patient to mobilize while minimizing further damage from vertical
and horizontal shear forces. Using this approach, with early
bedside interventions as part of an integrated approach (includ-
ing aggressive vascular/endovascular surgery), the major lower-
limb amputation rate and length of stay have both been
significantly reduced.91

TELEMEDICINE
Use of the Internet to access expert advice has been driven by
patients and clinicians with more limited experience in treatment
of frostbite, permitting a virtual opinion from anywhere in the
world.82 The United Kingdom–based service can be accessed
through the Diploma in Mountain Medicine or the British Moun-
taineering Council website (http://www.thebmc.co.uk/Category A
.aspx?category=19). The service is run by diploma faculty mem-
bers and serves climbers and physicians worldwide, often to
obtain a second opinion or to seek specialized advice. It is also
possible to follow patients in a “virtual clinic,” reviewing digital
images and discussing management options by telephone or
e-mail (see Figures 9-18 to 9-21).79,169 Digital images have been
used to assess wound healing in conjunction with HBOT.53,

LONG-TERM SEQUELAE OF FROSTBITE

Until 1957, minimal information was recorded about the long-
term sequelae of frostbite injuries. Blair and colleagues16 studied
100 veterans of the Korean conflict 4 years after their injuries. In
order of decreasing frequency, the patients reported excessive
sweating, pain, coldness, numbness, abnormal skin color, and
joint stiffness. The investigators noted frequent asymptomatic
abnormalities of the nails, including ridges and inward curving
of the edges. In general, the degree of long-term disability was
related to severity of the original injury. Symptoms were worse
in cold than in warm weather. This is attributed to blood vessels
that do not react as well to stress.180 Previously injured vessels
do not constrict when exposed to cold as effectively as do normal
vessels, and they do not dilate as effectively when vasoconstric-
tion is blocked.
Hyperhidrosis is probably both a cause and a result of frost-
bite. Hyperhidrosis suggests presence of an abnormal sympa-
thetic nervous response induced by cold injury and is abolished
by sympathetic denervation. Sensitivity to cold and predisposition
to recurrent cold injury should suggest hyperhidrosis. Blanching
and pain on subsequent cold exposure may be a nuisance or
may be dramatic enough to suggest a diagnosis of Raynaud’s
phenomenon (see Figure 9-12). Almost without exception, after
sympathetic interruption, a painful, shiny, cyanotic, and sweaty
limb becomes warm, dry, and useful.176,177 Schoning175 examined
changes in the sweat glands of Hanford miniature swine after
experimental frostbite injury to determine the etiology of hyper-
hidrosis. She noted that severe sweat gland changes were of two
types: degeneration with necrosis and squamous metaplasia.
Clearly, if hypohidrosis was a sequela of frostbite injury, mor-
phologically normal and active sweat glands would be an
expected finding. One can conclude that hyperhidrosis lacks
histologic documentation.
A beneficial effect of open cervicothoracic sympathectomy for
frostbite sequelae was described in 48 patients.93 The minimally
invasive endoscopic transthoracic sympathectomy approach
reduces surgical trauma, allows more rapid recovery (Figure
9-32), and may have a limited role in late, persisting palmar
hyperhidrosis. Iontophoresis may be of benefit in plantar
hyperhidrosis.
The late abnormalities of change in skin color, including
depigmentation of dark skin and an appearance resembling
erythrocyanosis in light skin, are most likely the result of isch-
emia.16 Similarly, the nail abnormality is comparable to that seen
with ischemia. Usually, neither of these sequelae requires
treatment.
Late symptoms of joint stiffness and pain on motion are rela-
tively common and are undoubtedly related to the underlying
scars and mechanical problems occasioned by the variety of
amputations. “Punched-out” defects in subchondral bone of
B
FIGURE 9-32  A, One of the two 3-mm thoracoscopic port insertions
into the axilla for a right endoscopic transthoracic sympathectomy
(ETS) performed under general anesthesia. B, View of right sympa-
thetic chain during ETS. (Courtesy Christopher H.E. Imray, MD.)
involved limbs have been noted. These localized areas of bone
resorption generally appear within 5 to 10 months after injury
and may heal spontaneously. Vascular occlusion is the probable
cause of these lesions. Such bone involvement close to joint
surfaces may help explain joint symptoms.
The effects of frostbite on premature closure of epiphyses in
the growing hand have been emphasized.205 Extent of premature
closure has been correlated with severity of frostbite and noted
in partial-thickness injuries. In the digits, premature closure is
more frequently from a distal to proximal direction (distal inter-
phalangeal > proximal interphalangeal > metacarpophalangeal).
The thumb is less often involved. In only 2% of cases does partial
epiphyseal closure cause angular deformity.
Cold-induced neuropathy may play an important role in the
long-term sequelae of cold sensitivity after local cold injury.
Alteration in somatosensory function was found to be more
pronounced in lower-limb injuries.8 Changes in nerve conduction
velocity measurements may provide objective findings in cold-
injured patients and in those with few or no conspicuous clinical
signs. Tissue that has recovered from frostbite is more susceptible
to further injury. This needs to be recognized when advising
individuals about a return to environments where they may be
at risk. Preventive measures remain the mainstay of primary and
secondary treatment.79
Malignant transformation of old frostbite scars is a rare but
well-recognized condition.190 The lesions are sometimes described
as “Marjolin’s ulcer,”194 but more often as squamous cell carcino-
mas.48 One of the largest series of patients found that the tumors
tended to be low grade and unlikely to metastasize; the physi-
cians advocated surgical excision.166
PREDICTION OF INDIVIDUALS AT RISK
Recent experimental techniques have been studied to predict
which individuals are susceptible to frostbite injury. Predicting

219
 those at risk would be helpful to assess risk for people planning
to work or travel to high altitude or into extreme cold, as well
as those who may be particularly valuable to military recruiting
and planning. It would also be especially helpful when trying to
advise persons who have sustained previous cold injury.
The RIF finger skin temperature response, determined in a
simple laboratory test, may be related to the risk for cold injuries
during operations in the field.36 The reproducibility of the time
course of CIVD suggests this methodology may be of value for
further studies examining the mechanism of the response.139
Kamikomaki88 proposed that a case of frostbite in a climber with
ACE DD allele was caused by genetic propensity for vasoconstric-
tion. Perhaps we will see the evolution of testing for genetic
predisposition to frostbite as a screening tool.
Thermography is an easy, noninvasive method for monitoring
thermal changes after experimental frostbite, but its clinical value
is as yet unknown.45,86,173 Laser Doppler techniques have been
used to assess efficacy of HBOT of frostbite. The number of
visible nutritive capillaries in frostbitten areas was shown to
increase.50
PREVENTION
In 1950, Herzog and Lachenal made a successful lightweight bid
without oxygen for the summit of Annapurna, the first 8000-m
(26,247-foot) peak to be climbed. Herzog77 lost his gloves near
the summit, and the summit team spent a night in a crevasse.
Both climbers suffered severe frostbite to their hands and feet.
In a heroic retreat, Dr. Jacques Oudot first gave intraarterial
COLD AND HEAT
vasodilators and then performed field amputations without
anesthetic.
Eleven of the 210 deaths on Mt Everest between 1921 and
2006 were attributable to hypothermia,51 and a significant pro­
portion of climbers attempting to climb to extreme altitude
develop frostbite,56 suggesting that climbing above 8000 m
(26,247 feet) carries significant risk for permanent cold injury (see
Figure 9-7).
PART 2
STRATEGY TO PREVENT FROSTBITE
Prevention of frostbite is one key to safe and successful travel
and work in cold environments. Box 9-4 summarizes general
prevention strategies. Sound pre-participation education, selec-
tion of proper clothing, optimal nutrition, and hydration are all
advised. Washburn’s recommendations, originally published in
1962, remain relevant203:
• Dress to maintain general body warmth. In cold, windy
weather, the face, head, and neck must be protected, because
enormous amounts of body heat can be lost through these
parts.
• Eat plenty of appetizing food to produce maximal output of
body heat. Diet in cold weather at low altitude should tend
BOX 9-4  Strategies for Prevention of Frostbite
Good experience is the base of core survival skills.
• Wear protective clothing—layers, loose, heat insulating
• Avoid constriction of body parts with clothing
• Stay dry
• Wear wind protection
Hands:
• Wear mittens instead of gloves
• Use chemical hand warmers
Feet:
• Avoid tight-fitting boots
• Wear suitably warm boots such as triple-layer extreme-
altitude boots
• Use electric-heated insoles
• Ensure adequate nutrition
• Maintain hydration
• Take aspirin (if not contraindicated)
• Use supplemental oxygen at extreme altitude
220
toward fats, with carbohydrates of intermediate importance
and proteins least important. As altitude increases above
3048 m (10,000 feet), carbohydrates become most important
and proteins remain least important.
• Do not climb under extreme weather conditions, particularly
at high altitudes on exposed terrain, or start too early in cold
weather. The configuration of a mountain can help a climber
find maximal shelter and solar warmth.
• Avoid tight, snug-fitting clothing, particularly on the hands
and feet. Socks and boots should fit closely, with no points
of tightness or pressure. When donning socks and boots, a
person should carefully eliminate all wrinkles in socks. Old,
matted insoles should be avoided.
• Avoid perspiration under conditions of extreme cold; wear
adequately ventilated clothing. If perspiring, remove some
clothing or slow down.
• Keep the feet and hands dry. Even with vapor-barrier boots,
socks must not become wet. All types of boots must be worn
with great care during periods of inactivity, especially after
exercise has resulted in damp socks or insoles. Wet socks in
any type of boot soften the feet and make the skin more
tender, greatly lowering resistance to cold and simultaneously
increasing the danger of other foot injuries, such as blistering.
Extra socks and insoles should always be carried. Light,
smooth, dry, and clean socks should be worn next to the skin,
followed by one or two heavier outer pairs.
• Wear mittens instead of gloves in extreme cold, although
gloves can be worn for short intervals when great manual
dexterity is required for specialized work such as photography
or surveying. In these situations, a mitten should be worn on
one hand and a glove temporarily on the other. If bare-finger
dexterity is required, silk or rayon gloves should be worn, or
metal parts that must be touched frequently should be covered
with adhesive tape. Occasionally, the thumbs should be
pulled into the fists and held in the palms of the mittens to
regain warmth of the entire hand.
• Be careful while loading cameras, taking pictures, or handling
stoves and fuel. The freezing point of gasoline (−57° C
[−70.6° F]) and its rapid rate of evaporation make it very dan-
gerous. Metal objects should never be touched with bare
hands in extreme cold, or in moderate cold if the hands are
moist.
• Mitten shells and gloves worn in extreme cold should be made
of soft, flexible, and dry-tanned deerskin, or moose, elk, or
caribou hide. Horsehide is less favorable because it dries stiffly
after wetting. Removable mitten inserts or glove linings should
be of soft wool.
• Mittens should be tied together on a string hung around the
neck or tied to the ends of parka sleeves. Oiled or greased
leather gloves, boots, or clothing should never be used in
cold-weather operations.
• Keep toenails and fingernails trimmed.
• Hands, face, and feet should not be washed too thor-
oughly or too frequently under rough weather conditions.
Tough, weather-beaten face and hands resist frostbite most
effectively.
• Wind and high altitude should be approached with respect.
They can produce dramatic results when combined with cold.
Exercise should not be too strenuous in extreme cold, particu-
larly at high altitude, where undue exertion results in panting
or very deep breathing. Cold inspired air will chill the whole
body and under extreme conditions may damage lung tissue
and cause internal hemorrhage.
• When a person becomes thoroughly chilled, it takes several
hours of warmth and rest to return to normal, regardless of
superficial feelings of comfort. A person recovering from an
emergency cold situation should not venture out into extreme
cold too soon.
• Avoid tobacco or alcohol at high altitudes and under condi-
tions of frostbite danger.
• A person who is frostbitten or otherwise injured in the field
must remain calm. Panic or fear results in perspiration, which
evaporates and causes further chilling.
• Tetanus immunity should be current.

FIGURE 9-33  Selection of gloves and mittens used on a frostbite-free
summit day on Mt Everest. (Courtesy Christopher H.E. Imray, MD.)
CHEMICAL OR OTHER WARMERS
The well-equipped sojourner at extreme altitude or in cold envi-
rons should have a wide selection of gloves and mittens, includ-
ing spares (Figure 9-33). In addition to protective clothing and
insulation, external heat sources are advisable. A recent paper
by Sands and co-workers172 assessed the efficacy of commercially
available, disposable, chemical hand and foot warmers. They
found variations between the devices, but a strong relationship
between the mass of the devices and duration of the heat pro-
duction. Despite concerns about whether the chemical hand
warmers function at the low levels of oxygen found at extreme
altitude, anecdotally these warmers function well (Figure 9-34).81
Electric foot warmers are probably more useful than chemical
foot warmers in extreme cold and at high altitude (Figure 9-35),
where removing boots to insert warmers may be not only imprac-
tical but unwise. New lithium batteries opened on summit day
are probably superior to rechargeable units. Chemical warmers
also occupy a significant volume, resulting in pressure points that
can either overheat and burn or lead to blistering.81
POTENTIAL FUTURE DEVELOPMENTS:
PREVENTIVE STRATEGIES
Over the past decade there has been substantial improvement in
available equipment; in part because of the increased number of
A B
FIGURE 9-35  Triple-layer, 8000-m mountaineering boots (A) rated to −55° C (−67° F) and electric boot
warmers (B) used on a frostbite-free summit day on Mt Everest. (Courtesy Christopher H.E. Imray, MD.)
CHAPTER 9  Frostbite
FIGURE 9-34  Chemical hand warmers for use in extreme cold used
on a frostbite-free summit day on Mt Everest. (Courtesy Christopher
H.E. Imray, MD.)
climbers attempting 8000-m (26,247-foot) peaks. Consequently,
there is considerable financial incentive for developing state-of-
the-art equipment. Current 8000-m boots are rated down to −50°
to −60° C (−58° to −76° F) (see Figure 9-35). As new technologies
are developed, such as “intelligent fabrics” and temperature-
responsive fibers, numerous outdoor applications will likely
occur. Newer insulating materials have already given rise to
significantly better boots, gloves, and mittens (see Figures 9-33
to 9-35). Climbing equipment has also improved. For example,
newer step-in crampons greatly reduce the time involved in
fitting the crampons and the likelihood of having to adjust them
while climbing, which substantially reduces the risk for cold
exposure.
POSSIBLE FUTURE TREATMENTS
TIMING OF INTRAARTERIAL THROMBOLYSIS
FOR FROSTBITE
Current opinion suggests that t-PA for acute frostbite may be
beneficial and thus should be used if it can be started within 24
hours of the initial injury. However, considerable evidence from
the treatment of both acute coronary syndrome26 and acute
stroke94 indicates a variable window of opportunity for successful
t-PA treatment. The timing of intervention for frostbite is yet to
be determined, but longer delays are likely to be associated with
221
less benefit44 and thus to increase the need for secondary inter-
ventions, such as fasciotomies for reperfusion injuries, or subse-
quent amputations.81
ULTRASOUND-ACCELERATED THROMBOLYSIS
In vitro work has shown that ultrasound accelerates transport of
recombinant t-PA into clots.55 Ultrasound is believed to reversibly
loosen fibrin strands and reduce their diameter, exposing more
individual strands, increasing thrombus permeability, and expos-
ing more plasminogen receptor sites for binding.20 More rapid
and complete thrombolysis has been reported with the use of
this technique than with standard catheter-directed thrombolysis.
Results of one study suggest that percutaneous ultrasound-
accelerated thrombolysis is more effective at clearing clots than
is catheter-directed thrombolysis in patients with acute massive
pulmonary embolism.108
ANTIPLATELET AGENTS
There have been significant advances in the understanding,
management, and outcomes of patients with acute coronary
syndrome with the introduction of IV antiplatelet agents, such
as glycoprotein IIb/IIIa inhibitors. Inhibiting platelet aggrega-
tion is a vital link in optimizing outcome.2 In a pilot study, out-
comes in unstable, symptomatic carotid endarterectomy patients
appeared to improve after using a glycoprotein IIb/IIIa inhibi-
tor.196 There likely will be a role in frostbite treatment for the
use of combination oral (aspirin and clopidogrel) and IV anti-
platelet agents to improve vessel patency after t-PA clearance of
thrombus.
TUMOR NECROSIS FACTOR-α
Evidence indicates that tumor necrosis factor (TNF)-α–induced
reactive oxygen species have a role in endothelial dysfunction
during reperfusion injury.58 Investigation into the effects of inhibi-
tion of phosphodiesterase type 4 and TNF-α on local and remote
injuries after ischemia and reperfusion injury suggests that these
processes may be modified.184 This particular approach might
offer improved outcome in early frostbite.
VACUUM-ASSISTED CLOSURE THERAPY
Vacuum-assisted closure therapy has been shown to be beneficial
in accelerating wound healing in partial diabetic foot amputa-
tions.6 This therapy can be used in community and specialty
hospitals, and in many tertiary care hospitals it is being admin-
istered through specialist tissue-viability nurses. One report has
shown a good outcome with frostbite.152
FROSTBITE MANAGEMENT REGISTRY AND
THE INTERNET
One of the persisting characteristics of frostbite research is the
lack of good evidence to support newer treatments. An interna-
tional frostbite management registry would allow pooling of data,
accelerating the learning process.
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 CHAPTER 10 
Nonfreezing Cold-Induced Injuries
CHRISTOPHER H.E. IMRAY, CHARLES HANDFORD, OWEN D. THOMAS,
AND JOHN W. CASTELLANI
Nonfreezing cold-induced injury (NFCI) is a clinical syndrome
that results from the damage caused to tissues exposed to cold
temperatures at or above freezing point (0° to 15° C [32° to 59° F).
NFCI does not involve tissue freezing, which distinguishes it both
clinically and pathologically from frostbite.45 The earliest descrip-
tions of this syndrome originated in the military. Baron Domi-
nique 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.115 Historically, infantry regiments have been decimated by
cold and wet conditions, and many medical advances in under-
standing the pathophysiology and clinical course of NFCI have
occurred after wars.1,44, However, the continuity of research tends
to lag during the periods between major military campaigns.123
Developments in the prevention of cold injury have flourished
as new clothing and footwear are designed, but little progress
has been made in the treatment of NFCI.
An increasing number of people are pursuing recreational
activities in harsh environments, and as a consequence, civilian
NFCIs are becoming more prevalent. However, because many
physicians are unfamiliar with these injuries, they may go undi-
agnosed during assessment of the cold-exposed patient.123 This
results in unnecessary hospital admissions and potentially harmful
and expensive therapy.49 Proper education and awareness of the
222
hazards innate to the cold environment should mean that NFCI
is preventable in most circumstances.
This chapter explores the history, epidemiology, pathophysi-
ology, and current prevention and treatment of NFCI and spe­
cifically discusses pernio (chilblains), cryoglobulinemia, cold
urticaria, and Raynaud’s phenomenon.
EPIDEMIOLOGY
Individuals with cold and wet extremities for extended periods
are at risk for nonfreezing cold injuries. During the 1800s, NFCI
was observed more frequently when the temperature hovered
around the freezing point—when the ground was muddy rather
than frozen.54,114 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.115
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.13,114 Ambient temperature and wind speed can both influence
cooling.39,140
In “shelter limb” (dependency without cold) and “paddy foot”
(wet but not cold), there is an injury that has no apparent dis-
tinguishing differential features from NFCI. This would suggest
that neither cold nor wet is a prerequisite required to develop
the injury. It appears more likely that NFCI is a reperfusion
injury that develops after a sustained period of peripheral
vasoconstriction.123
Epidemiologic studies relating to NFCI can be challenging
because the International Classification of Diseases (ICD-10)
does not offer a “code” for NFCI. However “Immersion hand and
foot” (T69.0), “Chilblains” (T69.1), “Other specified effects of
reduced temperature” (T69.8), and “Effect of reduced tempera-
ture unspecified” (T69.9) are available.142 Frostbite has a separate
and detailed ICD classification.
MILITARY
In combat settings, there is rarely the time, equipment, or oppor-
tunity 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.”114 In
November 1944, during World War II, American forces sustained
11,000 cases of trench foot.136
Nonfreezing cold injury has continued to affect armed forces.
A study of 3 Commando Brigade (UK) during the Falkland Islands
conflict in 1982 reported that 64% of the brigade appeared to
have NFCI, with the proportion being higher (76%) within infan-
try units.51 An evaluation of possible risk factors for NFCI during
the conflict found that 1 year after exposure, there were no cases
of cryoglobulinemia and no hematologic evidence to suggest
that any of those who had developed cold injury had abnormal
circulating proteins, plasma hyperviscosity, or indicators of
alcohol abuse.26 NFCI has been reported during operations in
Afghanistan.89
Cold injury is not unique to operational deployments. In the
1990s, both the U.S. Army and the Israeli Defense Forces recorded
that most NFCIs occurred during routine training exercises rather
than during combat operations.33,86,93
ETHNICITY
Historically, the first reports of increased susceptibility in certain
ethnic groups (i.e., African Americans) to cold-weather injury
(CWI) came from the American Civil War.109 Also, an increased
incidence of CWI was noted among African Americans in the
extremely cold winter conflict in the Ardennes in 1944 during
World War II.136
A major retrospective study of 2143 U.S. Army hospital admis-
sions for CWI between 1980 and 1999 found the injury rate for
men and women was similar, 13.9 and 13.3 per 100,000 soldiers,
respectively.33 Increased rank and experience were associated
with a decrease in CWI. There were 3.3 times more African
Americans than Caucasians hospitalized (95% confidence interval
[CI], 3.1-3.7), and infantry and gun crews appeared to be at
greater risk. Also, the number of soldiers admitted to the hospital
between 1980 and 1999 was greatly reduced, from greater than
30 cases per 100,000 soldier-years to almost zero.
Young male African Caribbean natives in the British Army
have a 30 times greater chance of developing peripheral cold
injury and are more severely affected than their Caucasian coun-
terparts following similar climatic exposure, using similar clothing
and equipment. Pacific Islanders are at a 2.6 times increased
risk, while being a Gurkha appeared protective.18 Peripheral
vascular responses to a local cold stress were studied in four
groups of Indians: South Indians, North Indians, Gurkhas, and
high-altitude natives (HANs) of 3500 m (11,483 feet). The heat
output and cold-induced vasodilation were highest in HANs, with
the lowest observed in South Indians.83
PREVALENCE
In most North Atlantic Treaty Organization (NATO) countries, the
prevalence of NFCI appears to be static or decreasing among
military personnel. In the British military, however, there appears
to be a marked increase in the incidence of reported CWI. Over
a 4-year period, the reporting rate increased from 9 to 30 per
CHAPTER 10  Nonfreezing Cold-Induced Injuries
1000 recruits, with the majority of cases (90%) reported during
field-based training. Independent factor analysis demonstrated
that African Caribbean recruits were 13.2 times (95% CI, 9.5-18.4;
p <0.01) more likely to report cold injury and 27.3 times (95%
CI, 16.3-45.9; p <0.01) more likely to be medically discharged
than were Caucasians.139
This increase in NFCI in the United Kingdom (UK) military
might be caused by greater exposure, lower threshold to diag-
nose the condition, increased awareness, or recruiting a different
and more sensitive population. Alternatively, the observed
increase may be incorrect and caused by a type I error (poor
specificity of the tests used to diagnose NFCI or excessive cre-
dulity) or type II error (poor sensitivity of the tests used to
diagnose NFCI). Also, other countries may be failing to diagnose
and report the condition.64
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 to the situation. Other civilian
populations at risk for NFCI include homeless people,143 older
adults,103 and alcoholic persons.123
Personal Factors
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 involve-
ment of the hands (26.4%) and feet (24.1%) were most common.
There was a significant correlation between lack of proper equip-
ment (odds ratio, 14.3) or guide (p <0.001) and the injury. Inap-
propriate clothing, lack or incorrect use of equipment, and lack
of knowledge of how to deal with cold and severe weather were
cited as the main reasons for the injury.58
Cold injury is uncommon in Antarctica. Despite this, NFCI
warrants a continued high profile because under most circum-
stances, it may be regarded as an entirely preventable occur-
rence.19 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. The contrary was
observed in the feet, where there was improvement in cold
acclimatization despite developing moderate trench foot.97
Civilian Case Reports
Laden and colleagues78 reported that cold injury occurred 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
(often in cold water) for longer periods, and “adventure tourism,”
it was suggested that this extremely painful condition would
likely increase in prevalence.
Elderly patients typically present to the hospital after collapse
and a period of immobilization on the floor. A case of bilateral
trench foot in an immobile elderly patient has been reported.138
PHYSIOLOGY
SKIN: A THERMOREGULATORY ORGAN
Thermoregulation as a major function of human skin is achieved
by large fluxes in cutaneous blood flow.80 The metabolic re­
quirements of skin are fixed and relatively modest. Large fluc­
tuations in cutaneous blood flow are primarily determined by
the individual’s thermoregulatory needs. Arteriovenous anasto-
moses (AVAs) abound in the extremities. AVAs are coiled, mus-
cular-walled vessels approximately 35 µm in diameter and
have minimal basal tone. They are under dual control: central
223
 hypothalamic via the sympathetic nervous system and direct local
control, dilating under warm conditions and constricting in reac-
tion to a cold stimulus. The two effects are additive. Cutaneous
vessels are controlled by sympathetic adrenergic vasoconstrictor
fibers, and vascular smooth muscles have both α- and β-
adrenergic receptors. When core temperature exceeds 37.5° C
(99.5° F), the hypothalamus reduces vasoconstrictor drive to
AVAs and vasodilation occurs. As a result, a low-resistance shunt
in the dermal venous plexus opens, which in turn increases local
heat loss. Under cold conditions, sympathetic tone increases,
resulting in local arteriovenous vasoconstriction and reduced
cutaneous blood flow.
Under basal conditions, a 70-kg (154-lb) person has total
cutaneous blood flow of 200 to 500 mL/min. With external
heating to maintain skin temperature at 41° C (105.8° F), this may
increase to 7000 to 8000 mL/min, while cooling the skin to 14° C
(57.2° F) may diminish it to 20 to 50 mL/min.
Cutaneous vascular tone is inversely related to ambient
temperature. Cold-induced vasoconstriction is attenuated by α2-
adrenergic blockers and by sympathetic inhibition. Reduction in
ambient temperature results in insertion of more α2-adrenergic
receptors from the myocyte Golgi apparatus into the plasma
membrane, raising the affinity for the sympathetic neurotransmit-
ter norepinephrine. At the same time, endothelial nitric oxide
synthase (eNOS) activity declines, resulting in vasoconstriction of
the AVAs. Core temperature has a strong influence over cutane-
ous sympathetic vasomotor activity.
The vascular endothelium regulates local vascular tone by
secreting vasoactive agents, including the vasoconstrictor endo-
COLD AND HEAT
thelin and the vasodilators nitric acid and prostacyclin. Endothe-
lin causes long-lasting vasoconstriction and is elevated in hypoxia,
preeclampsia, and hemorrhagic stroke.
ORTHOSTASIS
Orthostasis (standing upright) or lowering a limb below heart
level causes immediate reduction in local blood flow; cutaneous
perfusion is reduced by approximately two-thirds as a result of
PART 2
the poorly understood venoarteriolar response. It is thought 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 vaso-
constriction and minimal blood flow occur. If cooling continues
to 10° C (50° F), vasoconstriction is interrupted by periods of
vasodilation and an associated increase in blood and heat flow.
This cold-induced vasodilation (CIVD), or “hunting response,”
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. Eskimos, Lapps, and
Nordic fishermen have a strong CIVD response and short inter-
vals between dilations, which may contribute to maintenance of
hand function in the cold environment.55 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 to normothermia.28,29,98
Cheung and colleagues21 investigated if CIVD responses of one
finger can predict the responses of other fingers, as well as
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 phenomenon, the vessels of
the toes and fingers exhibit an exaggerated and sustained vaso-
constriction response, resulting in blanching numbness and par-
esthesias, and in severe cases can result in tissue loss.
Individuals with a weak CIVD response to experimental cold-
water immersion of the fingers in a laboratory setting have a
higher risk for local cold injuries when exposed to cold in real
life.30 A strong correlation exists between the mean temperature
of the fingers during cold-water immersion and toes during
224
cold-air exposure (r = 0.83; p <0.01), showing that a weak CIVD
response in the hand is related to a weak response in the foot.131
Felicijan and associates40 found evidence for significant enhance-
ment of the CIVD response after brief high-altitude acclimatiza-
tion; these changes were especially prominent in the feet of
Alpinists compared with controls.
Temperatures of the extremities can drop surprisingly quickly
in the field. Toe temperature of 10 individuals was 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 devia-
tion [SD], 10.2) at an ambient temperature of −21° C (−5.8° F).
One person experienced a toe temperature below 5° C (41° F) for
2.9 hours during a 27-hour period. Surprisingly, none of the
participants demonstrated clinical signs of cold injury, but this
does not mean that this exposure was without risk.127
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 CWI,
sustained during military service.7 Transcutaneous oxygen tension
was decreased, but oxygen reappearance time, oxygen recovery
index, postocclusive reactive hyperemia, and venoarterial reflex
were normal. No capillary nailfold abnormalities were found.
Local cold injuries appear to cause disturbances in the CIVD and
impair cold tolerance and may increase the risk for future cold
injuries. Evidence suggests disturbances of reflex mechanisms
mediated by the central nervous system. Neurophysiologic factors
seemed more important than ischemic mechanisms in the patho-
physiology of late sequelae with peripheral CWI.
PATHOPHYSIOLOGY
Continuous exposure to a cold, wet environment causes break-
down of skin, 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 nerve, fat, and muscle
cells.62,92,123 Pain, fear, constrictive footwear, and immobility inter-
act in maintaining vasoconstriction through a heightened sympa-
thetic nervous system response or by mechanically limiting blood
flow (Figure 10-1). The length or degree of exposure needed to
evoke these changes and thus NFCI is unclear. Nevertheless, the
level of risk appears to be inversely proportional to tissue tem-
perature and directly proportional to duration of insult.13,124
Lengthy exposure to a temperature of about 10° C (50° F) will
result in similar injury as a short exposure to a temperature of
1° C (33.8° F). Repeated exposure is likely to cause a more sig-
nificant injury than a single exposure of longer duration.72
Local nerve Swelling and
Cold-wet
cooling breakdown of
exposure
skin
Vasoconstriction Pain and fear
Constrictive
↓ Local blood flow footwear
Immobility
Local nerve Ischemia
damage
Endothelial
damage
Sensory Loss of Cold
impairment vasodilation sensitization
FIGURE 10-1  Schematic of factors and mechanisms that contribute to
nonfreezing cold injuries.
 VASCULAR INJURY

CHAPTER 10  Nonfreezing Cold-Induced Injuries

120 Vasoconstriction is mediated by presynaptic vesicle release of
norepinephrine and neuropeptide Y from sympathetic nerve
fibers that interact postsynaptically on smooth muscle at α2c–
Percent of NBF baseline
100
adrenergic receptors9,23 and Y1 receptors.118 Recent work dem-
onstrated that cold-induced vasoconstriction is mediated by rho
80 kinase.126 The prolonged decrease in blood flow caused by
Control vasoconstriction causes direct injury to capillary endothelium.
Experimental Studies indicate that the endothelial lining separates from under-
60
lying cells, leaving “gaps.”38 Leukocytes and platelets fill in
these gaps and accumulate, further decreasing capillary blood
40 flow and leading to ischemia and eventually tissue hypoxia
(Figure 10-6).
Microvascular thrombosis after reperfusion injury is believed
20 to play a pivotal role following cold injury, with cold-damaged
0 100 200 250 12h D1 D2 D3 D5 endothelial cells central to the process.91 Reperfusion results in
min min min formation of free radical species, leading to further endothelial
Time (min, hr, and day) damage and edema.71
Apparently, CIVD is a physiologic protective response attempt-
FIGURE 10-2  Laser Doppler mean nerve blood flow (NBF) in control ing to prevent vascular injury and tissue ischemia. Unfortunately,
and experimental animals at 10-minute intervals during nerve cooling this response is lost or impaired in certain situations, including
and rewarming (up to 250 minutes) and at follow-up examination (but not limited to) hypoxia,102 dehydration,28 sleep deprivation,50
immediately before sacrifice (at various times up to 5 days). Note that and hypothermia.28 There also appears to be a genetic compo-
the NBF falls steeply over 20 minutes and reaches its nadir (25% of nent, with African Caribbean persons possessing a blunted CIVD
baseline) 180 minutes after the onset of cooling. NBF remains signifi- response.63 In sickle cell patients, there is net vasoconstriction,
cantly reduced up to 5 days after cold injury. (Modified from Jia J, instead of the normal vasoconstriction response being overcome
Pollock M: The pathogenesis of non-freezing cold nerve injury: Obser- by activation of the alerting response–induced vasodilation.90
vations in the rat, Brain 120:631, 1997.)

NERVE INJURY
Nerve cooling has been suggested as contributing to the etiology
of NFCI. Large myelinated fibers (C fibers) are most susceptible
to prolonged cold exposure.67,75,76,110 In severe NFCI, characteristic
peripheral nerve damage and tissue necrosis occur.68 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
a decrease of oxygen to the nerve, resulting in the appearance
of a primary nervous system injury71,72 (Figures 10-2 to 10-5).
In NFCI, nerve injury is ultimately likely to be multifactorial,
consisting of both direct nerve fiber damage and a vascular
component.73
ANIMAL MODELS
Animal models have been developed to understand the underly-
ing pathophysiology of NFCI. Thomas and colleagues124 devel-
oped 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 as a
prolonged decrease in tail blood flow followed by increased
blood flow above baseline. This pattern is similar to that clinically
observed in humans during the prehyperemic phase followed by
the hyperemic phase.
Stephens and associates118 recently 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 endo-
thelial function and possibly a change in smooth muscle contrac-
tility. Irwin,67 using a rabbit hind limb model, demonstrated that

V
A

A B C D E
FIGURE 10-3  Sciatic nerve epineurial microvessels before, during, and following nerve cooling (1° to 5° C
[33.8° to 41° F]). A, Normothermia. Arteriole (A), venule (V), and metarterioles (M) have a normal appear-
ance. B, One hour after the commencement of nerve cooling, the diameters of both the arteriole and venule
are reduced by approximately 40%. Under a dissecting microscope, erythrocytes present a granular appear-
ance in both vessels (arrows). Note occlusive aggregations (open arrow) in metarteriole and the suggestion
of leukocyte clumping in the venule (arrowhead). C, Two hours after nerve cooling, segmental occlusive
aggregates are seen in the venule (arrows). The arterioles contain prominent rouleaux (open arrows).
D, Three hours after nerve cooling, there is stasis of flow in both vessels. An occlusive aggregate (arrow)
is now seen in the arteriole, and those in the venule have extended (open arrows). E, After 1 hour of nerve
rewarming (37.5° C [99.5° F]), the venule still exhibits multiple segmental occlusions (arrows). Erythrocyte
granulations (open arrows) in the arteriole indicate poor reperfusion. Bars represent 100 mm. (From Jia J,
Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)

225
 A B
COLD AND HEAT

C D
FIGURE 10-4  Electron micrographs of endoneurial vessels in cooled sciatic nerve. A, An empty capillary
with a degenerating pericyte 1 hour after nerve rewarming. Bar represents 2 µm. B, Aggregating platelets
(arrows) 24 hours after cooling. Bar represents 2 µm. C, Platelets, adherent to the endothelium of a venule,
show varying degrees of degranulation without pseudopod formation, 48 hours after nerve cooling. Two
red blood cells are trapped within this platelet thrombus. Bar represents 1 µm. D, A thrombus formed of
platelets, red blood cells, and fibrin 5 days after nerve cooling. The blood vessel wall is necrotic. Bar rep-
resents 2 µm. (From Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in
PART 2

the rat, Brain 120:631, 1997.)

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
to the skin, muscle, nerve, and bone.11,12,46 Muscles exhibit separa-
tion of the cells and damage of the muscle fibers, described as
acidophilic and hyalinized (Zenker’s hyaline degeneration). The
myoplasm within muscle loses its cross-striation, and the healing
muscle then appears to undergo fibrous tissue replacement.
One of the major pathologic processes in NFCI is progressive
microvascular thrombosis following reperfusion of the ischemic
limb, with cold-damaged endothelial cells playing a central role

A B
FIGURE 10-5  Electron micrographs of cooled sciatic nerve fibers. A, A rat sciatic nerve fiber, 12 hours after
nerve cooling, illustrating myelin unraveling and intramyelinic edema (arrow) . B, A rat sciatic nerve fiber 2
days after cooling, exhibiting a shrunken axon and marked periaxonal edema. Bars represent 1 µm. (From
Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631,
1997.)

226
 • Dehydration

CHAPTER 10  Nonfreezing Cold-Induced Injuries

Cold-wet exposure
• Altitude (hypoxia)
• Poor calorie intake
• Sleep deprivation and fatigue
NE NPY • Hypothermia
• Damp environments/wet clothing
• Increasing age
a2c Y1 • African Caribbean ethnicity
• Previous NFCI

CLINICAL PRESENTATION
DAG and IP3 Nonfreezing cold-induced injury should be considered a syn-
drome, and presentation is variable. NFCI is insidious in onset,
Blood flow Ca2+ influx often with few objective clinical signs at presentation, and one
must take into account the history and environment. After initial
exposure, there are three stages of progression: prehyperemic,
Intense and prolonged vasoconstriction hyperemic, and posthyperemic. These phases often overlap, and
the time course of each varies.
Decreased blood flow
• Nerves
• Muscle
PREHYPEREMIC PHASE
• Fat During the prehyperemic phase, the affected limb both during
and immediately after cold exposure appears blanched, yellowish
white, or mottled but seldom blistered130 (Figure 10-7). Whayne
and DeBakey136 state that the degree of edema during this
Endothelial injury
prehyperemic stage is less severe if the feet are intermittently
Hypoxia
to capillaries rewarmed during the course of exposure. Whereas muscle
Blood flow
cramps are common, pain is rare.54,115 The most important diag-
nostic criterion is loss of a sensory modality, most often complete
local anesthesia, which is distinct from premonitory feelings of
extreme cold in the affected periphery. This almost invariably
Opening of gaps Leukocyte adhesion to occurs in the foot, although hands can also be affected. With
between cells blood vessel walls with further exposure, the cold sensation leads to complete anesthesia
decrease in blood flow with loss of proprioception, resulting in numbness and gait dis-
FIGURE 10-6  Proposed hypothesis for the etiology of nonfreezing turbances. This sensation has been described as “walking on air”
cold-induced injury (NFCI). α2c, Norepinephrine (NE) α-adrenergic or “walking on cotton-wool.”130 Capillary refill is sluggish, and
receptor; Y1, neuropeptide Y (NPY) receptor; DAG, diacylglycerol; pedal arterial pulses are usually absent, except using Doppler
IP3, inositol triphosphate; Ca2+, calcium. examination.88 Intense vasoconstriction is the predominant fea-
ture of this stage.57

in the outcome.91 Reperfusion of previously ischemic tissues

causes free radical formation, leading to further endothelial
HYPEREMIC PHASE
damage and subsequent edema. With restoration of blood flow, Within several hours after rewarming, the extremities become
there is reintroduction of oxygen species within cells that further hot, erythematous, painful, and swollen (Figures 10-8 to 10-11),
damages cellular proteins, DNA, and the plasma membrane. Free with full bounding pulses.135 Impairment of the microcirculation
radical species may act indirectly in oxidation-reduction (redox) is evidenced by delayed capillary refill123 (Figure 10-12) and
signaling to turn on apoptosis. Leukocytes may build up in small petechial hemorrhages.56 Sensation returns first to proximal
capillaries, obstructing them and leading to more ischemia.72 regions and then extends distally, rapidly progressing to severe,
In an in vivo rabbit hind limb model subjected to 16 hours burning, or throbbing pain, and reaching maximal intensity in 24
of cold-water immersion (1° to 2° C [33.8° to 35.6° F]), there was to 36 hours.128,130 Affected areas have marked hyperalgesia to light
reduction in the number of myelinated nerve fibers of all sizes, touch. This pain is aggravated by heat and dependent positioning
most marked in large-diameter fibers, a feature consistent with and often worsens at night, when even the pressure of sheets
ischemic neuropathy and reperfusion injury.68 Unmyelinated
fibers showed only minor damage. The resulting evidence sug-
gests that both these mechanisms may contribute to the nerve
injury. There is further extensive supporting evidence to establish
that NFCI is associated with histologic and clinical evidence of
nerve damage.34,37,72,96
Das and co-workers31 demonstrated that quinacrine, an anti-
oxidant, decreased damage to cell membrane phospholipids on
their rewarming and reperfusion, although more recent studies
have shown no benefit from antioxidant use.121 Most importantly,
both these studies used models that assumed that cold-induced
nerve injury, rather than capillary or endothelial damage, is the
primary etiologic cause of NFCI.

RISK FACTORS
The risk factors associated with NFCI include the following (this
is not meant to be an exhaustive list)18,51,85,104,107,122,144:
• Inadequate clothing FIGURE 10-7  Prehyperemic phase of immersion foot. These feet are
• Immobility still mostly numb and very cold to the touch. (British Crown Copyright/
• Smoking MOD.)

227

FIGURE 10-8  Hyperemic phase of nonfreezing cold injury. This person
spent 18 hours in winter bailing out a boat that threatened to capsize
in Prince William Sound, Alaska. (Courtesy James O’Malley, MD.)
COLD AND HEAT
FIGURE 10-9  Hyperemic phase of immersion foot in mild nonfreezing
cold injury. Recruit of the British Royal Marines just returned from a
field exercise feeling well. While showering, his feet rapidly became
PART 2
swollen, red, and painful. (British Crown Copyright/MOD.)
may be unbearable.57 After 7 to 10 days, the nature of the pain
changes to “shooting or stabbing.”128 The sensory deficits usually
diminish, but paresthesias continue, and anesthesia may be
extensive on the toes and plantar surfaces.137 Vibratory sensation
is reduced or lost, whereas proprioception is usually retained.
Anhidrosis coincides with the extent of sensory loss.123
Vascular injury is evident in vessel reactivity. Skin tempera-
ture gradients are absent, with digits often as warm as or
warmer than the groin or axillae. When the affected limbs are
lowered, blood pools, turning the extremity a deep purple-red
FIGURE 10-10  Hyperemic phase of immersion foot. The characteristic
redness of the stage is absent due to the pigmented skin, but the feet
are swollen and painful. (British Crown Copyright/MOD.)
228
FIGURE 10-11  Hyperemic phase in moderately severe nonfreezing
cold injury. Swelling, redness, and persistent pain in the feet of an
infantry soldier from the Falklands War. (British Crown Copyright/
MOD.)
FIGURE 10-12  Hyperemic phase in mild nonfreezing cold injury. There
is delayed capillary refill in the dorsum of the foot. The examiner’s two
fingers resting on the skin for 10 seconds was sufficient to blanch the
capillaries. When the pressure was removed, the blanched patches
disappeared very slowly, reflecting impaired microcirculation. (British
Crown Copyright/MOD.)
color, whereas blanching occurs when the limb is raised. Tense
edema becomes marked during this stage. Blisters containing
serous or hemorrhagic fluid may form, indicating more severe
injury.123 The superficial epidermis becomes thick, indurated,
and desquamated. Eschars form (Figures 10-13 and 10-14) and
eventually slough, leaving a pink dermis (Figure 10-15). In more
severe cases, the skin may become gangrenous (Figure 10-16);
this is rare, and with appropriate care the gangrene is usually
minimal.3,135,136
Muscles may show weakness with impaired electrical
responses, slowing of plantar deep tendon reflexes, and intrinsic
muscle atrophy.128,130 In milder cases, this stage peaks at 24 hours;
in more severe cases, the hyperemic phase may take 6 to 10
weeks to resolve.123
FIGURE 10-13  Severe nonfreezing cold injury. This Argentinian soldier
had been unable to care for his feet for many weeks. (British Crown
Copyright/MOD.)

FIGURE 10-14  Severe nonfreezing cold injury in an Argentinian mine
worker who wore his boots for 47 straight days during the Falklands
War. (Courtesy M. P. Hamlet.)
FIGURE 10-15  Severe nonfreezing cold injury in a British sailor during
World War II. (Courtesy M. P. Hamlet.)
POSTHYPEREMIC PHASE
The posthyperemic phase lacks obvious physical signs. In mild
cases, this phase may be absent;130 in other patients, it may last
weeks, months, or years after the hyperemic phase has sub-
sided.88,128 The extremities transition from consistent warmth
to coolness, with affected areas having an abnormal cooling
FIGURE 10-16  The Argentinian mine worker seen in Figure 10-14,
several weeks later. (Courtesy M. P. Hamlet.)
CHAPTER 10  Nonfreezing Cold-Induced Injuries
FIGURE 10-17  Patient 24 months after nonfreezing cold injury. Ampu-
tation of third, fourth, and fifth toes on the left foot. (Courtesy
Christopher H.E. Imray, MD.)
response. Extremities become cold sensitive, remaining so for
hours after exposure despite normal warming processes.
After 6 to 10 weeks, patients often complain of spontaneous
hyperhidrosis, and sweat rashes are common in areas with heavy
perspiration.128 On a warm day, socks are quickly soaked;
extremities may sweat excessively, even when cold. Hyperhidro-
sis predisposes to chronic paronychial infections. Sweating may
be more pronounced at the margins of anhidrotic and analgesic
areas.130
During this posthyperemic phase, the paresthesias and
extreme pains consistent with the hyperemic phase have usually
resolved, replaced by dull aches and anesthesias that may persist
for months to years.136 Recurrent edema of the feet, return of
paresthesias, and further blistering are common, especially after
long walks. Intrinsic muscle and ligament atrophy tends to
resolve,130 but in severe cases, fibrous scarring may lead to rigidity
and permanent contracture of the toes.137 Decalcification of bones
as seen in osteoporosis is frequently observed, but this tends to
reverse.129 Immobility and pain in severe cases may lead to pro-
longed convalescence of 6 months or more.137
In the most severe cases, gangrene can develop, and ablative
surgery in the form of amputation of digits or occasionally major
lower-limb amputation becomes necessary. The neuropathic
tissue is susceptible to local trauma, ulceration, and eventually
local osteomyelitis and sinus development64 (Figures 10-17 to
10-19). Partial foot amputations result in significant alterations in
the functional biomechanics of the foot. Since this is often associ-
ated with alterations in the sensory nerve supply to the feet,
disabling problems can persist64 (Figure 10-20).
FIGURE 10-18  Same patient as in Figure 10-17, 24 months after NFCI,
with chronic discharging sinuses from osteomyelitis of first metatarsal.
(Courtesy Christopher H.E. Imray, MD.)
229

FIGURE 10-19  Magnetic resonance imaging scan of the patient in
Figures 10-17 and 10-18, 24 months after nonfreezing cold injury, with
chronic discharging sinuses from osteomyelitis of the first metatarsal
head. (Courtesy Christopher H.E. Imray, MD.)
TREATMENT
HYPOTHERMIA
The treatment required for the general effects of cold is different
from that needed for localized NFCI. Core temperature must be
COLD AND HEAT
peripheral circulation and the apparent noradrenergic sensitiza-
tion,45 it was thought that vasodilators or α-adrenergic blocking
drugs might be beneficial. To date, however, no evidence sup-
ports this approach.
Painful rewarming and persistent pain are features of NFCI,
so it is important to attempt to alleviate pain at an early stage.
Simple analgesics may be of benefit. In a pilot study, Thomas
and Oakley123 used quinine salts (200 to 300 mg, given at night),
which appeared more successful than regular analgesics, although
others since then have not supported their use. Since 1982, the
standard treatment in the UK armed forces, first proposed by
Riddell,106 has been amitriptyline hydrochloride, in doses of 50
or 100 mg at night. Incremental increases in dosage may be
required with both drugs if “breakthrough” pain occurs after
initial relief.43 In centers receiving major trauma or burn patients,
it is becoming increasingly standard practice to start a drug for
neuropathy treatment early in the patient’s care, to help minimize
chronic neuropathic pain.5,84 Although no specific trials have
studied this in NFCI, it is advisable to consider starting a neu-
ropathy agent as early as possible.
OCCUPATIONAL MEDICINE
Depending on the patient’s profession, occupational medicine
review may be required. This will be the case if patients work
in environments that put them at risk of repeated NFCI.

raised while the extremities are kept cool.135-137 Injured feet

should be elevated and exposed to steady, cool air from a fan.
Extremity cooling lowers the metabolic requirements to a point
where vascular oxygen supply can sustain tissue demand. Con-
tinuous cooling brings rapid improvement in pain, edema, and
vesiculation.135,137 Local cooling should be continued until pain is
relieved, circulation has recovered, and hyperemia subsides.137
The affected extremities should never be rubbed, which may
compound the injury.2
PART 2

REWARMING
Treatment is limited to symptomatic relief and reversing ischemia
while minimizing disease progression. Rewarming injured tissues
increases metabolic demand of damaged cutaneous cells to a
greater extent than the supply capability of the injured subcuta-
neous blood vessels.140 Tissue anoxia and endothelial cell injury,
coupled with reflex vasodilation, lead to fluid transudation,
increasing edema, skin necrosis, and worsening pain.135,137 Rapid
rewarming should be avoided.

SYMPATHECTOMY
Recovery during the posthyperemic phase may be hastened with
A
physiotherapy and exercise to rehabilitate atrophied intrinsic
muscles.136,137 Lumbar sympathectomy has been theorized to
reduce disabling contracture by decreasing vascular tone, increas-
ing circulation, and hastening collagen and fibrous tissue absorp-
tion. In severe cases of NFCI exhibiting atrophic rigid feet, small
case studies have shown symptomatic improvement after sym-
pathectomy,137 but other authors believe there is little therapeutic
advantage to the procedure.135

TISSUE-FREEZING COMPLICATIONS
Frostbite and NFCI injuries do not necessarily occur in isolation,
so when assessing an individual, both diagnoses need to be
considered as possibilities. After exposure to severe cold, careful
appraisal of the injury is required if optimal treatment is to be
given.
DRUGS
The diagnosis of an NFCI is often difficult or delayed. In view
of involvement of the α-adrenergic receptors in control of the
B
FIGURE 10-20  A guillotine transmetatarsal amputation of left foot was
undertaken 6 months after severe nonfreezing cold injury. The patient
was treated with delayed primary split-skin grafting. This photo was
taken 12 months after the original injury. The graft has taken but is
now ulcerated as a result of the shear forces generated by walking on
the insensate tissue. (Courtesy Christopher H.E. Imray, MD.)

230

36.0° C
36
34
32
30
28
26
24
20.9° C
FIGURE 10-21  Infrared thermography in the assessment of the con-
sequences of nonfreezing cold injury (NFCI). The upper sequence of
three images was taken from an uninjured, asymptomatic control; the
lower sequence from a patient who had sustained NFCI and was sub-
sequently complaining of sensitivity to the cold. In both control and
patient, the first (left) image was taken after resting in an ambient air
temperature of 30° C (86° F). The second (center) image was taken
immediately after the foot had been immersed in water at 15° C (59° F)
for 2 minutes. The final (right) image was taken 5 minutes after removal
from the water, again in 30° C (86° F) air. The upper series shows feet
that were warm at rest, which rewarmed briskly after mild cold stress,
recovering almost completely within 5 minutes after removal from the
water. The lower series shows a severe degree of cold sensitization;
the feet were much colder than the surrounding air at rest, and once
cooled, took a long time to rewarm, remaining much cooler than the
control foot at 5 minutes after immersion. The scale at far right indi-
cates the color-temperature relationship. (British Crown Copyright/
MOD. Reproduced with the permission of Her Britannic Majesty’s
Stationery Office. From Thomas J, Oakley H. Nonfreezing cold injury.
In Pandolf KB, Burr RE, editors: Textbook of military medicine: Medical
aspects of harsh environments. Vol 1. Washington, DC, 2002, Office
of the Surgeon General, Borden Institute, pp 467-490.)
ASSESSING INJURY SEVERITY
Following the initial injury, increased sensitivity to cold develops.
There are often surprisingly few objective clinical signs. A careful
history of appropriate cold-weather exposure, clear history of the
typical rewarming symptoms and signs, detailed examination,
and special investigations all build a picture consistent with NFCI.
Corroborative evidence from medical records is vital.
SPECIAL INVESTIGATIONS
Infrared (IR) thermography can be used to assess the individual’s
response to a standardized cold stress and may be helpful in
confirming the diagnosis, assessing injury severity, and monitor-
ing recovery (or otherwise) from NFCI (Figure 10-21). However,
FIGURE 10-22  British Army information “credit card.”
although used extensively by the UK military, IR thermography
CHAPTER 10  Nonfreezing Cold-Induced Injuries
is not widely used elsewhere or conclusively validated.65,130 There
appears to be significant variability in the response of some
individuals to the current IR thermography test. As a result, inter-
est is focusing on the use of gentle exercise before the cold
sensitivity test, as well as laser Doppler flowmetry to improve
the assessment used to classify NFCI.36 Careful experimental
design to validate any potential new tests against suitable controls
both before and after exposure will be required.
PREVENTION
The simplest way to prevent NFCI is to avoid prolonged exposure
to cold, wet environments. This can be difficult to implement
because of varying conditions and individual susceptibility. In
military conflicts, completing the assigned mission is most impor-
tant and may require performing in a cold, wet environment for
sustained periods in a cramped, immobile position. During
mountain rescues, individuals may be so focused on helping to
save others that they do not take adequate care of themselves.
Prevention can be achieved by encouraging people to remain
active and increase blood flow to the feet, rotating personnel out
of cold-wet environments on a regular basis, keeping feet dry by
early changing of wet socks, maintaining body core temperature
by limiting sweat accumulation into clothing and dressing in
layers, and educating personnel about the early signs and symp-
toms of NFCI. Changing socks two or three times throughout the
day is mandatory in cold, wet environments. Military sources
suggest that optimal care entails air drying feet for at least 8 hours
of every 24 hours.17,143 Vapor-barrier boots do not allow sweat
from the foot to evaporate, and in some situations, this increases
maceration.4 Boots should be taken off each day, wiped out, and
dried. Footwear should not constrict blood flow; sizing is impor-
tant, as is educating the user not to tie shoelaces too tightly. To
achieve an adequate level of self-care, education must impart a
sense of individual responsibility, while expedition leaders still
monitor and ensure that standards are maintained.
Prophylactic treatment with silicone preparations has proved
effective in clinical studies.48 The protective effect is thought
to result from prevention of hyperhydration of the stratum
corneum.17,35 However, stickiness, adherence of sand and grit to
the foot, and product bulkiness made it marginally acceptable to
infantrymen in combat situations.48 In small clinical trials, silicone
ointment applied only to the sole of the foot instead of to the
entire foot (thus reducing surface area exposed to dirt retention,
amount of material transported by the soldier, and dollar cost)
was sufficient to prevent NFCI.35
Because of the apparent increasing incidence of NFCI in
the British military, a number of additional preventive steps
have been taken, including improved education of personnel
about prevention measures, equipment, and early recognition
(Figure 10-22).
The severity of the injuries affecting the military appears to
be relatively mild compared with civilian NFCI injuries (see
Figures 10-17 to 10-19) and military historical controls (see
Figures 10-13 to 10-16). This raises the question as to whether
there is (1) a continuous spectrum of disease, (2) a bimodal
231
 distribution of the disease with milder and more severe forms of
NFCI, or whether (3) the commonly presenting form now seen
is the same disease process investigated in the past. Part of the
problem may lie in the UK military’s decision to use IR thermog-
raphy as one of the bases on which the diagnosis, severity, and
progression of NFCI are determined.
One approach to the high levels of NFCI noted would be to
consider screening potential recruits. This requires a test with
high sensitivity and specificity. However, individual variation in
the control of peripheral blood flow is so great that none of the
assessments currently available meets these requirements.15,28,30,123
Reducing the incidence of cold injury in military training
requires striking a delicate balance between training realism and
safety. While training in demanding environments runs real risks
of injuring personnel, the benefits to them in the development
of field-craft skills are vital if they are to avoid NFCI.123
MORE SEVERE INJURIES
Nonfreezing cold injury can vary in severity from mild to severe.
In severe cases, cold sensitization is so serious that individuals
are unable to work outside. Edema and hyperhidrosis often
occur, making the individual susceptible to fungal infections.
Chronic pain resembling causalgia or reflex sympathetic dystro-
phy may occur. The profound sensory loss may lead to minor
or major lower-limb amputation. Ongoing care within a specialist
foot clinic using custom-made shoes and insoles appears to
improve functional outcome. Multidisciplinary team approaches,
such as healing of the ulcerated neuropathic foot using patella
COLD AND HEAT
tendon–bearing orthoses, have been described.77 NFCI pain is
often so severe as to require tricyclic antidepressants, which
should be instituted at an early stage.66,123 Failure to do so
increases the risk of developing severe chronic pain resistant to
all subsequent treatment modalities. Early involvement of pain
specialists is important.
TRENCH FOOT (IMMERSION FOOT)
PART 2
Trench foot and immersion foot are clinically and pathologically
indistinguishable but have different etiologies. The term trench
foot originated during the trench warfare of World War I,136 when
soldiers wore wet boots and socks for prolonged periods.8
Immersion foot was first medically documented during World
War II among shipwreck survivors whose feet had been continu-
ously immersed in cold water.27 Both injuries occur when tissue
is exposed to cold and wet conditions at temperatures ranging
from 0° to 15° C (32° to 59° F). Colder temperatures decrease the
time required to induce NFCI.13,115 Severe nerve damage from
immersion foot has been seen after exposure periods of 14 to
22 hours.128,130 Immersion foot injury may extend proximally and
involve the knees, thighs, and buttocks, depending on the depth
of immersion.137
PERNIO (CHILBLAINS)
Pernio (perniones) or chilblains are localized, inflammatory,
bluish red lesions caused by an abnormal reaction to a cold,
damp environment. This mild form of cold injury is prevalent in
the temperate climates of northwestern Europe81 and is found
worldwide throughout temperate and northern zones.49,87,88,99
Pernio is less common in very cold climates, where well-heated
houses and adequate warm clothing are common.100
In a recent study of 111 patients, 67 (60.4%) were males and
44 (39.6%) females; 89 (80.2%), 90 (81.1%), and 90 (81.1%)
patients had onset in relation with lower temperature (<10° C
[50° F]), relatively low atmospheric pressure (<1500 kPa), and
higher relative humidity (>60%), respectively. Susceptibility to
chilblains appeared to increase when ambient temperature was
less than 10° C (50° F) and relative humidity was more than 60%.105
Acute pernio has a seasonal incidence, with reversible symp-
toms more common in cold weather. The acute form is seen
primarily in schoolchildren and young adults younger than 20,
with the highest incidence in adolescent females.81 It can occur
in mildly cold settings such as logging, kayaking, snowmaking,57
232
winter horseback riding, and hiking.101 Pernio can be caused by
brief cold exposure (30 minutes), often appearing several hours
after exposure, with the skin lesions fully developed within 12
to 24 hours.99 Characteristic locations for these lesions are the
feet, hands, legs, and thighs. Single or multiple, erythematous,
purplish, edematous lesions form, with vesicles in severe cases.
Symptoms include intense pruritus, burning, or pain, often wors-
ened by subsequent warmth. The lesions of acute pernio are
self-limited and usually resolve within a few days to 3 weeks,100
occasionally leaving residual hyperpigmentation.25 Although the
healing process appears to occur as the plaques resolve, pain
often persists. Subsequent mild cold exposure may trigger par-
esthesias, edema, and skin scaling.57
Chronic perniosis usually progresses over several winters after
repeated episodes of acute pernio, rarely progressing from the
initial injury to chronic irreversible skin changes within a single
season.81 Repeated episodic seasonal lesions may become edem-
atous, with permanent discoloration and subcutaneous nodule
formation. The nodules are firm and painful, ultimately rupturing,
which provides pain relief and leaves a shallow ulcer with pig-
mented atrophic skin. These ulcers may grow larger and coalesce,
remaining open, which leads to permanently swollen extremities,
scaly pigmented skin, and unremitting pain aggravated by light
pressure.
Pernio is thought to be caused by prolonged cold-induced
vasoconstriction with subsequent hypoxemia and vessel wall
inflammation.49,69 Subcutaneous arterial vasoconstriction is docu-
mented by both pathologic81 and arteriographic studies.116 Histo-
logic examinations show lymphocytic vasculitis and papillary
dermal edema with pervasive inflammatory changes.49,69,81 The
differential diagnosis includes lupus erythematosus, Raynaud’s
phenomenon, polycythemia vera, atheromatous embolization,
erythema nodosum, and livedo vasculitis with ulcerations.
Treatment of pernio is accomplished by drying and gently
massaging the affected skin. Active warming above 30° C (86° F)
significantly worsens the pain and should be avoided.57 Although
therapeutic regimens in the literature include nicotinic acid,53
ultraviolet irradiation,61 thymoxamine,70 intravenous calcium com-
bined with intramuscular vitamin K,42 corticosteroids,47 and sym-
pathectomy in severe cases,81 few have proved to be either
effective or universally accepted. Nifedipine (20 mg three times
daily) has been effective for treatment of severe perniosis.
Patients treated had a significantly reduced time for clearance of
lesions, decreased pain and irritation of existing lesions, and less
development of new pernio.49,108
Preventing pernio is relatively simple. Recommended prophy-
lactic measures include minimizing cold exposure with suitable
clothing when outdoors and maintaining adequate warm tem-
peratures indoors.
RAYNAUD’S PHENOMENON
This eponymous phenomenon was first identified by Maurice
Raynaud in 1862, who described “local asphyxia of the extremi-
ties.” Raynaud’s phenomenon is a paroxysmal vasospastic and
subsequently vasodilatory arteriolar response to temperate or
occasionally emotional stressors. This can include changes in
temperatures, not only cold exposure,52 and is essentially arterial
hyperresponsiveness and vasoconstriction in susceptible indi-
viduals.59 The classic observed color change, common in digits,
is white (following the initial vasospastic response) to blue
(indicating hypoxia) and finally to red, with subsequent vasodila-
tion on rewarming. The final stage is often associated with
burning pain.
Broadly, Raynaud’s can be divided into primary and second-
ary. Raynaud’s phenomenon is the primary form, typically affect-
ing women in their 20s to 30s, with no obvious underlying cause.
Raynaud’s syndrome, or secondary Raynaud’s, is when the phe-
nomenon has an underlying cause, sometimes presenting as
the first sign of a systemic condition, such as systemic sclerosis.52
The vascular defect in primary Raynaud’s is thought to be primar-
ily functional with a hyperresponsiveness causing symptoms,
whereas secondary Raynaud’s often has underlying vascular and
microvascular abnormalities.59
 Primary Raynaud’s is unlikely to cause digital ischemia and
usually has normal nailfold capillaries and erythrocyte sedimenta-
tion rate (ESR). By definition, it does not progress to irreversible
tissue damage,60 although the symptoms can be painful and
distressing. In contrast, general secondary Raynaud’s is more
likely to present in older age groups (>30), and individuals are
more likely to develop tissue damage.52
PREVALENCE
Prevalence varies with geography and gender. Surveys showed
15% of patients reporting Raynaud’s phenomenon,113 although
prevalence varies depending on the definition of the disease.
Higher altitude is thought to increase prevalence.82 It is two to
nine times more common in women.32 Although not fully under-
stood, a relationship to hormonal factors is believed to exist,
particularly in view of the gender predominance. Digital vascular
reactivity in the preovulation period similar to that seen with
Raynaud’s suggests a role for estrogen.79 Use of a vibratory tool
and a genetic component have also been implicated.60
PATHOGENESIS
The pathogenesis differs between primary and secondary Rayn-
aud’s and has not been fully elucidated. Intravascular factors
related to underlying conditions, such as increased viscosity in
Waldenström’s macroglobulinemia or platelet activation, are seen
in secondary Raynaud’s syndrome.52 Structural abnormalties in
the vasculature do not occur in primary Raynaud’s phenomenon,
although some seemingly primary Raynaud’s cases have later
been revealed to be secondary, with subsequent tissue damage.
Interestingly, Raynaud’s phenomenon preferentially affects the
digits, with the thumb less affected,22 possibly because of its
shorter length.60
As mentioned earlier, α2-adrenergic receptors attenuate cold-
induced vasoconstriction, as illustrated by the use of intraarterial
administration of α1- and α2-agonists and antagonists and effects
on finger blood flow.24 Thus, it is thought that abnormalities in
this control is responsible for Raynaud’s phenomenon.60 This
condition primarily affecting extremities can therefore by partly
explained by the increase in α2-receptor responsiveness in distal
arteries.24
Control of vasoconstriction and vasodilation is complex. It is
not known in Raynaud’s phenomenon whether the production
of vasodilators is reduced or their effects on receptors are
impaired.60 However, further work is directed at the use of exog-
enous nitric oxide (NO), which can be given topically to increase
digital microvascular blood flow.6 A more detailed discussion can
be found in a recent review.60
DIAGNOSIS
Primary Raynaud’s phenomenon does not usually require further
investigation, although if one suspects secondary Raynaud’s syn-
drome, perhaps because of the appearance of digital ulcers,
advice should be sought regarding further investigation.52
MANAGEMENT
Symptoms can be distressing and painful. Various strategies
involve initially reducing exposure to sudden temperature
changes by using gloves and hand warmers, and keeping hands
warm. Smoking cessation is important because smoking decreases
finger systolic pressures.59 Although a large study did not find an
association between Raynaud’s phenomenon and cigarette con-
sumption, smoking may impair delay physiologic improvement
and increase severity of symptoms.20
Mild cold injury can result in a sensitization process that may
resemble secondary Raynaud’s disease, in particular cumulative
cold injuries. Avoidance of further cold injuries until not sensi-
tized is recommended.
Recent recommendations include exercising regularly and
reducing stress.119 Pharmacologic management has traditionally
involved calcium channel blockers, particularly noncardioselec-
tive dihydropyridine for treatment and prophylaxis, and meta-
CHAPTER 10  Nonfreezing Cold-Induced Injuries
anaylsis has shown significant improvement (weighted mean
difference, −5; 95% CI, −9 to −0.99) for all calcium channel block-
ers and higher for nifedipine alone.125 Nifedipine is currently the
only medication licensed for use in the UK.52 Side effects such
as flushing and pedal edema can lead to poor compliance. No
drugs are licensed by the Food and Drug Administration (FDA)
for use in the United States. Others drugs being studied are
fluoxetine and topical nitrates. Ginkgo biloba has shown improve-
ment over placebo, with few side effects.52
CRYOGLOBULINEMIA
Cryoglobulins are cold-precipitable serum immunoglobulins.120
Cryoimmunoglobulins were first reported in a patient with mul-
tiple myeloma144 and subsequently recognized to occur in a
diverse group of hematologic malignancies, acute and chronic
infections, and collagen vascular diseases.117,132 Cryoglobulins are
classified as three types. Type I cryoglobulins (10% to 15% of
total) are composed of a monoclonal immunoglobulin, primarily
IgG. Type II cryoglobulins (50% to 60%) are polyclonal, most
frequently IgG and IgM. The IgM fraction usually has rheumatoid
factor activity. Type III cryoglobulins (25% to 30%) are also com-
posed of polyclonal IgG and IgM fractions.
In general, the higher the protein concentration, the higher is
the temperature at which precipitation begins. Of clinical rele-
vance is the composition of the cryoprecipitate. For example, IgM
is intrinsically more viscous than IgG, and patients with monoclo-
nal cryo-IgM have amplified hyperviscosity. Because extremity
temperatures can reach 30° C (86° F), in vivo cryoprecipitation
may directly contribute to impaired capillary blood flow.57
Many clinical conditions are associated with cryoglobuline-
mia.120 Infections (viral, bacterial, fungal, parasitic), hematologic
diseases (chronic lymphocytic leukemia, multiple myeloma), and
autoimmune diseases (rheumatoid arthritis, pulmonary fibrosis,
inflammatory bowel disease) are all associated with cryoglobuli-
nemia. Hepatitis C virus (HCV) is considered a principal trigger
of cryoglobulinemia. Serum cryoglobulin values do not usually
correlate with clinical severity or disease prognosis,120 but may
serve as a marker of the disease.
Cryoglobulinemia is characterized by a clinical triad of
purpura, weakness, and arthralgias. A large clinical trial showed
that two-thirds of patients diagnosed with cryoglobulinemia ini-
tially presented with symptoms of skin lesions or Raynaud’s
disease–like vasomotor attacks. Mucosal bleeding, visual distur-
bances, and abdominal pain were less common. Cold sensitivity
was apparent in less than half of these patients.16 Symptoms
associated with cryoglobulins include typical Raynaud’s phenom-
enon, dependent purpura, cutaneous vasculitis with ulceration,
retinal hemorrhages, coagulopathies, glomerulonephritis, renal
failure, and cerebral thrombosis.
Treatment of cryoglobulinemia should be directed at the
severity of symptoms and the disease causing the cryoglobuline-
mia. Because HCV is implicated in many cases of type II and III
cryoglobulinemia, targeting HCV is the treatment of choice to
eliminate cryoglobulinemia. Interferon, prednisone, and ribavirin
have all been used to treat HCV and associated cryoglobulinemia.
For non–HCV-associated cryoglobulinemia patients with mild to
moderate symptoms (purpura, arthralgia, sensory neuropathy),
immunosuppression with steroids and analgesics is the treatment
of choice.120 A low-antigen content diet (rice, fresh vegetables,
fruit, tea) has been shown to improve purpura.41 With severe
manifestations of disease, such as renal failure, neurologic impair-
ment, disabling paresthesias, or myalgias, plasmapheresis may
be helpful in reducing the cryoimmunoglobulin concentration
below a critical point to alleviate symptoms.16 Plasmapheresis is
used in conjunction with steroids or other drugs, since discon-
tinuing plasmapheresis treatment usually causes reappearance of
cryoglobulinemia.120
COLD URTICARIA
Cold urticaria is characterized by development of localized or
generalized wheals and itching after skin exposure (air, liquid,
233

FIGURE 10-23  Cold urticaria. The hive occurred within minutes of
holding an ice cube against the skin. (From Habif TP: Clinical dermatol-
ogy, ed 4, Philadelphia, 2004, Mosby.)
object) to cold111 (Figure 10-23). It most frequently affects young
adults, although primary cold urticaria can occur at any age.
Women are twice as likely to be affected.112 The incidence rate
is about 0.05% of the population.
Symptoms are usually limited to cold-exposed skin areas.111
Local symptoms include redness, itching, wheals, or edema of
exposed skin. The wheals last approximately 30 minutes. Sys-
temic reactions include fatigue, headache, dyspnea, and hypoten-
sion. Swimming in cold water is the most common trigger of
severe reactions. This may lead to hypotension, fainting, shock,
and possibly death.10,56 Suffocation may also occur after consum-
ing cold drinks because of pharyngeal angioedema.111
Secondary urticaria occurs in 5% of patients with cold urti-
caria.56 The wheals are more persistent and may be associated
with purpura and vasculitis on skin biopsy. This disorder is
associated with an underlying disorder such as cryoglobulinemia,
cold agglutinins, paroxysmal hemoglobinuria, or connective
tissue disease.133 In addition, a rare autosomal dominant familial
form has its onset in infancy and is associated with arthralgias
and leukocytosis.134
The cause of cold urticaria is unknown. Cold urticaria has
been associated with viral or bacterial infections,111,112 as well as
infections of the upper respiratory tract, teeth, and urogenital
tract. It has been reported to involve release of histamine,74 leu-
kotrienes, and other mast cell mediators,112 possibly mediated by
IgE and IgM. Support for an IgE-mediated mechanism comes
from successful treatment14 using an anti-IgE agent (omalizumab).
The diagnosis of cold urticaria is made through the ice cube test
in the majority of patients,94 where a hive is induced by holding
an ice cube to skin for 3 to 5 minutes. If the results are equivo-
cal, a cold-water immersion test of submerging a forearm for 5
to 15 minutes in water at 0° to 8° C (32° to 46.4° F) establishes
the diagnosis.
Treating cold urticaria with antihistamines is the most effective
option. To reduce symptoms sufficiently requires dosing up to
four times the recommended dose.95,111,112 In addition, other thera-
pies include leukotriene antagonists, cyclosporine, corticoste-
roids, and anti-IgE.112 Individuals with severe reactions should
have an emergency kit containing corticosteroids, antihistamines,
and epinephrine. Based on the finding that infectious disease
may be a trigger for cold urticaria, treatment with antibiotics may
also be warranted.112
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234.e3
 CHAPTER 11 
Polar Medicine
MARTIN RHODES AND HANS CHRISTIAN SØRENSON
As with much of wilderness medicine, polar medicine is largely
derived from its setting. Polar, however, can be defined in several
different ways. Geographically, the Arctic and Antarctic circles,
at latitudes 66 degrees, 33 minutes north and south, delimit areas
in which the sun does not rise or set on at least 1 day of the
year, and determine the North Polar region (“The Arctic”) and
South Polar region (“The Antarctic”). A definition based on tem-
perature is the 10° isotherm, which joins those areas in which
the average temperature in the warmest month of the year is
10° C (50° F); this correlates roughly with the tree line.
For medical purposes, the definition of polar is more complex.
Although climate and geography are clearly important, the salient
features of polar medicine are logistic and experiential. Unlike
high-altitude medicine or hyperbaric medicine, for example,
polar medicine is not unified by an underlying pathophysiology.
High-altitude medicine is a medical field because of the environ-
ment’s effect on the human organism, but polar medicine is
largely medical practice within a particular environmental setting.
Medical practice in isolated settings is paradigmatic of wilder-
ness medicine; the patient population is essentially, if not literally,
a small demographic island. A broad definition of polar medicine,
therefore, could be “the practice of medicine in isolated settings
234
within an extreme cold environment, distinguished by a scarce
population, limited resources, and challenging logistics.” It is the
cold, remoteness, hostility, and unforgiving nature of the environ-
ment in which humans struggle to survive, let alone work, that
make medicine in polar areas, and in particular Antarctica, so
challenging.69
The environment itself defines polar medicine in another
sense. So harsh are the poles that the simplest of mistakes can
lead to harm. The average temperature at the South Pole in winter
is −60° C (−76° F). At this temperature, exposed skin freezes within
minutes. Prevention is everything, and thus polar medicine can be
seen as example of preventive medicine in practice.
THE DISTINCTION BETWEEN ARCTIC
AND ANTARCTIC MEDICINE
Although the polar regions share the predominant attributes of
cold, dark, isolation, and severe weather, they display many
important contrasts. The Arctic has been described as a frozen
sea nearly surrounded by land, whereas Antarctica is a land and
ice mass circumscribed by ocean. The moderating effect of the
surrounding North Polar waters contrasts with the cooling effect
of altitude on the Antarctic plateau, which lies at approximately
2835 m (9301 feet) and accounts for the approximately 40° C
(72° F) difference in wintertime low temperatures between the
two polar regions. On a plot of temperature versus humidity, the
polar plateau is more similar to Mars than to the rest of the earth.
The flora and fauna are unique to each area. The Arctic has an
abundance of land- and sea-based animals as well as migratory
birds and plant life. On the other hand, the Antarctic has no
permanent land-based animals, although there are migratory
birds, as well as a rich marine life and limited plant life.
The differences in population patterns mark an important
north-south disjunction in polar studies in general and in polar
medicine in particular. The northern polar regions above 66
degrees latitude comprise a frozen sea that is surrounded by eight
countries, each with its unique set of populations and medical
care services. The countries of the Arctic are Canada, Finland,
Greenland (Denmark), Iceland, Norway, Russia, Sweden, and
the United States. Together, they make up approximately 8%
of the earth’s surface. Human population is scattered throughout
the Arctic, with several relatively large urban areas, but for the
most part, the Arctic is sparsely populated, totaling less than 1%
of the world’s population.128 The overall estimated population
of the Arctic as defined by the Antarctic Monitoring and Assess-
ment Programme (AMAP) is approximately 4 million; indigenous
peoples make up 10% of that population, and they constitute the
majority of the total population in Greenland and in sparsely
settled areas of northern Alaska and Canada.51,65 Within the Arctic
there are eight major indigenous peoples and more than 30
minority groups. Some of these peoples have separate govern-
ments, languages, and socioeconomic possibilities.
There are no indigenous peoples in Antarctica, which is regu-
lated by the Antarctic Treaty, with 12 original and currently a
total of 49 signatory countries, although only 28 contribute to the
decision-making process.5 This complex treaty helps delineate
the relationships of the countries that are active in Antarctica and
how the continent is to be best preserved and used for peaceful
purposes. Seven countries claim territorial rights, which are held
in abeyance while the treaty remains in force.5 Of the 79 stations
in Antarctica, 39 are operated year-round.25 The total population
living in Antarctica, all seasonal, now exceeds 4400 persons in
the summer and well over 1100 in the winter.20
In the Arctic, there are two distinct but interacting popula-
tions, the indigenous Arctic inhabitants and visitors and immi-
grants. These populations have distinct but overlapping spectra
of medical problems. Many of the medical problems among the
Inuit, Sami, Chukchi, Nenet, and other northern groups are those
of populations making the often Faustian demographic and cul-
tural transition to a Western industrialized society. Thus, medical
practice among these groups is similar to that among many other
displaced indigenous populations. In some senses, the current
illnesses and health risks of the indigenous Arctic populations
are the results of contamination from distant sources and contact
with other cultures.15 In contrast, all medical problems in Antarc-
tica occur in visitors, whether these visitors are staying for days
or a year or more. Until the 1980s, the vast majority of these
visitors, whether tourists, expeditioners, or scientists, were young
and fit, and the medical problems they encountered reflected
this. They were usually related to the environment or to trauma.
The Antarctic visitor demographic has changed remarkably since
then. Not only is there a steadily increasing number of older
visitors with age-related medical problems, but now younger
expeditioners and adventure sports participants visit on guided,
commercial trips. They generally have little, if any, polar experi-
ence and are increasingly from countries with no tradition of
polar life. This lack of experience renders them much more
susceptible to environmental risks.
IMPORTANCE OF POLAR MEDICINE
INCREASES IN TOURISM AND EXPEDITIONS
The combined geographic polar regions cover about one-sixth
of the earth’s surface. Their territory in the imagination has been
enlarged by several remarkable expeditions, and recent stunning
CHAPTER 11  Polar Medicine
photographic and video images have added to the popularity of
the polar regions. This was fueled by worldwide interest in the
celebrations of 2012 and 2013 marking the centenary of Amund-
sen and Scott’s arrival at the South Pole. Despite or because of
the forbidding environment, tourism of various sorts is increas-
ing.81 The Arctic is a trendy destination. An estimated 1.5 million
tourists visit the Arctic each year, up from 1 million in the prior
decade.127 In 1980, it was estimated that a total of 31,000 paying
tourists, adventurers, or guests of national scientific expeditions
had ever visited Antarctica, but its increasing lure has led to
explosive growth. According to International Association of Ant-
arctica Tour Operators (IAATO) statistics, 37,405 tourist, staff, and
crew visited Antarctica by air or ship in 2013-2014. Since 1989,
tourists have visited approximately 200 sites, including 20 research
stations in the Antarctic Peninsula region, the most common site
for tourists. About 50 of these sites have received more than 100
visitors in any one season, and about the same number have
been visited only once. Most visits are to one of 35 sites. Fewer
than 10 sites receive around 10,000 visitors each season. The
British Antarctic Survey (BAS) monitors Port Lockroy and main-
tains an ongoing program on the effects the 10,000 visitors per
year have on wildlife and ecology of the area.53,81
Concerns about the dramatic increase in tourism and its effect
on the ecosystem have led to a movement to limit the total
number of tourist visits per year. The World Wildlife Fund and
the United Nations have proposed guidelines to developing
ecofriendly tourism in the Arctic. The guidelines cover its impact
on the environment as well as on local populations. In April 2009
the consultative countries of the Antarctic Treaty endorsed a
proposal to limit the size of cruise ships and the number of tour-
ists who can go ashore at any one time and eventually make it
binding to all parties.127
This increasing number of visitors and expeditioners has cre-
ated interest in polar medicine, in particular as it relates to land-
based and extreme expeditions. Wilderness medicine courses
specific to polar medicine are now offered. Tourist vessels gener-
ally carry a physician and sometimes a nurse. The occasional
expeditioner who needs rescue or assistance from a scientific
station uses scarce resources.26,81 One peculiar phenomenon is
that when patients and medical/rescue/evacuation resources are
from different countries, a complex flurry of high-level diplomatic
interchange must often occur before help can be rendered.
Perhaps the most notable tourist fatalities were associated with
the ill-fated skydiving venture at the South Pole, which resulted
in the deaths of three of the four participants,48 and the Air New
Zealand Flight 901, a scheduled sightseeing DC10 that in 1979
crashed into Mt Erebus with death of all 257 people aboard.87
Hazards are inherent in any expedition and may well be the
attraction for some participants. To be allowed to participate in
risky activities, some tourists may fail to declare serious medical
problems that later precipitate emergency medical evacuation.
Thus, one real concern is increased risk taking and the conse-
quences, or the dilemma between what is reasonable and what
is foolhardy. From a medical perspective, making a risk assess-
ment is multifactorial and differs for people, places, and goals.
Hazards of an evacuation need to be assessed for both the patient
and rescuers. Setting guidelines and anticipating needs in pre-
event preparation are the keys to successful evacuation.49 Because
of the occasional tourist in need of expeditious medical evacua-
tion, IAATO and other governmental groups have suggested
requiring insurance to defray the costs associated with these
evacuations. An increasing number of travel companies now
insist on such insurance. A dedicated medical evacuation from
continental Antarctica will cost upward of $250,000. There is also
discussion of the ethical versus medicolegal implications of
whether to render aid. The overriding issue should be care of
the patient. In practice, there is a great deal of mutual assistance
between companies and governments when life is at risk.
GEOPOLITICAL CONCERNS
The interests of governments in polar regions have not lagged
behind those of tourists. Political and territorial concerns have
235
 been important in both polar regions. With increasing exploration
of mineral and oil reserves and fishing potential, migrating humans
will continue to bring medical problems with them. Although the
Antarctic Treaty of 1959 prohibits territorial or commercial claims,
seven nations have made sectoral claims on the continent. Some
of these claims overlap and in the future may lead to a less-than-
peaceful resolution. In early 2010, however, Australia failed to
pursue Japan legally for ramming and sinking an antiwhaling boat
in Antarctic waters supposedly governed by Australia. The most
common reason given was that Australia feared that the Interna-
tional Court of Justice would nullify all territorial claims to and
national governance over parts of the continent.
In 2007, the Russian minisubmarines Mir-1 and Mir-2
descended to 4300 m (14,108 feet) in the Arctic Ocean and
placed a Russian flag on the seabed under the North Pole. The
Russians were hoping that soil samples would prove that its
Siberian ridge was directly connected to the Lomonsov Ridge, an
underwater crest 1996 km (1240 miles) long running across the
Arctic, and would lend credence to their territorial claim.
Concern about the environmental impact of increasing human
activity in polar regions seems to be tempering the pace of
development. As national resources diminish, however, the Ant-
arctic may come under increasing pressure to open up to extrac-
tion industries, similar to the situation in the Arctic.
INCREASES IN RESEARCH ACTIVITIES
Scientific research has been a part of polar exploration through-
out this century. There are scientific and medical journals devoted
COLD AND HEAT
to the polar regions, and thousands of articles are indexed each
year in the Antarctic Bibliography (http://www.coldregions.org/
antinfo.htm). The International Journal of Circumpolar Health
(http://ijch.fi/Issues.htm) is a richer source for health issues in
polar regions. Antarctic research continues to expand. All the
continent’s permanent stations are primarily there to support
research. The largest study is the IceCube project at the South
Pole station, which uses a series of downward-looking detectors
spread over a square kilometer to look for traces of the notori-
PART 2
ously elusive neutrinos. Neutrinos are produced when neutrons
transform into protons during nuclear reactions. The detectors
do not detect the neutrinos themselves, but rather the blue light
emitted by the breakdown particle (a “muon”) produced when
a neutrino collides with an ice molecule. The source of these
neutrinos coming up through the ice to the detectors may be
black holes, gamma ray bursts, or supernova remnants and other
extragalactic events. The muon preserves the direction of the
original neutrino and thus points back toward its cosmic source.
The IceCube project is at the forefront of astronomy and particle
physics research. In 2014, a report on 3 years of analysis dem-
onstrated a total of 37 high-energy neutrino strikes. The largest
of these, detected on December 4, 2012, is nicknamed “Big Bird”
and is the highest-energy neutrino interaction ever observed.1
The South Pole also hosts two large telescopes.
Another huge project involving many countries at multiple
sites across the Antarctic continent is ice-core drilling, designed
to catalog climate change over tens of thousands of years. Other
scientific endeavors include marine biology and ocean dynamics
research; atmospheric and climatologic research, including air
cleanliness monitoring and ice sheet movements; medical re-
search (primarily at Japanese and Chinese stations)84; biologic
research (ecosystems, penguins, seals, bacteria, lichen); seismic
monitoring; aerial and sea floor mapping with unmanned vehi-
cles in the harsh environment; paleontology; meteorite searches;
and demonstrations of alternative power in extreme circum-
stances (e.g., wind generators at New Zealand’s Scott Base).
Some observers have discerned a north-south split, perceiving
research in Antarctica as having more of a political motivation
and that in the Arctic as being more practical. For both scientific
and political reasons, an important part of scientific research in
polar regions concerns environmental issues. The remoteness of
these regions enhances their value as benchmarks for studies of
pollution. Indeed, several worrisome facts have been revealed
about the contamination of formerly pristine wilderness, such as
widespread radioactive contamination, the prolonged effective
236
half-life of radioactive fallout deposits,120,129 and increased chemi-
cal contamination, particularly in animals high on the food chain,
with persistent organic compounds, heavy metals, and other
contaminants affecting the environment and food supply.71,129
Widening of the Antarctic ozone hole (discovered by BAS scien-
tists in 1985) carries implications of increased ultraviolet (UV)
radiation. As occupational and environmental health issues draw
more attention, this aspect of polar medicine assumes greater
importance.30,31
BRIEF HISTORY OF HUMAN
HABITATION IN POLAR REGIONS
A perspective on the contrasts between Arctic and Antarctic
medicine may be sharpened by a brief summary of human habi-
tation in polar areas. Humans are known to have inhabited Arctic
regions for at least 4500 years. Anthropologists have uncovered
evidence for several waves of population migration from Siberia
through northern Canada to Greenland. Each of these migrations
was probably linked to climatic conditions, and each resulted in
a distinct set of cultures. The general pattern was of a nomadic
life with population densities of approximately one person per
400 km2 (154.4 square miles).55,123 In more recent times, this long-
established and remarkable adaptation to a hostile environment
has been disturbed. The pace of cultural change increased dra-
matically during the second half of the 19th century, when the
whaling industry moved into Hudson Bay, leading to sustained
contact between Europeans and the Inuit. In the early part of
the 20th century, religious missions, trading company posts,
government stations, church missions, and eventually medical
clinics and schools began to encourage permanent settlements,
roughly quadrupling the population density.55 In some areas,
such as Eurasia, large industrial and mining cities arose. This
change in population distribution has at times led to conflict
between indigenous and European cultures, and it has had sig-
nificant environmental and medical consequences.130
The known history of human exploration of Antarctica, unlike
that of the Arctic, is quite recent. Recorded sightings of the con-
tinent date only to around 1800, and “winter-over” sojourns did
not occur for another century. Waves of settlement also occurred
in Antarctica: sealing in the early 19th century, whaling in the
early 20th century, and scientific exploration since the mid-20th
century.123 The heroic era of Antarctic exploration occupied the
early years of the 20th century, with exploits such as the highly
publicized race for the South Pole between Roald Amundsen and
Robert Scott in 1911; the extraordinary survival of the crew of
the 1914 Endurance expedition, led by Ernest Shackleton;64 and
the heroic survival of Douglas Mawson, an Australian geologist
who wintered alone after other expedition members perished.75
Perhaps because of these and other dramatic events, and the
absence of an indigenous population and a scarcity of easily
exploited resources, human activities in the Antarctic have
retained a somewhat more expeditionary flavor than in the Arctic.
This has helped shape the contrasts in medical practice between
the northern and southern polar regions.
ARCTIC MEDICAL PROBLEMS
EFFECTS OF CULTURAL AND
DEMOGRAPHIC TRANSITION
The Arctic is not a homogeneous region. Although the population
is only approximately 4 million, it is very diverse, with few fea-
tures in common except the latitude of residence and hours of
daylight. Medical problems among indigenous populations in the
Arctic, approximately 10% of the total population, are character-
istic of displaced aboriginal people elsewhere in the world. The
wide-ranging interrelated factors include demographics, socio-
economic and physical environments, personal health practices,
and availability of good-quality and culturally appropriate health
care services.13,56 Although increased contact with industrialized
cultures has brought benefits, it has also brought many problems.
Some of the benefits include greatly improved life expectancy,
largely because of a decrease in morbidity and mortality from
infectious diseases and diseases of childhood (prevented by vac-
cines). Nevertheless, in indigenous Arctic peoples of the United
States, Canada, and Greenland, infant mortality is higher and life
expectancy is lower compared with Arctic dwellers in Nordic
countries.101 For many years, health care has lagged behind
national norms in the Canadian Arctic, with infant mortality 2 to
3.5 times the national average.118 Age-adjusted death rates are
also telling, with 8.4 per 1000 Northern Canadian people, com-
pared with 5.8 per 1000 for the Canadian national average; 14.3
per 1000 in Greenland; and up to 29.2 per 1000 in parts of Russia.
Other striking statistics reveal a suicide rate in Nunavik six times
that of the southern provinces of Canada,63,124 and an uninten-
tional accidental death rate three to four times higher than the
national average. Tuberculosis has decreased but is still unac-
ceptably prevalent at 47 per 100,000 persons. Diabetes mellitus
has increased to 5% of the population of 30- to 39-year-olds,
compared with 1% in the general Canadian population. In a
population in whom dental caries were previously almost
unknown, the need for restorative dental work is up to 60%.
Widely prevalent alcoholism and tobacco use greatly contribute
to these problems.11,45,118
As the Arctic environment and indigenous Arctic populations
make the cultural and demographic transitions to a Western
industrialized way of life, the spectrum of medical problems
has shifted. Changing social patterns have resulted in disturbing
trends: increasing numbers of young adolescent mothers, rising
prevalence of gonorrhea and syphilis among Greenlanders, and
concerns about other transmissible diseases, such as viral hepa-
titis and acquired immunodeficiency syndrome (AIDS).80,134 The
unwanted pregnancy/birth rate ratio in Greenland is approxi-
mately 1 : 1. Changes from the traditional diet and lifestyle have
led to increased obesity, diabetes, cardiovascular disease, and
mental health problems, including depression, binge drinking,
alcoholism, and higher suicide rate.13,118,124
ENVIRONMENTAL AND OCCUPATIONAL
HEALTH PROBLEMS
Transboundary pollutants, primarily from Eurasia and the North
American continent, have made deep and lasting changes.11 The
Arctic, once viewed as pristine, is now considered a pollutant
sink. Even so, promising new data reflect that strict environ­
mental control (e.g., bans/restrictions on uses and emissions of
persistent organic pollutants [POPs]) is working.51 The nuclear
accident at Chernobyl in April 1986 led to cesium-134 and
cesium-137 levels in reindeer meat 50 to 100 times those consid-
ered safe, forcing destruction of the Sami reindeer herds. During
that same time, lake fishing and berry picking were curtailed
because of contamination.40,130 Fortunately, research 20 years after
this accident demonstrates thriving flora and fauna even in the
most contaminated areas, demonstrating a rebounding environ-
ment. Nevertheless, the young people exposed to the nuclear
accident have shown an impressive increase in thyroid cancers,
and those exposed to the highest doses of radiation show an
increase in leukemias, solid cancers, and circulatory system dis-
eases.119 Industrial emissions from neighboring regions, including
an estimated 100 million tons of sulfur dioxide, have led to the
“Arctic haze” phenomenon, a gradual whitening of the histori-
cally deep-blue Arctic sky.40
Environmental impacts have had direct health conse-
quences.11,45 During the last 500 years, industrial pollution has
led to a sevenfold increase in lead levels in human tissues in the
Arctic.40 Another survey found blood mercury levels above the
normative limit in more than 10% of Sami reindeer herders in
northern Finland. In North Greenland, a study revealed that in
84% of human mothers, blood mercury levels were above the
World Health Organization provisional limit.42 Oceans, rivers, and
lakes reveal contamination and concentration of heavy metals in
fish.130 Further contamination of the food chain with long-lasting
POPs, including polychlorinated biphenyls (PCBs) and many
organic pesticides, is increasingly identified.31 Long-term conse-
quences of environmental pollutants on the health of the Arctic
dwellers continue to be studied.30 Recent work suggests that
the endocrine-disrupting effects of PCBs may have changed the
CHAPTER 11  Polar Medicine
normal ratio of male-to-female births from 1.05 to 1.02 in the
past 30 years.13 It has been documented that the concentrations
of PCBs in breast milk are seven times higher in the Arctic than
in Quebec.118 As previously noted, fallout from radioactive testing
has caused river pollution, and other environmental degradations
have affected the food chain, with an increase in certain cancers
noted in both animals and humans.137 Fear of the effect of pol-
lutants has caused many to abandon or significantly limit their
consumption of traditional foods (e.g., marine mammals, fish,
terrestrial mammals, birds). Unfortunately, this can have negative
nutritional effects, such as obesity, diabetes, and increased car-
diovascular disease, and in some cases relative malnutrition.41
Tragically, POPs, even in low concentrations, have been shown
to cause increased risk for diabetes, so both consumption of
traditional foods and changes in diet to processed foods have
contributed to the increased rate of diabetes in these regions.51
In some areas, consumption of traditional marine foods has led
to blood levels of mercury exceeding current recommendations.
Local health departments have to weigh overall nutritional ben-
efits of traditional land and marine food sources against the
potential long-term risks of neuropsychological and other poten-
tial health problems, particularly in newborns and infants.71
Fortunately, new trends show human exposure to pollutants
in the Arctic is decreasing. For example, the number of Arctic
childbearing-age women with excessive levels of PCBs, mercury,
and lead is decreasing. This is believed to be a result of dietary
changes and increased awareness of the problem. However, new
research is demonstrating many additional chemicals, some
newly developed, that have the potential to collect in the Arctic
food chain, so ongoing research, identification of these chemi-
cals, and their regulation are essential to continue improving the
health of indigenous peoples.51
Nontoxicologic factors also make important contributions to
Arctic morbidity and mortality. Accidents are more prevalent in
the Arctic. In younger (up to age 35) Inuit groups, injuries
account for approximately one-third of all deaths.17 Although it
has continued to decline since the early 1990s, it is striking that
Alaska’s occupational mortality is just over twice that of the U.S.
national average mortality per 100,000 workers. However, this is
greatly improved from five times the national average in the
1990s.89 With establishment of the Alaska surveillance system in
1991, work-related deaths have decreased by approximately 65%,
including a significant reduction in commercial fishing deaths and
a sharp decline in helicopter logging–related deaths.24 These data
reflect in part the inherently hazardous working conditions and
occupations and possible demographic biases of a young popula-
tion. Other factors, however, may play a role. Because aircraft
are a predominant mode of transportation in polar regions, it is
not surprising that Alaska accounted for greater than one-third
of all air crashes in the United States and 20% of the fatalities
from 1990 to 2008.88 Nonscheduled or commuter plane (<30
seats) flights, commonly used in isolated areas, pose a risk for
fatal crash six times that of scheduled airline flights, a figure not
surprising given the often extremely challenging flying conditions
(terrain, weather, and isolated landing sites with limited naviga-
tional aids and operator error). In recent years, the pilot occu-
pational fatality rate has fallen from 298 to 148 per 100,000 (less
than twice the rate for all U.S. pilots), thought to result largely
from increased awareness and proactive intervention in the
industry, such as the implementation of automated remote
weather stations, Global Positioning System (GPS), and terrain
avoidance hardware and software.88 Overall, the mortality rate
for Alaska natives is 939 per 100,000 per year, compared with
the overall U.S. rate of 698.9 per 100,000 per year.51
PSYCHOSOCIAL HEALTH PROBLEMS
With social disruption and increased environmental and occupa-
tional health risks, psychological problems in the Arctic have
achieved greater visibility in recent years. For a variety of reasons,
stress seems to be higher in winter. One survey of over 7000
adults living north of the Arctic Circle found a prevalence of
midwinter mental distress of 14% in men and 19% in women.43
237
 Most other studies suggest that this figure may be low. One study
among Inuit found that 22%, or one in five, experience depression
during the winter months, and 7% appeared to have seasonal
affective disorder.39 Cultural stress, erosion of traditional lifestyles,
and substance abuse are all contributory factors.13 Studies inves-
tigating scientific staff at Arctic research stations are relatively
uncommon but show patterns of sleep disturbances, depression,
and alcohol use reminiscent of those in Antarctic stations.
The double apparent risk factors of high latitude and dis-
placed indigenous populations have made alcohol abuse and
concomitant violence a serious problem in the Arctic. In Green-
land, one in three Inuit dies a violent death, and about 25,000
adults consume 28 million cans of beer a year, one of the highest
per capita consumptions of alcohol in the world. Prevalence of
“binge drinking” among Arctic peoples ranges from 12% to 39%,
with male greater than female rates. Fetal alcohol syndrome is
13% higher in Alaska than in the continental United States.13 One
study compared alcohol consumption by the Greenland Inuit
with nonindigenous local inhabitants and found that alcohol
consumption was less among the Inuit. However, other studies
found the reverse.63
Accidents are the leading cause of death in the Arctic, and
one-third of these are estimated to be alcohol related. In the
Canadian Arctic, alcohol consumption is 1.5 times the national
average, and Inuit and Indians 15 to 24 years old have a suicide
rate up to 11 times the national average. In some communities,
for boys and men ages 15 to 29, suicides are the most common
form of injury leading to death. It should be no surprise that life
expectancy is lower, and infection rates for many diseases (e.g.,
COLD AND HEAT
tuberculosis, meningitis, syphilis) higher than in neighboring
countries. Inuit communities have significantly lower incomes,
and their housing is crowded and of poor quality. Traditional
hunting and fishing no longer provide sufficient food or income
to support many families. The association between poor health
and social deprivation is well established.63,86
CURRENT AND FUTURE TRENDS
PART 2
In summary, indigenous populations of the Arctic show lower
life expectancy, higher rates of infectious diseases, higher infant
mortality, and higher rates of injuries and suicides compared with
norms in their respective countries.51 Fortunately, there are
encouraging signs related to Arctic health care. The incidence of
low birth weight, 5.5% in the central Canadian Arctic, has
decreased, although it is still higher than that among non-Arctic
dwellers.13 Tuberculosis, which incapacitated up to 20% of the
Canadian Inuit by 1950, has largely been brought under control,
although the rate of occurrence is still as much as 10 times the
national average.17 In Greenland, there has been significant
reduction in perinatal deaths. Having been 40 per 1000 births
in 1975, it decreased to 25 per 1000 in 1995 and 15 per 1000 in
2009.16 This is as a result of national guidelines, improved train-
ing, and introduction of ultrasound screening. High-risk pregnan-
cies are identified as early as possible, with childbirth planned
to occur in the main hospital in Nuuk, West Greenland. Despite
these improvements, perinatal mortality is still significantly higher
than for the rest of the developed world. This is the inevitable
consequence of life in the polar regions. With long transfer-to-
hospital distances, weather-dependent logistics, and limited
medical resources, a sudden unexpected premature birth or
obstetric complication is at high risk for a poor outcome. Trends
in environmental and occupational health problems show
increased monitoring, intervention, and improvement. Unfortu-
nately, the age-adjusted incidence of diabetes mellitus is dramati-
cally rising among First Nations populations.28
An important development in recent years has been the insti-
tution of trauma registries to track and target significant causes
of morbidity and mortality. Recent research emphasizes that
injury prevention is not solely a function of safer design of equip-
ment but also a complex interplay of environment, activity, and
people, notably including personal risk-taking behavior. If current
trends continue toward greater economic independence and
education of Arctic peoples, such potentially modifiable adverse
health behaviors may recede in importance in coming years.61,62
238
There is increasing acknowledgment that isolated Inuit com-
munities offer rich grounds for research. For example, a 2014
study from Greenland demonstrated that bacille Calmette-Guérin
(BCG) vaccination significantly lowered the incidence of Myco-
bacterium tuberculosis infection and tuberculosis in Greenlandic
children and young adults. This study was possible because the
BCG vaccination, introduced there in 1955, was temporarily
halted from 1991 to 1996 because of nationwide policy changes.78
ANTARCTIC MEDICAL PRACTICE
Medical practice, problems, and their study in the Antarctic are
somewhat different from those in the Arctic. Extreme isolation
makes Antarctic medicine unique. Because of the remoteness, it
may not be possible to medically evacuate (medevac) a patient
for weeks or even months. It might be easier to medevac from
the International Space Station than from some of the more
remote Antarctic stations.36 In general, the population residing at
national Antarctic programs is adult, relatively young, and physi-
cally and mentally healthy. As previously, noted, however, the
number of tourists of all ages visiting the Antarctic has increased
dramatically, bringing with them a broad range of acute and
chronic medical conditions.
NATIONAL ANTARCTIC PROGRAMS
There are approximately 30 summer-only and 42 year-round
national Antarctic program bases spread around the Peninsula
and continent. The newest of these is the Chilean summer-only
base, Glacier Union.
Winter-over personnel, including those spending a year or
more at a time in Antarctica, are required to pass medical screen-
ing that varies in intensity with the various national programs.
Most stations only house adults. There are two exceptions: Chile
and Argentina have families living at their principal bases, Villa
las Estrellas and Esperanza on King George Island. To date, 11
children have been born there. Some believe that the decision
to house families here was politically driven to reinforce their
respective sovereignty claims. All stations have some form of
medical care, usually a station physician. The more temporary
camps have varied medical support, ranging from first-aid wilder-
ness responders to paramedics or midlevel providers with limited
medical supplies. In general, the permanent year-round bases
have more sophisticated facilities, with radiographic, laboratory,
surgical, and dental provisions and a reasonably well-stocked
pharmacy for expected emergencies. There is at least one physi-
cian and sometimes nurses and ancillary medical personnel.
MEDICAL STATIONS IN ANTARCTICA
Medical facilities in the Antarctic polar regions can be conve-
niently divided into permanent and expeditionary facilities. As a
result of community expectations and long-term commitment to
research in Antarctica, a notable shift from an expeditionary to
an operational attitude has occurred in many of the Antarctic
programs. Figures 11-1 to 11-3 show the expeditionary facilities
at Union Glacier field camp. This unit can be flown in and out
of Antarctica by cargo plane.
What type of physician is needed? To paraphrase Grant,36 the
physician cannot be too specialized in approach; broad knowl-
edge and a wide range of practical skills are necessary to provide
good Antarctic medical care. Specialization in emergency medi-
cine or the equivalent seems to be a suitable choice, especially
to deal with emergencies. Bases usually have no room for anes-
thetists, surgeons, dermatologists, or psychiatrists; one person
covers these roles. However, huge advances in satellite and video
teleconferencing (VTC) enable polar physicians to access advice,
counsel, and guidance. For a significant proportion of the Ant-
arctic population, it is still extremely difficult and costly to evacu-
ate patients.36
The following is a description of the personnel and facilities
in the U.S. Antarctic Program; other nations maintain similar
facilities. McMurdo Station (MCM) (Figures 11-4 to 11-8) has the
largest population: about 200 in the winter and 1200 in the
 CHAPTER 11  Polar Medicine
FIGURE 11-1  Medical facility, Antarctic Logistics and Expeditions FIGURE 11-2  Medical facility, Antarctic Logistics and Expeditions
Field Camp, Union Glacier. (Courtesy Martin Rhodes.) Field Camp, Union Glacier. (Courtesy Martin Rhodes.)

FIGURE 11-3  Medical facility, Antarctic Logistics and Expeditions FIGURE 11-4  McMurdo Station medical facility—main area. (Courtesy
Field Camp, Union Glacier. (Courtesy Martin Rhodes.) Kenneth V. Iserson.)

FIGURE 11-6  McMurdo Station medical facility—reception area.

(Courtesy Kenneth V. Iserson.)

FIGURE 11-5  McMurdo Station medical facility—pharmacy. (Courtesy

Kenneth V. Iserson.)

239
 All permanent U.S. medical facilities have digital radiograph
and ultrasound capabilities, laboratory equipment for blood
chemistries and cardiac enzymes, and the capability to perform
immunologic testing for β-hemolytic Streptococcus, infectious
mononucleosis, and influenza A, as well as common resuscitative
equipment, including Life Pak 12 and Zoll monitor/defibrillators,
portable ventilators, and crash carts similar to those in most
emergency departments.
The pharmacies are well stocked and cover a broad range of
potential medical problems. There is no blood storage, but in
the event of significant bleeding, a “walking blood bank” (walk-
in donor system) is activated. To facilitate this process, all winter-
over and most summer personnel are blood-typed and screened
for hepatitis B and C and human immunodeficiency virus (HIV).
After a series of acute cholelithiasis cases, South Pole winter-over
personnel are now screened with ultrasound for gallbladder
disease. The Australian physician undergoes prophylactic appen-
FIGURE 11-7  McMurdo Station medical facility—side view. (Courtesy
dectomy. Otherwise, the experience has been that early antibiotic
Kenneth V. Iserson.) therapy can abort an acute appendicitis attack, allowing the
appendix to be removed electively at a later time.
The South Pole does not have 24-hour satellite coverage, but
year-round stations have facilities for telemedicine, including live
camera, still photos, fax, and digital radiography for transmission
and consultation via satellite and the Internet. VTC, used for
many years in Antarctica by multiple programs,36 came of age at
the South Pole in 2002 with a midwinter repair of a patellar
tendon rupture. The tendon was surgically reattached by the base
physician under the direction of consultants at major medical
centers via live video and voice connection. Various physicians
COLD AND HEAT

at Antarctic stations are also able to consult with colleagues via

VTC, such as with the South Pole medical staff’s successful man-
agement of a severely hypotensive tourist in 2009 with VTC input
from MCM clinicians. In addition, telemedicine has been used
for diagnosis and consultation in the treatment of a wide variety
of ailments, including acute cholecystitis, ophthalmologic lesions,
pancreatitis, pericarditis, fracture treatment, psychological consul-
tations, radiologic reports, and many other situations. Telemedi-
cine has improved the quality and availability of sophisticated
PART 2

care in these and other remote, hostile environments.

FIGURE 11-8  McMurdo Station medical facility sign. (Courtesy Medevacs are frequently dangerous and costly. Summer is the
Kenneth V. Iserson.) only season during which some stations can be reached for an
evacuation. Winter evacuations are infrequent, very dangerous,
and costly. Logistically, it may be 2 or more weeks before a
summer. Whereas the winter MCM and South Pole populations rescue can take place, and for some stations, it may not even be
are isolated, their summer populations constantly have an influx
of rotating personnel that bring new diseases. In the summer
season, the medical component is staffed with two physicians, a
physician’s assistant or nurse practitioner, an Air Force flight
surgeon, a dentist, a radiologic technologist, a laboratory techni-
cian, and a physical therapist. In the winter, the staff is composed
of one physician, a physician’s assistant, and a physical therapist.
All are cross-trained on site. (Other large national stations provide
necessary additional training in advance.) In addition, MCM has
a full fire department with paramedics who respond to emergen-
cies on station. The South Pole population peaks at 250-plus in
summers and reaches a nadir of about 50 in the winter. There
is one physician, a physician’s assistant or nurse practitioner, and
a volunteer trauma team trained on station. Palmer Station is the
smallest, with a population of 45 in the summer and a low of 10
to 20 persons in the winter. There is one physician, and volun-
teers are trained on site to provide assistance. How well these
volunteers can function was demonstrated in 2009 when the sta-
tion’s physician developed a peritonsillar abscess. She had one
of the station emergency medical technicians needle-drain and
then incise it under topical and local anesthesia. She then used
VTC and an intraoral camera to consult with an otolaryngologist
based in the United States. She improved within a few days.29
The Australian stations have one physician. Before deploy-
ment, there is a 2-week training course for two of the crew in
operating-theater nursing skills and for two persons in anesthesia
assisting. The predeployment training has proved valuable, as FIGURE 11-9  Trauma and rescue teams are frequently composed of
was clearly demonstrated in the case of a scientist who fell into volunteers and at least one experienced, trained individual. This
a crevasse and suffered serious injuries, including internal bleed- rescuer is practicing for possible extrication of a victim from a crevasse.
ing, that required on-site surgery (Figure 11-9).106 (Courtesy Betty Carlisle.)

240
 Pregnancy

CHAPTER 11  Polar Medicine

Ophthalmic
1% 0%
Vascular
Diabetes
Pulmonary 1% 3%
4%
Neurological
2%
Genitourinary
4%
Infections
2%
Dental
7% Injuries
Anxiety/ 42%
depression
5%

Tissue mass/
FIGURE 11-10  Historic midwinter rescue at the South Pole. Twin Otter tumor
aircraft flown by pilots from Canadian Kenn Borek Air Service. 6%

possible. A historic medical evacuation from the South Pole was
undertaken in winter 2001 with the first successful landing of a
twin Otter aircraft in full darkness at a temperature of −68.9° C
(−92° F) (Figure 11-10). This event, while fraught with danger,
has opened new possibilities and has been repeated.18,21
To increase further the ability to provide medical assistance,
even during the winter months, the U.S. Air Force recently
proved their capability of landing C-17 aircraft at MCM using
night-vision goggles and made successful air drops of critical
equipment at the South Pole. Certainly, however, prevention
through careful screening of candidates and increased use of
telemedicine as a way to avoid medevacs still remains the ulti-
mate goal.
To reduce the number of medical crises and need for urgent
medical evacuations, all participants must pass a “physical quali-
fication test.” Medical clearance criteria are used as a screening
tool. To establish appropriate guidelines, evidence-based criteria
from the medical literature, historical data of the U.S. Antarctic
Program, and guidelines from other programs, such as the
National Aeronautics and Space Administration (NASA), the
Peace Corps, and the U.S. Navy, that have activities in remote
areas were used. What appears to be lacking is screening for
body mass index and alcoholism. However, up to 30% of all
medical evacuations (both emergent and urgent) have been for
trauma; that is, they were not related to the evaluation criteria.
Of emergent and urgent evacuations, 10% were for gastrointes-
tinal (GI) and 8% for cardiovascular reasons (Figure 11-11).
Considering only truly emergent medical evacuations, 28% were
for cardiovascular and 28% were for GI reasons. Figure 11-12 is
a chart showing the number of medevacs from MCM and the
South Pole station.
Cardiovascular
8% Altitude related
Gastrointestinal
5%
10%
FIGURE 11-11  Evacuations for medical reasons, with percentages of
5-year totals (1998-2003). (From Mahar H [Safety and Health Officer,
OPP/NSF]: Medical clearance criteria: Revalidation study. Personal
communication, 2003.)
completely clothed, from a 93.3° C (200° F) sauna to the Pole
outside at an ambient temperature of −73.3° C (−100° F) or lower.
Similarly, the quintessential polar first-aid story involves creative
solutions to the problem of finding warm fluids,3 but it would
be reckless to forget the ever-present danger of such a hostile
environment. Windchill typically drops the effective temperature
on exposed skin far below −73° C. It has been estimated that
under the most severe winter conditions, an inactive person in
full polar clothing could undergo a life-threatening drop in core
temperature in only 20 minutes. Airplane refueling crews and
others working with liquids at polar ambient temperatures are
constantly reminded that even a small splash can mean instant
frostbite.34
Rescue and treatment are complicated by the additional
need for both victim and rescuer to avoid hypothermia and
frostbite.55,57 Disorientation and confusion from hypothermia,
MEDEVACS BY LOCATION
100%

SOMATIC HEALTH PROBLEMS 80%

Percentage

Many of the primarily somatic health problems in Antarctica 60%

relate to cold, altitude, and trauma and are thoroughly covered
in the chapters on these topics. In a midwinter setting where a 40%
tossed mug of coffee freezes before the liquid hits the ground,
the dangers of frostbite are clear. Anyone gasping for breath after 20%
climbing the six flights of stairs with 92 steps from the tunnel to
the living area of the South Pole’s elevated station, or who has 0%
lost 5 kg (11 lb) in the first 2 weeks merely from resting tachy-
cardia and tachypnea, can appreciate the physiologic stresses of 000/ 01/ 02/ 04/ 05/ 06/ 07/ 08/ 09/
01 02 03 05 06 07 08 09 10
rapid ascent to an equivalent of 3200 m (10,499 feet). Likewise,
the dangers of UV exposure at altitude with an ozone hole and Season
snow surface reflectance of 80% to 90% can become painfully
evident to the unwary visitor.22,117 From other location
From NPX
Cold-Related Problems From MCM
Cold is a dominant factor in polar medicine. It can be a source
of humor, such as the infamous “300 Degree Club” at the South FIGURE 11-12  Number of medical evacuations (medevacs) from
Pole. Membership requires sprinting, while somewhat less than McMurdo Station (MCM) and the South Pole station (NPX).

241

FIGURE 11-13  Clothing is an important topic in polar medicine.
A researcher prepares to leave the station for an extended time at
−56.7° C (−70° F). The total weight of his clothes is 11.5 kg (25.4 lb).
COLD AND HEAT
Notice the multiple layers for each area of the body. (Courtesy Stephen
Warren.)
clumsiness from bulky clothing, and degraded performance char-
acteristics of equipment and intravenous (IV) fluids can compli-
cate otherwise straightforward procedures. A recent case report
describes almost immediate freezing of fluid in IV lines and shat-
tering of the plastic IV tubing despite vigorous attempts to warm
PART 2
them.57 Simple devices commonly used in warmer settings, such
as air splints and pneumatic antishock garments, would be simi-
larly unusable. In more sophisticated equipment, batteries rapidly
fail, unwinterized mechanical moving parts seize up, and metal
objects become dangerous sources of frostbite.
Clothing, not normally considered a medical topic, assumes
special importance in the polar environment76,104 (Figure 11-13).
Although the clothing used for many polar research programs in
the summer seems adequate, a strong argument can be made for
specialized winter gear, possibly adapted from the space program,
that would allow relatively delicate manipulation of scientific
equipment while offering protection from the cold. In fact, at
temperatures below those of most military specifications, material
properties of equipment, including plastic electrical insulation,
create unexpected hazards, such as splitting of insulation and
other plastics, and extreme rigidity of cables and hoses such that
they cannot be used. Fortunately, the importance of ergonomic
issues in the design of machinery and clothing for polar condi-
tions is receiving increased attention.47,132 There is new research
on use of personal heaters, which are particularly effective for
extreme cold and for sedentary work in the cold.110 Phase-change
material can store latent heat and then release it during periods
of low activity.104 These newer materials will allow thinner gloves
with high thermal protection to be worn for work in the cold
that requires dexterity, and they will be particularly effective for
persons whose efforts alternate between heavy work that can
produce sweating and light work with associated cooling (Figure
11-14). In addition, as phase-change material clothing becomes
readily available, clothing will be lighter and less bulky, particu-
larly advantageous when doing intricate work in the cold as well
as alternating active with sedentary work in the cold.
Altitude Illnesses
Altitude illness can be a major issue at many Antarctic stations,
camps, and research locations, including the South Pole, Vostok,
and Mt Erebus. A literature-based approach to preventing altitude
242
illness with the least possible adverse outcomes over the season
was to administer acetazolamide (Diamox), 250 mg twice per
day, starting 24 hours before altitude exposure. Participants vol-
untarily took this medication for an additional 3 days of exposure.
If the individual still had symptoms, such as observed periodic
breathing or headache, the dose would be increased to three
times a day. Dexamethasone (Decadron), 4 mg twice a day
beginning the day of ascent, was used as an alternative for
persons who had experienced serious side effects or allergic
reactions, who had an allergy to sulfa-containing medications, or
who had no notice before having to ascend to high altitude. This
was also continued for 3 days at altitude. After 3 days at altitude,
the body’s own compensatory mechanisms have had time to
adjust to the new environment, and the medication is no longer
needed.
Because medication use was voluntary, complications seen
from not taking it included high-altitude pulmonary edema
requiring use of a Gamow bag before urgent evacuation, relative
hypoxemia, and decreased work tolerance. Complications from
taking acetazolamide included dehydration and electrolyte abnor-
malities in patients who were already ill or had severe underlying
diseases.54 See Chapters 2 and 3 for current recommendations for
prophylaxis and treatment of high-altitude–related illnesses.
Nutritional Studies
Nutrition occupies a key niche throughout the history of polar
expeditions. Early expeditions in both polar regions provided
several examples of nutritional illnesses, including scurvy and
possible hypervitaminosis A and lead poisoning. More sophisti-
cated nutritional analyses have been possible during recent expe-
ditions,117,121 and advances continue to be made in development
of lightweight but nutritionally dense rations. When participants
in endurance events are well trained, it is possible to compete
without loss of lean body mass.73 Although many prolonged,
unsupported expeditions include an element of malnutrition or
even starvation, protein synthesis is still active.121,122
During a Canadian-Soviet transpolar ski trek, participants
skiing approximately 20 km/day (12.4 miles/day) at a speed of
about 3.5 km/hr (2.2 miles/hr) while carrying 37- to 45-kg (81.6-
to 99.2-lb) packs showed increased strength, decreased body fat,
and increased high-density lipoprotein cholesterol. A paradoxical
drop in aerobic power was noticed, perhaps because of intensive
pretraining and conditioning, as well as increased efficiency of
skiing as the trip progressed. More recently, in a nonsupported,
two-man, 86-day trans-Greenland trip, well-trained and experi-
enced skiers eating an adequate caloric diet had little if any
significant impairment. Their average energy intake in rugged
terrain was 28 to 34 kilojoules (kJ) per day (6688 to 8121 calories/
day) and in level terrain 14 to 16 kJ/day (3344 to 3822 cal/day).34
Although applicability of these figures to more sedentary polar
FIGURE 11-14  Frostbite on thigh with eschar. Newer phase-change
materials would have prevented this injury. This skier across Antarctica
suffered frostbite when he removed one layer of insulating clothing to
avoid sweating on a calm sunny day. When a wind came up, it caused
frostbite through the wind pants and light insulation. (Courtesy Borge
Ousland.)
sojourners is probably limited, work is being done to alter the
diets of more sedentary expeditions to improve the lipid profile
of participants.74 Better availability of common foods and fresh
fruits and vegetables during the summer and frozen foods in the
winter at the permanent stations allow participants to choose a
healthier diet. However, frequent fried and high-fat food intake
leads to elevation of lipid profiles and the associated increase in
cardiovascular risks. Some studies have demonstrated that it is
possible to make simple and acceptable changes in food prepara-
tion that have a significant impact on lowering cardiovascular
risk factors of winter-over personnel.7,74
An area that has received increased attention involves
the possibility that the prolonged low dose of sunlight may
have long-term effects on bone metabolism and immune and
cardiovascular systems. One study showed a decrease in the
25-hydroxy metabolite of vitamin D (25OHD) as UV radiation
ceased. However, the active metabolite 1,25-dihydroxyvitamin
D (1,25[OH]2D) did not show such variation.105 A few studies
have demonstrated significant decreases in serum vitamin D as
measured by 1,25(OH)2D and associated increases in serum
osteocalcin during the dark period, possibly indicating bone
remodeling.138 Another study, in which low doses of vitamin D
were given, showed increased bone mass in lumbar vertebrae
and leg bones, but no bone mass increase in the pelvis or upper
extremities. This was thought to be the result of vigorous activity
over the winter. The study also showed a decrease in serum
calcium and 25OHD levels during the winter.90 A study was
undertaken in the 2003-2004 Antarctic summer and followed 53
Australian expeditioners for 2 years. It showed that they became
vitamin D deficient after just a few months; after 12 months, this
began to result in loss of bone density. Further study is planned
to identify the minimal dose of supplementation needed to
prevent deficiency and whether these expeditioners have greater
risk for developing osteoporosis later in life.58 Because many
participants return for successive winters, further studies are
needed to delineate possible long-term effects of bone mass after
redeployment.
Infection and Epidemiology
With particular reference to the space station analogy, a number
of studies have taken advantage of the physical isolation of Ant-
arctic stations as a natural laboratory for infectious disease epi-
demiology. Because microorganisms are believed not to survive
the extreme cold long enough to be carried in by winds, mid-
winter respiratory tract infection outbreaks in the absence of
outside contacts have suggested that such organisms could persist
in clothing or other fomites.102
Despite a widely reported leukopenia, decrease in cell-
mediated immunity, and decreases in salivary IgA and IgM during
the isolation of wintering over, it is not clear whether persons
emerging from Antarctic stations are more susceptible to infec-
tion,33 or whether the changes in immunity are related to the
stress associated with a winter-over.
Circadian Rhythms, Endocrine Studies, and Sleep Research
Pioneering studies of Natani and colleagues83 on sleep electro-
encephalograms at the old South Pole station demonstrated clear
patterns of sleep disturbances and “free cycling” of the sleep–
activity cycle. Some of these findings have been extended in
more recent studies. For example, among four subjects at a small
winter-over camp, summer sleep cycles synchronized within the
group and with clock time. During 126 days of sunless winter,
rhythms free-cycled in all four people and then resynchronized
with reappearance of the sun.60 The degree of synchrony versus
free cycling appears to depend on a number of factors, notably
zeitgeber strength (an environmental agent or event that provides
the cue for setting or resetting a biologic clock, i.e., activities,
social contacts, and the most important zeitgeber in nature,
light).35 Studies in Indian stations also confirm continuing sleep
pattern changes.14
A number of studies have examined the effect of prolonged
polar residence on diurnal variations in the level of melatonin.
Its important role in free radical scavenging and sleep regulation
is beginning to be elucidated.59 Melatonin has been studied as a
chronobiotic and is used as a supplement to treat circadian
CHAPTER 11  Polar Medicine
rhythm disorders.6,113 Of the various studies using melatonin to
treat sleep disorders, including delayed sleep phase and for
night-shift workers, most have only small numbers of partici-
pants. Although the initial studies are promising, more research
needs to be done. It appears that exogenous melatonin can be
used effectively for most persons. The short-term side effects
(headache, nausea, drowsiness) are few. There are no long-term
studies. Use of blue-enriched white light in the workplace
improved alertness, performance, and sleep quality, as well as
daily resetting of the melatonin cycle.32,79,113
Other endocrine fluctuations also appear to be correlated with
the length of the day.127 Some endocrine studies have examined
the effects of prolonged residence in polar regions with a longer-
than-diurnal time constant. Twenty-four-hour urinary excretion
of catecholamines increases in the cold, but social stresses appear
to overwhelm climatic determinants of catecholamine metabo-
lism, correlating with increases in diastolic blood pressure and
pulse during the year.44 A more consistent pattern of elevated
thyroid-stimulating hormone (TSH), decreased free thyroid hor-
mones, and increased triiodothyronine (T3) clearance after several
months has been demonstrated. It has been suggested that rapid
clearance of T3 is caused by the cold. A pattern of increased
pituitary release of TSH in response to IV thyrotropin-releasing
hormone and increased serum clearance of orally administered
T3 has been identified and dubbed the “polar T3 syndrome.”27
The full clinical significance of these findings remains unclear,
but the T3 may well be related to the winter-over syndrome (see
later).91,99 Several studies that used thyroxine (T4) supplementa-
tion noted improvement in midwinter cognitive function, mood,
and vigor.106,109,131
Environmental Health Issues
Because of Antarctica’s isolation, it seems a particularly disturbing
site for litter and pollution. As in the Arctic, events such as the
early problems with a nuclear reactor at MCM (since removed)
and the 1989 oil spill from the Bahia Paraiso near Palmer Station,
as well as studies by groups such as Greenpeace, have focused
attention on environmental health risks in the Antarctic.82,129 Envi-
ronmental inspections at a broad range of Antarctic stations have
raised concern about toxic effluents and heavy-metal residues,
as well as radioisotopes used for research. To address these
issues, a number of countries have begun to implement more
responsible waste management and water-monitoring policies
and are taking corrective actions. Most have active recycling
programs in place, and many cleanups are in progress or have
been completed. Currently, most stations, including all U.S. sta-
tions, discharge raw sewage. Proposals are in place to find a way
to ameliorate the contamination from raw sewage that is dis-
charged into the sea and into large bubble holes in the ice for
the inland stations. The BAS Rothera Station installed a sewage
treatment plant, with significant improvement in the near-shore
marine environment.50,52,77
Occupational Health and Injury Prevention
Rigorous studies of risk are important for injury prevention. Un-
fortunately, they are complex and often bedeviled by challenges,
including controversial data, multiple variables, and biases. For
example, for purposes of occupational epidemiology, it may
ultimately prove useful to stratify the Antarctic sojourner popula-
tion into groups such as sport expeditions, military, commercial,
and scientific, but the health behaviors of these groups overlap,
and few studies have gone beyond aggregate descriptive statis-
tics. There is no current system for archiving these data, except
by individual programs or organizations; therefore much of the
data is not available for review. There were plans to address this
issue at the Council of Managers of National Antarctic Programs
(COMNAP) at the planning meeting for the International Polar
Year of 2007-2008.10 Unfortunately, because of funding issues,
this has not been done.37
Even from these broad statistics, some figures emerge that
may be useful cognitive anchors. There were 16 fatalities from
1947 to 1999 in the Australian Antarctic Program, but only one
fatality in the past decade. Among 3500 scientists and support
243
 personnel (2000 person-years), there were four medical deaths,
two myocardial infarctions, one case of appendicitis, one perfo-
rated gastric ulcer, and one cerebral hemorrhage. The remainder
of the events were accidents involving falls, head injuries, hypo-
thermia, drowning, crush injury, and burns.68,70
There have been 60 deaths in the U.S. Antarctic Program since
1946.2 These can be ranked by cause: aviation, 61%; vehicles,
11%; ships, 7%; recreational, 7%; station/industrial, 5%; field
activities, 5%; and other, 4%.72 Although it is difficult to adhere
to standard occupational safety practices when in a remote loca-
tion, new guidelines and serious efforts in some of the programs
have led to improved worker and participant safety.
A review of data for the Australian National Antarctic Research
Expedition (ANARE) 2002-2003 season listed the following
reasons for medical consultation: medical (e.g., upper respiratory,
GI), 39%; injuries (sprains, strains, dermatologic, lacerations, frac-
tures), 27%; follow-up visits, 24%; and preventive (immuniza-
tions, midyear examinations, wellness programs), 10%.19 For the
2004-2005 season, Antarctica New Zealand (ANZ) reported mus-
culoskeletal, 42%; medical (e.g., upper respiratory infections, GI),
22%; other injuries, 20%; dermatologic, 15%; and preventive,
dental, and other, 8%.103 Usually, most visits are related to injuries,
and the next most frequent medical clinic visits are attributable
to upper respiratory infections. Environmental problems include
dry skin and fissures, particularly on fingertips as a result of cold
and very dry conditions. Cyanoacrylate glue hastens healing of
disabling fingertip and heel fissures.8 Cold-induced urticaria,
frostnip, and frostbite are frequently underreported, except for
moderate to severe cases. Small nasal bleeds occur frequently,
COLD AND HEAT
but they rarely require treatment beyond instruction to use pet-
rolatum or antibiotic/antiseptic ointment once or twice daily to
protect the delicate nasal epithelium, which easily becomes dehy-
drated or can sustain frostnip. Although the bulk of care is limited
to routine visits, the pathologic conditions encountered even
among this carefully screened population have included myocar-
dial infarctions, massive GI bleeds, unreported Crohn’s disease,
bowel obstructions, acute cholelithiasis with pancreatitis, pulmo-
nary emboli, massive head injuries, fractures, crush injuries,
PART 2
newly diagnosed schizophrenia, and cancer.
Fire Safety
In light of the extreme cold, it is somewhat counterintuitive that
fire is a major concern and significant danger at all Antarctic
stations. This surprising assessment rests on a number of factors.
Cold temperatures severely limit the utility of water for fire
suppression. Firefighting equipment may become inoperative
in extreme cold, and frequent high winds can fan fires. The
extremely low absolute humidity in many polar regions results
in an even lower relative humidity when outside air is warmed
in station dwellings. This in turn leads to increased static electric-
ity and dryness of combustibles, already at risk from frequent
use of space heaters. In addition, alternative food, shelter, and
fuel are limited.
Elaborate predeployment training, frequent on-site drills, and
keen awareness of potential fire hazards have correlated with a
satisfactory fire safety record to date, but this good fortune cannot
be taken for granted. One of the most life-threatening events was
the explosion and fire at Vostok in 1982, leaving the station
essentially without power or adequate heat. Only one person
died, but there were several injuries, and the winter crew had to
endure 8 months without a power plant to supply heat.107 In 2001
the BAS Rothera Station lost its new Bonner Lab building when
an electrical short started a fire. No one was injured, but with
50- to 70-knot winds, little could be done to save the station.12
Although fire-suppression systems are built into the newer build-
ings, a historic A-frame building at New Zealand’s Scott Base
burned down in May 2009 and, much more seriously, a two-story
building at Russia’s Progress Station burned down in October
2008, killing one person and seriously injuring two others.
Because the building contained their radio equipment, they could
not contact the outside world for 4 days after the event. Fatal
fires continue; in 2012, two staff members died in a fire at Brazil’s
Comandante Ferraz base on King George Island. In Antarctica,
fire is an ever-present threat.
244
National Programs’ Responsibilities for Tourist Safety
As transportation increasingly opens up previously inaccessible
areas, this image attracts growing tourist traffic and, with it,
heated debate from both legal and environmental viewpoints.116
The essential medicolegal issue is the extent of governmental
organizations’ responsibility for medical care of participants in
nongovernmental activities, whether scientific, political, or com-
mercial. Although this discussion started much earlier, it is
ongoing.81 When a tourist group requires aid beyond its own
capabilities, whose responsibility is it? To what extent should a
research station with limited medical supplies be required to
divert some of those supplies to an individual who presumably
bears responsibility for planning his or her own medical cover-
age? By default, stations provide what assistance they can,
although they often try to bill tourist companies and their insur-
ance agencies for costs involved in patient treatment or transport.
The Antarctic Treaty Consultative Meeting XXXI provided attend-
ees with a list of guidelines recommended before trips to Ant-
arctica, including travel insurance, contingency plans, and other
necessary equipment.4
Air Safety
As in the Arctic, reliance on aircraft for transportation has high-
lighted the critical importance of air safety. The worst Antarctic
air accident was the crash of an Air New Zealand tourist “flight-
seeing” DC-10 on Mt Erebus in November 1979.87 This accident
killed all 257 people aboard and temporarily ended such flights,
although IAATO records indicate that overflights are now hap-
pening with new guidelines in place. There have been 35 air-
related fatalities in the U.S. Antarctic Program since 1946 from
crashes related to either fixed-wing or rotor aircraft.72,116 A ski-
equipped LC-130 Hercules crashed at the remote D-59 camp in
1971 (Figure 11-15). Fortunately, none of the 10 crew members
aboard was injured. During a salvage operation in 1987, however,
another LC-130 bringing supplies to D-59 crashed nearby, killing
two and injuring nine. More recently, a helicopter crash occurred
in the dry valleys; both the pilot and passenger were seriously
injured. After a weather delay, they were extricated and evacu-
ated to New Zealand for definitive care.19,85 With better weather
prediction and increased safety standards, the accident profile is
improving. However, in 2010, there was a fatal helicopter crash
near the Dumont d’Urville station that killed four persons. In
January 2013, a Kenn Borek Air DHC-6 Twin Otter crashed near
the summit of Mt Elizabeth in the Queen Alexandra range on a
flight from the South Pole to the Italian base at Terra Nova Bay.
All three crew members perished.
FIGURE 11-15  LC-130 Hercules partially stuck in a hidden crevasse,
demonstrating the inherent hazards of working in Antarctica. (Courtesy
National Science Foundation photo archive.)
PSYCHOSOCIAL HEALTH PROBLEMS
As the U.S. Polar Manual explained in 1965, “No psychiatric case
ever got better in the cold.”46 For many, polar living arrangements
and psychosocial issues may be more important than the strictly
medical or environmental factors. Psychiatric problems are men-
tioned even in reports of early expeditions, and almost any
participant in expeditions will recognize Thor Heyerdahl’s obser-
vation: “The most insidious danger on any expedition where men
have to rub shoulders for weeks is a mental sickness that might
be called ‘expedition fever’—a psychological condition that
makes even the most peaceful person irritable, angry, furious,
absolutely desperate because his perceptive capacity gradually
shrinks until he sees only his companions’ faults while their good
qualities are no longer recorded by his grey matter.”126
Most psychological problems, primarily sleep disturbances,
are minor and temporary. Many disturbances are more related to
the social environment than to the physical environment.93,112
Appropriate lighting or changes in photo periodicity (the dura-
tion of daylight and darkness in a 24-hour period) help improve
mood and sleep.95,133 In addition to appropriate exercise facilities,
opportunities for quality mental stimulation and frequent contact
with friends and family via the Internet and telephone can help
maintain stability. Except for insomnia, which may be endemic,
the incidence of psychiatric problems is lower than expected in
the overall population.
Not all psychiatric events are benign. One author witnessed
an acute psychosis in a worker who was threatening to set fire
to the base and kill a colleague with a shovel, apparently the
result of the stress of a dysfunctional work relationship.
Many nations use formal and informal psychological screen-
ing, especially for participants planning to winter-over in Antarc-
tica. How well the screens function is debatable. A British study
showed that an extensive psychological screening examination
weeded out many participants with problems with “defensive-
hostility” and “emotion-focused coping.” Simple interviews did
not identify these problems.38
Alcohol Abuse
Adjustment to psychosocial stresses in polar communities depends
on a complex array of sociocultural factors. One coping mecha-
nism is alcohol use. As in many isolated communities at high
latitudes, alcohol use can disrupt or lubricate social interactions.
In the U.S. Antarctic Program, summer support-staff members
have been terminated for alcohol abuse, and both summer and
winter-over staff are occasionally prohibited from purchasing
alcohol. In some cases, interventions with group support are
effective. At many Antarctic stations, alcohol is easily available
and may be subsidized. In some stations, rations can be excessive
or nonexistent. Observations are that at least 50% of recreational
injuries are alcohol related. Recommendations have called for
routine monitoring of alcohol levels of anyone involved in an
accident,116 or even prohibition of alcohol at Antarctic stations.
However, as with prohibition in other countries, this might create
more problems than it might solve. Judicious use of monitoring
can help identify persons who may need intervention before an
accident happens.
Psychoneuroimmunology
Psychological stress at research stations may arise from several
sources. One is the environment itself; environmental severity
has been found to be an independent predictor of hostility and
anxiety after wintering over.94 Perhaps more important is the
perception of the environment. Newcomers to the South Pole
station are usually observed wearing a full 12-kg (26.5-lb) polar
outfit at −20° C (−4° F) for several weeks after arrival. By midwin-
ter, the same individuals think little of walking short distances in
only workout shorts and a T-shirt at −60° (−76° F).
Stress can also result from disjunction between a person’s
original motivation for joining the program and the realities of
life in the station, that is, the sociocultural environment. This may
be the greatest determinant of difficulties.94 Studies suggest that
people who go to Antarctic stations to seek thrills or to challenge
themselves often have more difficulty sustaining their motivation
and performance than those who go to accomplish a scientific
mission or even those primarily motivated to earn money. In
CHAPTER 11  Polar Medicine
general, older individuals who are somewhat introverted are able
to set work goals and work toward them, and persons who have
broadly defined hobby interests seem to cope better with the
social isolation and dynamics of wintering over. One study found
that members with low social coherence reported significantly
more depression, anxiety, and anger than did individuals belong-
ing to expeditions with high social cohesion.92,134
SMALL-GROUP DYNAMICS
In addition to external climate and internal motivational factors,
stress can arise from interpersonal interactions. Although there
are many exceptions, participants in the Antarctic program often
speak of a tendency for personnel to form cliques or microcul-
tures. People may cluster according to ordinary personal chem-
istry, along lines of OAE (Old Antarctic Explorer) versus novice,
winter-over versus summer status, or according to scientific, civil-
ian, or military affiliation. With time, such social clusters can be
a source of support or of friction. In an attempt to unify the core
group, winter-overs participate in a mini–Outward Bound type
of group bonding experience before deployment.
Social isolation is an important factor in polar communities,
although this isolation has been lessened by modern communica-
tions and transportation. A number of studies have drawn paral-
lels between group processes in polar stations and those in other
isolated and confined environments, such as submarines or in
space. As space travel becomes a reality, studies on group selec-
tion, leadership style, and interaction between the isolated group
and headquarters take on urgency.36,66,97,135 Collaborative efforts
are being made between many stations and space agencies, in
particular the European Space Agency (ESA) and the NASA
program.112
Cross-cultural and cross-gender issues by research groups are
currently being studied at the international station, Concordia,
particularly as an analog for long-distance space missions.
Whereas in some areas cross-gender differences increase difficul-
ties, in others they are beneficial. Further studies on rigorous
selection criteria and training before deployment will avoid the
problems that have occurred with sexual harassment. It is thought
that the positive effect of better communication, less rude behav-
ior, and increased supportive environment outweigh the negative
effect. Other stations have already gone through this process.66,112
Winter-Over Syndrome
Stressors such as those mentioned previously can result in what
has been termed the winter-over syndrome. The historically oft-
mentioned “Big Eye” or “20-foot stare in a 10-foot room” seems
to be less common now, perhaps because the stations are
increasingly comfortable and have stimulating environments.
However, the constellation of depression, hostility, sleep distur-
bances, and impaired cognition still seems to be both common
and underreported.98,99,109 The winter-over syndrome is not a
static condition but a time- and individual-dependent process. At
the South Pole research station, for example, winter-over staff
characteristically report a recognizable pattern of fluctuating
activity and mood. There is often a mixture of relief, pride, and
fearful anticipation as the last LC-130 flight departs in mid-
February, followed by a period of frenetic activity to beat inven-
tory deadlines, file resupply orders, launch projects, and prepare
the station for winter. As work and recreation routines develop,
mood generally drops with the setting sun. A rise in mood occurs
toward sunrise but is followed with anticipation, increase in
anxiety, and stress as the arrival of the first return flight draws
near. Studies at the Australian stations of Mawson and Macquarie
Island suggest that the influx of new staff at station opening may
actually be associated with increased depression.
Seasonal Affective Disorder
A probable contributor to and confounder of the winter-over
syndrome is the apparently fairly consistent exacerbation of stress
and depression under conditions of winter or night, leading to
seasonal affective disorder (SAD). Subsyndromal SAD (S-SAD)
may be a better definition of what is experienced by many who
245
 winter-over in the dark latitudes.96 Further studies indicate that
S-SAD may be part of the T3 syndrome.99 Correlations with mela-
tonin levels have been shown to be associated with the frequent
sleep disturbances at higher latitudes, both with advanced or
delayed phases and with increased latency.6,133 In some studies,
melatonin’s chronobiotic properties are used to resynchronize
the individual’s sleep.6 Other studies have demonstrated the
effectiveness of light therapy in helping resynchronize the
body.133 SAD may be no more prevalent in Antarctica than at
lower latitudes; some of the depressive symptoms may well be
the result of social isolation or related to seasonal changes.100
Beneficial Effects of Isolation
An interesting point is that isolation may have positive as well
as negative effects.100 Isolation is not synonymous with loneliness
and depression, as Amundsen reported from his sojourn at Fram-
heim. In fact, a subset of “professional isolates” may actually
prefer polar stations to “normal” society.125 In some cases, reentry
and adaptation to the rest of the world can take up to 6 months.
The positive effect of isolation may be reflected in a 1992 study
of somatic complaints that compared U.S. Navy volunteers who
qualified for winter duty in Antarctica and wintered-over, with
those who were physically qualified but were assigned elsewhere
because of the limited number of winter assignments. Those who
spent the winter in Antarctica had fewer illnesses and hospitaliza-
tions after the winter-over period. These volunteers were fol-
lowed an average of 5.4 years after the winter period. It was also
noted that the complex psychophysiologic symptoms experi-
enced during the winter-over period were probably adaptive
COLD AND HEAT
coping mechanisms. Coping led to a process of negotiation
leading to compromise, which frequently led to finding new
strategies or resources that could be used for subsequent stress-
ful experiences. Newer studies confirm the salutogenic effect of
completing a long-term contract in an isolated environment.92,100
Screening and Selection
Based on the preceding findings, several attempts have been
made to refine the selection and screening processes for success-
PART 2
ful polar and space sojourners. It is not surprising that previous
successful polar experience seems to be among the best predic-
tors of subsequent high performance. Biographic data, peer
ratings, psychometric testing, and interviews all seem helpful in
selection, although each has weaknesses and inconsistencies.
Recent studies have suggested that team climate significantly
related to the perception of good leadership.115 More research
needs to be done to explore the characteristics and behaviors
that constitute effective leadership, in order to guide selection of
crew and leader.15,115 Early studies led to the tripartite “ability,
stability, compatibility” criteria for successful participation in the
Antarctic programs.38 This simple but useful scheme recognizes
that technical skill, emotional equilibrium, and interpersonal
skills all play important roles in an individual’s performance and
internal satisfaction. It would be desirable to improve measure-
ment and predictive usefulness of these factors; such studies
remain at the active frontier of Antarctic research.38
TOURISTS
The vast majority of tourists visit the Antarctic on ships around
the Peninsula. The International Association of Antarctic Tour
Operators has more than 100 members from 19 countries. A
wealth of information, guidance, and statistics about Antarctic
tourism is found on their website (www.iaato.org). Landing tour-
ists come on vessels carrying 6 to 500 passengers. There are some
larger ships (500 to 3000 passengers) that offer “cruise-by” sight-
seeing trips without landing. Visits usually take place at ice-free
coastal areas in the austral summer from November to March.
Landings of short duration (usually 1 to 3 hours) are made by
inflatable boat (Zodiac) and occasionally by helicopter. There are
currently three operators offering land-based trips. IAATO figures
show that in 2013-2014 there were 37,405 tourists by sea and
land.53 This is actually a reduction from the peak figure of 47,225
in 2007-2008 and results from the restrictions now placed on
larger vessels, although the figure is rising annually.
246
Tourist visitors can be broadly divided into two groups, “sight-
seeing” and “expedition/adventure sport.” Ship-based sightseers
make up approximately 98% of the visitor total. A very small
number travel to the continent itself, to visit, for example, the
South Pole or emperor penguin colonies. There is little if any
medical screening of ship-based tourists, and persons of all ages
may travel. The financial expense of these cruises means that
there is bias toward the older traveler who has accumulated
wealth and has the time to spend it. A recent paper showed that
more than half the respondents on an Antarctic cruise ship were
older than 50, and 25% were over 60.136
Medical facilities on board ship vary widely, as do the experi-
ence and competence of accompanying medical professionals.
The American College of Emergency Physicians published com-
prehensive guidelines to enhance medical care on board cruise
ships, including specific requirements for physicians, such as
3 years of postgraduate/postregistration experience in general
and emergency medicine. These are only guidelines and not
requirements.3a
The medical problems encountered mirror those found in an
urban setting, with additional risks of trauma (usually minor)
from, for example, falls in the unfamiliar environment.
The expedition/adventure sport group is primarily involved
in ski or mountaineering expeditions, with most professionally
guided. These visitors are generally a fitter and younger popula-
tion. In line with adventure sports worldwide, age and (lack of)
experience are bars to participation. Other visitors are involved
in sailing, kayaking, and scuba-diving trips. Some expeditions
deploy motorized vehicles. At Union Glacier in 2014, there were
two marathon and two ultramarathon running events.
MEDICAL PROBLEMS
Many medical problems of activity in the extreme cold, including
frostbite and hypothermia, are discussed elsewhere (see Chapters
6 through 10). Clinical entities particularly associated with polar
ski expeditions include polar thigh, skier’s thumb, and kite
skier’s toe.
Polar Thigh
The clinical picture of polar thigh in both genders is an erythema-
tous and frequently urticarial rash, predominantly on the anterior
thigh, although it can also be seen on the sides (particularly
medial) and back (Figures 11-16 and 11-17). If inadequately
treated, and if behavioral modifications and clothing adjustments
are not made, the rash progresses to frank ulceration. Despite
appearances, infection is rarely demonstrated when microbio-
logic samples are taken. The exact etiology is not known. We
believe that although cold may play a part, the main etiologic
factor is mechanical abrasion. The action of skiing drives the leg
into extension at the hip, and clothing is stretched over the leg.
The thighs also generate a great deal of heat when exercising.
Abrasion to the medial aspect is exacerbated in persons
with bulkier thighs. This causation theory is supported by the
FIGURE 11-16  Polar thigh. (Courtesy Ian Davis.)
 CHAPTER 11  Polar Medicine
FIGURE 11-19  Skier’s thumb.

thumb was exposed to the cold and wind at the top of the ski-
pole, away from the shared heat of the other digits enclosed in
a mitten. Skier’s thumb is not seen in persons who use “Pogies,”
which are neoprene and Velcro gloves (inspired by the handlebar
FIGURE 11-17  Polar thigh. mitts used by motorcycle and snowmobile drivers) fixed to the
ski pole that protect the whole hand (Figure 11-20).
observation that “polar thigh” is also seen where pulk (sledge)
pulling harnesses rub, and because it is not seen in the upper Kite Skier’s Toe
arm, which is exposed to the same temperature and winds and This condition is frostbite of the downwind hallux in kite skiers,
is likely to have the same clothing layers as the thighs. It is also as described in a 2013 case report114 (Figure 11-21).
neither seen in experienced skiers and guides nor reported in
the diaries of early explorers, who were meticulous in recording
details of their journey. These groups will have made suitable OVERVIEW AND FUTURE
adjustments to their clothing.
Polar thigh can be prevented by wearing long, silk shorts (or
DEVELOPMENTS
cut-off pajamas) and ensuring liberal use of an emollient or Aloe A point made early in this chapter is the challenge inherent
vera gel. In the early stages of the rash, there is usually good in meaningfully synthesizing Arctic and Antarctic medicine.
response to a topical corticosteroid cream (e.g., betamethasone
valerate 0.025% or 0.05%) combined with an emollient or Aloe
vera. If the skin breaks down, topical corticosteroids should not
be applied to ulcerated areas, which should be covered with a
hydrocolloid dressing. Granuflex is ideal (www.convatec.com).
Antibiotics are not routinely indicated. The key to management
is scrupulous wound care and dressing changes. Once out of the
field, a plastic surgery or burn unit may well be the appropriate
setting for severe cases (Figure 11-18).
Skier’s Thumb
Skier’s thumb does not refer to the ruptured ulnar collateral liga-
ment seen in skiers who fall while holding a skipole, but rather
refers to frostbite of the terminal phalanx of the thumb (Figure
11-19). This was often seen in returning expeditioners whose

FIGURE 11-18  Severe polar thigh. FIGURE 11-20  Pogies.

247

FIGURE 11-21  Kite skier’s toe.
Reflection on some of the issues raised previously suggests
several common areas of linkage and directions for future work.
ISSUES OF METHODOLOGY AND
MEDICAL EPISTEMOLOGY
The state of knowledge about the human factors involved in
living in the Antarctic is still rudimentary, although renewed
interest by NASA and ESA in Antarctica as a space analog has
COLD AND HEAT
led to increased research funding and should lead to better
information. Studies in polar settings are often handicapped by
extremely difficult research conditions and may never achieve
the statistical power and validity expected of counterparts in
more forgiving climes. Common methodologic problems most
notably include small sample sizes, unknown effect sizes, mea-
surement of proxy variables, and multiple confounders.
FOURTH WORLD MEDICAL DECISION MAKING
PART 2
Polar medical lore is replete with stories like that of Leonid
Rogozov, the physician of the sixth Soviet Antarctic Expedition
at Novolazarevskaya Station, who performed an appendectomy
on himself in April 1961 with assistance from the station mechanic
(Figure 11-22).111 Although the basic principles of emergency
medicine, epidemiology, occupational health, psychology, and
other disciplines still apply in polar settings, the spectrum of
health problems and some important aspects of their manage-
ment are undoubtedly skewed. However, with newer and
improved technical communication modalities and transporta-
tion, delivery of advanced care in the polar latitudes has improved,
and many lessons learned in Antarctica are applicable to space
exploration and settlement.
Fourth World medicine requires distillation of medical practice
into a compact yet comprehensive package that is sufficiently
FIGURE 11-22  Leonid Rogozov.
248
robust to travel well. Novel constraints and the inherently unpre-
dictable nature of a hostile environment further stretch the usual,
already tentative rules and thresholds of medical decision making.
Perhaps to a greater extent than in most settings, prevention and
preparation are paramount in polar medicine. As might be imag-
ined, cold and its effects on both humans and equipment exac-
erbate the risks from even minor mishaps, altitude impairs tissue
oxygenation and wound healing, and bulky clothing restricts
dexterity and vision. Isolation from medical facilities exerts a
multiplier effect on these risks. Patient extrication and resuscita-
tion that would be routine in most urban or suburban settings
present overwhelming challenges in polar settings.106
With lives at stake, arguments have been made for planning
for worst-case scenarios rather than only for likely situations.116
On the other hand, a realistic balance point on the cost-versus-
utility curve, based on estimated risks, must be set for each situ-
ation. Given existing fiscal and logistic constraints, preventive
measures should take priority over higher-cost options.9
A recurrent medical issue in polar stations involves con­
tingency planning and the optimal level of inventory. This ques-
tion applies equally to drugs, equipment, training, and personnel
and is faced immediately by any incoming physician. “Just
in time” principles of inventory management are unlikely to be
appropriate.9,116
Combined improvements in communications systems, the
Internet, and the powerful tool of telemedicine with its many
modalities have transformed what was once an extremely iso-
lated practice of medicine. The advantages of rapid access to
organized databases and remote consultations for radiology and
other specialties via video are realities. Telemedicine is in place
and functioning in many northern Arctic regions. The Australian,
British, Italian, and U.S. Antarctic Programs and many others have
been using it successfully for a number of years.36,59,67,108 Physi-
ologic, psychological, and occupational health data can be moni-
tored or retrieved, ultimately linking geography and information
flow and allowing almost real-time consultation and guidance
from multiple specialists. These promising tools are real solutions
to the problems of isolation faced by earlier physicians.
USE OF FROZEN MEDICATIONS
Although the medical literature is relatively sparse on the use of
frozen drugs, there is a useful consensus document from the
Union of International Alpine Associations (UIAA).23 Notable
points are that glass ampoules may have microscopic cracks
when frozen, and that drugs (e.g., insulin) that contain protein
or any emulsion should not be used once frozen. They will
degrade, and the products could cause a pulmonary embolus.
Morphine is a useful drug not covered in this guidance, although
it has been used to good effect in our experience after multiple
freeze-thaw cycles. A BAS study found that most medications
remained stable, even after multiple freeze-thaw cycles.107a The
exception was hydrocortisone cream, although the investigator
also recommended against subjecting eye medications to tem-
perature extremes. Medical devices, such as IV cannulas, worked
normally after rewarming, as did all forms of tape and dressings.
Frozen IV fluids expanded when frozen, may perforate the bags,
and thus leak when rewarmed.
ACKNOWLEDGMENTS
The authors would like to acknowledge Betty Carlisle, Lesley J.
Ogden, Ian Davis, and Kenneth V. Iserson for their excellent work
on this chapter in the previous edition, on which the current
chapter is based. Special thanks to Kenneth H. Willer, MLS,
Manager–Library Services, Samaritan Health Services, Corvallis,
Oregon, kwiller@samhealth.org.
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 CHAPTER 12 
Pathophysiology of
Heat-Related Illnesses
LISA R. LEON AND ROBERT W. KENEFICK*
Heat illnesses exist along a continuum, transitioning from heat
exhaustion to heat injury and the life-threatening condition of
heatstroke. Environmental heat exposure is one of the most
deadly natural hazards in the United States, with about 200 heat-
stroke deaths per year. The majority of heatstroke deaths are
observed in the very young and elderly populations during
annual heat waves, whereas fit, young athletes typically succumb
to heatstroke during strenuous exertion in hot or temperate
environments. Multiorgan system failure is the ultimate cause of
heatstroke death as a result of complex interplay among the
physiologic and environmental factors that compromise an indi-
vidual’s ability to respond adequately to heat stress. The patho-
physiology of heatstroke is thought to be caused by a systemic
inflammatory response to endotoxin leakage across ischemic,
damaged gut membranes, although our understanding of the
mechanisms causing morbidity and mortality remains limited.
This chapter provides an overview of the pathophysiologic
responses observed in patients and experimental animal models
at the time of heatstroke collapse and during long-term recovery.
A brief discussion is provided on current clinical heatstroke treat-
ments as well as promising avenues of research that may aid in
the development of more effective interventions and treatments
to prevent this debilitating illness.
HEAT STRESS AND
THERMOREGULATION
FOUR AVENUES OF HEAT EXCHANGE
Mammals and other homeotherms are capable of maintaining
body temperature within a fairly narrow range, approximately
35° to 41° C (95° to 105.8° F), despite large fluctuations in envi-
ronmental temperature. Environmental variables that have the
largest impact on heat exchange are temperature; humidity;
radiation from the air, water, or land; and air or water motion.98
To maintain stable body temperature, organisms rely on four
avenues of heat exchange: conduction, convection, radiation,
and evaporation.
Dry heat exchange is achieved by conduction, convection,
and radiation. Effectiveness of these mechanisms depends on
differences between the skin and environmental temperature.
Dry heat loss occurs when skin temperature exceeds that of the
environment, and dry heat gain occurs when environmental
temperature exceeds that of the body. Conduction occurs when
the body surface is in direct contact with a solid object and
depends on thermal conductivity of the object and the amount
of surface area in contact with the object. Conduction is typically
an ineffective mechanism of heat exchange because of behavioral
adjustments that minimize contact with an object. For example,
wearing shoes is an effective behavioral adjustment that mini-
mizes conduction of heat from a hot or cold surface (e.g., desert
sand to the foot). Within the body, conductive heat transfer
*The opinions or assertions in this chapter are the primary views of the
authors and are not to be construed as official or reflecting the views of
the U.S. Army or Department of Defense. Any citations or trade names
do not constitute an official endorsement of approval of the products or
services or these organizations.
occurs between tissues in direct contact with one another but is
limited by poor conductivity of the tissues. For example, subcu-
taneous fat has approximately 60% lower conductivity than the
dermis and impedes conductive heat loss.329 Convection is a
mechanism of dry heat transfer that occurs as air or water moves
over the skin surface. The windchill index is an example of the
convective cooling effect of wind velocity. The rate of convective
heat transfer depends on the temperature gradient between the
body and environment, thermal currents, bodily movements, and
body surface area exposed to the environment, which can vary
dramatically with different clothing ensembles. Within the body,
convective heat transfer occurs between blood vessels and tissues
and is most efficient at the capillary beds, which are thin-walled
and provide a large surface area for heat exchange. Radiative
heat transfer is electromagnetic energy exchanged between the
body and surrounding objects and occurs independently of air
velocity or temperature. Radiation is effective even when air
temperature is below that of the body. All objects within our
environment absorb and emit thermal radiation, but clothing can
reduce radiant heat impinging on the skin from various environ-
mental sources.
Evaporation represents a major avenue of heat loss when
environmental temperature is equal to or above skin temperature
or when body temperature is increased by vigorous physical
activity. In humans, evaporative cooling is achieved as sweat is
vaporized and removes heat from the skin surface, with approxi-
mately 580 kilocalories (kcal) of heat lost for each liter (L) of
evaporated sweat.104 The most important environmental variables
affecting evaporative cooling are ambient humidity and wind
velocity. Sweat is converted to water vapor and readily evapo-
rates from the skin in dry air with wind, whereas the conversion
of sweat to water vapor is limited in still or moist air. If sweat
accumulates and fails to evaporate, sweat secretion is inhibited
and the cooling benefit is negated. Small mammals, such as
rodents, do not possess sweat glands but achieve evaporative
cooling by grooming nonfurred and highly vascularized skin
surfaces, such as the ears, paw pads, and tail, with saliva that
evaporates in a manner similar to that of sweat in humans.114,295
BODY TEMPERATURE CONTROL
Regulation of a relatively constant internal temperature is critical
for normal physiologic functioning of tissues and cells. For
example, membrane fluidity, electrical conductance, and enzyme
functions are most efficient within a narrow temperature range.
By convention, thermal physiologists describe body temperature
control with a two-compartment model that consists of an inter-
nal core (viscera and brain) and an outer shell (subcutaneous fat
and skin) (Figure 12-1).81
The skin is the final barrier between the body and the envi-
ronment and functions as a conductive pathway for heat transfer,
while also serving as the primary site to sense changes in envi-
ronmental temperature. Skin temperature may fluctuate because
of changes in environmental temperature, relative humidity, wind
velocity, and radiation. Heat transfer mechanisms are evoked in
response to changes in body heat storage (S), which depends
on metabolic rate, work, and the four avenues of heat exchange,
as follows:
S = M − ( W ) − ( E) − (C) − ( K ) − ( R )
249

37° C 36° C 37° C
Core 32° C Core
Shell
28° C
34° C
31° C
COLD AND HEAT
Cold Warm
FIGURE 12-1  Distribution of temperatures within the human body into
core and shell during exposure to cold and warm environments. The
temperatures of the surface and thickness of the shell depend on the
environmental temperature: the shell is thicker in the cold and thinner
in the heat. (From Elizondo RS: Human adaptation to hot environ-
ments. In Rhoades RA, Pflanger RG, editors: Human physiology, ed 3,
Philadelphia, 1996, Saunders. Reprinted with permission of Brooks/
Cole, a division of Thomson Learning.)
PART 2
where M is metabolic rate, W is work, and E, C, K, and R are
evaporative, convective, conductive, and radiant heat transfer,
respectively.141 The impact of the four avenues of heat exchange
on total body storage depends on a variety of organismal (e.g.,
age, gender, adiposity), environmental (e.g., humidity, wind
velocity), and occupational (e.g., protective clothing, work inten-
sity) variables. Under conditions in which heat production and/
or heat gain exceeds heat loss, such as during exercise or heat
exposure, positive heat storage occurs (S >0) and body tempera-
ture increases. When heat loss exceeds heat production and/or
heat gain, such as during prolonged cold exposure, negative heat
storage occurs (S <0) and body temperature decreases.98
Endothermic animals use both autonomic and behavioral
thermoeffector mechanisms to regulate body temperature.
Autonomic thermoeffector responses are often referred to as
“involuntary” and include sweating, vasodilation, vasoconstric-
tion, piloerection (furred mammals), shivering, and nonshivering
thermogenesis (brown fat heat production). Behavioral thermo­
effector mechanisms are considered “voluntary” and include
clothing changes, use of heat or air-conditioning systems, hud-
dling or use of blankets, fan cooling, and seeking of shade or
shelter. Rather than working independently of one another, auto-
nomic and behavioral thermoeffector mechanisms typically func-
tion in concert to maintain temperature control. For example,
evaporative cooling in rodents requires autonomic stimulation of
salivation and behavioral spreading of saliva onto nonfurred
surfaces.114,295 Many large species in the wild use natural water
sources to facilitate cooling. Elephants spray water onto their skin
surface, and hippopotami and other species are often observed
near or in watering holes. Water is a more effective medium to
facilitate convective heat transfer because of its high heat transfer
coefficient, approximately 25 times greater than air,308 even if the
water temperature is tepid. However, voluntary suppression of
behavioral mechanisms of cooling in humans can increase the
250
risk for thermal injury. This is illustrated by older adults who
refuse to use air-conditioning systems or leave their residences
during heat waves, and highly motivated athletes and military
personnel who voluntarily dehydrate and sustain a high rate of
work in hot weather.
Regulation of body temperature is best conceptualized as a
negative feedback system consisting of sensors, integrators, and
effectors. In vertebrates, neurons in the skin, spinal cord, and
abdomen sense thermal stimuli and convert those signals to
action potentials that are transmitted by afferent sensory neurons
to the preoptic area of the anterior hypothalamus (POAH). The
POAH is considered the main central nervous system (CNS) site
for thermoregulatory control because it receives and integrates
synaptic afferent inputs and evokes corrective autonomic and
behavioral thermoeffector responses for body temperature
regulation.38 This negative feedback loop is diagrammed in
Figure 12-2.
The concept of a temperature set point was developed as a
theoretical framework to examine regulated and unregulated
changes in body temperature.28 The temperature set point is
analogous to a thermostat that controls a mechanical heating
device; under homeostatic conditions, body temperature is
approximately equal and oscillates around the temperature set
point. Environmental perturbations, such as heat and exercise,
cause body temperature to deviate from the set-point tempera-
ture as heat gain and/or production exceeds heat loss and the
organism becomes hyperthermic (S >0). During prolonged cold
exposure, heat loss exceeds heat gain and/or production and the
organism becomes hypothermic (S <0) (Figure 12-3).
Heat stress Exercise
↑ Temperature
Heat gain/production > heat loss
∆S>0
Thermal receptors
(skin, spinal cord, abdomen)
Sensory afferent
signals
Preoptic anterior hypothalamus (POAH)
Thermoregulatory Integration Center
Motor efferent
signals
Behavioral and autonomic thermoeffectors
Heat loss > heat gain/production
↓ Total body heat storage
FIGURE 12-2  Diagrammatic representation of the negative feedback
pathway regulating core temperature in homeotherms. Climatic heat
stress and exercise (metabolic work) cause heat gain/heat production
to exceed heat loss (ΔS >0) and increase body temperature above
baseline. Increase in total body heat storage is sensed by thermal
receptors in the skin, spinal cord, and abdomen, which transmit action
potentials via sensory afferent nerves to the preoptic area of the ante-
rior hypothalamus (POAH). The POAH receives and integrates synaptic
afferent inputs and evokes corrective behavioral (e.g., fanning, removal
of clothing) and autonomic (e.g., vasodilation, sweating) thermoeffec-
tor responses to decrease total body heat storage and return body
temperature to baseline. Solid line indicates stimulatory pathway;
dashed line indicates inhibitory pathway.

HYPERTHERMIA
HP = HL HG/HP > HL HL > HG/HP HP = HL
Tset
Tc Heat stress, exercise
FEVER
HP = HL HC/HP > HL HP = HL HL > HC/HP
Tset
Tc Infection, inflammation
FIGURE 12-3  Theoretical concept of core temperature (Tc) changes
mediated by a change in the temperature set point (Tset). Hyperthermia
represents an increase in Tc in the absence of a change in Tset. In
response to climatic heat stress, exercise, or the combination of these
factors, heat gain (HG) and/or heat production (HP) exceed heat loss
(HL) and Tc rises above Tset as the organism becomes hyperthermic. In
response to removal from the heat, cooling, or cessation of exercise,
HL exceeds HG/HP and Tc returns to baseline. Fever is defined as a
regulated increase in body temperature that is actively established and
defended by behavioral and autonomic thermoeffector responses that
increase heat conservation (HC) and/or HG, and decrease HL, to
increase Tc to a new elevated level. The rising phase of fever is associ-
ated with shivering (increases HP) and the donning of blankets
(increases HC). The individual feels “cold” until a new elevated level of
Tc is attained. Note that while fever is maintained, Tc oscillates around
Tset and the individual is considered normothermic with HP = HL. Once
fever breaks, HL exceeds HC/HP as the individual sweats, removes
clothing, and so forth, to return Tc to the baseline level.
Regulated increases and decreases in the temperature set
point are referred to as fever and regulated hypothermia (also
called anapyrexia), respectively, and are protective immune
responses to infection, inflammation, or trauma. Fever is defined
as a regulated increase in the temperature set point and is actively
established and defended by heat-producing (e.g., shivering and
nonshivering thermogenesis) and heat-conserving (e.g., periph-
eral vasoconstriction, huddling to reduce exposed body surface
area) thermoeffectors (Figure 12-3).141 An individual is considered
normothermic (S = 0) once fever is established and body tem-
perature oscillates around the new, elevated temperature set
point. The highly regulated nature of fever was first suggested
by Liebermeister in the 1800s when it was observed that individu-
als actively reestablished an increase in body temperature after
experimental warming or cooling.185,287 Fever is a protective
immune response used by invertebrates, fish, amphibians, rep-
tiles, and mammals to survive infection or injury.163 The protective
effects of fever are mediated by increased mobility and activity
of white blood cells,215,308 increased production of interferon (IFN;
antiviral and antibacterial agent) antibodies,75 and reduced plasma
iron concentrations; all these effects inhibit the growth of patho-
gens.98,160 In mammals, inhibition of fever with nonsteroidal anti-
inflammatory drugs (NSAIDs; e.g., aspirin) increases mortality
from bacterial and viral infections, emphasizing the importance
of fever as an immune response.134,310
Many species exploit regulated hypothermia as a means of
CHAPTER 12  Pathophysiology of Heat-Related Illnesses
surviving severe environmental insults. Regulated hypothermia is
elicited in response to a decrease in the temperature set point
and is actively established and defended by behavioral and auto-
nomic heat loss mechanisms.137 The Q10 effect states that each
10° C (18° F) change in body temperature is associated with a
twofold to threefold change in enzymatic reaction rates. Based
on this relationship, a regulated decrease in body temperature is
thought to protect against injury and inflammation by reducing
production of reactive oxygen species that compromise tissue
function under conditions of low oxygen supply. In bumblebees,
infected worker bees spend significantly more time in cooler
temperatures outside the nest than healthy worker bees; this
cold-seeking behavior is associated with increased survival from
parasitic infection.128 Mice inoculated with influenza virus also
show cold-seeking behavior and develop regulated hypothermia,
which is associated with improved infection outcome.162 Other
environmental insults that induce regulated hypothermia in small
rodents include hypoglycemia,43,109 hypoxia,199,255 hemorrhage,129
dehydration,138 infection,162,181,260 and heatstroke.180
Mechanisms of Heat Dissipation during Thermal Stress
Cardiovascular mechanisms have evolved to shunt warm blood
from the body core to the skin surface to facilitate an increase
in heat loss during thermal stress. Arteriovenous anastomoses
(AVAs) are collateral connections between adjacent blood vessels
that increase the volume of blood delivered to a particular tissue.
Mean skin blood flow can vary approximately 10-fold in humans,
depending on the thermal environment. The hands and feet are
concentrated with AVAs that serve as effective areas for dry heat
loss. The nonfurred surfaces of small rodents, such as the ears,
tail, and paw pads, also have an abundance of AVAs and a large
surface area to facilitate convective heat transfer.101 During exer-
cise heat stress, increased blood flow to the skin surface is
accompanied by sweat secretion. The density, secretion rate, and
activation threshold of regional sweat glands determine the
volume of sweat loss at a body site. In humans, the back and
chest have the highest sweat rates for a given body temperature
change, whereas only about 25% of total sweat is produced by
the lower limbs.218 Additional factors affecting sweat rate include
clothing characteristics, environmental conditions, and rate of
metabolic heat production. Panting is an effective method of
evaporative heat dissipation in animals, such as birds, dogs,
sheep, and rabbits, and occurs at a resonant ventilation frequency
that requires minimal energy expenditure.116,261 Humans and
rodents do not pant, but breathing frequency and minute volume
increase during severe heat exposure to facilitate evaporative
cooling from the respiratory surfaces. In humans, the contribution
of respiratory evaporative cooling is small compared with skin
evaporative cooling (Figure 12-4).
DEHYDRATION AND ELECTROLYTE IMBALANCE
Water requirements during heat exposure are primarily deter-
mined by a person’s sweat losses. Water depletion dehydration
develops when the rate of water replacement is not adequate,
which can result from a mismatch between fluid intake and
sweat loss, lack of water availability, or use of diuretic medica-
tions. Sweat rates may range from 0.3 to about 3 L/hr during
athletic or occupational activities, depending on the environmen-
tal conditions and type, duration, and intensity of work.57,150 If
high sweat rates are maintained without adequate replenishment
of lost water, this can cause electrolyte imbalances that impede
the efficiency of autonomic mechanisms of thermoregulatory
control. For example, hyperosmolarity alters heat responsiveness
of warm-sensitive neurons in the POAH and limits the effective-
ness of evaporative heat loss.303,304,335 Severe hypernatremic
dehydration is associated with brain edema, intracranial hemor-
rhage, hemorrhagic infarcts, and permanent brain damage
(Figure 12-5).214
Severe reductions in electrolytes can have a profound impact
on heatstroke outcome. Symptomatic hyponatremia (decreased
serum sodium concentration) is a relatively rare condition but
has been observed during marathon running and military training
251

A 12-1). Heat cramps are often mistaken as a form of heat illness
COLD AND HEAT
PART 2
B hot environments and may progress to a moderately severe con-
C Heat injury is a more recent classification of heat illness char-
FIGURE 12-4  Infrared images of various surface regions; the brighter
the color, the warmer the surface temperature. A, Female runner after
45 minutes of exercise in a 23° C (73.4° F) environment. Note that the
palms of the hands and the face are substantially warmer than the rest
of the body surface. B, Two polar bears. Note that only the snout,
eyes, ears, and footpads are noticeably different from the surround-
ings. C, Sled dog relaxing shortly after completing the 17.7-km (11-
mile) ceremonial starting leg of the 2005 Iditarod Trail Sled Dog Race.
The course of the Iditarod is greater than 1850.7 km (1150 miles) from
Anchorage to Nome, Alaska. Ambient conditions were 0° C (32° F),
with a lightly overcast sky and no wind. The infrared shot shows that
the dog’s entire snout is white, meaning it is the hottest part of the
body surface. The armpits and ears also are warmer. This may explain
why dogs roll around in the snow, face first, on a warm day. (A and B
from Grahn D, Heller HC: The physiology of mammalian temperature
homeostasis, Trauma Care 14:52, 2004, with permission; C courtesy D.
Grahn; photo by Matthew Grahn.)
252
due to overconsumption of hypotonic fluids without adequate
replacement of sodium losses.214,227 Hyponatremia is associated
with intracellular swelling that can lead to CNS dysfunction.
Hypokalemia (decreased serum potassium concentration) may
be caused by overproduction of aldosterone, excessive sweating,
or respiratory alkalosis. Any cause of overproduction of urine
(polyuria) potentially causes urinary potassium loss. Potassium is
a potent vasodilator of blood vessels to the skeletal and cardiac
muscles. Excessive loss of this electrolyte can have detrimental
effects, such as decreased sweat volume, cardiovascular instabil-
ity, and reductions in muscle blood flow that predispose to
skeletal muscle injury (i.e., rhabdomyolysis).164,278
HEAT ILLNESSES
Heat illnesses are best viewed as existing along a continuum
transitioning from the mild condition of heat exhaustion to heat
injury and the life-threatening condition of heatstroke (Table
because they occur during or in response to physical activity in
warm environments. However, the muscle soreness associated
with heat cramps is transient and rapidly resolves with no per-
manent disability, so this condition is not regarded as a true heat
illness. Cramps may be recurrent but are typically confined to
the skeletal muscles that are involved in vigorous exercise in the
heat. Skeletal muscle spasms in the extremities may be sporadic
but are painful and develop most frequently in persons who are
not acclimatized to physical exertion. However, heat cramps may
also occur in fit athletes who are salt depleted. Although their
cause is not fully understood, heat cramps are thought to occur
in response to increased intracellular calcium release that stimu-
lates actin-myosin filaments and muscle contraction. Current
treatments include rest and replacement of electrolytes with fluids
or salted food. Salt tablets should be avoided because they can
cause gastrointestinal irritation and may stimulate excess potas-
sium loss in the distal tubules of the kidneys.
Heat exhaustion is characterized by elevation in body tem-
perature and the potential for collapse because of an inability to
maintain adequate cardiac output.333 The signs and symptoms of
heat exhaustion include fatigue, dizziness, headache, nausea,
vomiting, malaise, hypotension, and tachycardia with possible
collapse. Heat exhaustion can occur with or without exercise in
dition without associated organ damage. Heat exhaustion is often
observed in older adults as a result of medications (e.g., diuret-
ics), inadequate water intake that leads to dehydration, or pre-
existing cardiovascular insufficiency that predisposes to collapse.
Treatment should consist of placing the individual in a recumbent
position in a cool environment to normalize blood pressure. Oral
fluid ingestion with electrolytes is often adequate for recovery,
whereas intravenous (IV) fluid administration may be warranted
in severely dehydrated individuals.
acterized by an elevation in body temperature in the presence
of organ (e.g., kidney, liver) or tissue (e.g., gut, skeletal muscle)
dysfunction that resolves with proper treatment.333 Heat injury
may be difficult to distinguish from heat exhaustion during the
early time course of heat exposure and can progress to heatstroke
if not properly diagnosed and treated. A lack of mental status
changes distinguishes heat injury from heatstroke. Rapid cooling
is the most effective treatment because the reduction in body
temperature mitigates organ injury, although it does not prevent
dysfunction in all victims.
Heatstroke is clinically recognized by a triad of symptoms that
include (1) a severe elevation in body temperature (typically, but
not always, >40° C [104° F]); (2) CNS dysfunction that may include
combativeness, delirium, seizures, and coma; and (3) a history
of exposure to hot and humid weather or vigorous physical exer-
tion.333 The onset of heatstroke may be gradual (over hours or
sometimes days) with nonspecific symptoms that are similar to
heat exhaustion (e.g., weakness, dizziness, nausea, headache)
but may also occur rapidly with no warning signs. CNS dysfunc-
tion is the hallmark clinical sign of heatstroke that requires
immediate medical intervention to prevent permanent neurologic
 CHAPTER 12  Pathophysiology of Heat-Related Illnesses
100 100
r = 0.53 r = −0.76

Change in sweating rate (g·m−2·h−1)

Change in sweating rate (g·m−2·h−1)
0 0

−100 −100

−200 −200

−300 −300

−30 −20 −10 0 15 −4 −2 0 2 4 6 8 10

Change in plasma volume (%) Change in osmolarity (%)

FIGURE 12-5  Effect of reduced plasma volume or increased osmolality on the sweat rates of six individuals.
(Modified from Sawka MN, Young AJ, Francesconi RP, et al: Thermoregulatory and blood responses during
exercise at graded hypohydration levels, J Appl Physiol 59:1394, 1985.)

damage. However, CNS dysfunction is not the sole determinant
of heatstroke severity; injury to the gut, kidney, lung, spleen,
liver, and skeletal muscle (specific to exertion) often occurs
within days or weeks of clinical presentation.
Heatstroke may be classified as “classic” or “exertional”
depending on the etiology of the condition. Classic heatstroke is
observed in very young or elderly persons who are often immu-
nocompromised before heat exposure and experience high mor-
tality during annual summer heat waves. Classic heatstroke
occurs at rest during exposure to high environmental tempera-
ture, with patients often presenting with hot, dry skin caused by
failure of the normal sweating response (e.g., anhydrosis). Up to
60% of patients with classic heatstroke are hospitalized or found
dead within 1 day of the reported onset of illness, underlying
the life-threatening nature of this condition.145 Several intrinsic
factors may predispose infants to heatstroke death, including
increased surface area–to–body mass ratio (accelerates heat
gain), limited effective mechanisms of thermoregulation (e.g.,
suppressed behavioral adjustments), increased risk for dehydra-
tion (e.g., lack of water availability), and preexisting respiratory
infections. On the other hand, older individuals have preexisting
conditions, such as mental illness, prescription drug use (e.g.,
diuretics, anticholinergics), or infections, that predispose to
passive heatstroke10,69,315 (Box 12-1).
Exertional heatstroke (EHS) occurs primarily in young, physi-
cally fit individuals who collapse during exercise from heat
stress.333 Physical effort unmatched to physical fitness is a signifi-
cant risk factor for EHS.256 Anhydrosis is an uncommon finding
in these patients; rather, continuation of sweating after cessation
of exercise facilitates spontaneously cooling of EHS patients after
collapse. Behavioral influences may increase the risk for EHS;
highly motivated individuals may ignore the physiologic signs of

TABLE 12-1  Heat Illness Symptoms and Management

Condition Symptoms Management

Heat cramps Brief, painful skeletal muscle spasms
Heat rash (miliaria rubra) Blocked eccrine sweat glands
Heat exhaustion Mild to moderate illness with inability to sustain
cardiac output; moderate (>38.5° C [101.3° F])
to high (>40° C [104° F]) body temperature;
often accompanied by dehydration
Heatstroke Profound CNS abnormalities (agitation, delirium,
stupor, coma) with severe hyperthermia (>40° C
[104° F])
Rest; replacement of electrolytes; avoid salt tablets.
Cool, dry affected skin area; topical corticosteroids, aspirin
Move supine individual to cool, shaded environment, and
elevate legs; loosen or remove clothing, and actively
cool skin; administer oral fluids.
Ensure an open airway, and move to a cool environment.
Immediately cool to <39° C (102.2° F) using ice packs,
water bath, wetting with water and continuous fanning;
IV fluid administration; reestablish normal CNS function;
avoid antipyretics or drugs with liver toxicity.

Data from Bouchama A, Knochel JP: Heat stroke. N Engl J Med 346:1978, 2002; and Winkenwerder W, Sawka MN: Disorders due to heat and cold. In Goldman L,
Ausiello DA, Arend W, et al, editors: Cecil textbook of medicine, ed 23, Philadelphia, 2007, Saunders, pp 763-767.
CNS, Central nervous system; IV, intravenous.

253
 BOX 12-1  Predisposing Risk Factors for Serious
Heat Illness
Environmental Factors
High ambient temperature
High humidity
Lack of air movement
Trees and shrubbery
Access to air-conditioning
Lack of shelter
Heat wave (≥3 days of temperatures >32.2° C [90° F])
Individual Factors
Age (small children, older adults)
Obesity
Poor physical fitness level
Lack of acclimatization
Dehydration
Drug Use
Diuretics
Anticholinergics (e.g., atropine)
β-Adrenergic blockers (e.g., propranolol)
Antihistamines
Amphetamines (e.g., Ecstasy)
Ergogenic aids (e.g., ephedra)
Antidepressants
Alcohol consumption
Compromised Health Status
Viral infection (e.g., pneumonia, mononucleosis)
COLD AND HEAT
Inflammation (e.g., fever)
Skin disorders (e.g., miliaria rubra, burns)
Cardiovascular disease
Diabetes mellitus
Malignant hyperthermia
Sickle cell trait
fatigue that would normally cause them to stop exercising.2 EHS
PART 2
may occur in temperate conditions because of high physical
demand or clothing that inhibits cooling (e.g., firefighter uni-
forms). Mortality from EHS is relatively low (~3% to 5%) com-
pared with classic heatstroke (~10% to 65%), which is likely a
consequence of preexisting medical conditions and chronic use
of medications in the classic form that increase thermoregulatory
and cardiovascular strain.49,281,284,286
COMPENSABLE VERSUS UNCOMPENSABLE
HEAT STRESS
Heat stress refers to conditions that increase body temperature,
whereas heat strain refers to the physiologic consequences of
heat exposure. Heat stress is typically described as compensable
heat stress (CHS) or uncompensable heat stress (UCHS), with
both these conditions affected by biophysical (environment,
clothing) as well as biologic (hydration status, acclimatization)
factors. CHS occurs when the rate of heat loss maintains balance
with heat production, and steady-state body temperature can be
sustained during physical activity or heat exposure. A physically
fit individual wearing light clothing while exercising in moderate
heat and low humidity would typically experience CHS. Under
these conditions, elevated body temperature (<40° C [104° F]) can
be sustained for a relatively long period until dehydration or
energy depletion occurs.
Uncompensable heat stress is a consequence of an individu-
al’s evaporative cooling requirements being ineffective because
of environmental or other conditions that impede cooling. For
example, an individual wearing heavy protective clothing while
exercising in a hot, humid environment would be expected to
experience UCHS. Under UCHS conditions, body temperature
will increase to the point of exhaustion. Even for individuals at
low risk for UCHS, the physiologic demands for increased heat
dissipation during prolonged exercise and heat stress cannot be
endured indefinitely and often lead to circulatory insufficiency
and collapse at relatively mild temperatures.
254
HEATSTROKE EPIDEMIOLOGY AND
RISK FACTORS
The ability to perform strenuous work in a hot environment is
inversely related to the heat stress level, which can be assessed
using the wet bulb globe temperature (WBGT) index. The WBGT
for indoor or outdoor environments is determined as follows:
Indoor WBGT = 0.7 Tw + 0.3 Tamb
Outdoor WBGT = 0.7 Tw + 0.2Tbg + 0.1Tamb
where Tw is the natural wet bulb temperature, Tbg is the black
globe temperature, and Tamb is the dry bulb temperature. Tbg
determines the radiant heat load with a specialized thermometer
that is surrounded by a 15-cm (6-inch)–diameter blackened
sphere. The WBGT is the most widely used index to determine
safe limits of physical activity and establish strategies that will
minimize the incidence of heat illness during military, athletic,
or occupational tasks. The WBGT index does not take into con-
sideration different clothing ensembles or exercise intensities, so
the most practical and safe application of this measurement
requires adjustment for these factors.
Heat waves are defined as three or more consecutive days
during which the environmental temperature exceeds 32.2° C
(90° F).50 In summer 2003, Europe experienced 22,000 to 45,000
heat-related deaths during a 2-week period in which the average
temperature was 3.5° C (6.3° F) above normal.59,274 The European
continent has experienced an increase in minimum daily tem-
peratures over the last 30 years, and this trend will likely increase
if average global temperatures continue to rise. A 1.4° to 5.8° C
(2.5° to 10.4° F) increase in minimum daily temperatures in
Europe is predicted over the next century.59 Most prediction
models suggest more severe and longer-duration heat waves,
suggesting that the incidence of heatstroke will increase in future
decades. Predictions based on climate variability data from the
1995 Chicago and 2003 Europe heat waves suggest that by 2090,
heat waves in these cities will be 25% to 31% more frequent and
last 3 to 4 days longer.204 Another prediction model suggests a
253% increase in annual heatstroke deaths in the United Kingdom
by 2050.74
The impact of climate change is not equally distributed across
the globe because of regional variability in thermal tolerance that
influences the incidence of heatstroke mortality. A study of
11 U.S. cities showed that threshold temperatures for heatstroke
mortality are higher in warmer southern cities than in cooler
northern cities.63 A comparison of temperature-mortality relation-
ships in southern Finland, southeastern New England, and North
Carolina indicated that lower temperature thresholds in cooler
climates are coupled with steeper temperature-mortality relation-
ships.73 Similarly, the upper safety limit of environmental tem-
peratures in The Netherlands, London, and Taiwan are 16.5°, 19°,
and 29° C (61.7°, 66.2°, 84.2° F), respectively.193 A case study of
15 Marine Corps recruits who collapsed from heatstroke during
training exercises in South Carolina showed that 73% previously
resided in northern states and that 60% of cases occurred during
the second week of training during the hottest summer months.229
From 1980 to 2002, the highest EHS incidence in military recruits
was in unacclimatized individuals from northern, cold-climate
states who were enlisted for less than 12 months.49 During July,
many regions of the world have a WBGT index that is greater
than 29° C (84.2° F), and military training often occurs in environ-
ments with a WBGT index that is greater than 35° C (95° F).
During peacetime exercises, approximately 25% of fatal military
EHS cases occur during the hottest summer months in recruits
who have been in training camp less than 2 weeks.197 Individuals
from northern states are expected to be less acclimatized to hot,
humid summer conditions than those from southern states. Heat
acclimatization improves thermotolerance but requires several
days to weeks of exposure to similar heat stress and exercise
conditions to be fully effective. This likely accounts for hot days
early in the summer showing a greater impact on heatstroke
morbidity and mortality than those cases occurring later in the
training process, after the protective effects of heat acclimatiza-
tion have been realized.115
 Humanity’s impact on the landscape in conjunction with
increased production of greenhouse gases may be creating the
largest climate change. Urban heat islands are created in cities
when vegetation is removed and blacktop roads and concrete
buildings are erected. Temperatures may be 30° to 40° C (54° to
72° F) higher on asphalt roads and rooftops compared with those
of the surrounding air.95 Since 1978, urban sprawl has accounted
for an increase in city temperatures in southeastern Asia of
approximately 0.05° C (0.09° F) per decade.147 Across the entire
land mass of the United States, the surface temperature has
increased approximately 0.27° C (0.49° F) per century because of
changes in the land cover arising from agricultural and urban
development.147 Concrete and asphalt surfaces cool slowly at
night when air temperature decreases, and this increase in urban
heat storage magnifies the intensity of heat exposure experienced
by individuals living in concrete urban structures.57,171
Several social factors predispose older adults to heatstroke
mortality, including living alone, inability or unwillingness to
leave one’s home, residing on the top floor of buildings (heat
rises), and annual income of less than $10,000.32,219 Most heat
wave early-warning systems emphasize use of air-conditioning,
but availability and use of the units are limited by socioeconomic
status because they are expensive to operate. A working air
conditioner was the strongest protective factor against mortality
during the 1999 heat wave in Chicago; fan cooling did not afford
protection.219 High mortality rates were recorded in Chicago
despite extensive programs to educate high-risk populations,
such as advising older adults to seek cool shelters or use air-
conditioning. Approximately 10,000 elderly persons died during
the France heat wave of 2003 primarily because of lack of air-
conditioning units in residences and hospitals.75,315 In 2005, Hur-
ricane Katrina ravaged the U.S. Gulf Coast, and electrical failures
caused high heatstroke mortality of older adults confined to resi-
dences, retirement homes, and hospitals because local tempera-
tures exceeded 43° C (109.4° F). Increases in the average human
life span, global climate change, and use of medications that
compromise cardiovascular adjustments to heat stress will neces-
sitate increased reliance on artificial cooling systems and educa-
tion programs to prevent heatstroke deaths in vulnerable
populations such as older adults.
The death toll of older adults from excessive heat may be
small compared with that caused by aggravation of a preexisting
illness. Heat strain imposes large cardiovascular demands on the
body. Blood flow is shunted from the viscera to the skin to dis-
sipate excess heat to the environment, making cardiovascular
fitness a more important factor than age in determining an indi-
vidual’s susceptibility to heatstroke. Austin and Berry14 examined
100 cases of heatstroke during three summer heat waves in St.
Louis and reported cardiovascular illness in 84% of patients.
Levine183 found that heatstroke deaths are associated with arte-
riosclerotic heart disease (72%) and hypertension (12%). Cardio-
vascular deficiency impedes heat loss and compromises the
ability to maintain cardiac output during prolonged heat expo-
sure, leading to circulatory collapse and death. Older individuals
may have impaired baroreceptor reflex modulation, lower sweat
rates, longer time to onset of sweating, and diminished sympa-
thetic nerve discharge, all of which increase the risk for heat-
stroke morbidity and mortality.139,151,293 Minson and colleagues212
demonstrated reliance on a higher percentage of cardiac chro-
notropic reserve in older than in younger men.
Preexisting illness is thought to compromise an individual’s
ability to respond appropriately to heat stress and can be a com-
plicating factor, regardless of age. During a Chicago heat wave
in 1995, 57% of heatstroke patients older than 65 had evidence
of infection on clinical admission.69 In Singapore, a young EHS
victim had been ill for 3 days before heatstroke collapse.53 It has
been proposed that acute illness causes transient susceptibility
to heatstroke in young, fit individuals exercising in the heat. For
example, idiosyncratic episodes of hyperthermia were associated
with acute cellulitis and gastroenteritis in soldiers exercising in
the heat.48,154 Four male Marine recruits presented with viral
illness (mononucleosis, pneumonia) before collapse from exer-
tional heat illness (EHI) during training exercises associated with
“the Crucible” at Parris Island, South Carolina.290 Peripheral
blood mononuclear cells (PBMCs) from these recruits expressed
CHAPTER 12  Pathophysiology of Heat-Related Illnesses
higher levels of IFN-inducible genes than did those from con-
trols who participated in the training event but did not col-
lapse.290 High plasma levels of IFN-α and IFN-γ mediate flulike
symptoms during viral infection and are often associated with
EHI/EHS.29,290 In rats, exposure to lipopolysaccharide (LPS), a
cell wall component of gram-negative bacteria, exacerbated
inflammation, coagulation, and multiorgan system dysfunction
from heat exposure.187
Several mechanisms may account for increased heatstroke risk
in individuals who recently experienced a mild illness. Respira-
tory or gastrointestinal illness may cause mild dehydration, which
is known to compromise reflexive thermoregulatory control
mechanisms. However, euhydrated individuals also experience
exacerbated hyperthermia, indicating that other factors are affect-
ing body temperature control.48 Fever is a common response to
infection that may contribute to the rise in body temperature
during heat exposure. Rapid development of hyperthermia
leading to heatstroke in otherwise low- to medium-risk individu-
als is caused by activation of neuronal pathways of fever in the
liver after pathogen exposure.27 The liver reticuloendothelial
system (RES) is composed of monocytes, macrophages, and
Kupffer cells that detect pathogens and stimulate the complement
cascade for rapid, local production of prostaglandin E2 (PGE2, a
main fever inducer27). Binding of locally produced PGE2 to recep-
tors on afferent (vagal) neurons projecting to the POAH evokes
behavioral and autonomic mechanisms of heat production/heat
conservation and inhibits mechanisms of heat loss for rapid
generation of fever.27 Neuronal thermogenesis is an effective
mechanism for rapid fever development during infection and
could rapidly increase body temperature during heat exposure
with mild illness. Regardless of the mechanism(s) for increased
vulnerability, use of NSAIDs is contraindicated for alleviation of
fever because of toxic organ effects. This suggests that monitor-
ing of sickness symptoms and medication use before a predicted
heat wave or an athletic or other physical event may be an effec-
tive method to identify individuals at high risk for both classic
heatstroke and EHS.
The annual Muslim pilgrimage to Mecca (the Hajj) is associ-
ated with high heatstroke incidence each year and provides many
lessons regarding etiologic factors that increase susceptibility. The
Hajj takes place in the hot desert environment of Saudi Arabia
during the extreme-weather months of May to September, with
temperatures ranging from 38° to 50° C (100.4° to 122° F).156 Hot
weather combined with physical exertion (first day consists of
a 3.5-km [2.2-mile] jog), heavy clothing that is traditional to
the region (limits heat dissipation), and an older population
(~50 years is an advanced age for this region) predispose many
individuals to heatstroke. Clothing has a significant impact on
Muslim women because they are required to wear darker cloth-
ing that covers a larger body surface area than clothing worn by
men.122 Medical conditions such as diabetes, cardiovascular
abnormalities, and parasitic disease are common.122 Heatstroke is
a major concern, but heat exhaustion with water or salt depletion
is also prevalent. Overcrowding and congestion impose large
demands on sanitation services, as exemplified in the 1980s,
when approximately 2 million people participated in the Hajj.
Advances in modern technologies, such as more rapid transport,
will likely introduce additional factors (e.g., lack of acclimatiza-
tion, increased greenhouse gas production, increased congestion)
to this already complex situation.
Protective clothing is a significant predisposing factor to EHS
during athletic (heavy uniforms), military (chemical protective
clothing), or occupational activities (e.g., pesticide application,
firefighting, race car driving). Protective clothing often consists
of multiple layers that insulate anatomic sites from heat exchange,
including the skin and head.254 Protective clothing in combination
with strenuous work can cause rapid elevation in body tempera-
ture. Fifty-one cases of EHI were observed in military trainees in
San Antonio, Texas, during participation in a 9.3-km (5.8-mile)
march in full battle dress uniform and boots.286 Lack of acclima-
tization to athletic uniforms and high environmental temperatures
result in the majority of EHS cases in athletes occurring on the
second or third day of exposure to hot weather before these
255
 individuals are acclimatized to uniforms and environmental
temperatures.108,263
SKIN DISORDERS
Miliaria rubra (also known as “prickly heat” or “heat rash”)
occurs when the sweat gland ducts become blocked with dead
skin cells or bacteria. Obstruction of the sweat glands causes
eccrine secretions to accumulate in the ducts or leak into the
deeper layers of the epidermis, causing a local inflammatory
reaction consisting of redness and blister-like lesions. Miliaria
rubra can increase body heat storage, reduce exercise perfor-
mance in the heat (with as little as 20% of the body surface
affected), and persist for up to 3 weeks after the rash appears to
have resolved.241,242 If heat illness is expected, the affected area
of the skin should be cooled and dried to control infection.
Topical corticosteroids or aspirin may be effective in reducing
swelling and irritation.
Sunburn is a common reaction to ultraviolet (UV) radiation
that causes epidermal and dermal injury and limits efficiency of
the sweating response.105 Sweating sensitivity as well as sweat
rates on the forearm and back were significantly reduced 24
hours after artificial sunburn compared to responses observed in
body regions that were protected from UV exposure.240 Severe
sunburn to major portions of the body can cause systemic toxicity
that manifests as chills, fever, nausea, and delirium.132 Sunburn
effects on sweating are locally mediated at the sweat glands and
dermal vasculature and can persist after the skin appears to be
completely healed.240 If the sunburn covers more than 5% of the
COLD AND HEAT
body, heat exposure should be avoided until the skin has healed.
Sunburn is a preventable disorder with the use of sun-blocking
lotions, protective clothing, and shelter from sun exposure.
In the past decade, burn-related injuries requiring extensive
skin grafts affected about 180,000 individuals in the United
States.7 Split-thickness skin grafts require transplantation of the
entire epidermis as well as a portion of the dermis from a non-
injured body site to the burned area. Because most split-thickness
grafts do not contain functional sweat glands, revascularization
PART 2
and neural control of blood flow must be reestablished at the
grafted site to support thermoregulatory control. Higher rectal
temperature and a diminished tolerance for heat were observed
in patients with healed burns over 40% of the body.20,269,279,280
Interestingly, grafted burn patients showed diminished cutaneous
vasodilation during heat exposure for more than 4 years after
surgery, whereas the vasoconstrictor responses to cooling
remained intact.64,65 These findings suggest that grafted skin loses
vasodilator control of body temperature while the vasoconstrictor
response remains intact. A comprehensive review of the cutane-
ous vascular and sudomotor responses in human skin grafts is
available.62
PATHOPHYSIOLOGY OF HEATSTROKE
The pathophysiologic responses to heatstroke range from condi-
tions experienced immediately after collapse to long-term changes
that persist for several weeks, months, or years after hospital
treatment and release. Clinical records documenting the immedi-
ate symptoms of heatstroke have provided most information
regarding the severity of this syndrome. Case reports and epide-
miologic studies from major heat events highlight the long-term
outcomes, although the mechanisms mediating permanent organ
dysfunction, which often leads to death, remain poorly under-
stood. It is now believed that the long-term pathophysiologic
responses to heatstroke are caused by a systemic inflammatory
response syndrome (SIRS) that ensues after heat-induced damage
to the gut and other organs.34 Following damage to the epithelial
membrane of the gut, endotoxin normally confined to the gut
lumen is able to “leak” into the systemic circulation and elicit
immune responses that cause tissue injury. The thermoregulatory,
immune, coagulation, and tissue injury responses that ensue
during long-term progression of heatstroke closely resemble
those observed during clinical sepsis and are likely mediated by
similar cellular mechanisms. Figure 12-6 provides an overview of
the current understanding of the pathophysiologic responses that
256
Climatic heat stress and exercise
Heat strain
Cardiovascular Heat cytotoxicity
responses
(Intestine, kidney,
Gut Skin spleen, endothelium)
constricts dilates
Ischemia HSPs
↑ Gut epithelial Systemic inflammatory
membrane permeability response syndrome
Increased tight (fever, DIC, rhabdomyolysis,
junction permeability tissue injury)
Endotoxin Anergy
(Th1 > Th2
response)
Innate immune system
Multiorgan
TLR4 Cytokines system failure
Adaptive immune system
FIGURE 12-6  Summary of heatstroke pathophysiologic responses that
culminate in multiorgan system failure. An increase in heat strain stimu-
lates a reflexive increase in cutaneous blood flow and decrease in
splanchnic blood flow to facilitate heat dissipation to the environment.
Gut ischemia causes increased epithelial membrane permeability and
leakage of endotoxin into the systemic and portal circulation. Toll-like
receptors (e.g., TLR4) detect pattern-associated molecular patterns on
the cell membrane of endotoxin and stimulate proinflammatory and
antiinflammatory cytokine production. Heat is toxic to several organs
and stimulates secretion of heat shock proteins (HSPs) that interact
with cytokines and other proteins to mediate the systemic inflamma-
tory response syndrome (SIRS) of the host. Peripheral and central
nervous system actions of cytokines and other mediators of SIRS are
thought to mediate many of the adverse consequences of the heat-
stroke syndrome that lead to multiorgan system failure and death. DIC,
Disseminated intravascular coagulation.
are thought to initiate and mediate heat-induced SIRS, as dis-
cussed in detail here.
BODY TEMPERATURE RESPONSES
The severity of hyperthermia varies widely between heatstroke
patients at the time of collapse with values ranging from approxi-
mately 41° C (105.8° F) to 47° C (116.6° F).36,51,118,285 During a
summer heat wave in St. Louis in 1954, the core temperature of
100 heatstroke patients ranged from 38.5° to 44° C (101.3° to
111.2° F), with 10% of fatalities occurring below 41.1° C (106° F).14
In some cases, individuals may tolerate hyperthermia without
adverse side effects. During a competitive marathon race in Cali-
fornia, a 26-year-old man maintained a rectal temperature of
41.9° C (107.4° F) for approximately 45 minutes without clinical
signs of heat illness.202 However, there are several reports of
athletic, military, and occupational workers with core tempera-
tures below 41.9° C who were hospitalized, experienced perma-
nent CNS impairment, or died from EHS (Table 12-2).
Hypothermia and fever are often observed in patients
and experimental animal models during heatstroke recovery.
Hypothermia is not a universal heatstroke recovery response
in humans, but it has been anecdotally observed following
aggressive cooling treatment. Hypothermia manifests as a rapid
 CHAPTER 12  Pathophysiology of Heat-Related Illnesses
TABLE 12-2  Clinical Characteristics of Exertional Heat Illness Cases

Activity Body Temperature °C (°F) Age (Years) Duration of Symptoms Outcome

Military Training
Army (aviation) >39.0 (102.2) 18-59 10 min CNS dysfunction*
Army (basic) 40-41.1 (104-106) 18-41 24 hr to 12 d Death
Army (basic) 41.1 (106) 20 5d Recovery
Army (Singapore) 40-42 (104-107.6)† 18-29 45 min to 99 hr Death
Marine Corps <38.9-40.0 (102-104) 17-30 None Recovery
Marine Corps 39-42.5 (102.2-108.5)†‡ 17-19 >1 d Recovery
Marine Corps 41.1 (106) NR ≤12 hr Hospitalization
NBC 41.3 (106.3) 25 12 d Recovery
Athletic Events
6-mile run 39.2 (102.6)§ 29 10 d Death
Marathon run 40.7 (105.3)‡ Late 30s 5d Recovery
Marathon run 41.9 (107.4) 26 None Recovery
Hajj rituals <42 (107.6) 32-80 NR Ataxia, infarction, death
≥42 (107.6) NR NR Death
43.9 (111) NR NR Recovery
Migrant farming 42.2 (108) 44 None Death
Firefighter training 42.6 (108.7) 22 9d Death

CNS, Central nervous system; d, day(s); NR, not reported; NBC, nuclear, biologic, and chemical protective clothing.
*CNS dysfunction includes agitation, confusion, disorientation, delirium, poor memory, convulsions, and/or coma.
†Indicates patient cohorts with documented prodromal illness before heatstroke collapse.
‡Body temperature measured several minutes after collapse or cooling.
§Patient temperature increased to 41° C (105.8° F) on day 10 of hospitalization before death.

undershoot of body temperature below 37° C (98.6° F) and is
thought to represent a loss of thermoregulatory control after
heat-induced damage to the POAH. However, evidence in
support of this hypothesis is lacking. That is, histology and
magnetic resonance imaging (MRI) studies have failed to detect
damage to the POAH despite extensive damage in other
organs.5,180,197,235,298,340 In experimental animals, hypothermia is a
natural heatstroke recovery response associated with behavioral
and autonomic thermoeffector responses that support a decrease
in core temperature. Mud puppies are ectothermic species that
rely on behavioral adjustments, such as the selection of differ-
ent microclimates, to control body temperature. Mud puppies
heat-shocked to about 34° C (93.2° F) behaviorally selected a
cooler microclimate and maintained a significantly lower body
temperature than did nonheated controls during 3 days of
recovery.137 This study did not determine the impact of hypo-
thermia on survival, but the association of decreased body tem-
perature with the selection of cool microclimates indicated this
was a regulated response to a decrease in the temperature set
point. Small rodents, such as mice, rats, and guinea pigs,
showed reductions greater than 1.0° C (1.8° F) in body tempera-
ture that were associated with improved survival after passive
heatstroke. In mice, hypothermia was associated with a 35%
decrease in metabolic heat production and with the behavioral
selection of microclimates that precisely regulated the depth
and duration of this response.180 Exposure of mice to warm
ambient temperatures that prevented heat-induced hypothermia
caused increased intestinal damage and mortality.179,331 Hypo-
thermia likely provides protection against heat-induced tissue
injury in a manner similar to that shown for protection against
other extreme environmental insults based on the temperature
coefficient (Q10) effect.
A common heatstroke recovery response observed in patients
and animal models is recurrent fever during the days and weeks
of recovery.14,179,197,210 In mice, fever was observed within a day
after passive heatstroke collapse and was associated with a 20%
increase in metabolic heat production and increased plasma
levels of the proinflammatory cytokine interleukin-6.177,179,180 IL-6
is an important regulator of fever during infection and inflam-
mation and may regulate fever during heatstroke recovery,
although this hypothesis remains to be experimentally tested.175
In patients, fever is reestablished after clinical cooling.197 This is
reminiscent of Liebermeister’s experimental observations of the
recurrence of fever after experimental cooling of the POAH of
rats.185 This suggests that fever may provide protection against
some aspect of the SIRS and development of multiorgan dys-
function. The argument against this hypothesis is that recurrent
hyperthermia in heatstroke patients has been anecdotally associ-
ated with poor outcome.197,210,285 For example, an amateur long-
distance runner was hospitalized for 10 days after collapsing
from EHS during a 9.6-km (6-mile) foot race. This patient dis-
played moderate fever (>38° C [100.4° F]) during the first 4 days
of hospitalization, but on the 10th day, convulsions induced a
rapid increase of body temperature to 41° C (105.8° F). Rapid
cooling and aspirin therapy were ineffective in reducing body
temperature, and the patient died.210 NSAIDs are potent inhibi-
tors of prostaglandin production within the POAH, which is the
mechanism by which these drugs normally inhibit fever during
infection. Lack of an effect of aspirin on recurrent hyperthermia
suggests this was not a true fever response, but rather a patho-
logic response to increased metabolic heat production induced
by convulsions. Indomethacin is an NSAID with potent anti-
pyretic actions in mice, but it failed to reduce fever during
heatstroke recovery.24 Unfortunately, prostaglandin production
within the POAH has never been examined in animal heatstroke
models, so it remains unknown if activation of these signaling
pathways is associated with development of recurrent hyperther-
mia during heatstroke recovery. Physicians may attempt to treat
recurrent hyperthermia episodes with NSAIDs, but these drugs
are toxic to the liver and have been associated with the need
for liver transplantation.102,123,124,271,318
IMMUNE RESPONSES
During heat stress, blood flow to the skin is increased to facilitate
heat loss to the environment and reduce the rate of total body
heat storage. Increased skin blood flow is accompanied by a fall
in splanchnic (i.e., visceral organ) blood flow as a compensatory
mechanism to sustain blood pressure. Endotoxin is normally
confined to the gut lumen by tight junctions of the epithelial
membrane, but these junctions can become “leaky” following
prolonged reductions in blood flow that cause ischemic stress.117,170
Several lines of evidence support the hypothesis that endotoxin
leakage from the gut lumen into the systemic circulation is the

257
 initiating stimulus for heat-induced SIRS. First, systemic injection TABLE 12-3  Toll-Like Receptors of the Innate
of LPS into experimental animals induces symptoms similar to
those observed in heatstroke, including hyperthermia, hypother- Immune System
mia, fever, hypotension, cytokine production, coagulation, and
tissue injury.166,265,266 Second, increased portal or systemic endo- Toll-Like
Receptor Ligand Cell/Tissue Types
toxin levels are observed in heatstroke patients and animal
models. In primates, circulating endotoxin was detected at rectal
TLR1 Triacyl lipopeptide Monocytes, macrophages,
temperatures above 41.5° C (106.7° F), with a precipitous increase
DCs, polymorphonuclear
at approximately 43.0° C (109.4° F).99 Splanchnic blood flow
shows an initial decrease at 40° C (104° F); the liver, which is leukocytes, B and T
an important clearance organ for endotoxin, shows damage at cells, NK cells
body temperatures of approximately 42° to 43° C (107.6° to TLR2 Lipopolysaccharide Monocytes, granulocytes
109.4° F).39,40,53,117,223 In a young athlete with a body temperature Peptidoglycan Brain, heart, lung, spleen
of 40.6° C (105.1° F) on the second day of football practice, high Lipoteichoic acid
circulating levels of endotoxin were associated with hemorrhagic Measles virus
necrosis of the liver.108 In heatstroke patients, endotoxin was Human cytomegalovirus
detected at approximately 42.1° C (107.8° F) and remained ele- Hepatitis C virus
vated despite cooling.36 Third, rats rendered endotoxin tolerant Zymosan
after systemic injection of LPS are protected from heatstroke Necrotic cells
mortality. The protective effect of endotoxin tolerance is related TLR3 Viral double-stranded DCs, T cells, NK cells,
to enhanced stimulation of the liver RES, which is composed of RNA monocytes, granulocytes
monocytes, macrophages, and Kupffer cells that are important Placenta, pancreas
for endotoxin clearance.77,78 RES stimulation reduced and RES TLR4 Lipopolysaccharide B cells, DCs, monocytes,
blockade increased mortality of heat-stressed rats.78 Fourth, anti- Fibrinogen macrophages,
biotic therapy protects against heatstroke in several species. In Heat shock proteins granulocytes, T cells
dogs, antibiotics reduced gut flora levels and improved 18-hour High-mobility group Spleen
survival by more than threefold when provided before heat
box 1
exposure.46 In rabbits with heatstroke, hyperthermia and endo-
TLR5 Flagellated bacteria Monocytes
toxemia were reduced after administration of oral antibiotics.45
COLD AND HEAT

Anti-LPS hyperimmune serum reversed the heatstroke mortality Ovary, prostate

of primates and returned plasma LPS levels to baseline, but it TLR6 Diacyl lipopeptide B cells, monocytes
was ineffective at the highest body temperature of 43.8° C Thymus, spleen, lung
(110.8° F), indicating hyperthermia alone may cause irreversible TLR7 Single-stranded RNA Monocytes, B cells, DCs
organ damage and death.100 Lung, placenta, spleen,
The heat-induced SIRS is initiated by the innate and adaptive lymph node, tonsil
immune systems, which interact to sense the presence of endo- TLR8 Single-stranded RNA Monocytes
toxin and orchestrate an immunologic response. The innate Lung, placenta, spleen,
immune system comprises monocytes, macrophages, and neu- lymph node, bone
PART 2

trophils that use pattern recognition receptors (PRRs) on their
cell surfaces to recognize pattern-associated molecular patterns
(PAMPs) on the cell surface of endotoxin and other invading
pathogens.144,310 Toll-like receptors (TLRs) are a class of PRRs that
have been widely studied in the immune response to infec-
tion.209,310 Ten mammalian TLRs have been identified, and the
specific pathogenic ligands that activate these PRRs are known
(Table 12-3).
Toll-like receptor 4 (TLR4) is the principal receptor for LPS
that stimulates gene transcription factors, such as nuclear factor
(NF)–κB, to increase the synthesis of a variety of immune modu-
lators in response to endotoxin. Endotoxin infection (i.e., sepsis)
is associated with increased expression of TLR4 on circulating
human PBMCs, as well as on mouse liver and spleen macro-
phages.310,311 In the 1960s, a spontaneous mutation in the TLR4
gene was discovered in C3H/HeJ mice, which has been an
important animal model to determine the role of TLR4 in endo-
toxin and heatstroke responsiveness. C3H/HeJ mice experienced
mortality during the SIRS to bacterial infection, which was caused
by inability to induce the full complement of immune responses.113
These mice also experienced more severe classic heatstroke
responses than did wild-type mice. These included profound and
sustained hypothermia, rapid induction of circulating IL-1β, IL-6,
tumor necrosis factor (TNF)–α, high-mobility group box 1
(HMGB1), more severe liver damage, and increased mortality
through 3 days of recovery.67 HMGB1 is a classic alarmin that
binds a wide range of molecules to dictate the resulting immune
response. On binding LPS, HMGB1 induces a SIRS composed of
elevated IL-1β and IL-6 secretion.135 Given that TLR4 polymor-
phisms exist in humans, this may be one of several genetic factors
that predispose to mortality during the SIRS to heatstroke.7,85
Specificity of immune responses is provided by B and T cells
of the adaptive immune system. These cells respond to antigens
by secreting cytokines, which are intercellular immune signals
that elicit proinflammatory (T helper type 1 [Th1]) and antiinflam-
matory (T helper type 2 [Th2]) actions during the progression of
marrow, PBLs
TLR9 CpG DNA B cells, DCs
Spleen, lymph node, bone
marrow, PBLs
TLR10 Unknown B cells
Spleen, lymph node,
thymus, tonsil
Data from Medvedev AE, Sabroe I, Hasday JD, et al: Tolerance to microbial TLR
ligands: Molecular mechanisms and relevance to disease, J Endotoxin Res
12:133, 2006; and Tsujimoto H, Ono S, Efron PA, et al: Role of Toll-like
receptors in the development of sepsis, Shock 29:315, 2008.
CpG, Deoxycytidylate-phosphate-deoxyguanylate; DC, dendritic cell; DNA,
deoxyribonucleic acid; NK, natural killer; PBL, peripheral blood leukocyte; RNA,
ribonucleic acid.
the SIRS. The actions of cytokines depend on the nature of the
danger signal, the target cells with which they interact, and the
cytokine “milieu” in which they function. Th1 and Th2 cytokines
function in a negative feedback pathway to regulate each other’s
production and maintain a delicate balance of inflammatory reac-
tions. Anergy is thought to be a consequence of inadequate Th2
cytokine production late in the SIRS. For example, increased
patient mortality from peritonitis is associated with the inability
to mount a Th2 cytokine response127 (see Figure 12-6).
Alarmins are endogenous PAMPs released from stressed or
injured tissues that initiate restoration of homeostasis after an
infectious or inflammatory insult.23 HMGB1 is a highly conserved
nuclear protein that functions as an alarmin after release from
necrotic (but not apoptotic) cells.273 Necrosis is premature death
of cells in a tissue or organ in response to external factors, such
as pathogens and toxins. Because necrosis is detrimental to the
host, it is associated with an inflammatory response. Apoptosis
refers to genetically programmed cell death that does not elicit
an inflammatory response because it is beneficial to the host.

258
Release of HMGB1 from necrotic cells stimulates Th1 cytokine when platelets and coagulation proteins are consumed faster than

CHAPTER 12  Pathophysiology of Heat-Related Illnesses

production late in the sepsis syndrome and is a purported media- they are produced.13,16 Hemorrhagic complications in heatstroke
tor of lethality; this shift in the balance of cytokines from a Th2 patients include prolonged bleeding from venipuncture sites or
to Th1 phenotype is a potential mechanism of sepsis lethality. In other areas (e.g., gums), which can have a fatal outcome.156 The
human PBMCs, HMGB1 interacts with TLR2 and TLR4 to enhance primary event that initiates coagulation in heatstroke patients is
Th1 cytokine production in synergy with LPS.135 Elevated serum thermal injury to the vascular endothelium.30,34,217 In vitro studies
HMGB1 levels are observed 8 to 32 hours after LPS injection have shown the ability of heat (43° to 44° C [109.4° to 111.2° F])
in mice. Anti-HMGB1 antibodies did not protect against LPS- to directly activate platelet aggregation and cause irreversible
induced mortality unless the antibodies were provided 12 and hyperaggregation despite cooling.97,330 Cancer patients treated
36 hours after LPS exposure.323 The delayed kinetics of HMGB1 with whole-body hyperthermia (41.8° C [107.2° F] for 2 hours)
and the association of elevated serum levels of this protein with showed decreased fibrinogen and plasminogen at body tempera-
poor outcome in sepsis patients suggest that HMGB1 detection tures as low as 39° C (102.2° F), alterations in factor VII activity
late in the SIRS may be a sensitive clinical marker of disease at 41.8° C (107.2° F), and decreased platelet concentrations from
severity.125,299,323 the time of maximum body temperature through 18 hours of
recovery.296
Several proteins, including HMGB1, IL-1, TNF, and activated
COAGULATION protein C (APC), affect the coagulation, anticoagulation, and
Disseminated intravascular coagulation (DIC) is a common clini- fibrinolytic pathways. In rats, HMGB1 in combination with throm-
cal symptom of heatstroke that manifests as two distinct forms bin caused excess fibrin deposition in glomeruli, prolonged clot-
(Figure 12-7). Microvascular thrombosis is a form of DIC charac- ting times, and increased sepsis mortality compared with thrombin
terized by fibrin deposition and/or platelet aggregation that alone.140 As demonstrated in vitro, the effect of HMGB1 protein
occludes arterioles and capillaries and predisposes to multiorgan is caused by inhibition of the APC pathway and stimulation of
system dysfunction.182 Microvascular thrombosis is frequently tissue factor expression on monocytes.140 Cytokines stimulate
observed in response to sepsis or trauma. DIC associated with microvascular thrombosis by interacting with neutrophils, mac-
consumptive coagulation is characterized by excessive blood loss rophages, platelets, and endothelium to increase expression of
intracellular adhesion molecules. Increased expression of cell
adhesion molecules, neutrophil adhesion, and release of reactive
oxygen species cause endothelial activation and injury.207 APC is
an important component of the anticoagulation pathway that
Extrinsic pathway Intrinsic pathway
inactivates factors Va and VIIIa to inhibit fibrin clot formation.
In septic patients, reduced APC production was associated with
TISSUE INJURY CONTACT ACTIVATION
increased risk of mortality from systemic inflammation and
Tissue Factor (TF) DIC.88,184 In addition to its anticoagulation properties, APC pos-
sessed antiinflammatory and antiapoptotic properties that pro-
Factor VII Factor VIIa Factor XIIa Factor XII tected against experimental sepsis and heatstroke.54,305
Typical clinical measures of coagulation include prothrombin
Factor XIa Factor XI time (PT), activated partial thromboplastin time (aPTT), and
fibrinogen. PT in combination with aPTT assesses the time for
plasma clot formation to occur in response to exogenous tissue
Factor IXa Factor IX factor and is a sensitive measure of responsiveness of the coag-
ulation pathway. The reference range for PT is approximately
VIIIa 12 to 15 seconds and may be prolonged several-fold in heat-
stroke patients. The aPTT normally ranges from 30 to 40
Anticoagulation
Factor Xa Factor X seconds and is used clinically to monitor treatment effects of
Protein C anticoagulants such as heparin. Fibrinogen is an acute-phase
Factor V Factor Va
Protein S protein synthesized by the liver that is normally in the range of
2 to 4 g/L. Low fibrinogen levels indicate liver damage or DIC,
Activated protein C (APC) whereas elevated levels are a clinical sign of systemic inflam-
mation. DIC can be difficult to diagnose, but low fibrinogen
levels and prolonged PT or aPTT are strong clinical indicators
Prothrombin Thrombin Factor VIIIa Factor VIII in critically ill patients.

TISSUE INJURY
Fibrinogen Fibrin Clot Multiorgan system failure is the ultimate cause of heatstroke
mortality and is a result of SIRS, which ensues after heat-induced
damage to the gut and other tissues.34 A variety of noninfectious
Fibrinolysis
and infectious clinical conditions are associated with SIRS, and
Plasminogen
Plasminogen activator similar physiologic mechanisms are thought to mediate the
Inhibitor 1 tPA Fibrin pathogenesis of these conditions (Box 12-2).
degradation The term sepsis refers to SIRS associated with the presence of
Plasmin products infection. Much of the understanding of pathophysiologic mecha-
nisms mediating heat-induced SIRS has been obtained from
FIGURE 12-7  Pathways of disseminated intravascular coagulation
sepsis studies. This section provides an overview of the responses
(DIC). The coagulation cascade is stimulated by the extrinsic pathway
(also known as the tissue factor [TF] pathway) and the intrinsic pathway
that constitute heat-induced SIRS and our current understanding
(also known as the contact activation pathway). Both pathways repre- of the pathophysiologic mechanisms that mediate the adverse
sent a series of enzymatic reactions that result in formation of a fibrin events of this syndrome.
clot. Fibrinolysis represents the pathway by which the fibrin clot is The severity of heatstroke is primarily related to the extent of
resorbed through the actions of plasmin. The major physiologic anti- damage to the brain, liver, and kidneys and is clinically identified
coagulant is protein C, which is activated by protein S and inactivates by elevations in serum biomarkers, such as creatine kinase
factors Va and VIIIa to inhibit clot formation. Lipopolysaccharide, (CK), blood urea nitrogen (BUN), aspartate aminotransferase/
interleukin-1, and tumor necrosis factor affect DIC by stimulating TF transaminase (AST), and alanine aminotransferase/transaminase
formation and inhibiting the inactivation of factors Va and VIIIa, which (ALT). CK is released from muscle and is a marker of skeletal
prolong clot formation. muscle injury (also known as rhabdomyolysis), myocardial

259
 BOX 12-2  Predisposing Risk Factors for Serious
about 30% of heatstroke survivors experience permanent decre-
ments in neurologic function.10,34,69 CNS dysfunction is often
Heat Illness associated with cerebral edema and microhemorrhages at autopsy
in heatstroke patients.5,53,197,301 The blood-brain barrier (BBB) is a
Clinical
semipermeable membrane that allows selective entry of sub-
Neurologic symptoms (fatigue, weakness, confusion, stupor, coma,
stances (e.g., glucose) into the brain while blocking entry of other
dizziness, delirium)
Tachycardia
substances (e.g., bacteria). Hyperthermia increases BBB perme-
Nausea, vomiting, diarrhea ability in experimental animal models, which permits leakage of
Headache proteins and pathogens from the systemic circulation into the
Hypotension brain. Computed tomography (CT) scans have been used to
Oliguria, multiorgan system failure examine CNS changes in heatstroke patients. In the 1995 Chicago
Hyperventilation heat wave, atrophy, infarcts of the cerebellum, and edema were
Shock evident in older adult victims. CT scans also revealed severe loss
Laboratory of gray-white matter discrimination (GWMD), which was associ-
Metabolic acidosis
ated with headache, coma, absence of normal reflexive responses,
Elevated hematocrit and multiorgan dysfunction.301 Loss of GWMD is a result of
Elevated blood urea nitrogen (BUN), aspartate transaminase (AST), increased brain water content, which is in line with occurrence
and alanine transaminase (ALT) of edema in heatstroke victims. If GWMD provides an early,
Elevated lactate sensitive measure of brain injury, it will be a powerful prognostic
Disseminated intravascular coagulation indicator of outcome for heatstroke patients.
Elevated cytokines Exertional heatstroke is often associated with rhabdomyolysis,
Circulating endotoxin which is a form of skeletal muscle injury caused by leakage of
muscle cell contents into the circulation or extracellular fluid.
Myoglobin released from damaged muscle cells is filtered and
metabolized by the kidneys. When severe muscle damage occurs,
the renal threshold for filtration of myoglobin is exceeded, and
infarction, muscular dystrophy, and acute renal failure. BUN is a this protein appears in the urine in a reddish brown color.96
measure of the amount of nitrogen in the blood in the form of Myoglobin is toxic to nephrons and causes overproduction of
urea, which is secreted by the liver and removed from the blood uric acid, which precipitates in the kidney tubules to cause acute
COLD AND HEAT

by the kidneys. A high BUN concentration is typically regarded
as an indication of impaired renal function, although BUN levels
may be altered by conditions unrelated to heat illness, including
malnutrition, high-protein diets, burns, fever, and pregnancy.2,270,321
AST is released by the liver and skeletal muscle and may be a
clinical sign of congestive heart failure, viral hepatitis, mononu-
cleosis, or muscle injury. ALT is released by the liver, red blood
cells, cardiac muscle, skeletal muscle, kidneys, and brain tissue.
AST and ALT are common clinical markers of liver function in
PART 2
renal failure, coagulopathy, and death if not rapidly detected and
treated.15,96,190,244,322 Not all cases of rhabdomyolysis are associated
with myoglobinuria; many patients can be asymptomatic. Clinical
markers of rhabdomyolysis include elevated myoglobin, CK,
aldolase, lactate dehydrogenase, ALT, and AST, which are influ-
enced by a variety of factors (type, intensity, and duration of
exercise; gender; temperature; altitude) and released by more
than one organ or tissue.58,211,270 If a clinical diagnosis of rhabdo-
myolysis is confirmed, immediate medical attention is imperative

heatstroke patients despite multiple tissue sources of these

enzymes and occasional false-negative results that complicate
interpretation. Unfortunately, all these biomarkers are released
by a variety of tissues and altered by heat-exhaustive exercise
and thus do not always provide a precise measure of the extent
of tissue injury.106,112,283 The extent and time course of organ injury
vary widely between individuals. Tissue injury manifests as
primary and/or secondary multiorgan dysfunction, depending on
whether heat toxicity alone or in combination with a SIRS causes
cellular damage.8 Gut epithelial barrier disruption is an example
of primary organ dysfunction evident at the time of heatstroke
collapse. Hyperthermia degrades epithelial membrane integrity
and causes microhemorrhages, dilation of the central lacteals of
the microvilli, and blood clots within the stomach and small
intestine37,117,177,234 (Figure 12-8).
15 min 30 min
It is often difficult to determine if organ injury is caused by
primary or secondary factors.30,69,108,177,197 For example, protein
clumping in kidney tubular epithelial cells may be a result of
heat toxicity, elevated myoglobin levels, or DIC.37,53,108,177,252,322 A
conscious mouse model has shown that kidney damage is present
within approximately 2 hours following heatstroke collapse and
remains elevated through 24 hours of recovery.177 In heatstroke
patients, acute renal failure is a nearly universal finding that is
accompanied by decrements in function within 24 hours of
admission to the intensive care unit.246 In patients who survive
more than 24 hours, severe hypotension, dehydration, BUN, and 45 min 60 min
oliguria are associated with tubular necrosis or intertubular
FIGURE 12-8  Effect of heating on villus structure. Representative light
edema.197 Primary changes in the spleen are even less well micrographs of rat small intestinal tissue over a 60-minute course at
understood, but cytoplasmic protein clumping is thought to be 41.5° to 42° C (106.7° to 107.6° F). Note the generally normal-appearing
a consequence of this organ being “simply cooked and villi at 15 minutes (slight subepithelial space at villous tips), compared
coagulated.”53 with initial sloughing of epithelia from villous tips at 30 minutes,
A hallmark of heatstroke, CNS dysfunction is dominant early massive lifting of epithelial lining at top and sides of villi at 45 minutes,
in the disorder. Patients are often confused, delirious, combative, and completely denuded villi at 60 minutes. Bars represent 100 µm.
or comatose at clinical presentation. Hyperthermia with exercise (From Lambert GP, Gisolfi CV, Berg DJ, et al: Selected contribution:
is also associated with reduced cerebral blood flow, which may Hyperthermia-induced intestinal permeability and the role of oxidative
account for these CNS abnormalities.226 Despite rapid treatment, and nitrosative stress, J Appl Physiol 92:1750, 2002, with permission.)

260
because 50% mortality rates from acute renal failure have been
documented for this condition.
Liver failure is one of the most common causes of morbidity
and mortality in patients during the later stages of recovery. The
time course of liver damage differs from that of the other organs
and often does not peak until approximately 24 to 48 hours after
heat exposure. For example, liver damage consisting of centri-
lobular degeneration and necrosis with parenchymal damage was
only evident in EHS patients who survived more than 30 hours.197
In addition, enhanced breakdown of fat or inability of the mito-
chondria to use fat results in heatstroke-associated fatty liver
changes.53 Disturbances in plasma glucose homeostasis are a sign
of liver damage that may cause hyperglycemia or hypoglycemia
as a result of dysfunction of phosphoenolpyruvate carboxyki-
nase, which is a regulatory enzyme of the liver’s gluconeogenic
pathway.30,177 Liver dysfunction may also contribute to increased
circulating endotoxin levels because of the important bacterial
clearance function of this organ.40,223 Unfortunately, many heat-
stroke patients require liver transplantation. Use of antipyretic
drugs, such as acetaminophen (Tylenol), has been associated
with hepatic failure.102,123,124,263,318
Many patients are released from the hospital after several days
or weeks of treatment and continue to experience organ dysfunc-
tion during the ensuing years of recovery. Following the 2003
heat wave in France, mortality increased from 58% at day 28 of
hospitalization (mean hospital stay, 24 days) to 71% by the
second year of recovery.10 An epidemiologic study of military
EHS patients showed a twofold increased risk of death from
cardiovascular, kidney, and liver disease within 30 years of hos-
pitalization.320 Several of the clinical responses (hyperthermia,
dehydration, kidney/liver damage) occurring during progression
or shortly after heatstroke collapse are clinically recognized and
treated. However, those occurring during the months and years
after hospitalization are underreported. The mechanisms respon-
sible for long-term decrements in organ function remain poorly
understood.
CYTOKINES
Cytokines are a class of intercellular protein messengers
released from macrophages, T and B cells, endothelial cells,
astrocytes, and other cell types that mediate inflammatory reac-
tions to disease and injury.55,148,200,282,312 Cytokine-inducing stimuli
include bacterial and viral infection,76,245 psychological stress,196,232
heat stress,29,37,45,126,177,186 whole-body hyperthermia,220 and exer-
cise.47,213,222,300 The defining characteristics of cytokines include a
lack of constitutive production, the ability to regulate each other’s
production, and overlapping actions that depend on the target
cell type and cytokine milieu in which they function. Cytokines
act over short distances and time spans (half-life, generally <60
minutes) and are usually present at low concentrations in the
circulation. Cytokines bind reversibly to high-affinity cell surface
receptors and stimulate intracellular signaling pathways (e.g.,
NF-κB) that alter the transcription of genes involved in immune
responses.
Several lines of evidence link cytokines with symptoms of the
heat-induced SIRS. These include induction of heatstroke symp-
toms by cytokine injection in experimental animal models, asso-
ciation of increased circulating cytokine levels with heatstroke
morbidity/mortality, and effectiveness of cytokine neutralization
in altering heatstroke mortality in animal models. Peripheral
injection of IL-1β, IL-2, IL-6, IL-10, TNF-α, and platelet-activating
factor into experimental animals replicates the pathophysiologic
responses observed in heatstroke, including hyperthermia, hypo-
thermia, fever, increased vascular permeability, DIC, and
death.163,174,233,237,276,309 Simultaneous injection of multiple cytokines
(e.g., IL-1 and TNF) is most effective in mimicking heatstroke
symptoms and has shed light on cytokine interactions in vivo
that orchestrate SIRS. Increased circulating levels of IL-1α, IL-1β,
IL-1 receptor antagonist (IL-1ra, a naturally occurring antagonist
of IL-1), IL-6, soluble IL-6 receptor (sIL-6R), IL-8, IL-10, IL-12,
IFN-γ, TNF-α, and soluble TNF receptor (sTNFR) concentrations
are typically observed at the time of heatstroke collapse or shortly
after cooling.29,36,37,118,122,177 Sustained high IL-6 levels during
cooling correlate with heatstroke severity, tissue injury, and
CHAPTER 12  Pathophysiology of Heat-Related Illnesses
death, whereas high circulating IL-8 levels are implicated in leu-
kocyte activation and coagulation in EHS patients.33 The recipro-
cal regulation of IL-12 and IL-10 production suggests complex
interactions in heat-induced SIRS, but the function of these cyto-
kines has not been clearly delineated. As previously mentioned,
high IFN-inducible gene expression and IFN-γ levels are clinical
measures of viral or intracellular bacterial infection and are
evident in EHS patients with preexisting infections.291
Failure of clinical and animal studies to correlate cytokine
production with specific heatstroke responses probably results
from the short half-life of these proteins, local tissue concentra-
tions exceeding those in the circulation, and/or the presence of
soluble cytokine receptors that mask detection or alter cytokine
action(s).3,29,33,36,118,122,165,275 For example, sTNFR inhibits the actions
of TNF and is often higher in heatstroke survivors than in non-
survivors, suggesting TNF might mediate lethality.118 On the other
hand, sIL-6R might potentiate endogenous IL-6 effects by increas-
ing concentration of available IL-6 signaling receptors on cell
membranes (known as a trans-signaling effect) or reducing IL-6
signaling through competitive binding with IL-6 receptors that
are already present on the cell membrane (Figure 12-9).
Although cytokines are known to interact with one another,
their soluble receptors, and other endogenous stress hormones
(e.g., glucocorticoids) during SIRS, it remains unknown how
these interactions in vivo affect heatstroke outcome. Taken
together, results from the few antagonism/neutralization studies
conducted to date indicate that high levels of cytokines may be
detrimental for heatstroke recovery; however, baseline (permis-
sive) actions of some cytokines (e.g., IL-6, TNF, or proteins
affected by their actions) appear to be essential for survival.175
Clearly, more research is required in this area to determine the
multitude of cytokine actions in heat-induced SIRS and determine
protective versus detrimental effects of the proteins on multior-
gan system function.
HEAT SHOCK PROTEINS
Heat shock proteins (HSPs) are molecular chaperones that
prevent misfolding and aggregation of cellular proteins during
exposure to stressful stimuli.86,121,142,189 HSPs are found in organ-
isms ranging from bacteria to humans. Their chaperoning activi-
ties protect against environmental (heavy metals, heat stress),
physiologic (cell differentiation, protein translation), and patho-
logic (infections, ischemia/reperfusion) stimuli that cause cellular
damage.142,167,189 HSPs were originally discovered in Drosophila
melanogaster, when puffs associated with novel protein synthesis
appeared on the giant chromosomes of the salivary glands in
response to heat stress.262,306 It was later discovered that heat
denaturation of mature proteins inside the cell was the cellular
signal that increased protein synthesis in response to heat stress
in Drosophila.130
Heat shock proteins are grouped into families according
to their molecular mass, cellular localization, and function
(Table 12-4).
Also referred to as sHSP, HSP 27 is a constitutively expressed
cytosolic and nuclear protein with cytoskeletal stabilization and
antiapoptotic functions.12,173,243 HSP 60 exists in the mitochondria
and cytosol, is released from PBMCs on LPS stimulation, and
functions as a “danger” signal for the innate immune system.
HSPs interact with PAMPs (e.g., TLRs) to stimulate monocytes,
macrophages, and dendritic cells to produce cytokines.44,224 The
HSP 70 family has been extensively studied for protective
function(s) against thermal stress,149,338 ischemia/reperfusion,201,251
tissue injury,42 glucose deprivation,332 and sepsis.172,316 HSPs 70
function in concert with other molecular chaperones, such as
HSP 90 and HSP 110, to facilitate LPS and antitumor responses.136
Gene expression of HSPs is mediated primarily at the level of
gene transcription by a family of heat shock transcription factors
(HSFs) that interact with the heat shock regulatory element (HSE)
in the promoter region of genes. HSF-1 is the major stress respon-
sive element in mammalian cells that is activated by febrile-range
temperatures.317,336 HSF-1 interacts with HSEs on cytokine genes
to alter transcription and confer protection against endotoxin and
261
 IL-6

sIL-6R

IL-6 IL-6
IL-6R sIL-6R
gp130 gp130 gp130

Signal Signal

Classic signaling Trans-signaling

FIGURE 12-9  Interleukin-6 receptor signaling pathways. Classic signaling involves binding of IL-6 to the
membrane bound IL-6 receptor (IL-6R), which stimulates an interaction between the IL-6:IL-6R complex and
the membrane-bound glycoprotein 130 (gp130) to initiate intracellular signaling. Trans-signaling occurs
when the extracellular domain of the membrane-bound IL-6R is proteolytically cleaved, leading to genera-
tion of the soluble IL-6R (sIL-6R) that binds IL-6. The IL-6:sIL-6R complex can stimulate cells that only express
gp130 (i.e., do not normally possess the transmembrane IL-6R) to transmit an intracellular signal. Cells that
express gp130 only would not be able to respond to IL-6 in the absence of sIL-6R.
COLD AND HEAT

other infectious and inflammatory stimuli. In gene-transfected
human PBMCs, inhibition of TNF-α, IL-1β, IL-10, and IL-12 in
response to LPS was specific to HSPs 70 overexpression.71 A lack
of effect of HSP 70 on IL-6 gene transcription may be an indirect
mechanism of protection, because IL-6 functions in a regulatory
feedback loop to inhibit IL-1 and TNF production, which are
Th1 cytokines with potent proinflammatory activities.71,82,83,324 In
PART 2
murine macrophages, HSP 70 inhibited IL-12 (Th1) and stimulated
IL-10 (Th2) production in response to LPS.324 The shift from Th1
to Th2 cytokine production may be a mechanism by which HSP
70 protects against bacterial infection.
Heat strain is a consequence of the time and intensity of heat
exposure. These factors interact in vivo to influence the magni-
tude and kinetics of HSP expression. In human PBMCs, maximal
expression of intracellular HSPs 70 was observed between 4 and
6 hours after a brief heat shock (43° C [109.4° F] for 20 minutes).289

Increased expression of HSPs 10, 20, 40, 60, 70, 90, and 110 was
TABLE 12-4  Heat Shock Protein (HSP) Structure observed in PBMCs from EHS patients or following exposure to
and Function hypoxia in vitro.288,291 Anatomic differences in the magnitude and
kinetics of in vivo expression have also been observed, with HSP
Family Function Attributes 70 expression occurring within 1 hour in the brain, lungs, and
skin and being delayed until 6 hours after heat exposure in the
HSP 27 (sHSP) Antiapoptotic Constitutively liver of rats.26 In mice, liver expression of HSP 70 showed pro-
expressed gressive increase beginning approximately 6 to 24 hours after
Cytoskeletal Cytosolic and collapse from passive heatstroke.176 In rats, a high rate of passive
stabilization nuclear heating (0.175° C [0.315° F]/min) induced greater HSP 70 expres-
HSP 60 Protein refolding Mitochondria sion in the liver, small intestine, and kidneys than did a lower
Prevents aggregation and cytosol rate of heating (0.05° C [0.09° F]/min), despite attaining the same
of denatured maximum body temperature (42°C [107.6° F]).90 Differences in
proteins tissue blood flow and metabolic activity likely account for
Immune responses regional differences in HSP expression during passive and exer-
HSP 70 family tional heat exposure.
  HSP 72 Thermotolerance Highly inducible Thermotolerance is the term used to describe the noninher-
HSP 73 (HSC 70) Molecular chaperone Constitutively itable, transient resistance to a lethal heat stress that is acquired
expressed after previous exposure to a nonlethal level of heat stress.
  HSP 75 Molecular chaperone Mitochondrial
Increased HSP 70 expression is a mechanism of thermotolerance
that protects against heat-induced increases in epithelial perme-
HSP 78 (GRP 79, Bip) Cytoprotection Endoplasmic
ability. A unique in vitro model system consisting of high-
reticulum
resistance Madin-Darby canine kidney (MDCK) epithelial cell
HSP 90 family: HSP 90 monolayers was developed to examine the relationship between
  GRP 96 Glucocorticoid Cytosolic and HSP 70 expression and changes in epithelial integrity with heat
receptor functioning nuclear exposure. Following heat stress to 38.3° C (100.9° F), MDCK
Glucose regulation Endoplasmic monolayers showed increase in permeability that was reversible
reticulum with cooling.216 If the monolayers were preexposed to a condi-
HSP 110/104 Molecular chaperone Cytosolic tioning heat stress of 42° C (107.6° F) for 90 minutes, subsequent
Tumor antigen exposure to a higher temperature of 39.4° C (102.9° F) was
presentation required to increase monolayer permeability.216 Association of a
thermotolerant state with increased HSP 70 expression suggests
Data from Hartl FU, Hayer-Hartl M: Molecular chaperones in the cytosol: From that HSPs shift the temperature threshold upward to prevent
nascent chain to folded protein, Science 295:1852, 2002; and Kregel KC: Heat
shock proteins: Modifying factors in physiological stress responses and acquired heat-induced disruptions in epithelial permeability.216 Follow-up
thermotolerance, J Appl Physiol 92:2177, 2002. studies showed that HSPs interact with proteins in the tight junc-
Bip, Binding protein; GRP, glucose-regulated protein; HSC, heat shock cognate. tions of the epithelium to regulate permeability. Occludin is a

262
plasma membrane protein located at tight junctions that was
increased, along with HSPs 27, 40, 70, and 90, in intestinal epi-
thelial monolayer (Caco-2) cells exposed to 39° or 41° C (102.2°
or 105.8° F). Treatment of Caco-2 cells with quercetin (an inhibi-
tor of HSF-1) inhibited HSPs and occludin expression and
reversed the thermotolerant state of these cells.72 These studies
demonstrate a complex interaction between HSPs and tight-
junction proteins for modulation of epithelial barrier function
during thermal stress.
It is interesting to speculate that differences in HSP expres-
sion profiles may be a sensitive marker of heat stress susceptibil-
ity among different populations. During the life of an organism,
there is accumulation of protein damage caused by continual
oxidant and free radical activity within cells. The life span of
Drosophila was extended by heat shock treatment or the addi-
tion of HSP 70 gene copies, suggesting that increased protein-
chaperoning activity may protect against aging.155 In rats, aging
was associated with a significant reduction in liver HSP expres-
sion after passive heat exposure, which was associated with
greater liver damage compared with that observed in young
rats.168,339 Older animals do not appear to have a global inability
to express HSP, because exertional heat stress can induce
expression profiles similar to those of mature rats.168 Rather,
aging is associated with reduction in the threshold for HSP
stimulation.168 Similarly, Fargnoli and co-workers83 showed that
global reduction in protein synthesis was not responsible for
decreased HSP induction in aged lung fibroblasts. Alzheimer’s
disease is thought to be a consequence of decreased HSP func-
tion that results in increased deposition of abnormally folded
proteins.215 It is anticipated that screening for altered HSP titers
will help to identify individuals with reduced thermotolerance
caused by aging, infection, or other conditions that may predis-
pose to heatstroke.159
HEATSTROKE TREATMENTS
(See Chapter 13)
Current heatstroke therapies fall into two categories: supportive
therapies directed at the immediate clinical symptoms and thera-
pies directed at the causative mechanisms of injury. The primary
objectives of clinical heatstroke treatments are to reduce body
temperature as rapidly as possible, reestablish normal CNS
function, and stabilize peripheral multiorgan system function.
Supportive therapies consist of rapid cooling and IV fluid admin-
istration for restoration of normal blood pressure and tissue
perfusion. Advanced therapies are directed at coagulation and
inflammatory disturbances that cause organ failure. Despite thera-
peutic efforts, heatstroke morbidity and mortality rates remain
quite high, and multiorgan system dysfunction continues to claim
the lives of heatstroke patients during ensuing years of recov-
ery.10,320 This section discusses conventional clinical treatments of
heatstroke, as well as innovative treatment strategies targeted at
SIRS to mitigate injury and death.
COOLING
Rapid cooling is considered the single most important treatment
for protection against permanent CNS damage and death from
heatstroke. To facilitate cooling, the individual should be placed
into a supine position and as many clothes as possible removed
to expose a large surface area of the body to facilitate heat
transfer. If comatose, the individual should be placed onto his
or her side (recovery position) to facilitate an open airway. Ice-
water immersion is an effective cooling technique that requires
placement of a heatstroke patient in a tub of ice water while the
extremities are massaged to promote increased skin blood flow
for heat dissipation. This technique relies on conductive heat
transfer and is currently recommended by the American College
of Sports Medicine and the National Athletic Trainer’s Association
for treatment of EHS.11,25 Ice-water immersion of military heat-
stroke patients was effective in reducing body temperature to
approximately38.5° C (101.3° F) within 10 to 60 minutes.19,61,229
Using an ice bath or ice packs on the skin surface has met with
some resistance because it is thought that cooling of the skin will
CHAPTER 12  Pathophysiology of Heat-Related Illnesses
elicit peripheral vasoconstriction and shivering.157,248,337 Young, fit
test volunteers were heat-stressed to 40° C (104° F) and experi-
enced shivering and cold sensations during immersion in cold
water.337 However, the threshold for activation of shivering is
probably increased in heatstroke patients, such that the risk of
cold-water or ice-water immersion eliciting such a response and
compromising the benefits of cooling is unlikely. Ice-water
immersion of young, healthy individuals is a safe and effective
method of cooling, whereas this technique is not well tolerated
in elderly patients with classic heatstroke.120 Additional limitations
to consider with ice-water immersion include inability to admin-
ister external defibrillation in an immersed individual and the
need for multiple assistants for placement into and removal from
the bath.
Evaporative cooling is based on the premise that conversion
of 1.7 mL of water to a gaseous phase will remove 1 kcal of
heat. Efficiency of this cooling technique is improved by remov-
ing all clothing and spraying tepid water on the patient while
evaporation and convection are facilitated with fanning. To
reduce peripheral vasoconstriction, a body-cooling unit was
designed to spray atomized water (15° C [59° F]) and blow hot
air (45° C [113° F]) over the entire body surface to maintain skin
temperature at 32° to 33° C (89.6° to 91.4° F).327 However, effi-
ciency of this method for rapid cooling of classic heatstroke
patients was similar to conventional methods that involved cover-
ing patients in a wet sheet sprayed with tap water accompanied
by fan blowing.4 Fanning is used to accelerate convective and
evaporative cooling by increasing conversion of water to the
gaseous phase. Helicopter downdraft is another method of evap-
orative cooling that was reported to have better results than the
body-cooling unit, but availability and feasibility of this technique
are limited.248 Evaporative cooling techniques are reasonable
alternatives to ice-water immersion for classic heatstroke patients
because they are easily applied, readily accessible, and well toler-
ated by frail elderly individuals.
Dantrolene and NSAIDs have been tested for their effects on
prevention of heat illness and for body cooling, but neither class
of drugs has shown efficacy for protection against heatstroke.
Dantrolene protects against malignant hyperthermia by lowering
intracellular calcium concentrations in skeletal muscle to decrease
muscle tone. Dantrolene is effective for the treatment of malig-
nant hyperthermia, which is a genetic mutation that predisposes
to involuntary muscle contractions and rigidity after exposure to
general anesthetics or muscle-depolarizing agents. Dantrolene
has been considered a treatment for heatstroke, but animal and
human heatstroke studies have failed to validate its use for this
condition. A randomized, double-blind, placebo-controlled trial
of Hajj heatstroke patients failed to show a cooling advantage of
dantrolene over traditional cooling methods.31,52 As discussed
later, malignant hyperthermia is distinct from exertional or passive
heatstroke, so it is not surprising that dantrolene does not protect
equally against these diverse conditions.
The NSAIDs have been considered therapeutic drugs based
on their potent antiinflammatory and antipyretic effects. The
actions of classic NSAIDs, such as aspirin, ibuprofen, and
acetaminophen, are attributed primarily to blockade of the
cyclooxygenase (COX) pathway of eicosanoid metabolism
(Figure 12-10).
Prostaglandins are synthesized by the COX pathway in
response to a variety of stimuli (e.g., bacterial infection, heat
shock) and regulate a multitude of physiologic responses, includ-
ing fever, inflammation, and cytokine production. During fever,
prostaglandins are released in response to proinflammatory cyto-
kines (e.g., IL-1, IL-6) and stimulate an increase in the tempera-
ture set point to induce fever.294 Inhibition of prostaglandin
production by NSAIDs is the primary mechanism for the anti-
pyretic (i.e., fever-reducing) actions of these drugs. However,
hyperthermia in response to heat exposure is not caused by an
increase in the temperature set point, but rather by an unregu-
lated increase in body temperature that occurs when heat gain
exceeds heat loss in the absence of a change in the temperature
set point. Furthermore, aspirin and acetaminophen may aggra-
vate gut bleeding tendencies and accelerate liver damage,
263
 Cell membrane
Phospholipids
NSAIDs
PLA2
Acetaminophen Arachidonic acid (AA)
Salicylic acid
Ibuprofen COX LOX
Liver toxicity
Prostaglandins
Leukotrienes
Thromboxanes
Leukocyte aggregation
Fever
Vascular permeability
Platelet aggregation
Vasomotor changes
Induce IFNγ, IL-1, IL-2
Inhibit IL-1, IL-2
FIGURE 12-10  Eicosanoid metabolism is initiated when cell mem-
brane phospholipids are converted to arachidonic acid (AA) by enzy-
matic actions of phospholipase A2 (PLA2). Cyclooxygenase (COX)
converts AA to prostaglandins and thromboxanes, whereas the lipo-
oxygenase (LOX) pathway is responsible for production of leukotri-
enes. Nonsteroidal antiinflammatory drugs (NSAIDs) block the action
of COX enzymes with potential toxic effects on the liver. IFNγ,
Interferon-γ; IL-1, interleukin-1; IL-2, interleukin-2.
respectively. In a mouse model of heatstroke, an acute oral dose
of indomethacin (a potent antipyretic NSAID) provided immedi-
ately before heat exposure resulted in a 40% increase in heat-
stroke mortality because of extensive gut hemorrhaging.178
Increased mortality was also observed in heat-exposed rats
COLD AND HEAT
injected peripherally with aspirin.153 Aspirin has also been shown
to attenuate protective, reflexive skin blood flow responses
required for adequate heat dissipation.131,206 Aspirin will therefore
predispose to heatstroke collapse. Given that NSAIDs do not
attenuate hyperthermia and that organ (e.g., gut, liver) toxicity
of these drugs is exacerbated with heat, they are contraindicated
for prophylaxis or treatment of heatstroke patients.
Alcohol sponge baths are inappropriate under any circum-
stances, because transcutaneous absorption of alcohol may lead
PART 2
to poisoning and coma.
FLUID RESUSCITATION (See Chapter 89)
One of the first lines of defense against permanent tissue damage
is treatment with resuscitation fluids. The objective of IV fluid
administration is to restore intravascular volume and rehydrate
the interstitium to stabilize cardiovascular functioning, improve
tissue perfusion, and maintain immune function. The resuscita-
tion fluid optimally needs to be safe, efficacious, and easy to
transport for use in military or athletic settings and have the
capability to restore tissue oxygen perfusion and minimize cel-
lular and tissue injury. Blood provides oxygen-carrying capacity
and volume, but supply is limited, with a risk for allergic or
infectious reactions, difficulties with crossmatching, and potential
for high hemoglobin levels to increase blood viscosity and reduce
nutrient flow to the tissues.259 Balanced salt solutions, such as
saline and lactated Ringer’s, have a long shelf life and are inex-
pensive and in unlimited supply, with a minimal risk for disease
transmission. However, they are able freely to cross semiperme-
able capillary membranes, which increases the risk for tissue
edema and makes frequent transfusions necessary to maintain
adequate plasma volume.119,152,307 Tissue edema increases the
distance from blood vessels to tissue mitochondria and limits
oxygen delivery to the tissues. There is a greater risk for edema
in heatstroke patients because of increased capillary permeability
and lack of muscle movement that limits lymph flow following
collapse.
To minimize the adverse consequences of balanced salt solu-
tions, these fluids may be replaced with colloid solutions. Natural
colloids, such as albumin, possess antioxidant properties that
reduce tissue injury during times of oxidant stress, but carry a
risk for infection.94,341 Dextran is an artificial colloid that was used
after World War II until adverse hemostatic effects restricted its
use to specific clinical conditions, such as deep vein thrombosis
and pulmonary embolism.21,66 Hydroxyethyl starch (HES) is a
264
blood plasma substitute that exerts high colloidal pressure to
stimulate movement of fluid from the interstitial space into the
blood vessel lumen for plasma volume expansion.238,334,341 Small-
volume treatment with HES protected against heatstroke mortality
in rats, but use of HES in other heatstroke animal models and
humans has not been validated.192 Because of severe dehydration
and acute renal failure with heatstroke, fluid shifts from the
interstitial fluid into the vessel lumen may mean HES will not be
well tolerated in patients with severe heatstroke patients (see
Chapter 13).
ANTICOAGULANTS
Anticoagulants (e.g., heparin, aspirin) have been examined for
heatstroke protection, with mixed results. Heparin therapy has
been associated with positive heatstroke outcome in patients,
although it is difficult to dissociate the direct effects of this
therapy from other clinical treatments.247,292 The mechanisms of
heat-induced DIC may include prostaglandin synthesis, because
aspirin has shown protection against platelet hyperaggregation
in vitro and in animal models. In human volunteers, ingestion of
aspirin 12 to 15 hours before blood sampling or heat exposure
of cells was effective in inhibiting platelet hyperaggregation.
However, aspirin was ineffective if provided after heat exposure,
even though complete inhibition of the arachidonic acid pathway
was achieved.97 The ability of aspirin to protect guinea pigs from
DIC induced by Staphylococcus aureus suggests that similar
activities function in vivo to control platelet reactivity.225 However,
there is currently insufficient evidence to support the use of
aspirin as a preventive measure in heatstroke patients. Given the
hormonal and metabolic alterations that accompany heatstroke,
including dehydration, increased catecholamine levels, and
hypoxia, the mechanisms responsible for DIC extend beyond
those mediated by prostaglandins alone. Furthermore, aspirin
and other antiinflammatory drugs can cause liver damage if con-
sumed in large quantities, as previously mentioned.
Recombinant activated protein C (APC) is an effective antiin-
flammatory drug for treatment of sepsis and may also hold
promise as a treatment for heatstroke patients. APC efficacy
appears to depend on a variety of patient conditions, including
age (most effective in patients >50), extent of organ dysfunction
(benefit not apparent if failure of only one organ), and the pres-
ence of shock at infusion, which improves its efficacy.326 In rat
heatstroke models, the efficacy of APC depends on the time of
treatment. A single dose of recombinant human APC provided
at the onset of heatstroke inhibited inflammation and coagulopa-
thy, prevented organ failure, and improved survival; however, if
treatment was delayed for 40 minutes after onset of heatstroke,
there was no beneficial effect on survival time.54 The efficacy of
APC was less obvious in a baboon heatstroke model. Infusion
for 12 hours after heatstroke onset attenuated plasma IL-6, throm-
bomodulin, and procoagulant components but had no effect on
mortality.35 APC is the first biologic agent approved in the United
States for the treatment of severe sepsis based on two decades
of research,326 but there is insufficient evidence to justify use of
this treatment in heatstroke patients.
ANTICYTOKINE THERAPIES
As previously described, attenuations in splanchnic blood flow
during heatstroke contribute to increased gut permeability and a
rise in circulating endotoxin. This series of events is hypothesized
to stimulate the increased plasma cytokine levels implicated in
the adverse consequences of SIRS. Based on these findings, the
question arises: Do anticytokine therapies represent an effica-
cious treatment strategy for heatstroke? No controlled studies
have examined the efficacy of anticytokine therapies on patient
outcome with heatstroke. However, clinical sepsis trials indicate
that potential protective effects of anticytokine therapies need
to be viewed with cautious optimism. Sepsis patients display
high circulating IL-1 levels that correlate with morbidity and
mortality, but IL-1ra treatment has been unsuccessful in reducing
mortality.236,257 A comparison of 12 randomized, double-blind
multicenter trials of more than 6200 sepsis patients showed
no significant benefit of antiendotoxin antibodies, ibuprofen,
plasminogen-activating factor receptor antagonist, anti-TNF
monoclonal antibody, or IL-1ra on all-cause mortality.68
There are several explanations for negative results from anti-
cytokine therapies, including the possibility that the mediator has
no pathophysiologic role in the response, the agent failed to
neutralize the protein (because of a lack of biologic activity,
competition by other mediators, or inadequate anatomic distribu-
tion), compensatory increase of other mediators with similar
activities, administration too early or too late in the course of
disease, too-short therapy duration, or need for combination
therapy.203 Kinetic studies have shown that the half-life of IL-1ra
is approximately 20 minutes, and Phase III clinical trials showed
that circulating IL-1β levels at the time of clinical treatment were
undetectable in 95% of the patient population.87,249 Exposure to
anticytokine therapies before sepsis onset is thought to be desir-
able (but practically is infeasible), although this may suppress
shifts in Th1/Th2 immune responses that are important for resolu-
tion of infection. On the other hand, anticytokine therapies given
too late in sepsis progression may shift the Th1/Th2 milieu in an
unpredictable manner or may have no effect because of the
overwhelming nature of the septic event.110 The transient nature
of cytokine production and/or clearance and lack of correlation
between serum levels and disease severity further complicate
treatment scenarios. Given the short half-life of TNF-α (~6 to 7
minutes)22 and biphasic clearance patterns of IL-1β and IL-6
(rapid disappearance in first 3 minutes followed by attenuated
clearance over next 1 to 4 hours),161 the narrow protective
window in which anticytokine therapies may be effective is a
difficult obstacle to overcome.
Interleukin-10 is a potent antiinflammatory cytokine that sup-
presses production of several proinflammatory cytokines, includ-
ing IL-1β, IL-6, and TNF-α, and is part of an important negative
feedback loop during infection and disease.111,314 Few, if any,
studies have investigated efficacy of IL-10 treatment for heat-
stroke recovery, although the cytokine has been frequently used
in treatment of multiple autoimmune diseases, including rheu-
matoid arthritis, Crohn’s disease, multiple sclerosis, and sepsis.41,231
As with other cytokines, timing of IL-10 administration must be
carefully considered. IL-10 decreases IFN-γ production by natural
killer and Th1 cells, which may suppress clearance of infectious
organisms (via IFN-γ).258,319 Consistent with anticytokine thera-
pies, beneficial effects of exogenous IL-10 administration depend
on multiple factors, including time of administration, route, and
site where the cytokine is targeted.231,267 These considerations,
along with the immunosuppressive and unpredictable nature of
IL-10–based therapies, have resulted in diminished enthusiasm
for anticytokine therapies for sepsis.
HEATSTROKE PREVENTION
Heatstroke is currently a more preventable than treatable disease.
The most effective preventive measures include acclimatization
to the heat, reductions in duration and extent of physical activity,
rescheduling of activities to cooler times of the day, increased
consumption of nonalcoholic fluids, and removing vulnerable
populations, such as those with preexisting viral or bacterial
infections, from the heat stress environment. Fan cooling has not
shown protection against heatstroke and is associated with
increased thermal discomfort at temperatures higher than 38° C
(100.4° F).158
HEAT ACCLIMATIZATION
Climatic heat stress and exercise interact synergistically to increase
body temperature (core and skin) and cardiovascular strain, and
to decrease performance in the heat. Heat acclimatization is one
of the within-lifetime changes in an organism (vs. evolutionary
changes) that protect against the negative effects of heat strain.
Heat acclimatization occurs after exposure to the natural envi-
ronment, whereas heat acclimation develops after exposure to
artificial conditions. However, these terms are used interchange-
ably because they induce similar physiologic adaptations.328 Heat
acclimation occurs after repeated bouts of heat exposure that are
CHAPTER 12  Pathophysiology of Heat-Related Illnesses
BOX 12-3  Heat Acclimation Strategies
Must Mimic Climate of Athletic Event or Occupational Setting
and Include Adequate Heat Stress
• Heat must be sufficient to cause heavy sweating.
• Use exercise/rest cycles to intensify or diminish the effect of the
heat stress on bodily functions.
• Include at least 6 to 14 days of adequate heat stress.
• Exercise daily for at least 90 minutes.
Start with Acclimation and Exercise Training
• Be flexible in scheduling training.
• Build confidence.
• Performance benefits may take longer to achieve than
physiologic benefits.
Methods of Heat Acclimation
• Use a climate-controlled room (sauna or heat chamber) or hot
weather.
• Incorporate training by including additional acclimation
sessions.
Days Leading to Athletic Performance or Event
• Start slowly, and decrease training duration and intensity; limit
heat exposure.
• Acclimatize in heat of the day.
• Train in coolest part of the day.
• Use appropriate work/rest cycles.
• Be vigilant of salt and fluid needs, especially during the first
week of acclimation.
of sufficient intensity, frequency, duration, and number to elevate
core and skin temperature and induce profuse sweating. Heat
acclimation may be achieved after exercise or rest in the heat,
although the former method is more effective. It is important to
note that heat acclimatization is specific to the climate and activity
level; therefore, if individuals will be working in a hot, humid
climate, heat acclimatization should be conducted under similar
conditions (Box 12-3).
Although heat acclimation does not require daily exposure to
heat and exercise, the rapidity with which biologic adaptations
are achieved is slower with less frequent exposures. This was
shown experimentally in human volunteers in whom heat accli-
mation was achieved after 10 days of daily heat exposure, but
required 27 days when the frequency of exposure was reduced
to every third day of experimentation (conditions: 47° C [116.6° F],
17% relative humidity).84 Continual 24-hour exposures are also
not required, because daily 100-minute periods of exposure were
adequate to produce heat acclimation in participants exposed to
dry heat.188 However, because of the transient nature of the
biologic adaptations, continued heat exposures are required to
maintain the acclimated state. Aerobically trained athletes retain
heat acclimation benefits longer than unfit individuals because
they are exposed to high body temperatures during training
exercises.239
Improvements in thermal comfort and exercise performance
are achieved in heat-acclimated individuals through a variety of
physiologic mechanisms, including a lower threshold and higher
rate of skin blood flow, reduction in metabolic rate, earlier onset
and rate of sweating, and improvements in cardiovascular func-
tion and fluid balance.272 Figure 12-11 illustrates the effect of 10
days of heat acclimation on heart rate, core temperature, and
mean skin temperature responses of individuals walking on a
treadmill in a desert type of environment.80 On the 10th day of
acclimation, heart rate was lower by approximately 40 beats/min,
and rectal and skin temperatures were reduced approximately
1° C (1.8° F) and 1.5° C (2.7° F), respectively.
Once heat acclimation is achieved, skin vasodilation and
sweating are initiated at a lower core temperature threshold, and
higher sweat rates can be sustained without the sweat glands
becoming “fatigued.”60,91 Whereas an unacclimated individual will
secrete sweat with a sodium concentration of approximately
60 mEq/L (or higher), the concentration of secreted sodium from
the sweat glands of an acclimated individual is significantly
265

160
Heart rate (bpm)
140
120
100
80
39
temperature (° C)
Rectal
38
37
38
37
temperature (° C)
36
35
Skin
34
33
32
31
COLD AND HEAT
1 2 3 4 5 6 7 8 9 10
Cool
control Acclimation (days)
FIGURE 12-11  Effect of 10 days’ acclimation on heart rate and rectal
and skin temperatures during a standard exercise (five 10-minute
periods of treadmill, separated by 2-minute rests) in dry heat. Large
PART 2
circles, Values before start of the first exercise period each day; small
circles, successive values; squares, the final values each day. Controls
of exercise in cool environment before and after acclimation. (Modified
from Eichna LW, Park CR, Nelson N, et al: Thermal regulation during
acclimatization in a hot, dry (desert type) environment, Am J Physiol
163:585, 1950.)
lower, at about 5 mEq/L.264 This effect of heat acclimation on salt
conservation is thought to be caused by increased aldosterone
secretion or responsiveness of the sweat glands to this steroid
hormone, which is released by the adrenal cortex and increases
resorption of ions and water in the distal tubules and collecting
ducts of the kidneys.92,160
Overall improvements in fluid balance with heat acclimation
include reduced sweat sodium losses, better matching of thirst
to body water needs, and increased total body water and blood
volume.195 Provided that fluids are not restricted during physical
activities, heat-acclimated individuals will be better able to main-
tain hydration during exercise and show a marked reduction in
“voluntary” dehydration.17,80,272 Although controversy surrounds
the ability of heat acclimation to alter the maximum temperature
that can be tolerated during exercise in the heat,221 individuals
who live or train in hot environments may experience reduced
incidence of syncope17,107,250 (Figure 12-12).
An essential cellular adaptation of heat acclimation is altered
expression or reprogramming of genes that encode constitutive
and stress-inducible proteins.133 Heat acclimation is associated
with downregulation of genes associated with energy metabo-
lism, food intake, mitochondrial energy metabolism, and cellular
maintenance processes and upregulation of genes that are linked
with immune responsiveness.133 The HSPs are the most exten-
sively studied heat-inducible proteins and show faster transcrip-
tional response and elevated cellular reserves (HSP 72 specifically)
in heat-acclimated versus nonacclimated individuals.133,134,198,205
266
That is, whereas nonacclimated individuals require de novo HSP
72 synthesis for cellular protection, individuals who reside in hot
climates maintain elevated HSP 72 levels.194 The cellular mecha-
nisms of heat acclimation are not fully understood, but are
thought to involve global and tissue-specific changes in genes
involved in thermal responsiveness, DNA repair and synthesis,
free radical scavenging, and apoptosis.133
GENETIC POLYMORPHISMS
Heatstroke susceptibility is influenced by complex interactions
between environmental and host genetic factors. Emerging
molecular technologies have improved our understanding of the
genetic mutations and polymorphisms that might predispose to
heat illness or inhibit resolution of SIRS. It is anticipated that
ability to prescreen individuals for genetic polymorphisms that
may prevent resolution of SIRS will help in developing more
effective therapies to alleviate morbidity/mortality in these
individuals.
SINGLE NUCLEOTIDE POLYMORPHISMS
Single nucleotide polymorphisms (SNPs) are variations in the
nucleotide sequence of DNA that can affect physiologic responses
to environmental stimuli. SNPs have been implicated in a variety
of diseases, including sepsis, type 1 diabetes, arthritis, inflamma-
tory bowel disease, and rheumatic fever.89,143,253,297 The identifica-
tion of SNPs in the promoter region of genes suggests that disease
susceptibility may be affected by altered transcription of immune
determinants of clinical outcome. SNPs have been identified in
IL-1, IL-2, TNF, IFN-γ, IL-10, IL-1ra, TLR2, and TLR4. The risk for
death from sepsis is significantly increased in patients with a
genetic polymorphism in the TNF-α or TNF-β gene.93 Even for
Cool
cytokine polymorphisms located distal to a critical promoter
control
region that do not directly affect gene transcription rates, coin-
heritance of multiple immune-responsive genes by a process
known as linkage disequilibrium can alter immune function.
Some TNF-α polymorphisms exist in linkage disequilibrium with
human leukocyte antigen (HLA) haplotypes that encode cell
surface antigens. Coinheritance of these genes may ultimately be
responsible for poor sepsis outcome.146,297
20
experiencing syncope
15
Subjects
10
5
1 2 3 4 5 6 7 8 9
Days of heat acclimation
FIGURE 12-12  Incidence of syncope among 45 participants who lived
in and trained at cool ambient temperatures and could complete a
physical training regimen without mishap. They were then relocated
to a hot environment, where they carried out the same physical training
regimen. (Modified from Bean WB, Eichna LW: Performance in relation
to environmental temperature: Reactions of normal young men to
stimulated desert environment, Fed Proc 2:144, 1943; and Hubbard
RW, Armstrong LE: The heat illness: Biochemical, ultrastructural, and
fluid-electrolyte considerations. In Pandolf KB, Sawka MN, Gonzalez
RR, editors: Human performance and environmental medicine at ter-
restrial extremes, Indianapolis, 1988, Benchmark Press, pp 305-359.)
MALIGNANT HYPERTHERMIA
Malignant hyperthermia (MH) is a genetic disorder that causes
muscle rigidity, hyperthermia, tachycardia, and metabolic acido-
sis during exposure to volatile anesthetics or depolarizing skeletal
muscle relaxants. Exercise, heat stress, and emotional stress also
trigger reactions in 5% to 10% of MH patients.70,325 MH reactions
result from massive release of calcium from the type 1 ryanodine
receptor (RyR1) of the sarcoplasmic reticulum, which overwhelms
cellular mechanisms of calcium homeostasis and activates actin-
myosin filaments to cause muscle rigidity and hyperthermia.230
RyR1 is the most common mutation in skeletal muscle, but addi-
tional isoforms have been identified in B and T cells, thalamus,
hippocampus, and heart.169,208,302 Activation of RyR1 by a variety
of pharmacologic compounds, including caffeine, halothane, and
the muscle relaxant 4-chloro-m-cresol, has led to development
of an in vitro contracture test of skeletal muscle biopsies to
identify MH individuals.268,342 Dantrolene is used to treat MH reac-
tions by lowering intracellular calcium stores, decreasing muscle
metabolic activity, and preventing hyperthermia. Using dan-
trolene, in combination with improved monitoring standards and
early detection with the in vitro contracture test, has helped
reduce mortality from greater than 70% to less than 5% in MH
patients.191
Malignant hyperthermia has been identified in several animal
species, including dogs,228 boars,277 cats,18 and horses,6 but the
most common experimental animal is a porcine MH model that
possesses a single mutation in the skeletal muscle RyR1 gene.
These animals develop the MH syndrome in response to inhala-
tional anesthetics, exercise, heat, and other stressors.313 Mild
exercise exacerbates MH symptoms in response to anesthetics in
MH pigs, suggesting that inflammatory mediators released by
skeletal muscle may contribute to the MH syndrome.313 MH
patients show an approximately fivefold higher expression of
IL-1β when stimulated with caffeine and 4-chloro-m-cresol com-
pared with control cells.103 Recent development of a transgenic
mouse model that overexpresses the RyR1 receptor has proved
useful to study the MH/EHS link and could shed light on the
role played in this syndrome by inflammatory cytokine produc-
tion from skeletal muscle or other organs.79 Association of RyR1
mutations with EHS incidence suggests that screening young,
healthy individuals (e.g., athletes, military personnel) for the MH
mutation could be a powerful tool to determine heatstroke
susceptibility.
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CHAPTER 13 
Clinical Management of
Heat-Related Illnesses
KAREN K. O’BRIEN, LISA R. LEON, ROBERT W. KENEFICK, AND FRANCIS G. O’CONNOR
This chapter discusses definitions, clinical manifestations, medical
management from the field through hospital discharge, return-
to-activity considerations, and prevention of heat-related ill-
nesses. The spectrum of injuries ranges from milder conditions
such as heat cramps to fatal manifestations such as arrhythmias.
Heat-related illnesses generate complications such as rhabdomy-
olysis and multiorgan dysfunction syndrome and may result in
death from overwhelming cell necrosis caused by a lethal heat
shock exposure. Exertional heatstroke (EHS) is usually character-
ized by development of mental status changes or collapse during
physical activity in a warm environment. Severity of heat illness
depends on degree and duration of elevation in core temperature
(Tco). Heatstroke is an extreme medical emergency that can be
fatal if not treated promptly with rapid cooling. To prevent and
minimize complications and save lives, proper prevention, man-
agement, and clinical care are essential.
EXERTIONAL HEAT ILLNESS
Dehydration and heat exposure can impair exercise performance
and contribute to various illnesses. Exertional heat illnesses
include both minor and serious disorders. Minor heat and
dehydration-related illnesses include heat cramps, erythromelal-
gia, and heat syncope. Heat cramps are characterized by intense
muscle spasms, typically in the legs, arms, and abdomen. Heat
cramps result from fluid and electrolyte deficits and occur most
often in persons who have not been fully acclimated to a com-
bination of intense muscular activity and environmental heat.
CHAPTER 13  Clinical Management of Heat-Related Illnesses
Individuals susceptible to heat cramps are often believed to be
profuse sweaters who sustain large sodium losses.16,114 Heat
syncope (fainting) is characterized by dizziness and weakness
during or after prolonged standing or after rapidly standing up
from a lying or sitting position during heat exposure. Heat
syncope results from blood pooling in the cutaneous and skeletal
vasculature and occurs most often in dehydrated and inactive
persons who are not acclimated.101 Erythromelalgia is character-
ized by pain and swelling of the feet and hands, triggered by
exposure to elevated temperatures.70
Serious illnesses include exertional heat injury (EHI) and EHS.
These illnesses have many overlapping diagnostic features; it has
been suggested that they exist along a continuum on the severity
scale.20 Heat exhaustion is characterized by inability to sustain
cardiac output in the presence of moderate (>38.5° C [101° F]) to
high (>40° C [104° F]) body temperature and is frequently accom-
panied by hot skin and dehydration. EHI is a moderate to severe
illness characterized by injury to an organ (e.g., liver, kidneys,
gut, muscle) and usually (but not always) involves a high Tco of
more than 40° C (104° F). EHS is a severe illness characterized by
central nervous system (CNS) dysfunction (e.g., confusion, dis-
orientation, impaired judgment) and is usually accompanied by
a Tco above 40.5° C (105° F). EHI and EHS can be complicated
by cardiac arrhythmia, liver damage, rhabdomyolysis, coagulopa-
thy, fluid and electrolyte imbalances, and kidney failure. Rhab-
domyolysis is most often observed with novel and strenuous
overexertion. Clinical evidence suggests that dehydration in-
creases the likelihood or severity of acute renal failure associated
267
 with rhabdomyolysis.22,99 Among U.S. soldiers hospitalized for
serious heat illness, 25% had rhabdomyolysis and 13% had acute
renal failure.25
Exertional heatstroke is usually associated with prolonged
exertion in a warm climate; in many cases, however, EHS occurs
within the first 2 hours of exercise and not necessarily at high
ambient temperatures.20,40 This is because exertion and environ-
mental heat stress during the 72 hours that precede such an event
strongly influence the individual’s susceptibility to heat illness.43
Using Tco of 40.5° C (104.9° F) as a critical temperature initially to
diagnose EHS is arbitrary. Mental status changes in an individual
performing exertion in the heat should be the defining charac-
teristic of heatstroke unless the individual has sustained head
trauma. At the stage of collapse, profuse sweating is still likely
to be present unless heatstroke develops in an already anhidrotic
individual. Dry skin may be evident either in situations where
the climate is very dry and sweat evaporates easily or when
heatstroke coincides with a severe degree of dehydration.39
Heatstroke is often categorized as either classic or exertional,
with the classic form primarily observed in elderly individuals or
otherwise sick or compromised populations and EHS in appar-
ently healthy and physically fit persons.
CLINICAL MANIFESTATIONS
Clinical manifestations of heatstroke vary, depending on whether
the person experiences classic heatstroke, which is a common
disorder of older adults during heat waves and occurs in the
form of epidemics, or EHS,1 which occurs when excess heat
COLD AND HEAT
generated by muscular exercise exceeds the body’s ability to
dissipate it (Table 13-1). Some overlap in presentation may occur;
treatment with a medication (e.g., antihypertensive or antipsy-
chotic) that places an older adult at risk for classic heatstroke
also places an exercising individual at risk for EHS. The clinical
picture of heatstroke usually follows a distinct pattern of events
with three phases: (1) acute, (2) hematologic or enzymatic, and
(3) late.41
Acute Phase
PART 2
The acute phase of heatstroke is characterized by CNS manifesta-
tions. Because brain function is very sensitive to hyperthermia,
this phase is present in all heatstroke patients. Early signs of CNS
dysfunction are typically cerebellar and include ataxia, poor
coordination, and dysarthria.124 Advanced signs of CNS depres-
sion include irritability, aggressiveness, stupor, delirium, and
coma.2,24,110 Mental status changes usually resolve after return to
TABLE 13-1  Comparison of Classic and Exertional Heatstroke
Characteristics Classic
Age group Young children and older adults
Health status Chronically ill
Concurrent activity Sedentary
Drug use Diuretics, antidepressants, antihypertensives,
anticholinergics, and antipsychotics
Sweating May be absent
Lactic acidosis Usually absent; poor prognosis if present
Hyperkalemia Usually absent
Hypocalcemia Uncommon
Hypoglycemia Uncommon
Creatine phosphokinase Mildly elevated
Rhabdomyolysis Unusual
Hyperuricemia Mild
Acute renal failure <5% of patients
Disseminated intravascular coagulation Mild
Mechanism Poor dissipation of environmental heat
Modified from Knochel JP, Reed G: Disorders of heat regulation. In Kleeman CR, Maxwell MH, Narin RG, editors: Clinical disorders of fluid and electrolyte
metabolism, New York, 1987, McGraw-Hill.
268
normal Tco. After a return to normothermia, persistence of coma
is a poor prognostic sign.62,110 Other symptoms include fecal
incontinence, flaccidity, and hemiplegia. Cerebellar symptoms
may persist beyond the acute phase.77,110,124
Other common disturbances during the acute phase occur in
the gastrointestinal (GI) and respiratory systems. GI dysfunction,
including diarrhea and vomiting, often occurs. However, the
vomiting may reflect translocation of toxic gram-negative bacte-
rial lipopolysaccharide from the lumen of the intestines because
of poor splanchnic perfusion as a result of hypotension caused
by increased skin blood flow and from CNS impairment.21,44,110
Hyperventilation and elevation of Tco primarily lead to respiratory
alkalosis, which in EHS may be masked by metabolic acidosis
as a result of increased glycolysis and hyperlacticacidemia.29,82
Hypoxemia may be present in patients with respiratory complica-
tions.31,82,113 Also, oxygen consumption is elevated during hyper-
thermia, with a 10% to 13% increase for every degree Celsius
above euthermia.35
Exertional heatstroke shares many common findings with
systemic inflammatory response syndrome (SIRS).20,105 Endotox-
emia, hyperthermia, and other risk factors (e.g., preexisting infec-
tion) and stressors associated with EHS can trigger this exaggerated
inflammatory response. Patients should be assessed for SIRS after
admission with the use of the following criteria19: body tempera-
ture less than 36° C (98.6° F) or more than 38° C (100.4° F); heart
rate greater than 90 beats/min, tachypnea, or an arterial partial
pressure of carbon dioxide (PaCO2) less than 4.3 kPa (32 mm
Hg); and white blood cell count less than 4000 cells/mm3 (4 ×
109 cells/L) or of more than 12,000 cells/mm3 (12 × 109 cells/L),
or the presence of more than 10% immature neutrophils. When
two or more of these criteria are met, SIRS can be diagnosed.
The presence of systemic inflammatory response markers during
the acute phase predicts the severity of subsequent phases.
Hematologic and Enzymatic Phase
Hematologic and enzymatic disorders peak 24 to 48 hours after
collapse. In the hematologic and enzymatic phase of EHS, hema-
tologic, enzymatic, and other blood parameters are altered. In
humans and experimental animals, hyperthermia results in leu-
kocyte activation49 and changes in lymphocyte subpopulations,
both in absolute numbers and percentages.2 Leukocytes may
range from 20 to 30 × 103/mm3 or higher.13,54 In severe cases,
leukocyte activation is associated with systemic activation of
coagulation cascades.59 In one study, all fatal cases of EHS
involved disturbances in the blood coagulation system.13,109 Pro-
thrombin time, partial thromboplastin time, and the level of fibrin
Exertional
Men ages 15 to 45
Healthy
Strenuous exercise
Usually none
Usually present
Common
Often present
Frequent
Common
Greatly elevated
Frequently severe
Severe
25%-30% of patients
Marked; poor prognosis
Excessive endogenous heat production and
overwhelming heat loss mechanisms
split products increased, with a fall in thrombocytes.41 Clotting
dysfunction peaked 18 to 36 hours after the acute phase of heat-
stroke; 2 to 3 days after heatstroke, prothrombin levels fell to
17% to 45% of normal. Depending on the severity of heatstroke,
thrombocyte values ranged between 110 × 103/mm3 and 0.108,109
This systemic inflammatory response state resembles gram-
negative bacterial sepsis, and it appears that lipopolysaccharide
(a cell wall component of gram-negative bacteria) participates in
the pathophysiology of EHS.46
Enzymes
One of the prominent and almost pathognomonic characteristics
of EHS is appearance of exceptionally high levels of certain cel-
lular enzymes, which implies cell damage or death. Most patients
with EHS show elevation of serum creatine phosphokinase (CPK)
activity and myoglobinuria, which suggests damage to skeletal
muscle.40 CPK values in the range of 103 to 104 international units
(IU) were typically found, with peak values occurring 24 to 48
hours after collapse.33,104 At Tco of 41.8° to 42.2° C (107.24° to
107.96° F), aspartate aminotransferase/transaminase (AST) and
alanine aminotransferase/transaminase (ALT) levels rose by
factors of 25 and 8, respectively, and bilirubin levels approxi-
mately doubled to 1.56 mg/dL.90
These rises in enzyme levels are related to tissue damage,
which in turn depends on Tco and its rates of rise and duration.81
CPK was the most sensitive indicator of increases in Tco, followed
by lactate dehydrogenase (LDH), which is an index of general-
ized tissue damage. CPK levels in EHI and EHS typically peak at
24 to 48 hours. Rising values after this point should alert the
clinician to possibility of an occult compartment syndrome. An
EHI patient may complain of lower-extremity pain that manifests
as a compartment syndrome. During the 1994 Hajj, 26 heatstroke
victims admitted to a heatstroke treatment unit had elevated
levels of CPK, AST, ALT, and LDH; these levels remained high
after 24 hours. Those who died had higher enzyme levels than
the survivors. LDH concentration was useful for distinguishing
between those who died and those who had a rapid recovery.
The enzymes were better prognostic indicators than Tco, anion
gap, and serum potassium level.
Late Phase
The late phase of heatstroke manifests 3 to 5 days after collapse
and is characterized by disturbances in renal and hepatic func-
tions. These abnormalities are consistent with multiorgan dys-
function syndrome as a result of SIRS.
Acute renal failure is a common complication of severe cases
and occurs in 25% to 30% of EHS patients.65,73,108 Oliguria and
anuria are characteristic features. During this phase, urine has
been described as being like machine oil, with a high specific
gravity.89,92,100,108 Usually present in the urine are red and white
cells, hyaline and granular casts, and mild to moderate protein-
uria.100 The etiology involves multiple causes,89 but a major factor
is reduced renal blood flow caused by heat-induced hypotension,
hypohydration, and peripheral vasodilation. In addition, direct
thermal injury may lead to widespread renal tissue damage.100
Myoglobinuria and elevated blood viscosity that result from dis-
seminated intravascular coagulation (DIC) may further contribute
to acute oliguric renal failure.92,100,112,119
Usually, EHS is manifested by increased serum levels of liver
enzymes, although acute liver failure has also been reported.42,123
High bilirubin levels, which may last for several days, reflect
hepatic dysfunction and hemolysis. In most cases of EHS, liver
injury is usually asymptomatic and exhibits reversible elevation
in plasma transaminase levels.51 Acute liver failure is documented
in 5% of patients with EHS.66 Hypophosphatemia (<0.5 mmol/L)
at admission may predict occurrence of acute liver failure.42
Despite limited experience and that EHS patients with extensive
liver damage may recover spontaneously, orthotopic liver trans-
plantation had been suggested as a potential treatment.15,50,97
Among 16 reported cases of EHS-induced liver failure,48 three
patients underwent liver transplantation. In the conservatively
managed group, eight patients recovered spontaneously, and five
died. Concomitantly, all three patients who received transplanta-
tion died. Hadad and co-workers48 concluded that, because of
the poor and limited results of liver transplantation after heat-
CHAPTER 13  Clinical Management of Heat-Related Illnesses
stroke, interpretation of prognostic criteria is crucial before listing
a patient for such surgery.
ON-SITE EMERGENCY MEDICAL TREATMENT
Early diagnosis of heat illness can be critical to therapeutic
success. Early warning signs include flushed face, hyperventila-
tion, headache, dizziness, nausea, tingling arms, piloerection,
chilliness, incoordination, and confusion.82 If the patient is alert
and has no mental status changes, he or she can rest in the shade
or indoors, and oral rehydration can be instituted with cold water
or an electrolyte replacement beverage. The concentration of
carbohydrates in such a beverage should not exceed 6%; other-
wise, gastric emptying and fluid absorption by the intestines may
be delayed. Responders should target an intake of 1 to 2 L (1.05
to 2.11 qt) over 1 hour. If the patient does not improve or in
fact worsens, he or she should be evaluated by a medical pro-
vider. All persons with suspected heat injuries should be observed
to ensure that decompensation does not occur. The patient
should continue to rest and drink over the next 24 hours. As a
general rule, for every pound of weight lost by sweating, 0.5 qt
(2 cups or ~500 mL) of fluid should be consumed. It may require
36 hours to completely restore lost electrolytes and fluid volume
to all body compartments via oral intake. After the acute episode,
a medical provider should determine any possible host risk
factors for heat illness and review with the patient the signs of
heat illness and preventive measures to consider.
Any athlete who is performing exercise in warm weather and
who develops mental status changes in the absence of trauma
should be treated as an EHS patient until proved otherwise.39
EHS is a medical emergency. Rapid reduction of elevated Tco is
the cornerstone of EHS management; duration of hyperthermia
may be the primary determinant of outcome.64,108 Cooling should
not be delayed so that a temperature measurement can be
obtained. Cooling measures should be only minimally delayed
for vital resuscitation measures. Nevertheless, it is important to
follow the ABCs (airway, breathing, and circulation) of stabiliza-
tion while cooling efforts are initiated; see Box 13-1 for basic
first-aid information. Before 1950, mortality with EHS was 40%
to 75%.7,38 Long-term survival is directly related to rapid institution
of resuscitative measures.52
In the field, the sick individual should be placed in the shade
and any restrictive clothing removed. There are multiple ways to
cool patients in the field, with cold-water immersion (CWI) being
the most effective modality.27,94 In a remote setting, this can be
accomplished by using a small children’s pool filled with iced
water. The patient should be submerged up to the shoulders and
kept under immediate hands-on supervision at all times. Another
expedient method in the field is to keep bed sheets soaked in a
cooler full of iced water; the person can then be wrapped in the
cold sheets. Particular care should be given to covering the head
and submerging the sheets every few minutes to recool them.85
Ice packs can be applied to the groin, axillae, sides of the neck,
and head to augment iced-sheet cooling. Cooling should con-
tinue until emergency medical services (EMS) providers arrive.
Nonmedical first responders should not attempt to evacuate
heatstroke patients themselves, because this may distract from
cooling efforts. If CWI or iced sheets are not available, the patient
BOX 13-1  Basic First Aid for Heat Illnesses
1. Place the patient in the shade.
2. Assess airway, breathing, and circulation.
3. Initiate cardiopulmonary resuscitation if the patient is pulseless
or apneic.
4. Remove any restrictive clothing.
5. Initiate rapid cooling measures.
6. Activate emergency medical services (EMS).
7. Measure the patient’s rectal temperature to confirm the
diagnosis.
8. Evacuate the patient to the nearest medical facility via EMS.
269
 should be kept wet by applying large quantities (20 to 30 L [5.3
to 7.9 gal]) of tap water or water from any source, and the per-
son’s body should be constantly fanned. Cooling blankets are
generally ineffective as a single modality for inducing rapid low-
ering of body temperature required for treating heatstroke.
EMERGENCY MEDICAL SERVICES TREATMENT
During evacuation, CWI is often not a viable method for treat-
ment. Iced sheets and ice packs can be easily used en route
during transport. Many EMS vehicles now carry refrigerated intra-
venous (IV) fluid to initiate induction of therapeutic hypothermia
in cardiovascular emergencies. When used, chilled IV fluid (4° C
[39° F]) should be peripherally administered.68 Vascular access
should be established without delay by inserting a 12- or 14-gauge
IV catheter. Administration of normal saline or lactated Ringer’s
solution should be started. Recommendations vary regarding
administration rate of fluids. Some clinicians advise a rate of
1200 mL (1.26 qt) over 4 hours,87 whereas others encourage a
2-L (2.11-qt) bolus over the first hour and an additional liter of
fluid per hour for the next 3 hours.106 Patients should be placed
on a cardiac monitor. Administration of supplemental oxygen
may help to meet the patient’s increased metabolic demands and
may also be used to treat the hypoxia often associated with
aspiration, pulmonary hemorrhage, pulmonary infarction, pneu-
monitis, or pulmonary edema.37,73 Blood glucose determination
should be performed, and adults with blood sugar level less than
60 mg/dL should be treated with one ampule of 50% IV dextrose
solution. Children should be treated with 2 to 4 cc/kg of 25% IV
COLD AND HEAT
dextrose solution.
Antipyretics are not effective and may potentially be harmful
to heatstroke patients. Aspirin and acetaminophen lower Tco by
normalizing the elevated hypothalamic set point that regulates
the fever response caused by pyrogens; in heatstroke, the set
point is normal, with Tco elevation reflecting a failure of normal
cooling mechanisms. Furthermore, acetaminophen may induce
additional hepatic damage, and administration of aspirin may
aggravate bleeding tendencies. Aspirin has also been shown to
PART 2
attenuate protective, reflexive skin blood flow responses that are
required for adequate heat dissipation,57,75 which will predispose
to heatstroke collapse. In a mouse model of heatstroke, an acute
oral dose of indomethacin (a potent antipyretic nonsteroidal
antiinflammatory drug [NSAID]) provided immediately before
heat exposure resulted in about a 40% increase in heatstroke
mortality because of extensive gut hemorrhage.69 Similar results
were observed in rats injected peripherally with aspirin.61 Because
NSAIDs do not attenuate Tco during environmental heat exposure,
and their toxicity on the gut and liver is exacerbated with heat,
using these drugs prophylactically or for treatment of heatstroke
patients is not warranted. Alcohol sponge baths are inappropriate
under any circumstances, because transcutaneous absorption of
alcohol may lead to poisoning and coma.
In a comatose patient, airway control should be established
by inserting a cuffed endotracheal tube. Positive-pressure ventila-
tion (PPV) is indicated if hypoxia persists despite supplemental
oxygen administration.
The patient’s altered mental status may adversely affect the
ability of emergency department (ED) personnel to obtain a
detailed history of precipitating events. Lack of such information
may delay diagnosis. EMS transport personnel should attempt to
obtain this history before evacuating the patient and should com-
municate the information to medical staff. Of particular impor-
tance is the duration, and when available, maximum degree of
hyperthermia.
HOSPITAL EMERGENCY MEDICAL TREATMENT
Patients with suspected heatstroke should be placed in a large
treatment room to accommodate the needed number of staff.
Patients are often combative and disoriented before reestablish-
ing their baseline mental status. Aggressive cooling measures
should continue until mental status returns to normal and Tco is
39° C (102° F).27 After discontinuation of cooling, Tco should be
monitored every 5 minutes to ensure that it does not increase.
270
The Tco reported in the field for heatstroke patients may be
significantly higher (e.g., 41.1° C [106.9° F]), than those docu-
mented in the hospital ED (e.g., 37.8° C [100° F]) because Tco may
fall during transport to the hospital.107 Documenting only a mild
elevation in Tco on arrival does not exclude the diagnosis of
heatstroke. CNS disturbances (coma, convulsions, confusion, or
agitation) that accompany hyperthermia may also result from CNS
infection, sepsis, or other disease process. Other diagnoses
should be considered when the patient does not regain normal
mental status after the Tco is normalized in less than 30 minutes.
When Tco remains elevated longer, there is a decreased likelihood
that mental status will normalize with euthermia.20
Core temperature can be measured at several anatomic sites,
but oral, tympanic, esophageal, and rectal temperatures show
regional variations as a result of differences in tissue metabolic
activity, local blood supply, and temperature gradients between
neighboring tissues. During exercise, active skeletal muscle tem-
perature differs dramatically from that of other areas of the body
not directly involved in the activity. Oral temperature is consid-
ered to be similar to blood temperature as a result of the rich
blood supply of the tongue, but it is also influenced by hyper-
ventilation and drinking fluids. Rectal temperature is a highly
reliable indicator of body temperature, but it has a slower
response rate and gives slightly higher readings than do other
sites in the body.
The comparison of oral and rectal temperature values in heat-
stressed underground miners showed a difference of approxi-
mately 1° C (2° F), with oral temperatures underestimating rectal
values.116 Tympanic temperature responds more rapidly to
cooling or heating than does rectal temperature, but it is influ-
enced by changes in the skin temperature of the head and
neck.47,74 The ear should be insulated from the environment to
prevent cool ambient temperatures (<30° C [86° F]) from affecting
this measurement. Esophageal temperature is the most accurate
and responsive to changes in blood temperature, but its instru-
mentation is impractical in severely injured or unresponsive
patients.
If airway control was not previously established and the
patient is still unconscious, a cuffed endotracheal tube should be
inserted to protect against aspiration of oral secretions. Supple-
mental oxygen should be provided, as well as PPV when hypoxia
(PaO2 <55 mm Hg) or hypotension is present. Overvigorous fluid
resuscitation may precipitate pulmonary edema, so careful moni-
toring is indicated. Ideally, 1 to 2 L (1.05 to 2.11 qt) of fluid
should be administered during the first hour after collapse, and
additional fluids should be administered until satisfactory urine
output (0.5 cc/kg/hr in adult and 1.0 cc/kg/hr in child) is estab-
lished.41 Most heatstroke patients arrive with a high cardiac index,
low peripheral vascular resistance, and mild right-sided heart
failure with elevated central venous pressure (CVP). Only moder-
ate fluid replacement is indicated if effective cooling results in
vasoconstriction and increased blood pressure. Providers should
consider noninvasive intravascular volume monitoring or the
minimally invasive monitoring of systolic volume variation and
pulse pressure variation. If these methods are not adequate, a
Swan-Ganz pulmonary artery catheter may be necessary to assess
appropriate fluid supplementation. Some patients have a low
cardiac index, hypotension, and elevated central venous pres-
sure. These persons have been successfully treated with an
isoproterenol drip (1 mg/min).87 Patients with low cardiac index,
low CVP, hypotension, and low pulmonary capillary wedge
pressure should receive fluid. Unless the patient has rhabdomy-
olysis, aggressive fluid hydration is seldom required after initial
treatment.
Cardiac monitoring should be maintained during at least the
first 24 hours of hospitalization. Arrhythmia is most likely to occur
during hyperthermia, but it may also occur as a result of elec-
trolyte abnormalities. Using norepinephrine and other α-adrenergic
drugs should be avoided because they cause vasoconstriction,
thereby reducing heat exchange through the skin. Anticholinergic
drugs that inhibit sweating (e.g., atropine) should also be avoided.
Cooling techniques are ineffective when the patient has sei-
zures that increase body heat storage; therefore, convulsions
should be controlled. IV benzodiazepines are preferred for their
efficacy and renal clearance. Initial dosing is either 4 to 8 mg of
IV lorazepam or 10 mg of IV diazepam. If seizures persist for
more than 10 minutes after the first dose, an additional 4 mg of
lorazepam or 10 mg of diazepam should be administered.
As a result of drastic cooling, skin temperature may decrease
enough to cause shivering. Administration of 12.5 mg of meper-
idine via slow IV push111 or 5 mg of IV diazepam is effective to
suppress shivering and prevent additional rise in Tco from meta-
bolic heat production. If CWI is used, the increase in metabolic
rate as a result of shivering will be more than offset by the high
rate of heat transfer. Therefore, presence of shivering should
not be a cause for concern when this method of cooling is
used.27,91
Severe muscle cramping may be caused by electrolyte imbal-
ances. Magnesium levels should be obtained. If magnesium levels
are low, consideration may be given to the use of 50% IV mag-
nesium sulfate (4 g in 250 mL of 5% dextrose injection at a rate
that does not exceed 3 mL/min).17,18
A Foley catheter should be placed to monitor urine output.
Renal damage from myoglobinuria and hyperuricemia can be
prevented by promoting renal blood flow by administering IV
mannitol (0.25 mg/kg) or furosemide (1 mg/kg).106 If CPK levels
exceed 100,000 IU, alkalinize the urine of patients with exertional
rhabdomyolysis; there is no advantage to alkalinization when
levels are lower. Hemodialysis should be reconsidered if anuria,
oliguria (<0.5 mL/kg/hr of urine for >6 hours), uremia, or hyper-
kalemia develops. Cooling and hydration usually correct acid-
base abnormalities; however, serum electrolytes should be
monitored and appropriate modifications of IV fluids made.
Glucose should be monitored repeatedly, because either hypo-
glycemia or hyperglycemia may occur after EHS.103 Oral and
gastric secretions are evacuated via a nasogastric tube connected
to continuous low suction. Although antacids, proton pump
inhibitors, and histamine-2 (H2) blockers have been used to
prevent GI bleeding, no studies to date demonstrate their efficacy
for heatstroke patients.
Induced Hypothermia
Induced hypothermia is increasingly being used for many neu-
rologic and cardiovascular emergencies, including acute stroke,
neonatal hypoxic-ischemic encephalopathy, and after cardiac
arrest.12,53,84,102 This therapeutic modality has not been evaluated
for effectiveness in individuals with EHS, but may have a role in
cooling severe refractory cases. There may be a role for a period
of induced hypothermia after severe EHS.
Dantrolene
No drug has been found to have a significant effect for reducing
Tco. Antipyretics are ineffective because the thermoregulatory set
point is not affected in heatstroke. Furthermore, antipyretics
might be harmful because they cannot be readily metabolized in
the heat-affected liver, and interactions between NSAIDs and heat
can cause extensive gut injury. However, dantrolene has been
used quite successfully for treatment of several hypercatabolic
syndromes, such as malignant hyperthermia, neuroleptic malig-
nant syndrome, and other conditions characterized by muscular
rigidity or spasticity.115,122 Dantrolene stabilizes the calcium ion
(Ca2+) release channel in muscle cells, thereby reducing the
amount of Ca2+ released from cellular calcium stores. This lowers
intracellular Ca2+ concentrations, muscle metabolic activity,
muscle tone, and thus heat production.30,83 In some studies, dan-
trolene was claimed to be effective for treatment of heatstroke,
whereas in others it improved neither rate of cooling nor sur-
vival.28,34,72,117 In six patients with rhabdomyolysis, intramuscular
Ca2+ concentrations were 11 times higher than in controls, and
dantrolene successfully lowered the elevated Ca2+ level.71 Col-
lectively, the limited data available are at best inconsistent.
Despite growing evidence for a possible benefit of dantrolene
treatment in patients with heatstroke, justification for its routine
use in such cases is not proved, although future clinical trials
may change this assessment.
Moran and colleagues79 studied dantrolene in a hyperthermic
rat model, and found it to be effective as a prophylactic agent
in sedentary animals only. Dantrolene induced more rapid
cooling by depressing Ca2+ entry into the sarcoplasm; this led to
CHAPTER 13  Clinical Management of Heat-Related Illnesses
relaxation of peripheral blood vessels with attenuated production
of metabolic heat. Dantrolene may also be effective in treating
heatstroke by increasing the cooling rate. In other animal models,
however, dantrolene was not superior to conventional cooling
methods.125 As such, dantrolene is not recommended.
Antibiotic Therapy
As previously discussed, in the clinical manifestations of EHI,
EHS shares many common findings with the SIRS.20,106 This rela-
tionship has created an interest in recognition and treatment of
occult or comorbid infection. Numerous systematic reviews and
case reports have identified infection as a risk factor for EHS. In
addition, others postulate that bacterial translocation from the gut
microbiome may take part in the pathophysiology of heatstroke.
Therefore, individual patients with EHS need to be carefully
examined for overt and occult infection so that appropriate
therapies can be initiated. Most importantly, future research is
warranted to address the issue of whether antibiotic treatment
should be evaluated in all heatstroke patients.
SEQUELAE
The combination of the rapid reduction of Tco, control of seizures,
proper rehydration, and prompt evacuation to an emergency
medical facility results in a 90% to 95% survival rate in heatstroke
patients, with morbidity directly related to duration of hyperther-
mia.20,106 A poor prognosis is associated with Tco of more than
41° C (105.8° F), prolonged duration of hyperthermia, hyperkale-
mia, acute renal failure, and elevated serum levels of liver
enzymes. Therefore, misdiagnosis, early inefficient treatment, and
delay in evacuation are the major causes of clinical deterioration.
Full recovery without evidence of neurologic impairment has
been achieved even after coma of 24 hours’ duration and sub-
sequent seizures.109 Persistence of coma after return to normo-
thermia is a poor prognostic sign.110 Red blood cell apoptosis
(i.e., cell blebbing, asymmetry, and shrinkage) on early periph-
eral blood smears is a sign of a very poor prognosis and may
indicate extensive cellular necrosis. Neurologic deficits may
persist, but usually only last for a limited period of 12 to 24
months, and only rarely for longer.
Central nervous system dysfunction becomes increasingly
severe with prolonged duration of hyperthermia and associated
circulatory failure. Nevertheless, coma that persists for up to 24
hours, even with subsequent seizures, is usually followed by
complete recovery without evidence of mental or neurologic
impairment.2,96 However, chronic disability may prevail for several
weeks or months in the forms of cerebellar deficits, hemiparesis,
aphasia, and mental deficiency.2,65,96 Only in exceptional cases,
when coma persisted for more than 24 hours, did mental and
neurologic impairment become chronic and prevail for years.
However, in one study of classic heatstroke, 78% of patients had
minimal to severe neurologic impairment, such as ataxia or dys-
arthria.33 Long-term EHS patients may have increased mortality
from heart, liver, and kidney disease.121
RETURN TO ACTIVITY
Return-to-play/activity (RTP) decision making for the individual
with a history of EHI can be complex. Although the final decision
is most often left in the hands of the providing physician, the
assessments, in particular with athletes, frequently require incor-
poration of both information and execution from the athletic
trainer, physical therapist, coach, and family members, as well
as the athlete. An American College of Sports Medicine (ACSM)
guideline on RTP identified the following key considerations to
assist in safely returning athletes to activity3:
• Status of anatomic and functional healing
• Status of recovery from acute illness and associated sequelae
• Status of chronic injury or illness
• Whether the athlete poses an undue risk to the safety of other
participants
• Restoration of sport-specific skills
• Psychosocial readiness
271
 • Ability to perform safely with equipment modification, bracing,
and orthoses
• Compliance with applicable federal, state, local, school, and
governing-body regulations
The cornerstone assessment in the RTP decision requires
fundamental understanding of the anatomic as well as functional
healing of the particular disorder that affects the athlete. Exer-
tional heat illness RTP is especially challenging because there
is incomplete understanding of the pathophysiologic processes
involved in development of and recovery from EHI.26,76
Despite the frequency of EHI, current civilian and military RTP
guidelines for a particular athlete are largely based on anecdotal
observation, prudence, and caution.76,86 At this time, no evidence-
based guidelines or recommendations exist for returning indi-
viduals, athletes, or soldiers to play or duty. Most guidelines are
commonsense recommendations that require an asymptomatic
state and normal laboratory parameters, coupled with a cautious
reintroduction of activity and gradual heat acclimatization. Current
suggestions range from 7 days to 15 months before EHS patients
return to full activity.8 This lack of consistency and clinical agree-
ment can negatively impact athletes and soldiers and makes it
difficult for medical providers to determine the best solution for
each individual; the inconsistencies also can directly impact mili-
tary readiness. Additionally, whereas current guidance states that
EHS patients may return to practice and competition when they
have reestablished heat tolerance, no evidence-based tools are
available to assess when the body’s thermoregulatory system has
returned to normal.76
This lack of clear evidence-based guidance has allowed some
COLD AND HEAT
medical professionals to clear individuals and athletes for RTP
after EHS without considering exercise heat tolerance deficits,
neuropsychological impairments, or the altered fitness status and
acclimatization status from not being actively engaged in training
during recovery.11,77,96 As with any other injury, RTP should
involve a carefully planned and incrementally increased physical
challenge that is closely supervised by an athletic trainer and
physician, as previously identified in the ACSM conference state-
ment. Current research indicates that most individuals eventually
PART 2
recover fully from EHS; indeed, this occurs in the vast majority
of cases when the athlete is treated promptly with aggressive
cooling strategies (i.e., ice-water immersion).11,26,95
Current Civilian Recommendations
In our opinion, the consensus RTP guidelines set forth by the
ACSM are clear and succinct and provide a rational process for
guiding athletes who have sustained an EHI. Current recommen-
dations from the ACSM for returning an athlete to training and
competition follow8:
1. Refrain from exercise for at least 7 days following release from
medical care.
2. Follow up about 1 week after the incident for a physical
examination and laboratory testing or diagnostic imaging of
the affected organs, based on the clinical course of the
heatstroke.
3. When cleared for RTP, begin exercise in a cool environment
and gradually increase the duration, intensity, and heat expo-
sure over 2 weeks to demonstrate heat tolerance and to initi-
ate acclimatization.
4. If RTP is not accomplished over 4 weeks, a laboratory
exercise–heat tolerance test should be considered.
5. Clear the athlete for full competition if heat tolerant between
2 and 4 weeks of full training.
PREVENTION
Prevention of heat illness relies on an awareness of host risk
factors, a change in behavior and physical activity to match these
risk factors and environmental conditions, and a requirement for
appropriate hydration during physical exercise in the heat. More
aggressive educational activity that explains heat illness and its
prevention to the public should be strongly promoted. Primary
care physicians should incorporate this information into the
anticipatory guidance of routine health assessment. Despite a
wealth of medical literature about heat injury, some athletic
272
coaches continue to use physical or psychological methods to
force athletes to compete or train under intolerably hot condi-
tions. This practice should be viewed as irresponsible, dangerous,
and possibly criminally negligent.
The importance of recognizing milder forms of heat illness
cannot be overstated. Any time heat injuries occur, coaches and
trainers should reassess all athletes and determine what other
measures can be implemented to prevent occurrence of addi-
tional or more serious injuries.
Awareness of Host Risk Factors
Shapiro and Moran104 studied 82 cases of EHS in Israeli soldiers
and concluded that at least one factor that predisposes an indi-
vidual to heatstroke (e.g., diarrhea, lack of acclimatization, poor
fitness) was associated with each case. Correcting individual risk
factors should lead to strategies that can prevent heatstroke. Any
underlying condition that causes dehydration or increased heat
production or that causes decreased dissipation of heat interferes
with normal thermoregulatory mechanisms and predisposes an
individual to heat injury. Older individuals are less tolerant to
EHI than younger persons and are more susceptible to classic
heatstroke because of decreased secretory ability of their sweat
glands and decreased ability of their cardiovascular systems to
increase blood flow to the skin. When healthy young adults
exercise strenuously in the heat, EHS may occur despite the
absence of host risk factors.
Elite and professional athletes, the general public, and the
military have widely used ergogenic aids (e.g., the herb ephedra
[ma huang]) that contain ephedrine to improve performance and
for weight loss. Because ephedra increases metabolic rate, it has
caused numerous cases of heat illness and deaths worldwide and
has been banned by reputable sports authorities. Because there
are no clear ergogenic benefits to ephedra alone, use of ephedra-
containing substances should be discouraged.88
The ratio of basal metabolic rate to surface area is higher in
children than in adults. As a result, a child’s skin temperature is
higher for any given Tco. Although the secretory rates of their
sweat glands are lower, children have greater numbers of active
sweat glands per area of skin than adults and overall greater
sweat rates per unit area.58 Any reduction in the rate of sweating
puts children especially at risk. The primary mechanism for heat-
stroke in young children is hot-vehicle entrapment. Between
1998 and 2010, 462 children died from heatstroke as a result of
vehicular hyperthermia.
The primary means of heat dissipation is production and
evaporation of sweat. Any condition that reduces this process
places the individual at risk for thermal injury. Poor physical
conditioning, fatigue, sleep deprivation, cardiovascular disease,
and lack of acclimation all limit the cardiovascular response to
heat stress.43,60 Obesity places an individual at risk as a result of
reduced cardiac output, the increased energy cost of moving
extra mass, increased thermal insulation, and altered distribution
of heat-activated sweat glands.80 Older adults and younger indi-
viduals show decreased efficiency of thermoregulatory functions
and increased risk for heat injury.
Several congenital or acquired skin abnormalities affect sweat
production and evaporation. Ectodermal dysplasia is the most
common form of congenital anhidrosis. Widespread psoriasis,
poison ivy, sunburn, scleroderma, miliaria rubra (“prickly heat,”
caused by the plugging of sweat ducts with keratin), deep burns,
and prior skin grafting may also limit sweat production.
Dehydration affects both central thermoregulation and sweat-
ing. A mere 2% decrease in body mass through fluid loss pro-
duces increased heart rate, increased Tco, and decreased plasma
volume. In an otherwise healthy adult, GI infection with vomiting
and diarrhea may cause sufficient dehydration to place the indi-
vidual at risk for EHS.
Chronic conditions that may contribute to heat illness include
diabetes mellitus, diabetes insipidus, spinal cord injury, eating
disorders (especially bulimia), and mental retardation. Alcohol-
ism and illicit drug use are among the 10 major risk factors
for heatstroke in the general population.63 An important effect
of alcohol consumption is inhibition of antidiuretic hormone
secretion, which leads to relative dehydration. Autonomic

BOX 13-2  Drugs That Interfere with Thermoregulation
Drugs That Increase Heat Production
• Thyroid hormone
• Amphetamines
• Tricyclic antidepressants
• Lysergic acid diethylamide
Drugs That Decrease Thirst
• Haloperidol
Drugs That Decrease Sweating
• Antihistamines
• Anticholinergics
• Phenothiazines
• Benztropine mesylate
Data from references 15, 34, 53, 72, 113, and 115.
dysfunction, which is present with many chronic diseases, impairs
thermoregulation.55
Despite evidence that hypohydration limits physical perfor-
mance, voluntary dehydration continues to be routine in certain
athletic arenas.6,9,23,118 Wrestlers, jockeys, boxers, and bodybuild-
ers typically lose 3% to 5% of their body mass 1 to 2 days before
competition. In addition to restricting fluid and food, they use
other pathogenic weight control measures, such as self-induced
vomiting, laxatives, diuretics, and exposure to heat (e.g., saunas,
hot tubs, “sauna suits”). Athletes undergoing rapid dehydration
are at risk not only for heat injury but also for other serious
medical conditions, such as pulmonary embolism.32
Box 13-2 highlights common medications that interfere with
thermoregulation. Special attention should be paid to the role of
antihistamines in reducing sweating. This class of medications is
often obtained over the counter, so the general population
should be warned about the dangers of exercising in the heat
when they are taking antihistamines.
Although it has been widely believed that sustaining an
episode of heatstroke predisposes the individual to future heat
injury, this has been refuted in a recent study of heatstroke
patients.10 Ten heatstroke patients were tested for their ability to
acclimate to heat; by definition, the ability to acclimate to heat
indicates heat tolerance. Nine of the patients demonstrated heat
tolerance within 3 months after the heatstroke episode; the
remaining patient acclimated to heat 1 year after injury. In no
patient was heat intolerance permanent. Although individuals
may show transient heat intolerance after thermal injury, evi-
dence for permanent susceptibility to thermal injury is lacking.
ADAPTATION TO ENVIRONMENTAL
CONDITIONS
Appropriate adaptation to hot environmental conditions encom-
passes many forms of behavior, including modifying clothing,
degree of physical activity, searching for shade, anticipatory
enhancement of physical conditioning, acclimation to heat stress,
and paying attention to level of hydration.
CLOTHING
Different regions of the body are not equivalent with regard to
sweat production.56 The face and the scalp account for 50% of
total sweat production, whereas the lower extremities contribute
only 25%. When exercising under conditions of high heat load,
maximal sweat evaporation is facilitated by maximal skin expo-
sure. Clothing should be lightweight and absorbent. Although
significant improvement has been made in fabrication of athletic
uniforms, uniforms and protective gear required by certain
branches of the military and public safety officers continue to
add to the risk of heat injury. Developing protective clothing that
permits for more effective heat dissipation is indicated. Uniforms
should be modified to decrease the amount of extra protective
equipment and head gear needed as much as is safely possible
during the first week of training and during times of high heat
CHAPTER 13  Clinical Management of Heat-Related Illnesses
stress conditions.
ACTIVITY
Behavioral actions can effectively minimize occurrence of classic
heatstroke. Lack of residential air conditioning places indigent
persons at risk during heat waves. By sitting in a cool or tepid
bath periodically throughout the day, the individual can decrease
heat stress and thereby prevent heat injury. The more than 10,000
deaths during the 2003 heat wave in Europe could have been
reduced by simple announcements by public health officials of
this preventive measure. This type of “heat dumping” activity can
also include taking cool showers instead of warm showers. In
addition, forearms and hands can be immersed into water that
has been cooled to 10° to 20° C (50° to 68° F) for 10 minutes.
This action will achieve reduction in Tco of 0.7° C (1.3° F) and
provide the athlete with sustained capability to train in the heat.45
In addition to forearm and hand immersion in cool or cold
water, the concept of cooling the palm by various devices, some
of which add vacuum pressure to the palm in addition to cooling,
has recently become popular. A comprehensive review of cooling
rates of various cooling modalities shows that this methodology
is no more effective in lowering body core temperature than limb
immersion in tap water (15° C [59° F]).26 Recent research on these
devices reports that the addition of negative pressure with cooling
did not enhance any cooling effect.67 In addition, these devices
have been shown to be ineffective in slowing development of
hyperthermia when used between exercise bouts5 and in improve-
ment of high-intensity, intermittent exercise.120 Cold or ice water
has been reported to have a cooling power five to eight times
greater than hand/palm cooling devices.26 Given the low cooling
power of these devices, their use in a field or athletic setting,
especially for treatment of heat injury or illness, should be ques-
tioned. This is also true when viewed in terms of cost when
compared with limb immersion modalities. Regarding use in a
wilderness setting, these devices have additional drawbacks,
including the need for electrical power with batteries and the
added weight of transport.
Athletes should be placed in the shade whenever possible
during periods of rest and instruction. If shade is not available
in areas where warm-weather training is routinely conducted,
consideration should be given to constructing overhead shelters.
If toilets/latrines are not easily accessed at training areas, consid-
eration should be given to placing portable toilets nearby to
prevent voluntary fluid restriction. We recommend spacing
runners widely apart during group runs to allow for optimal heat
dissipation.
Modification of physical activity should not be based solely
on any individual parameter of ambient temperature (Tamb), rela-
tive humidity, or solar radiation, because all these contribute to
heat load. The wet bulb globe temperature (WBGT) is an index
of heat stress that incorporates all three factors. This value may
be calculated (Table 13-2) or obtained directly from portable
digital heat stress monitors that measure all three parameters
simultaneously to compute WBGT. When heat stress monitors
are used, care should be taken to ensure that they are calibrated
TABLE 13-2  Determination of Wet Bulb Globe
Temperature Heat Index
Temperature (T [°F]) Factor Example
Wet bulb T ×0.7 78 × 0.7 = 54.6
Dry bulb T ×0.1 80 × 0.1 = 8.0
Black globe T ×0.2 100 × 0.2 = 20.0
Heat index 82.6
Wet bulb reflects humidity, dry bulb reflects ambient air temperature, and black
globe reflects radiant heat load; the heat index is the sum of the three.
Alternative equation: Wet bulb globe temperature = (0.567 Tdb) + (0.393 Pa) +
3.94, where Tdb is dry bulb temperature and Pa is water vapor pressure.
273
 TABLE 13-3  Modification of Sports Activity Based on
Wet Bulb Globe Temperature
Index Limitation
<10° C (50° F) There is a low risk for hyperthermia but
a possible risk for hypothermia.
<18.3° C (65° F) There is a low risk for heat illness.
18.3°-22.8° C (65°-73° F) There is a moderate risk toward the
end of the workout.
22.8°-27.8° C (73°-82° F) Those at high risk for heat injury should
not continue to train; all athletes
should practice in shorts and T-shirts
during the first week of training.
27.8°-28.9° C (82°-84° F) Care should be taken by all athletes to
maintain adequate hydration.
28.9°-31.1° C (85°-88° F) Unacclimated persons should stop
training; all outdoor drills in heavy
uniforms should be canceled.
31.1°-32.2° C (88°-90° F) Acclimated athletes should exercise
caution and continue workouts only at
reduced intensity; they should wear
light clothing only.
≥32.2° C (90° F) Stop all training.
COLD AND HEAT
yearly and are not left out in the heat for long periods without
use. Care should also be taken to ensure that the device measures
radiant heat, humidity, air movement, and shaded temperature
to calculate WBGT. Devices that measure the heat stress index,
relative humidity, and wind speed should not be used to estimate
WGBT. Current recommendations from the ACSM for preventing
EHI during workouts and competition are based on the WBGT.4
Most heat injuries occur during cooler WBGT periods as a result
of cumulative heat exposure from preceding days. Some clini-
PART 2
cians propose that heat-warning systems base their alerts on
cumulative heat stress rather than solely on the current WBGT.121
Other clinicians suggest using syndromic surveillance to help
alert the public about periods of high heat stress.14
Table 13-3 presents a suggested modification of sports activity
that is also based on the WBGT. Although ACSM guidelines for
the summer indicate that vigorous physical activity should be
scheduled in the morning or evening, individuals should be
cautioned that the highest humidity of the day is usually early
morning. In 1999, Montain and co-workers78 updated fluid
replacement guidelines for warm-weather training (see Chapter
89, Table 89-5). It is important to note that compliance with these
recommendations does not remove all risk of heat injury. The
development of another index of heat stress that provides a better
basis for the prevention of EHS is indicated.
Rav-Acha and colleagues93 assembled a case series of six fatal
cases of EHS in the Israeli Defense Forces and examined the
circumstances that led to the deaths. A significant association
between accumulation of predisposing factors and EHS totality
was found. In almost all the fatal cases, seven predisposing
factors were noticed: (1) low physical fitness, (2) sleep depriva-
tion, (3) high heat load, (4) high solar radiation, (5) physical
exercise unmatched to physical fitness, (6) absence of proper
medical triage, and (7) training during the hottest hours. These
fatality factors primarily concerned organizational training regula-
274
tions and not individual factors, which emphasizes the impor-
tance of proper guidelines and safety measures in a warm climate
for preventing EHS fatalities. It follows that a combination of
predisposing factors that were already found to impair heat toler-
ance43 is a strong predictor of a poor prognosis. Dehydration was
found in only two of the six fatal cases reported.
CONDITIONING
The contribution of cardiovascular conditioning to thermoregula-
tion is discussed in Chapter 6. Ideally, an individual should train
under temperate or thermoneutral conditions before exercising
in the heat. For the previously sedentary individual, an exercise
regimen that incorporates 20 to 30 minutes of aerobic activity
3 to 4 days a week will improve cardiovascular function after
8 weeks.
It is important to remember that even physically active indi-
viduals may lack physical conditioning relative to a particularly
stressful competition or activity. Heat illness in runners usually
occurs when novices exceed their training effort during races or
when well-trained athletes increase their pace above normal
during long-distance events.
ACCLIMATIZATION
During initial exposure to a hot environment, workouts should
be moderate in intensity and duration. A gradual increase in the
time and intensity of physical exertion over 8 to 10 days should
allow for optimal acclimatization.36 Early-season high school heat-
stroke deaths are most likely to occur during the first 4 days of
practice.95 Children and teenagers require 10 to 14 days to achieve
an appropriate acclimatization response. Acclimatization can be
induced by simulating hot environmental conditions indoors.
Aerobic activity should be conducted during exposure to the hot
environment so that the individual can achieve optimal acclima-
tization.98 If symptoms of heat illness develop during the acclima-
tion period, all physical activity should be stopped and appropriate
interventions begun. Acclimatization is not facilitated by restrict-
ing fluid intake; in fact, conscious attention to fluid intake is
required to prevent dehydration. As with physical conditioning,
there are limits to the degree of protection that acclimatization
provides from heat stress. Given a sufficiently hot and humid
environment, no one is immune to heat injury.
RESEARCH
Areas for future research include improved clarification of when
athletes can safely return to play; role of autonomic nervous
system dysfunction in EHS; benefit of induced hypothermia for
EHS treatment; and roles of clonidine, activated protein C, and
antibiotics during initial treatment.
ACKNOWLEDGMENTS
The authors extend much appreciation to the previous authors of
this chapter, Daniel S. Moran and Stephen L. Gaffin.
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Complete references used in this text are available
online at expertconsult.inkling.com.
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PART 3

Burns, Fire,
and Radiation
 CHAPTER 14 
Wildland Fires: Dangers and Survival
MARTIN E. ALEXANDER, ROBERT W. MUTCH, KATHLEEN M. DAVIS,
AND COLIN M. BUCKS

There can be few natural physical phenomena with the scope and complexity of a forest fire. The fuel that
powers it is found in a huge range of sizes, quantities, and arrangements in space. The weather affects
the current condition of this fuel array in a bewildering maze of drying and wetting effects, each fuel com-
ponent responding to a “different drummer.” The combustion process itself, once under way, responds
to a complex blend of fuel variation, moisture status, topography, wind speed, and other atmospheric
factors. Its frontal intensity varies over an immense range, from tiny flickers easily stepped over, to dense
sheets of flame whose fierce radiation keeps the observer at a distance.  —van Wagner (1985)

In describing the 13 wildland firefighter fatalities that occurred
on the Mann Gulch Fire near Helena, Montana, on August 5,
1949, Norman Maclean285 wrote in his award-winning 1992 book
Young Men and Fire, “They were still so young they hadn’t
learned to count the odds and to sense they might owe the
universe a tragedy.” Three years later, Canadian folksinger-
songwriter James Keelaghan, inspired by Maclean’s book, paid
tribute to the fallen firefighters in a haunting ballad entitled “Cold
Missouri Waters.” The Mann Gulch Fire has been called “the race
that couldn’t be won.”418 Although the crew increased their pace
ahead of the fire, the fire accelerated faster than they did until
fire and people converged. Miraculously, three people were able
to survive the fire’s wrath. Smoke jumper foreman Wagner Dodge
ignited an “escape fire” by burning off a patch of cured grass,26
into which he tried to move all his crew, while two others found
a route to safety and escaped injury on a nearby rockslide.
Many improvements in a firefighter’s odds of surviving an
entrapment or burnover encounter with a wildland fire have
occurred since 1949. These advances include improved under-
standing of fire behavior, increased emphasis on fire safety and
fire training, and development of personal protective equip-
ment.143 However, as incidents such as the 14 firefighter fatalities
on the 1994 South Canyon Fire in western Colorado (Figure 14-1)
and in 2015 in Washington have shown, tragedies can and con-
tinue to occur.178 Norman Maclean’s son, John, would in turn
write about this fatal fire 50 years later.286 Grief over lost loved
ones can sometimes lead to further tragedies. For example, one
of the smoke jumpers killed on the 1949 Mann Gulch fire, Stan
Reba, had been married less than a year. His widow grieved for
him and never remarried, then 10 years later took her own
life.247,299
The latest major multiple-casualty wildland firefighter fatality
event to occur, the Yarnell Hill Fire in central Arizona, took place
on the last day of June 2013. Nineteen members of the 20-person
Granite Mountain Hotshots perished during the fire’s major run.532
Wildland fires are a threat to human life, property, and natural
resources in many regions of the world (Figure 14-2). Although
the total number of deaths among the general public caused by
wildland fires in modern times pales in comparison with the
death toll and destruction from other natural hazards (e.g., hur-
ricane, tornado, flood, earthquake, tsunami, avalanche)86 and
human-made disasters, the fatalities are frequent and nevertheless
devastating.488
There are very few comprehensive summaries of deaths from
wildland fires on a worldwide basis. The compilation of U.S.
wildland firefighter fatalities begun in the early 1970s536 is
unique.353 Statistics on the number of civilian or wildland fire-
fighter fatalities from being trapped or overrun by wildland fires
on a global basis are unfortunately not kept in any systematic
manner.245 It is, however, well known that more than 300 deaths
caused by bushfire entrapments and burnovers occurred in the
state of Victoria in Australia alone during the 20th century.259 On
Saturday, February 7, 2009, Australia experienced a bushfire
disaster of unparalleled portions491:
In the wake of a long drought, and on a day of high temperatures, strong
winds and low humidity, bushfires swept through residential and farming
communities in Victoria. Some 430,000 hectares [one million acres] of
forest and farmland, countless homes and other buildings were burnt,
and hundreds of millions of dollars damage were done to economic and
community assets. Far more tragically, it was Australia’s worst civil disas-
ter: 173 lives were lost. February 7th 2009 has become Black Saturday,
to be (one imagines) seared into the Australian psyche for generations
to come.
On the fatal day, more than 300 fires were reported across
the state. Fifteen of these developed into major incidents, with
the most extensive damage and loss of life resulting from four
fires.142,203,311 The Kilmore East Fire alone was responsible for 70%
of the 173 deaths that occurred.162 A royal commission was estab-
lished soon afterward to investigate the causes and responses
to these fires (www.royalcommission.vic.gov.au/). The commis-
sion’s final report, issued at the end of July 2010, sets out 67
recommendations for protecting human life, “designed to reflect
the shared responsibility that governments, fire agencies, com-
munities, and individuals have for minimizing the prospect of a
tragedy of this scale ever happening again.”477 In their report, the
commissioners offered a warning: “It would be a mistake to treat
Black Saturday as a ‘one-off’ event” because “the risks associated
with bushfires are likely to increase.”
Given the occurrence of other major wildfire disasters involv-
ing significant loss of life among civilian populations in recent
years—for example, Greece in August 2007 (84 fatalities),545,546
western Russia during the 2010 summer fire season (63 fatali-
ties),218 Mount Carmel in northern Israel in December 2010 (44
fatalities),531 and Valparaiso, Chile, in April 2014 (15 fatalities)412—
this prediction has global application.
This chapter describes the current look at fire as a historical
force and discusses fire management policies, the nature and
scope of wildland fire hazards, behavior of fires, typical injuries,
fatality fire statistics, several fatal fire incidents, and survival
techniques. Although the emphasis is on North America, refer-
ence is made to other regions of the globe, most notably Aus-
tralasia and Europe. Wildland fire, like many other disciplines
and subjects, has its own unique terminology, so readers may
need to consult glossaries.198,313,359,456
WILDLAND FIRE MANAGEMENT
AND TECHNOLOGY
Programs for dealing with the overall spectrum of fire are col-
lectively termed fire management.58 They are based on the
concept that fire and the complex interrelated factors that influ-
ence fire phenomena can and should be managed to the extent

276
 Idaho, in 1992; Garnet Fire near Penticton, British Columbia, in

CHAPTER 14  Wildland Fires: Dangers and Survival

1994; Millers Reach Fire in Alaska in 1996; Virginia Hills Fire in
Alberta in 1998; Florida fires of 1998; Silver Creek Fire in British
Columbia in 1998; Cerro Grande fire in New Mexico in 2000;
Valley Complex in Montana in 2000; Chisholm Fire in Alberta in
2001; Biscuit Fire in Oregon in 2002; Hayman Fire in Colorado
in 2002; Rodeo/Chedeski Fire in Arizona in 2002; House River
Fire in Alberta in 2003; “Firestorm 2003” season in British Colum-
bia; record-setting fire seasons in Alaska and the Yukon Territory
in 2004 (Figure 14-6); the Slave Lake Fire in Alberta in 2011; and
the 2014 fire season in the Northwest Territories, Canada. Similar
incidents have occurred in other regions of the world. The hard
lesson learned from these and other incidents is that conflagra-
tions or large wildfires are inevitable unless mitigation measures
are taken. Several factors have coincided to produce massive
forest mortality, including drought, epidemic levels of insects and
diseases,250,333,337 and unnatural accumulations of fuels at the stand
level and at a growing landscape scale in some but not neces-
sarily all vegetation types,252 as a result of policies and practices
of attempted fire exclusion.16,221 The resulting dry forest type of
areas in the western United States was foreshadowed by a for-
ester, Harold Weaver,517 in the early 1940s. Many agencies are
now using prescribed fire more frequently, deliberately burning
under predetermined conditions to reduce accumulations of fuels
and to protect human life, property, and other values that are at
risk by wildfire.315,334,368
Research has indicated that fires are not categorically “bad.”432
In fact, many plant communities in North America are highly
flammable during certain periods in their life cycle.84 For example,
annual grasses, ponderosa pine, and chaparral plant communities

FIGURE 14-1  Flame front spreading upslope through Gambel oak

(Quercus gambelii) and pinyon (Pinus edulis)–juniper (Juniperus mono-
sperma) fuel complex during the major run of the South Canyon fire
in western Colorado on the afternoon of July 6, 1994. Approximately
2 12 minutes after this photograph was taken, the first of 14 firefighters
was overtaken by the advancing flames, estimated to have traveled
110 to 165 m/min (360 to 540 ft/min). (Courtesy USDA Forest Service;
photo by S. Archuleta.)

that they can. The scientifically sound fire management programs

that respond to the needs of people and natural environments
must also maintain full respect for the power of fire.
Since the early 1900s, federal, state, and local fire protection
agencies in the United States, for example, have routinely extin-
guished wildfires to protect watershed, range, and timber values,
as well as human lives and property. The basic methods of
fire suppression219,280 have changed very little, although new
technologies have gradually been implemented (Figure 14-3).
However, improvements in fire detection, fire danger rating
systems, and fire suppression methods have been developed by
fire science laboratories and two equipment development centers
maintained by the U.S. Department of Agriculture (USDA) Forest
Service, as well other organizations (e.g., state agencies and
universities). Patrol planes, some with infrared heat scanners,
other fixed-wing aircraft (Figure 14-4), and helicopters (Figure
14-5), can deliver firefighters, equipment, and fire-retarding
chemicals or water to the most remote fire. These firefighting
resources are organized under an Incident Command System that
can easily manage simple to complex operational, logistic, plan-
ning, and fiscal functions associated with wildfire suppression
actions.117,192,346 Many other countries have followed a somewhat
similar path in their evolution with regard to wildland fire sup-
pression and supporting research and development.396-398,401
Modern fire suppression technology, however, cannot indefi-
nitely reduce the area burned by wildfires, as demonstrated by FIGURE 14-2  Wildland-urban interface fire in the Amarante region of
numerous large fires and major fire seasons in the past 35 years Portugal on August 5, 2005. Drought conditions contributed to an
or so in North America, specifically the United States and Canada. exceptionally severe fire season in southern Europe during 2005.
This includes, to name a few: Mack Lake Fire in Michigan in Twelve firefighters and 10 civilians were killed in Portugal. Eleven
1980; the “Siege of ’87” in California in 1987; Silver Complex in firefighters were killed in one separate incident in a nature reserve in
Oregon in 1987; Greater Yellowstone Area fires in 1988; Stan- the Guadalajara area east of Madrid, Spain, on July 17, 2005. (Courtesy
islaus Complex in California in 1989; Foothills Fire near Boise, Publico newspaper; photo by Paulo Ricca.)

277

A Significant wildfire tragedies in the western United States have
BURNS, FIRE, AND RADIATION
B • Where wildland fire cannot be safely reintroduced because of
FIGURE 14-3  A helitorch, or flying drip torch, is a specialized aerial
ignition device slung below and activated from a helicopter (A). It
dispenses and ignites gelled fuel. The use of a helitorch in wildfire
suppression operations can take many forms (e.g., to reduce fire inten-
PART 3
sity; to slow or steer a fire; to remove potentially dangerous fuel
concentrations; to widen and strengthen control lines; to expedite
mop-up operations). Regardless of its specific purpose, the main
objective of this application of “fighting fire with fire” is to speed up
or strengthen control actions (B). Aerial backfiring and burning out with
a helitorch can be one of the safest, most economic, fastest, and least
damaging means of widening control lines and constitutes one of the
major innovations in wildland fire suppression technology in the past
35 years. The helitorch is also used in prescribed burning operations.
(Courtesy Alberta Sustainable Resource Development and Wildfire
Consulting Ltd, Edmonton, Alberta; photos by O. Spencer and W.
Bereska.)
are flammable during almost every dry season. Other communi-
ties, such as jack pine or lodgepole pine forests, although fire
resistant during much of their life cycle, eventually become fire
prone when killed by insects, diseases, and other natural causes.
The spread of non-native grasses, such as cheatgrass and red
brome, in the arid regions of the western United States has
increased the frequency of fires in desert shrublands.549
Wildland fires can benefit plant and animal communities.
Evolutionary development produces plant species well adapted
to recurrent fires. Fire tends to recycle ecosystems and maintain
diversity.279,543 Thus, there is growing consensus that fire should
be returned to many wildland ecosystems, where appropriate, to
perpetuate desirable fire-adapted plant and animal communities
and to reduce fuel accumulations.251
A landmark report in 1963 to the U.S. National Park Service
by the Advisory Board on Wildlife Management described how
the western slope of the Sierra Nevada had been transformed by
a policy of forest fire protection over the preceding approxi-
mately 100 years271:
When the forty-niners poured over the Sierra Nevada into California,
those that kept diaries spoke almost to a man of the wide-spaced columns
278
of mature trees that grew on the lower western slope in gigantic mag-
nificence. Today much of the west slope is a dog-hair thicket of young
pines, white fir, incense-cedar, and mature brush—a direct function of
overprotection from natural ground fires. Not only is this accumulation
of fuel dangerous to the giant sequoias and other mature trees, but the
animal life is meager, wildflowers are sparse, and, to some at least, the
vegetative tangle is depressing, not uplifting.
It must also be acknowledged that in some cases, past logging
practices contributed to the resulting fuel structure. Nevertheless,
the board recommended that the Park Service recognize in man-
agement programs the importance of the natural role of fire in
shaping plant communities.422
WILDLAND FIRE MANAGEMENT POLICIES
focused attention on the need to reduce hazardous fuel accumu-
lations.460 The events associated with the 1994 fire season created
a renewed awareness and concern among federal land manage-
ment agencies about wildfire impacts, leading to a combined
review of fire policies and programs. The result was enactment
of a new interagency federal wildland fire management policy,
which provided a common approach to wildland fire among
federal agencies and called for close cooperation with tribal,
state, and other jurisdictions.351 The principal points of the 1995
federal wildland fire policies are as follows:
• Firefighter and public safety remains the first priority in wild-
land fire management. Protection of natural and cultural
resources and property is the second priority.
• Wildland fire, as a critical natural process, must be reintro-
duced into the ecosystem, accomplished across agency
boundaries, and based on the best available science.
hazardous fuel accumulations, pretreatment must be consid-
ered, particularly in the wildland-urban interface.
• Wildland fire management decisions and resource manage-
ment decisions are connected and based on approved plans.
Agencies must be able to choose from the full spectrum of
actions, from prompt suppression to allowing fire to have an
ecologic function.
FIGURE 14-4  Specialized fixed-wing aircraft such as the amphibious
CL-415 “superscooper” are capable of delivering water and chemical
fire retardants on or near a wildfire. Although such planes are used in
sustained-action situations on isolated sectors of large fires, they are
most effective in initial attack operations during the incipient phase of
fire growth. In such cases, their primary purpose is to slow down the
progress of the fire until such time as ground suppression resources
are able to arrive and effect direct containment. Wing-tip vortices are
created in the wake of low-flying aircraft. These vortices gradually dis-
sipate as they descend to the ground level. They can cause a sudden,
unexpected increase in fire activity as a result of the momentary wind
gust. This can pose a threat to anyone located near the fire perimeter.
(Photo by T. Nebbs.)

FIGURE 14-5  Several different sizes and models of rotary-wing aircraft
or helicopters are used in a wide variety of direct roles as well as
support functions in wildland fire suppression, including the dropping
of water or fire-retarding chemicals directly on the fire. Helicopters also
create wake vortices while in forward motion, just like airplanes, but
generally these vortices are much weaker. A more common safety issue
with helicopters is the downward induced air flow or rotary downwash.
Some downwash effects are unavoidable when helicopters are engaged
in direct attack on the fire with water or chemicals. Anyone located
near the fire perimeter during such operations could be at risk. Even
with a “long line” delivery system operated from a Bell 212 helicopter,
as illustrated here on the Anarchist Mountain Fire near Osoyoos in
southern British Columbia on July 16, 2003, rotary downwash can 
still be a significant issue. (Courtesy Alberta Sustainable Resource
Development.)
• All aspects of wildland fire management will involve all part-
ners and have compatible programs, activities, and processes.
• The role of federal agencies in the wildland-urban interface
includes firefighting, hazardous fuel reduction, cooperative
prevention and education, and technical assistance. Ulti-
mately, the primary responsibility rests at the state and local
levels.
• Structural fire protection in the wildland-urban interface is the
responsibility of tribal, state, and local governments.
• Federal agencies must better educate internal and external
audiences about how and why we use and manage wild-
land fire.
The 1995 U.S. federal wildland fire management policy was
reviewed and updated in 2001,356 following a particularly severe
fire season in the western United States the previous year; about
2.8 million hectares (7 million acres) were burned over by about
89,000 fires during the 2000 fire season in the United States.497
Results of the 2001 review and update were defined in the “2003
Interagency Strategy for the Implementation of Federal Fire Man-
agement Policy.”266 This strategy broadened the scope of fire
management to balance fire suppression with management for
ecologic benefits and supports the use of the full range of fire
management activities to achieve ecosystem stability, including
fire use. The 2003 implementation strategy stresses the need to
complete or revise fire management plans that are more effec-
tively and directly integrated with other natural resource goals.80
One of the other outgrowths of the 2000 fire season was the
National Fire Plan (www.forestsandrangelands.gov/resources/
overview/), which calls for the following actions:
• Ensuring that necessary firefighting resources and personnel
CHAPTER 14  Wildland Fires: Dangers and Survival
are available to respond to wildland fires that threaten lives
and property
• Conducting emergency stabilization and rehabilitation activi-
ties on landscapes and communities affected by wildland fire
• Reducing hazardous fuels (dry brush and trees that have
accumulated and increase the likelihood of unusually large
fires) in U.S. forests and rangelands
• Providing assistance to communities that have been or may
be threatened by wildland fire
• Committing to the Wildland Fire Leadership Council, an inter-
agency team created to set and maintain high standards for
wildland fire management on public lands
It is clear from these objectives that one of the major foci of
the U.S. National Fire Plan is the human dimension of wildfire
(i.e., rural homeowners and communities).246,283
The 2003 implementation strategy was further revaluated in
2008, leading to another review and update. This resulted in the
2009 Guidance for Implementation of Federal Wildland Fire
Management Policy (www.nifc.gov/policies/policies_documents/
GIFWFMP.pdf). This update reaffirmed that the 1995 Federal Fire
Policy remains sound and presents a single, cohesive federal fire
policy for the USDA and Departments of the Interior. It provides
the highest degree of flexibility ever afforded to managers and
facilitates their ability to respond to changing conditions and
complexities of a wildfire event. However, some communications
issues were identified involving inconsistent terminology, which
this update corrected. One of the most significant changes
was removal of the distinction between “wildland fire use” and
“wildfire.”266
The latest development in the evolution of wildland fire man-
agement policy in the United States is a comprehensive strategic
plan, the National Cohesive Wildland Fire Management Strategy
(NCWFMS) (www.forestsandrangelands.gov/strategy/). Its focus
is to promote a collaborative working relationship among all
stakeholders and across all landscapes, using the best science to
make meaningful progress toward the following goals:
1. Restored and maintained landscapes
2. Fire-adapted communities
3. Safe and effective wildfire response
FIGURE 14-6  Swan Lake Fire in northern British Columbia (near border
with Yukon Territory) during midafternoon on June 23, 2004. Such
high-intensity fire events continue to spread until such time as burning
conditions ameliorate, as when a change in weather conditions (e.g.,
winds die down) or fuel type (e.g., leafed-out hardwood stand) occurs,
or a wide, natural barrier to fire spread is encountered (e.g., large lake
or river). The natural fire regime in the boreal forest of Canada and
neighboring Alaska is characterized by the periodic occurrence of large
crown fires. In the Yukon, for example, the average area burned over
the past 25 years has been about 120,000 hectares (297,000 acres) per
year. During the 2004 fire season, a record-setting 1.7 million hectares
(4.2 million acres) and 2.7 million hectares (6.7 million acres) were
burned over in the Yukon and Alaska, respectively. (Courtesy Yukon
Government, Department of Energy, Mines, and Resources; photo by
M. Clark.)
279
 The NCWFMS’s stated vision is, “To safely and effectively
extinguish fire when needed; use fire where allowable; manage
our natural resources; and as a nation, to live with wildland fire.”
The final phase of the NCWFMS was completed in April 2014.232
Both the Federal Wildland Fire Management Policy and the
NCWFMS emphasize the importance of risk and risk management
as a sound foundation for wildland fire programs.
In 2005 the Canadian Council of Forest Ministers issued the
Canadian Wildland Fire Strategy Declaration (www.ccmf.org/
english/coreproducts-cwfs.asp),111 which is based on principles
of risk management and hazard mitigation. This strategy strives
to balance public safety, forest protection and health, and fire
management expenditures, to maintain a strong and effective fire
suppression organization, but it also includes innovative hazard
mitigation, preparedness, and recovery programs. In other words,
this is a more holistic view of wildland fire envisioned about 45
years ago as land management agencies made the transition
from fire control to fire management. This strategy recognizes
the need for shared responsibility among the various stakehold-
ers (i.e., property owners, industries, and local, provincial, and
federal governments).241 One of the guiding principles of this
new declaration was that “public safety—including the safety of
firefighters—is paramount.”
BURNS, FIRE, AND RADIATION

Fire management policies similar to those of the United States

and Canada exist in other parts of the world.199 The Food and
Agriculture Organization of the United Nations200 prepared a
generic set of fire management guidelines to serve as a basis for
developing policies. The Fire Paradox project, a research initia-
tive supported by the European Commission from 2006 to 2010,*
examined wildland fire from multiple perspectives as a basis for
influencing policies on integrated fire management.443

PRESCRIBED FIRE AND WILDLAND FIRE USE

Prescribed fire, the intentional ignition of grass, shrub, or forest
fuels for specific purposes according to predetermined condi-
tions, is a recognized land management practice.36,512,525 The
objectives of such burning vary: to reduce fire hazards after
PART 3
FIGURE 14-7  Lightning-ignited fires in some wilderness areas and
national parks in the United States that meet certain criteria have been
allowed to burn freely under observation since the early 1970s as part
of a fire management strategy to allow natural ecosystem processes

logging, expose mineral soil for seedbeds, regulate insects and

to operate more freely. (Courtesy USDA Forest Service.)
diseases, perpetuate natural ecosystems, and improve range
forage and wildlife habitat.321,518 In some areas managed by the
National Park Service, USDA Forest Service, and Bureau of Land
Management, naturally ignited fires may be allowed to burn the sacrifice of relatively safe perimeter fire suppression strategies
according to approved prescriptions; fire management areas have in favor of directly protecting people and their possessions.535
been established in national parks and wildernesses from the Direct suppression actions within the fire’s perimeter place fire-
Florida Everglades to the Sierra Nevada in California (Figure fighters at a greater disadvantage from a safety standpoint. The
14-7). Planned-ignition prescribed fires are also carried out. new interagency policy that emphasizes firefighter and public
Similar policies exist in Canadian National Parks.235 Visitors are safety as the first priority will result in less effort to save structures
increasingly aware that wildland fires can be an important part in dangerous situations. Thus, what is known of fire behavior
of the natural cycle of an ecosystem, and that the future health
of wilderness areas and parks may depend in part on today’s
managed fires.314

WILDLAND-URBAN INTERFACE: NEW

LOOK AT A HISTORICAL PROBLEM
Just as resource agencies are attempting to provide a more
natural role for fire in wildland ecosystems, the general public is
increasingly living and seeking recreation in many of these same
areas. The area where houses and other human-made structures
meet or are intermingled with wildland vegetation is regarded as
the wildland-urban interface, or intermix (WUI; pronounced
“woo-ee”), although other names have been used (Figure 14-8).
It is a growing problem from a wildland fire perspective in the
United States,76,405,485 Canada,220,239 and many other regions of the
world,175,263 As mentioned earlier, past fire exclusion practices in
the United States have allowed abnormal fuel accumulations in FIGURE 14-8  Fire in the wildland–urban interface, or intermix. This
some forest types and regions, and this fact has combined with particular wildfire occurrence took place on the outskirts of Kamloops,
British Columbia, during the afternoon of July 26, 2007. The fire is
spreading through ponderosa pine (Pinus ponderosa) in the “red
attack” stage as a result of being killed by mountain pine beetle (Den-
*www.researchgate.net/publication/253642532_FIRE_PARADOX_A droctonus ponderosae) following attack one year earlier. (Courtesy
_European_initiative_on_Integrated_Wildland_Fire_Management). British Columbia Ministry of Forests and Range; photo by J. Hodge.)

280
and fire survival principles must be readily available to emer-
gency medical personnel, wildland dwellers, and recreationists.
In fact, fire protection agencies and others have been making
such information more readily available to the general public for
some time now,118,169,201,519 although much more needs to be
done.17
NATURE OF THE PROBLEM
Hot, dry, and windy conditions annually produce high-intensity
fires that threaten or burn homes where wildland and urban areas
converge (Box 14-1). Can the historical levels of destruction,
injury, and fatality be repeated today in the face of modern fire
suppression technology? The answer to this question requires an
analysis of the conditions, for example, that created such high-
intensity fire behavior events in the forests of northern Idaho and
northwestern Montana during late August 1910, in which 85
people, including 78 firefighters, were killed.139,187,399,455 (Figures
14-9 and 14-10).
The earliest fire incident of note involving a large loss of
human life was the series of conflagrations in the Miramichi
region of New Brunswick and adjacent areas in Maine in early
October 1825, in which at least 160 people144,388 perished.282,489
This was followed by several fatality fires in the U.S. Lake States
BOX 14-1  What Is It Like to Experience a Wildland-Urban Interface Fire? A Town That Nearly Went . . . Up in Smoke
by D. Blasor-Bernhardt71
Tok, Alaska, July 1, 1990, 15 to 30 minutes after the lightning strike
that started the Tok Fire. (Photo by D. Blasor-Bernhardt.)
July 1, 1990, started out like any other Sunday, but it quickly turned
Tok, Alaska, into a near raging inferno. I was working at the
Chamber of Commerce Main Street Visitor Centre when an
otherwise beautiful day suddenly turned black and foreboding.
Blowing in, a huge thundercell hung just southeast of town.
I stepped outside just in time to see a long, crooked finger of
electricity split from an ominous cloud and drill its way into Earth.
Minutes later, where the lightning had hit, a mushroom-shaped
cloud began to grow. I grabbed my camera and snapped a few
shots.
Five days later, and in spite of several thousand firefighters and
equipment from all over Alaska, Canada, and the States, Tok was
completely under siege and at risk of being cremated. The
wind-blown inferno licked greedily at several unoccupied dwellings,
then consumed them. East-side residents were evacuated. We, on
the west side, were told to pack our things, to be ready to leave,
and to await further instructions.
Tok was enveloped on two sides by fire—from the eastern and
northern directions. My log home was about a mile from the north
front of the fire. I stood on the cabin’s sod roof, watching the fire,
when the kids and extended family converged there about the same
From Blasor-Bernhardt D: A town that nearly went . . . up in smoke, Guide to the Goldfields and Beyond (Harper Street Publishing, Dawson City, Yukon Territory)
Summer: 52, 1997.
region, including the Peshtigo and area fires (www.peshtigofire
CHAPTER 14  Wildland Fires: Dangers and Survival
.info/) in eastern Wisconsin in October 1871 (about 1300 fatali-
ties),238,272,526 the Lower Michigan fires of September 1881 (169
fatalities),243 the Hinckley Fire in east-central Minnesota in Sep-
tember 1894 (418 fatalities),264 the Baudette Fire in northern
Minnesota in October 1910 (42 fatalities),388 and the Cloquet Fire
in Minnesota in October 1918 (538 fatalities).112,243 The western
United States experienced other fatality fires, such as in western
Washington and Oregon in mid-September 1902 (38 fatali-
ties).83,309 Canada suffered similar tragedies.24 For example, the
province of Ontario experienced several significant settler-related
wildfire fatalities in 1911, 1922, and 1938, including the 1916
“Matheson Holocaust” in which as many as 400 people were
killed.56,166,308 In 1908, a forest fire destroyed the city of Fernie,
British Columbia; 22 people were reported killed.289
Other countries, such as New Zealand312 and France,201 are
reported to have suffered similar but varying losses in the 20th
century. In Australia, for example, possessing some of the world’s
most fire-prone environments,119 71 lives were lost in the state
of Victoria on “Black Friday” in January 1939.201,364 On August 1,
1959, 48 people were reported killed by a forest fire northeast
of Massif des Aures, Algeria.245 In early September 1963, forest
fires swept about 2 million hectares (4.9 million acres) in Paraná
State in southern Brazil, destroying more than 5000 homes and
time, looking to me for instructions. All day, I had the sprinklers and
hoses running full blast over the cabins, garage, and surrounding
area. By now, the area looked like a swamp. Good. I’d leave them
on, even if we evacuated, in the hope that it would help save some
of our place from destruction.
Smoke stifled each breath. Helicopters screamed back and forth
carrying people, equipment, and large buckets of water.
There was no fear, no panic, in anyone—just resignation. And
there was no way our town would be destroyed.
I told the kids to first pack up whatever was closest to their
hearts—it didn’t matter how silly an item seemed if that made them
feel good. The first thing I placed in my own car was my late
husband’s ashes. I couldn’t bear to leave him behind. Next, we
would take irreplaceable things: photo albums, mementos. Then
down to brass tacks: the necessary things for survival and rebuilding
in the event we were burned out. Bombers loaded with retardant
flew directly overhead. We were in a war zone—man against fire.
The girls loaded their cars with personal items. Mine was loaded
with blankets, groceries, and clothing. The boys readied our
tandem-axle trailer, loading it with items from the garage—
chainsaws, tools, portable generator, water jugs. If the fire drew too
near and we had to evacuate, the plan was for the girls and I to
load our pets while the boys quickly cut the trees down around the
cabins, hopefully providing a bare, wet perimeter between them
and the fire.
Fully loaded, we assembled in the driveway, ready for word to
come. Besides myself, six young adults, a baby, half a dozen dogs,
numerous cats, a snake, six vehicles, and a trailer comprised the
Bernhardt entourage. We were ready. We waited in the foul air, our
eyes smarting from the smoke. An ember hit me on the shoulder,
burning a hole though my shirt. Sadly, I turned to look at our homes
one last time. Tomorrow they would be gone.
Imperceptibly at first, a slight shift in the wind began. I held my
breath. “Mom?” my son said. “Yes,” I answered, “but I’m afraid to
hope.” The wind, definitely shifting now, was no longer blowing
toward us. A sweet, light rain began to fall. While the eight of us
stood together, soaking wet in the rain, a trooper came by to tell us
the worst was over.
In all, the fire burned 109,501 acres (44,314 hectares) at a cost of
over $35 million (U.S.), yet not one person had been injured, not
one occupied dwelling destroyed, and Tok had been spared by a
miracle wind.
281

BURNS, FIRE, AND RADIATION
FIGURE 14-9  These burned-over and wind-thrown trees resulted from
the intense fire behavior associated with a forest fire near Falcon,
Idaho, in August 1910. (Courtesy USDA Forest Service; photo by J.B.
Halm.)
PART 3
killing 110 people.451 More than 100 people were killed by exten-
sive forest and savannah fires in Cote D’Ivoire (Republic of Ivory
Coast) on the southern coast of western Africa during the 1982–
1983 fire season.431
On October 8, 1871, the same day that fire wiped out the
town of Peshtigo, Wisconsin, and surrounding communities, the
Great Chicago Fire devastated urban Chicago.526 Comparative
FIGURE 14-10  Burned ruins of the foundry in Wallace, Idaho, furnish
mute testimony to the destructive force of the 1910 fires. The cottage
on the terrace was the only one left standing in that part of town. Of
the 85 people reported killed in the “Big Blowup of 1910,” 78 were
firefighters. (Courtesy USDA Forest Service; photo by R.H. McKay.)
282
statistics for those two fires highlight the destructive potential of
wildland fires. In every way, the Peshtigo conflagration was far
worse than the Chicago blaze. The Peshtigo Fire covered about
518,000 hectares (1,280,000 acres) and as indicated earlier, killed
approximately 1300 people, whereas 906 hectares (2240 acres)
burned and some 200 lives were lost as a result of the corre-
sponding urban fire.227 The Great Chicago Fire is generally
acknowledged as the birthplace of modern urban fire prevention.
As Lloyd277 notes, “Mention the name Peshtigo to most people
and all you get is a blank stare. Mention Mrs. O’Leary’s cow to
the same person and they will think right away of the Great
Chicago fire,” and “Some of the same social misconceptions that
allowed Peshtigo to be all but forgotten persist today.” So, it is
perhaps fitting to consider the following poem entitled “The
Peshtigo Calamity”243:
As the years roll along and the ages have sped
O’er the charred, blackened bones of the Peshtigo dead,
And the story is told by the pen of the sage,
In letters immortal on history’s page—
No fancy can compass the horror and fright
The anguish and woe of that terrible night.
The August 1910 wildfires in northern Idaho and western
Montana had several elements in common with the Peshtigo fires
of 1871: many uncontrolled fires burning at one time; prolonged
drought, high ambient air temperatures, and moderate to strong
winds; and mixed conifer and hardwood fuels with slash from
logging and land clearing. These large fires occurred primarily
in conifer forests north of the 42nd meridian, or roughly across
the northern quarter of the contiguous United States.83 One of
these critical elements that is not as likely to occur currently as
formerly is the simultaneous presence of several hundred uncon-
trolled fires. The effectiveness of modern fire suppression orga-
nizations is now able to reach even the most remote wildland
locations. High-velocity winds and more than 1600 individual
fires contributed to the spread of the fires in 1910; it is unlikely
that a multifire situation of that magnitude would occur today.82,119
However, multiple fire starts are still possible because of human-
caused ignitions (e.g., arson, power lines). For example, on
October 16, 1991, 92 separate fires occurred in the Spokane
region of eastern Washington343 in the space of a few hours under
the influence of exceedingly strong winds.32 Prolonged drought,
high winds, and flammable fuel types, however, remain signifi-
cant to the behavior of high-intensity fires.
Some of the fires most potentially damaging to human lives
and property occur in areas rich in the chaparral shrub fuel
complexes in southern California. Wilson535 and Phillips386
described the severe 1970 fire season in California, in which
official estimates showed that 97% of 1260 fires occurring between
September 15 and November 15 were held to less than 121
hectares (300 acres). The other 3% of the fires, fueled by a pro-
longed drought and fanned by strong Santa Ana winds, produced
14 deaths, destroyed 885 homes, and burned about 243,000
hectares (600,000 acres), as chronicled in the 1971 film Count-
down to Calamity. Ten years later, the situation recurred over
9550 hectares (23,600 acres) in southern California, the Panorama
Fire in November 1980, which resulted in the deaths of four
people and loss of more than 325 structures.108
On October 20, 1991, a devastating fire “of unprecedented
force blew out of control”4 in the hills above Oakland and Berke-
ley, California. Burning embers carried by high winds from the
perimeter of a small fire resulted in a major WUI conflagration.
The impact on people and their possessions was enormous.4,469
The fire resulted in direct deaths of 25 people, including a police
officer and a firefighter, injured 150 others, destroyed 2449 single-
family dwellings and 437 apartment and condominium units,
burned about 650 hectares (1600 acres), and did an estimated
$1.5 billion in damage.342 The scenario for disaster included a
5-year drought that had dried out overgrown grass, shrubs, and
trees, making them readily ignitable. Other factors included
untreated wood shingles, unprotected wooden decks that pro-
jected out over steep terrain, low relative humidity, high ambient
air temperatures, and strong winds that averaged 32 km/hr (20
miles/hr) and gusted up to 56 to 80 km/hr (35 to 50 miles/hr).
The area had not experienced any rain for 67 days before the
major fire run, although mean monthly maximum air tempera-
tures in the 6 months preceding the fire were not appreciably
high, 18° to 23° C (64° to 73° F).33 These severe conditions pro-
duced a voracious fire that consumed 790 homes in the first hour.
Winds lessened to 8 km/hr (5 miles/hr) by the first evening,
which assisted with the containment of the fire. Firefighters had
the situation under control by the fourth day, but not before they
had been given an awful glimpse of the nature of WUI fires in
the future. In late October 2003, fires in southern California
burned over 300,000 hectares (742,000 acres) in 1 week alone,
taking 23 lives and destroying more than 3300 homes.107,253,336
In recent times, wildland fire fatalities among the general
public have not been restricted to just California, or the United
States for that matter. Four civilians were killed as a result of the
massive forest conflagration that converged on the outskirts of
Canberra, Australia, in January 2003.3 During summer 2003 in
Portugal, 21 people lost their lives in 18 different fire inci-
dents.506,509 On January 11, 2005, nine people (including four
children and two firefighters) perished on the Eyre Peninsula of
South Australia as a result of being overrun by an extremely
fast-spreading grass fire in what is now referred to as “Black
Tuesday” in the state.129,447,454 Mutch and Keller338 give a compel-
ling account of the wildfires that occurred in Texas and Okla-
homa during late 2005 and early 2006, in which 19 civilians and
six firefighters died.
In many parts of the world, but especially in the United States
and Canada, the primary response has been to evacuate all
people threatened by wildfires.1,140,404 For example, more than
200,000 people were evacuated in Canada between 1980 and
2007 in more than 500 separate incidents.70 The pros and cons
of evacuation are extensively discussed in Chapter 12 of Web-
ster’s seminal work,519 The Complete Bushfire Safety Book, entitled
“The Decision—Evacuate or Stay? Safety or Suicide?” In this
regard, Phil Cheney,123 a renowned Australian bushfire research
scientist, states, “What it comes down to is a civil right to risk
your own life to save your house. I personally am in favor of
TABLE 14-1  Approximate Probabilities of a House Surviving a Wildland Fire*
Scenario A: Total disregard for any fire safety precautions
Scenario B: Fire safety precautions taken only in regard to fuels surrounding house
Scenario C: Fire safety precautions taken only in regard to the house itself
Scenario D: All reasonable fire safety precautions to and near the house taken
Without Persons in Attendance Fire Intensity
Class (kW/m)
Scenario 500-1500 1500-10,000 10,000-60,000
A 14.4% 1.2% 0.3%
B 16.0% 4.9% 1.0%
C 26.1% 8.7% 1.9%
D 59.1% 28.1% 7.4%
kW/m × 0.29 = BTU/sec-ft
The following attributes were considered in the above scenarios:
House and Surrounding Fuel Conditions A B
Flammable objects nearby (e.g., firewood heap)? Yes
Wooden shingle roof? Yes
Nonwooden or nontile roof with pitch >10 degrees? No
External walls made of brick, stone, or concrete? No
Trees (5+ m high) within 40 m of house? Yes
From Alexander ME: Proposed revision of fire danger class criteria for forest and rural areas in New Zealand, ed 2, Christchurch, New Zealand, 2008, Scion Rural Fire
Research Group. www.scionresearch.com/fire.
m × 3.3 = feet.
*Based on a logistic regression model as developed from an analysis of 455 houses, which were completely destroyed, threatened, or sustained minor damage by the
bushfire that swept through the township of Mount Macedon in Victoria, Australia, on the evening of Ash Wednesday (February 16) in 1983.537,540
people taking risks in their lives provided that they also bear the
CHAPTER 14  Wildland Fires: Dangers and Survival
responsibility for the consequences.”
Some amazing logistic feats have taken place to date without
incident using both ground and air transportation. A good
example of the latter occurred in early June 1995 as the residents
of Fort Norman and Norman Wells in Canada’s Northwest Ter-
ritories were airlifted to Yellowknife, the territorial capital.167
However, statements later on from the public (e.g., “I think they
took us away just in time”) suggest that this approach is not
infinitely infallible. Coupled with this reality is the fact that
modern fire records indicate that the vast majority of area burned
by wildfires is the result of a small percentage of fires.466 Thus,
on some days, adverse fuel and weather conditions, coupled with
an ignition source, will conspire to produce conflagrations that
occur despite our best fire prevention, detection, and initial attack
efforts. Climate change will only exacerbate the situation.196
Recent research involving simulations of evacuations in response
to a threatening wildfire has revealed that strategic planning is
essential.157-159,170 Communities need to ensure that they are fully
prepared well in advance of a threatening wildfire occurrence
by developing individual and local government emergency action
plans.378 Taylor473 has emphasized that managing the fire risk at
the WUI is a shared responsibility involving both private citizens
and numerous government agencies.
Past fire experiences in Australia374,519 have demonstrated that
often “houses protect people and people protect houses.”
Research had demonstrated that a well-prepared house can
provide protection from fire, and that the presence of people
prepared to defend against their home burning down is the most
significant factor in determining its survival (Table 14-1). Obvi-
ously, zones of defendable space around homes must be estab-
lished in advance of fires; young people, older adults, and infirm
persons are generally encouraged to leave well ahead of the fire.
Communities at risk from wildfires should be encouraged to be
responsible for their own safety, because fire service personnel
may not be available when burning conditions are severe. The
major issue is whether able-bodied residents should stay and
With Persons in Attendance Fire Intensity Class (kW/m)
Scenario 500-1500 1500-10,000 10,000-60,000
A 29.9% 10.3% 2.3%
B 63.6% 32.1% 8.9%
C 76.5% 46.8% 15.3%
D 93.0% 78.2% 42.6%
Scenario
C D
No Yes No
Yes No No
No Yes Yes
No Yes Yes
No Yes No
283
 defend or “fight” for their homes, or “flee” in the hopes of escap-
ing an advancing fire.539
In the late 1990s, the Tasmania Fire Service had a policy that
provided guidance on bushfire safety and evacuation decision
making called “Prepare, Stay, and Survive.”213 When there was a
threatening wildfire, people were told to go home and assist in
the protection of their property. Because human lives and prop-
erty values are at risk when threatened by wildfires, exemplary
cooperation and teamwork are required to ensure adequate
safety margins. Team members identified for reducing the loss
of life and property include state agencies, local government, the
communities, and individuals.
The “Stay or Go” policy concerning evacuation was advocated
by the Australasian Fire Authorities Council (AFAC)48 as a funda-
mental component of community bushfire safety in Australia.233
Variants to this general theme exist (e.g., “prepare, leave early,
or stay and defend”). However, the essence of the approach
urges people to make the decision to prepare themselves and
their properties to “stay” and defend when a wildfire is likely, or
to “go” well before a fire is likely to arrive. Although early evacu-
ation may contribute to increased personal safety, bushfire prop-
erty losses are likely to increase. Conversely, late evacuation may
put people at greater risk than had they stayed in the house as
BURNS, FIRE, AND RADIATION
the fire passed around them.
An evaluation of this policy was the focus of Project C 6—
Evaluation of Stay or Go Policy undertaken by the Australian
Bushfire Cooperative Research Centre (www.bushfirecrc.com/),
led by co-project leaders John Handmer, RMIT University, and
Alan Rhodes, Country Fire Authority of Victoria. Fire management
agencies and the public alike will find the final results of this
research project of great interest. The preliminary results gener-
ally supported the 2005 AFAC position, while recognizing that
implementation issues remained.90,92,231,236,278,482 However, the fires
of February 7, 2009, in Victoria, Australia, and in turn the Royal
Commission’s report477 have changed the context for this approach
quite significantly. There are a number of emerging issues (e.g.,
limit of validity), so the policy is most likely to evolve in coming
years414 in the aftermath of the Black Saturday fires, as evidenced
PART 3
by AFAC’s revised position on bushfire community safety based
on emergency risk management principles.52
The 2009 Black Saturday fires have placed an urgent emphasis
on the continuing debate over what constitutes the safest strate-
gies for survival in the WUI. The Victorian fires led to the creation
of a catastrophic, or “Code Red,” level of fire danger. When this
category of fire danger is forecast for the next day, it is recom-
mended that people in a high-risk bushfire area leave the night
before or in the early morning (www.cfa.vic.gov.au/warnings-
restrictions/). At the next two lower levels (“Extreme” and
“Severe”), it is recommended to stay only if one’s home is well
prepared, well constructed, and can be actively defended.
Testimony by John Handmer before the 2009 Victorian
Bushfires Royal Commission,477 coupled with analyses pro-
duced by his research team,230 indicate that only a small per-
centage of homes and property were adequately prepared to
be fire resistant. Without preparing a fire-resistant home and
property in advance, the only prudent course of action is to
evacuate early.
This issue of whether to “prepare, stay, and defend” or evacu-
ate early is a subject considered worthy of more open debate
and discussion in North America.17,307,339,379,459 Two communities
in the United States—Painted Rocks in Montana and Rancho
Sante Fe in California—have adopted variations of the original
Australian model of “Prepare, Go Early or Stay and Defend.”339
Both communities have had the “Stay and Defend” practice suc-
cessfully tested by wildfires. Both U.S. communities are carefully
monitoring the lessons learned from the 2009 Black Saturday fires
to determine if any change is needed in their approach. Mean-
while, Ready, Set, Go! (RSG) was rolled out as a full-scale pilot
program by the Ventura County Fire Department and the Orange
County Fire Authority for the 2009 fire season in Southern Cali-
fornia. Other fire departments, such as Los Angeles County,156
Los Angeles City, San Bernardino County, Riverside County, Santa
Barbara County, and Cal Fire, have adopted the basic approach.
The RSG approach involves preparing one’s house to withstand
284
a wildfire, preparing one’s family for evacuation, and finally,
leaving earlier. The program is now endorsed by the International
Association of Fire Chiefs (www.iafc.org/displaycommon.cfm?an
=1&subarticlenbr=1229).
In many regions of the world, people are warned that wild-
fires are dangerous and that they always need to evacuate. This
“scare tactic” approach reinforces the concepts that wildland fires
are always dangerous and that people must leave their homes.
Perhaps one solution to dealing with fires in the WUI in the
future would be to embrace the concept of “A Dream, a Team,
and a Theme.”335 The “dream” would be one where houses are
able to survive fires even when fire services personnel are not
available. The “team” would consist of the effective partnership
between the fire services and home dwellers. The “theme” would
comprise the dual strategy of adequate defensible space coupled
with the home dweller’s motivation to remain on site as an
important factor in suppressing fires initiated by ember attack.
In order for this approach to work, rural homeowners must
understand that although wildfires can be dangerous, with proper
precautions, people can remain with their homes and be an
important part of the solution to the WUI fire problem. Empow-
ering communities at risk from wildfire to play an active part in
their own protection is viewed as a viable long-term strategy to
enable safe and harmonious coexistence with fire as an element
of nature.121
During the 2000 fire season in western Montana, some indi-
viduals opted to stay with their homes as flame fronts advanced.
They created defensible space, installed sprinkler systems,
engaged in fire suppression activities, and provided local intel-
ligence to incoming fire service personnel. No home was lost as
people demonstrated responsibility for their personal well-being.
A similar “prepare, stay, and defend” action was successfully
carried out during the 2003 fire season on the Wedge Fire along
the North Fork of the Flathead River in western Montana. The
property was prepared in advance to be “fire safe,” the home-
owner remained with volunteer fire department officials, and
the home survived the passage of a high-intensity crown fire
(Figure 14-11).
Wildland fires that threaten human lives and property are not
exclusively located in southern California because the exodus
to wildland regions has become a national phenomenon. Fires
burned about 81,000 hectares (about 200,000 acres) in Maine
in October 1947, killing 16 people;93,180 another area of about
81,000 hectares (about 200,000 acres) burned in New Jersey in
April 1963.55 Wildland fire disasters have not always been large
in size. On September 26, 1936, most of the coastal town of
Bandon in western Oregon was destroyed, and 11 people were
killed by a wildfire that covered probably no more than about
4000 hectares (10,000 acres).243 The prevalence of gorse, a non-
native plant, was considered a key contributing factor to the
resulting devastation (Figure 14-12). On July 16, 1977, the Pattee
Canyon Fire that occurred near Missoula, Montana, destroyed six
homes and charred about 500 hectares (1200 acres) of forests
and grasslands in only a few hours.195 Similarly, more than 70
homes were damaged or destroyed by fires in the southern Cape
Peninsula region of South Africa that burned about 8000 hectares
(about 19,800 acres), during January 16 to 20, 2001.109,504 A host
of other cases have occurred in North America242 and are steadily
accumulating.
Fires at the WUI are also increasing internationally. For
example, the Ash Wednesday fire disaster in southeastern Aus-
tralia on February 16, 1983 burned about 340,000 hectares
(840,000 acres) of urban, forested, and pastoral lands in the states
of Victoria and South Australia, killing 77 people, injuring about
3500, and destroying more than 2500 homes.59,237,366 Phenomenal
fire spread rates in both forests and grasslands occurred,254,407 and
flame heights of almost 200 m (650 feet) were observed.472 In
May 1987, wildfires in northeastern China425 added a new per-
spective regarding the devastating impact wildland fires may
have on human lives, property, and natural resources. These fires
reportedly burned about 1.34 million hectares (3.31 million
acres), killed 212 people, seriously injured another 226, and left
about 56,000 homeless.173 Clearly, it was a disaster of major pro-
portions. These fires resulted from a combination of plentiful

FIGURE 14-11  Homeowners and firefighters successfully prepared,
stayed, and defended this rural home in western Montana from a high-
intensity flame front associated with the Wedge fire in July 2003.
(Courtesy Big Fork Volunteer Fire Department.)
fuels, sustained drought, low fuel moistures, and strong winds.465
Rates of spread during the major runs reached 20 km/hr (12
miles/hr). Protecting lives and property from wildfires at the WUI
represents one of the greatest challenges faced by wildfire pro-
tection agencies.
Large forest fires during the intense El Niño drought condi-
tions of 1997 and 1998 focused public and media attention once
again on the need to evaluate public policies and practices in
the forestry and nonforestry sectors that directly or indirectly
contribute to the impact of wildland fires. The size and damage
attributed to these fires were so immense that the Christian
Science Monitor termed 1998 “The Year the Earth Caught Fire.”
At times, that seemed to be literally true, as smoke palls blan-
keted large regional areas, disrupted air and sea navigation, and
caused serious public health threats.214,403,430,542 At least 60 people
were killed in Mexico as a result of the fires,486 and ecosystems
CHAPTER 14  Wildland Fires: Dangers and Survival
that generally are not subjected to fires, such as the Amazon rain
forest and the cloud forest of Chiapas, Mexico, sustained consid-
erable damage. A global fire conference sponsored by the Food
and Agricultural Organization of the United Nations in October
1998 brought together specialists from 33 countries to review the
C
FIGURE 14-12  A, Old man’s gorse (Ulex europaeus) is probably the
worst fuel type in the world from the standpoint of wildland fire man-
agement for two main reasons. B, Density of the vegetation and its
sharp spines or thorns make it extremely difficult if not nearly impos-
sible to physically engage in any kind of fire suppression activity. Vigor-
ous stands grow outward, crowding out all vegetation and forming a
center of fine, dry, dead, elevated fuel. C, This fuel structure, coupled
with the plant’s oil content, readily contribute to the development of
high-intensity flame fronts even under relatively mild fire weather con-
ditions. Gorse is native to central and western Europe, where it has
long been cultivated for hedgerows. It has been introduced to Austra-
lia, New Zealand, the U.S. West Coast (California, Oregon, and Wash-
ington), and southwestern British Columbia. It has also been reported
in Costa Rica and the Hawaiian Islands. In the northeastern United
States, it has established itself along the Atlantic Coast from Virginia
to Massachusetts. (Courtesy Ensis Bushfire Research Group, New
Zealand.)
285
 serious nature of worldwide vegetation fires.199 Participants at the
conference in Rome concluded that governments needed to enact
more sustainable land use policies and practices to reduce the
impacts of wildfires on people and natural resources.
It is becoming increasingly rare to have a wildland fire situa-
tion or incident that does not involve people and their homes.
However, people are not fully aware of the fire risks and hazards
of living and traveling in or near wildlands.65,224 “Risk,” in the
jargon of the wildland fire specialist, is the probability that a fire
will occur. “Hazard” is the likelihood that a fire, once started,
will cause unwanted results. Risk deals with causative agents or
ignition sources; hazard deals with the fuel complex.205 The
results of two surveys carried out in the western United States
during the 1970s indicated a general feeling of overconfidence
by most residents toward the potential danger or threat of a
wildland fire. About 80% of Seeley Lake, Montana, forest resi-
dents interviewed thought that the forest fire hazard was low to
moderate in their area.204 About 75% of Colorado residents inter-
viewed thought that the forest fire hazard was low or moderate
in mountain subdivisions of their state.244 Forest fire hazards in
these two areas were much higher than these public estimates.
A survey of attitudes toward bushfires in the Dandenong Ranges
of Victoria, Australia, found that people who had experienced
BURNS, FIRE, AND RADIATION
bushfires tended to rank their area with a higher rating than did
people without such experience.183 However, the survey also
revealed that 40% of the people with recent severe bushfire
experiences still did not rate bushfires as one of the three most
important environmental problems in their area. Dr. Sarah McCaf-
frey,306 a research social scientist with the USDA Forest Service
who has studied the social dynamics of fire management for
many years, suggests that the general public is much better
informed of the issues dealing with the WUI fire problem than
during the 1970s and 1980s.304,305 She attributes this fundamental
change to programs such as Firewise, fire safe councils, and
media coverage. No doubt the large number of conflagrations in
the past 25 years has also contributed to an increased awareness
regarding the realities of wildland fire.
In more recent surveys carried out in Florida and Minnesota362
PART 3
of homeowners’ preferences for vegetation and defensible space
near their homes, people recognized the wildfire threat but
varied in their perceptions of effective wildfire prevention mea-
sures and willingness to take actions to reduce the potential
threat to themselves and their homes. Most supported the use of
planned fire to reduce fire potential, especially if wildland fire
experts who understand the local ecology and fire behavior
conducted the prescribed burns. In-depth interviews conducted
with homeowners along the northern part of the Colorado Front
Range revealed that these people face difficult decisions regard-
ing implementation of wildfire mitigation measures.79 Perceptions
of wildfire mitigation options were found to be possibly as
important as perceptions of risk in determining likelihood of
implementation. These mitigation options were often viewed as
trade-offs between wildfire risk and preferred landscapes. The
study participants also reported, however, that one-on-one infor-
mation sharing with wildland fire experts, as well as increased
understanding of the flexibility of mitigation options, encouraged
implementation. Personalized contact appears to be a key factor
in educating homeowners about the realities of living in a wild-
land environment.303
Participants in a survey conducted in Michigan541 considered
wildland fires as inherently uncontrollable and the resulting
damage essentially random. Thus, they only weakly supported
investments in fire suppression infrastructure but strongly sup-
ported fire prevention programs that reduced the number of fire
starts, were unlikely to take all possible steps to safeguard their
own properties, and exhibited a negative view of prescribed
fire to the extent that it could preclude its use as a risk manage-
ment tool.
There is a growing need for the general public, emergency
medical personnel, and fire suppression organizations to be well
prepared to deal with wildland fire encounters (Box 14-2). As
Reitz and Geissler410 noted, “The old model of individual home­
owners and neighborhoods depending solely on government
provided firefighting resources is gone. Recent wildland fires
286
BOX 14-2  Recommendations to Reduce Loss of Life
and Property in the Wildland-Urban Interface (WUI)
Fire Protection Services
Remember that firefighter and public safety is the first priority in
every fire management activity.
Ensure that all personnel receive regular cross-training in fighting
wildfires and structural fires.
In urban departments, in particular, recognize the need to
extinguish fires in wildland fuels by using thorough mop-up
procedures.
Recognize the need for close coordination of response efforts
among neighboring departments or agencies.
Develop specific mutual-aid plans for coordinating resources to
attack fires in the WUI.
Schedule and conduct regular mutual-aid training exercises.
Regularly schedule and conduct fire prevention and fire
preparedness education programs for the general public and
homeowners.
Conduct an assessment of fire risks, and prepare a strategic plan
to reduce these risks.
Work effectively with lawmakers and other government officials to
help prevent unsafe residential and business development.
Legislators
Examine existing laws, regulations, and standards of other
jurisdictions that are applicable locally in mitigating hazards
associated with wildland fires.
Adopt National Fire Protection Association (NFPA) guidelines in
the form of NFPA 1144 (formerly NFPA 299, 1991 edition),
Standard for the Protection of Life and Property from Wildfire.344
The purpose of this standard is to provide criteria for fire
agencies, land use planners, architects, developers, and local
government for fire-safe development in areas that may be
threatened by wildfire. NFPA 1144 provides minimum planning,
construction, maintenance, education, and management
elements for the protection of life, property, and other values
that could be threatened by wildland fire. It is designed to
assist local, state, and federal fire agencies in dealing with the
escalating challenges presented by the proliferation of WUI
communities and the monetary losses of structures in WUI
areas. These guidelines address the following topics:
assessment and planning; access, ingress, egress, and
evacuation; fuel modification area; water supply; and residential
development design, location, and construction.
Provide strong building regulations that restrict untreated wood
shingle roofs and other practices known to decrease the fire
safety of a structure in the wildlands.
Planners and Developers
Create a map of potential problem areas based on fuel type and
known fire behavior.
Evaluate all existing or planned housing developments to
determine relative wildland fire protection ratings, and advise
property owners of conditions and responsibilities.
Ensure that all developments have more than one ingress-egress
route.
Offer options for fire-safe buildings.
Provide appropriate firebreaks, fuel breaks, or greenbelts in
developments.
Ensure that adequate water supplies exist in developments.
Follow specifications in NFPA 1144 Standard for the Protection of
Life and Property from Wildfire.344
Public and Homeowners
Determine the wildfire hazard potential of the immediate area
before buying or moving into any home.
Contact federal, state, and local fire services for educational
programs and materials regarding fire protection.
Provide a fuel-modified area or defensible space around
vulnerable structures to reduce the likelihood of ignition by an
advancing wildfire.
Design and build nonflammable homes.
Urge lawmakers to respond with legislative assistance to require
appropriate fire safety measures for communities.
have demonstrated that community firefighting resources are
easily outpaced when multiple structures are burning simultane-
ously. The cure is to move most structure protection responsibil-
ity to the homeowner and community.”
In 2000, 450 residents of Strathcona County, Alberta, Canada,
were randomly selected to test which three educational methods
would produce the greatest change in homeowner behavior with
respect to the WUI.461 The study showed that residents could be
influenced to change their behaviors when provided with the
information materials that enabled them to select between fire
safety alternatives.
A 2003 study evaluated workshops for the adult public featur-
ing experimental learning about wildland fire.377 Participants used
hands-on activities to investigate fire behavior and ecology and
to assess hazards in the WUI. Effectiveness was examined using
a pretest, a post-test following the program, and another post-test
30 days later. Participants’ knowledge increased after the work-
shop, and attitudes and beliefs became more supportive of fire
management. The study concluded that hands-on activities can
help adults become better informed about wildland fire and more
positive about fire management.
WILDLAND-URBAN INTERFACE
LESSONS LEARNED
Recommendations to reduce the loss of life and property in the
WUI will be useless unless they are implemented at the grassroots
level by all stakeholders. An excellent example of a community-
based program is one implemented at Incline Village and Crystal
Bay in the Lake Tahoe basin in Nevada.448 The objective of this
program is to “reduce the potential for natural resource, property,
and human life losses due to wildfire by empowering the com-
munities’ residents with the knowledge to address the hazard,
providing the resources necessary to correct the problem, and
encouraging the cooperative efforts of appropriate agencies.” The
three major components of this defensible-space program include
neighborhood leader volunteers, a slash removal project, and
agency coordination. The key to protecting life and property in
the WUI is property owners’ realization that they have a serious
problem and that their actions embody a significant part of the
solution. In the Incline Village and Crystal Bay community fire
plan, neighborhood leader volunteers are trained in defensible-
space techniques and are expected to teach these techniques to
their neighbors and to coordinate neighborhood efforts. Such
concerted community action will greatly minimize threats from
the southern California type of “fires of the future,” as discussed
earlier.
It is also wise to have sensible land development practices,
because tragedies arise not only from ignorance of fuels and
fire behavior (Figure 14-13), but also from a greater concern
for the aesthetics of a home site than for fire safety.345 The fol-
lowing aspects of development detract from fire safety in the
WUI141,195:
• Lack of access to adequate water sources
• Firewood stacked next to houses
• Slash (i.e., branches, stumps, logs, and other vegetative resi-
dues) piled on home sites or along access roads
• Structures built on slopes with unenclosed stilt foundations
• Trees and shrubs growing next to structures, under eaves, and
among stilt foundations
• Roads that are steep, narrow, winding, unmapped, unsigned,
unnamed, and bordered by slash or dense vegetation that
makes them extremely difficult if not impossible for fire appli-
ances to negotiate
• Subdivisions on sites without two or more access roads for
simultaneous ingress and egress
• Roads and bridges without the grade, design, and width to
permit simultaneous evacuation by residents and access
by firefighters and emergency medical personnel and their
equipment
• Excessive slopes, continuous or heavy fuel situations, struc-
tures built in box canyons, and other hazardous situations
• Lack of constructed firebreaks and fuel breaks around home
sites and in subdivisions
CHAPTER 14  Wildland Fires: Dangers and Survival
FIGURE 14-13  This permanent residence, located in west-central
Alberta, Canada, is unlikely to survive exposure to even a low-intensity
wildland fire, and it would be difficult to stay and defend it for a
number of reasons. There is dense forest vegetation immediately adja-
cent to the structure. Cedar shakes have been used for roofing. This
has been shown time and time again to be the “kiss of death” in
wildland-urban interface fires (at the time this photo was taken in 1997,
the shingles were in such bad shape that they had lichens growing on
them). The homeowner also liked to store flammable materials under
his deck. (Courtesy Yukon Wildland Fire Management; photo by A.K.
Beaver.)
• Living fuels that have not been modified by pruning, thinning,
landscaping, or other methods to reduce cured vegetation,
and litter that readily contribute to spot fire development and
fire intensity
• Homes constructed with flammable building materials (e.g.,
wooden shake shingles)
• Propane tanks exposed to the external environment
• Inability to deliver water effectively before and during passage
of a fire front around the home property (e.g., lack of proper
equipment, such as sprinklers)
In many cases, simply cutting the grass and keeping the yard
cleaned up will dramatically increase the chances of the house
surviving a wildfire.130
WHAT SOME ORGANIZATIONS HAVE TO OFFER
THE GENERAL PUBLIC
The National Disaster Education Coalition is a group of U.S.
federal agencies and nonprofit organizations that support
common goals in disaster and hazards education. This group
worked with leading social scientists in this area to produce a
state-of-the-art guide for public risk education. The group devel-
oped a standardized guide341 on hazard safety messages, provid-
ing information that all organizations agreed on for national use.
The guide covers many different hazards, including wildland
fires, as well as general preparedness issues.
Firewise Communities is a national mitigation planning pro-
gram that encourages communities to include land use planning,
building codes, landscaping codes, zoning, and fire protection
in developing new communities and in retrofitting existing
communities.54,390 Firewise Communities is a national initiative
designed to reach beyond the fire service and involve homeown-
ers, community leaders, planners, developers, and others in the
effort to protect people and property from the dangers of wild-
land fire. Firewise Communities programs include the Firewise
Communities Workshop series, Firewise Communities/USA Rec-
ognition Program, and support for fire organizations and com-
munity groups. The Firewise Communities program is part of the
Wildland-Urban Interface Working Team of the National Wildfire
Coordination Group (NWCG), a consortium of wildland fire
agencies that includes the USDA Forest Service, U.S. Department
of Interior, National Association of State Foresters, U.S. Fire
Administration, Federal Emergency Management Agency (FEMA),
and National Fire Protection Association (NFPA). Firewise
Communities emphasizes that everyone in every community is
287
 responsible for fire protection. Firewise Communities workshops
help define responsibilities for a network that includes many
partners. The intent is to undertake planning and actions to
ensure that people live more compatibly in every neighborhood
situation in a wildland fire environment. Toward this end, a
website has been developed (www.firewise.org), and several
publications and books345,445 have been published to assist home­
owners living in the WUI.
A team of scientists from across the United States has been
visiting communities to identify the activities they need to under-
take to increase their wildfire preparedness and the resources
necessary to support these activities. This research was funded
by the National Fire Plan and is led by the Social and Economic
Dimensions of Ecosystem Management Research Work Unit
of the USDA Forest Service’s North Central Research Center.
Research partners include the USDA Forest Service’s Pacific
Northwest Research Station, University of Minnesota, Southern
Oregon University, and University of Florida. Sixteen community
preparedness case studies were completed between 2002 and
2004 in a variety of locations throughout the continental U.S.
(jfsp.fortlewis.edu).527,534
In 1990, Partners in Protection (PiP) of Alberta, Canada, was
established. PiP is a coalition of professionals representing
BURNS, FIRE, AND RADIATION
national, provincial, and municipal associations and organiza-
tions committed to raising awareness, providing information, and
developing forums to encourage proactive, community-based
initiatives regarding fires at the WUI. In 2008, PiP was invited by
the Canadian Council of Forest Ministers to develop a proposal
for a nationally oriented effort. In response, PiP developed the
FireSmart Canada program that addresses the goals necessary to
protect lives and properties across Canada. PiP has produced a
comprehensive manual with respect to the WUI fire problem
entitled FireSmart: Protecting Your Community from Wildfire.378
This well-illustrated guide focuses on how individuals and com-
munities can work together to reduce the risk for loss from
wildfires in the WUI. It provides practical tools and information
for use by residents and by individuals and organizations that
operate in the WUI. The primary topics are description of
PART 3
interface issues, evaluation of hazards, mitigation strategies and
techniques, emergency response for agencies and individuals,
training for interface firefighters, community education programs,
and regional planning solutions. The manual, available in both
book form and CD-ROM, can be viewed online (www.firesmart
canada.ca/resources-library/protecting-your-community-from-
wildfire) and covers almost every facet of fire preparations in the
WUI. In the chapter on communications and public education,
for example, the following principles are cited for effective
communication:
• Begin with clear, explicit objectives.
• Do not make assumptions about what people know, think,
or want done. Take time to find out what people are thinking
by using surveys, focus groups, or other research.
• Involve all parties that have an interest in the issue. Identify
and address the particular interests of different groups.
• Identify with your audience. Put yourself in their place, and
recognize their emotions.
• Take time to coordinate with other organizations or groups.
• Choose your spokespeople carefully, and ensure they have
the training to communicate your messages effectively.
• Practice and test your messages.
• Do not either minimize or exaggerate the level of risk.
• Promise only what you can do. Do what you promise.
• Plan carefully, and evaluate your efforts.
Kumagai and colleagues261 also offer some excellent advice
with respect to wildland fire education and communication with
the general public.
Most local, state, provincial, territorial, and federal fire man-
agement agencies now have some type of outreach program
related to the WUI. For example, the State of Alaska offers
teachers both face-to-face wildland fire workshops and an
online training course.468 In 1993 the Country Fire Authority of
Victoria, Australia, developed a program called “Community Fire-
guard,” which assists communities in developing wildfire survival
strategies.74
288
C
B
A
FIGURE 14-14  In an attempt to avoid the intense heat of the Battle-
ment Creek Fire in southwestern Colorado on July 17, 1976, four
firefighters took refuge in the fire line, in the foreground at point A.
Affected by intense convective and radiant heat and dense smoke, one
individual ran into the fire and died at point B. Another individual ran
about 300 m (1000 feet) down the ridge, where his body was found
at point C. The third fatality was a person who remained at point A;
he died a short time after this position was overrun by fire. The only
survivor also remained in a prone position at point A with his face
pressed to the ground. At one point he reached back and threw dirt
on his burning pants legs. The survivor sustained severe burns to the
backs of his legs, buttocks, and arms. The deaths of the other three
individuals were attributed to asphyxiation. (Courtesy USDA Forest
Service.)
WILDLAND FIRE BEHAVIOR
URBAN AND WILDLAND FIRE THREATS
Safety precautions for wildland firefighting crews are continually
upgraded as new knowledge is gained about fire behavior and
human behavior. The sites where people were injured or killed
by fire are routinely examined afterward to assess fuel conditions,
terrain features, probable wind movements at the time of the fire,
and actions of firefighters294,329,530 (Figure 14-14). In this regard,
Maclean285 has noted:
It is hard to know what to do with all the detail that rises out of fire. It
rises out of a fire as thick as smoke and threatens to blot out everything.
Some of it is true but doesn’t make any difference. Some of it is just
plain wrong. And some doesn’t even exist, except in your mind, as you
slowly discover long afterwards. Some of it, though, is true—and makes
all the difference.
The information gleaned from past wildland firefighter fatali-
ties, as well as data about hazards in the WUI, are now included
in training programs and safety briefings.
In reviewing many past wildland fire tragedies, a sobering
observation is that crew members are almost always experienced
and well-equipped firefighters, trained to anticipate “blowup” fire
conditions (i.e., a temporary escalation in fire behavior). However,
when visibility is lowered to 6 m (20 feet), noise levels preclude
voice communication, eyes fill with tears, and wind blows debris
in all directions, a person’s judgment is greatly impaired. For
many members of the general public, the first wildland fire they
may experience will in all likelihood be a high-intensity confla-
gration. As Cheney122 notes:
The approach of a major fire can appear ominously threatening to those
directly in its path, but is often viewed with curiosity and with little
concern if it appears that the wind will direct the fire past their proper-
ties. Thus, when a combination of circumstances, often associated with
a frontal wind passage, exposes residents to a high-intensity fire environ-
ment, they are very much unprepared. Their senses are assaulted by
sudden darkness, thick blinding and choking smoke, buffeting winds and
unexpected calm periods, searing heat and flames which illuminate the
smoke-obscured scene and a roaring noise of wind and explosive com-
bustion. In all this activity they observe flames which change from a
metre or two to engulfing whole trees. In such a dramatic and emotional
situation, many people are apt to invent phenomena (such as, houses
exploding, the air burning, fantastic spread rates and the like) to explain
the extent of the devastation that confronts them when the smoke
clears away.
Even for experienced firefighters, previous training can give
way to panic-like attacks and poor decision making, leading to
actions that can result in serious injury or death.370 This scenario
is most evident in urban fires; the pattern of hysteria affecting
people trapped in burning buildings is all too familiar to urban
firefighters.452 The way fire kills in the urban setting can be com-
pared with wildland fires, as summarized here373:
1. Heat rises rapidly to upper stories when a fire starts in the
basement or on the ground floor. Toxic gases and smoke rise
to the ceiling and work their way down to the victim—a vital
lesson for families planning protective measures. Smoke poses
the double problem of obscuring exit routes and contributing
to pulmonary injury and oxygen deprivation.
2. As the fire consumes oxygen, the ambient oxygen content
drops, impairing neuromuscular activity. When the oxygen
content drops below 16%, death by asphyxiation will ensue
unless the victim is promptly evacuated. Asphyxiation, not fire
itself, is the leading cause of fire deaths.
3. Ambient air temperatures may rise extremely rapidly from
even small fires. Temperatures of 150° C (300° F) will cause
rapid loss of consciousness and, along with toxic gases, will
severely damage lung tissues. Warning devices may offer the
only possibility for survival because of the rapid onset of
debilitating symptoms.
Obvious similarities and differences are seen between wild-
land fires and urban fires:
1. Smoke, heat, and gases are not as concentrated in wildland
situations as in the confined quarters typical of many urban
fires.
2. Flames are not a leading killer in either the urban or the
wildland situation, although admittedly, autopsies are gener-
ally not performed, so this assertion awaits confirmation.
3. Although oxygen levels may be reduced near wildland fires,
there is usually sufficient replenishment of oxygen in the
outdoor environment to minimize deprivation. Asphyxiation,
however, can also be an important cause of death in wildland
fires.
4. Inhalation of superheated gases poses as serious a threat to
life in wildland fires as in urban fires.
5. Wildland smoke does not contain toxic compounds produced
by combustion of plastics and other household materials, but
it does impair visibility, contains carbon monoxide, and carries
suspended particulates that cause severe physical irritation of
the lungs.
6. Sprinkler systems and automatic early-warning devices to
detect smoke or heat may protect people from serious injury
or death in the urban environment, but in the wildland envi-
ronment, people must rely on their experience, senses, knowl-
edge, and skills or ingenuity to provide early warning of an
impending threat to life.
The general public needs to appreciate that fires occurring
under certain fuel, weather, and topographic situations may result
in explosive fire growth on an area basis (Figure 14-15). The fire
that burned through Faro, Yukon, on June 13, 1969, is a good
example of this type of behavior.255 The Faro Fire, which burned
about 15,500 hectares (38,300 acres) resulted from a lightning
strike that occurred 8 km (5 miles) west of town at 5:04 PM. The
fire started to spread fairly quickly in an easterly direction. Fire
crews were dispatched from town by vehicle to take suppression
action, but little could be done because of crowning activity. By
8:30 PM, the fire had burned through town and was continuing
to spread farther east. In other words, the fire had traveled 8 km
(5 miles) in less than 3.5 hours. This equates to a rate of spread
of around 2.3 km/hr (1.4 miles/hr) or 40 m/min (131 ft/min).
This would not be considered an unusual situation in many
regions of the North American boreal forest.30,160 How wide
would the fire have likely been when it hit the edge of town? A
rough rule of thumb is to divide the separation distance by a
factor of 2 to 4 based on an assumed wind-driven fire shape.475
CHAPTER 14  Wildland Fires: Dangers and Survival
FIGURE 14-15  View of the Crutwell Fire as it burned toward the city
of Prince Albert, Saskatchewan, during its initial major run that started
during the late afternoon of June 28, 2002. This photo was taken from
a building in the downtown area when the fire was about 18 km (11
miles) away. The fire was started by lightning during the morning of a
day of extreme fire danger. On escaping initial containment, this wind-
driven fire advanced by crowning through jack pine forests at rates of
about 2.3 km/hr (1.4 miles/hr) at the height of activity. Spotting up to
1 km (0.6 mile) was observed. Fortunately, changes in fuel types and
less severe fire weather conditions during the night contributed to the
effectiveness of the fire suppression operations. (Courtesy Saskatch-
ewan Health; photo by G. Matchett.)
The fire would have thus been about 2 to 4 km (1.2 to 2.5 miles)
wide when it hit the western edge of Faro.
Fire Behavior Knowledge: a Wildland Fire
Early-Warning System
Fire behavior is defined as the manner in which fuel ignites,
flame develops, and fire spreads and exhibits other related phe-
nomena as determined by the interaction of fuels, weather, and
topography. The science of fire behavior describes and predicts
the performance of wildland fires in terms of ignition probabili-
ties, rates of spread, intensity levels, spotting distances and densi-
ties, and crowning potentials.
To the layperson, a wildland fire can be a perplexing event.
As Countryman and Schroeder155 note:
A casual observer seeing a forest fire for the first time would probably
decide there is little rhyme or reason to the way a fire burns. Its sudden
variations in direction of travel, its quick change from a seemingly mild,
slow-burning fire to a raging inferno, all seem to add up to erratic behav-
ior without local explanation. Actually a fire behaves in accord with
changes in its surroundings—the character and condition of the burnable
vegetation, the topography, and the meteorologic factors—that affect
fuel flammability, fire intensity, and fire spread. This complex of envi-
ronmental factors that control the behavior of fire is what we call “fire
environment.”
Understanding one’s fire environment151 is considered a key
factor for safe and effective action in dealing with wildland fires.
For example, 4 of the 32 civilians killed in Victoria during the
1983 Ash Wednesday fires in southeastern Australia were caught
outside their homes tending to or attempting to herd up live-
stock,259 apparently unaware of the change in wind direction and
speed that accompanied passage of the cold front through their
area.407 In such situations in southeastern Australia, the strong
prefrontal winds are from the northwest. With the passage of the
front, the wind direction changes sharply to the southwest, and
winds increase markedly in strength. Had these people under-
stood or been aware of the implications of the cold front passage
on fire behavior and received some information on the timing of
the change, they may have chosen to stay inside their homes.259
An excellent overview of the fire environment concept has been
prepared by the National Wildfire Coordinating Group.350
Experienced firefighters routinely monitor the fire and the fire
environment and assess the probable behavior of fires using fire
289
 behavior guidelines and experienced judgment35,57 based on
current and expected fire weather conditions in relation to local
fuel type information, topographic conditions, and moisture
levels.88,273,475 This is also referred to as situational awareness,
that is, understanding what the fire is doing and what you are
doing in relation to the fire and being able to predict where the
fire and you will be in the future.391
In the conclusions to their detailed case study report on the
1994 South Canyon fire in Colorado, USDA Forest Service fire
researchers98 noted:
None of the findings and observations discussed in this study represent
new breakthroughs in wildland fire behavior understanding. Rather, the
findings support the need for increased understanding of the relations
between the fire environment and fire behavior. We can also conclude
that fire managers must continue to monitor and assess both present fire
behavior and potential future fire behavior given the possible range of
environmental factors.
The emergency medical person, backcountry recreationist,
and wildland homeowner must also understand certain basic fire
behavior principles to provide for adequate personal safety. A
cardinal rule in wildland fire suppression is to base all actions
on current and expected fire behavior.300,322 Attention to simple
BURNS, FIRE, AND RADIATION
principles, indicators, and rules should enable wildland users to
anticipate and avoid wildfire threats.
Heat, oxygen, and fuel are required in proper combination
before ignition and combustion will occur57,209 (Figure 14-16). If
any one of the three is absent, or if the three elements are out
of balance, there will be no fire (Box 14-3). Fire control actions
are directed at disrupting one or more elements of this basic fire
triangle.14
PHYSICAL PRINCIPLES OF HEAT TRANSFER
Heat energy is transferred by conduction, convection, radiation,
and spotting, but generally only the last three processes are
significant in a wildland setting.106 Although conduction through
solid objects is important in the burning of individual logs,57 this
PART 3
process does not transfer much heat outward from a flaming
front, unless there is a substantial accumulation, such as is found
in blowdown fuel complexes.208
Convection, or the movement of hot masses of air, accounts
for most of the heat transfer upward from the fire. Convective
Heat
O2
Oxygen Fuel
FIGURE 14-16  Combustion is a process involving the combination of
heat, oxygen, and fuel. An understanding of the variations of these
three factors is fundamental to an understanding of wildland fire
behavior. (Modified from Barrows JS: Fire behavior in Northern Rocky
Mountain forests, Station Paper No 29, Missoula, Mont, 1951, USDA
Forest Service, Northern Rocky Mountain Forest and Range Experi-
ment Station.)
290
BOX 14-3  Requirements for Wildland Fire Spread
Certain universal principles apply to all spreading fires in
vegetation, living or dead. These really have nothing to do with
biology but are based purely on the physics and chemistry of
combustion:
1. There must be sufficient fuel of appropriate size and
arrangement in space.
2. This fuel must be of sufficient dryness to support a spreading
combustion reaction.
3. There must be an agent of ignition.
In practical terms, the primary requirement is a continuous layer
of finely divided fuel or minor vegetation on the surface of the
ground. This material may be conifer needles, hardwood leaves,
grass, lichen, moss, finely divided shrubs, or other minor
vegetation. However, it must be present and it must be
continuous, or the possibility of spreading fire does not really
exist. The second requirement is that the material be dry enough.
The maximum moisture content at which fire will spread is hard to
specify; for any given fuel or vegetation complex, it will depend on
the amount of fuel, its arrangement in space, and the wind speed.
Thus, fire spreads poorly or not at all in surface litter of various
kinds at moisture contents over 25% or 30% (dry weight basis),
whereas fine shrubby fuels or conifer foliage may support
fast-spreading fires at moisture contents of 100% or more.
The two limiting criteria common to all spreading fires are as
follows:
1. The fire must transfer enough heat forward to dry out the
unburned fuel and raise it to ignition temperature by the time
the flame front arrives.
2. Enough fuel must pass through the moving flame front to
produce a continuous solid flame.
The behavior of any fire is the result of a complex process that
results in a dynamic equilibrium among all elements of mass and
energy flowing in and out of the flame zone. However difficult this
whole process may be to describe and predict, the above two
criteria run like threads through the whole range of fires in
vegetation, whether the fuel itself is dead or live.
From Van Wagner CE: Fire behaviour in northern conifer forests and shrublands.
In Wein RW, MacLean DA, editors: The role of fire in northern circumpolar
ecosystems, Chichester, England, 1983, John Wiley & Sons.
currents usually move vertically unless a wind or slope generates
lateral movement (Figure 14-17). Convection preheats fuels
upslope and in shrub and tree canopies, which contributes
further to a fire’s spread and the onset of crowning forest fires.
Through radiation, heat energy is emitted in direct lines or
rays; about 25% of combustion energy is transmitted in this
manner. Radiated heat on exposed skin can cause discomfort
and severe pain (Figure 14-18), and even death at elevated
levels.118,147 The amount of radiant heat transferred decreases
inversely with the square of the distance from a point source.
More radiant heat is emitted from a line of fire than from a point
source. Radiant heat travels in straight lines, does not penetrate
solid objects, and is easily reflected. It is believed to account for
most of the preheating of surface fuel ahead of the fire front and
poses a direct threat to people who are too close to the fire (see
Figure 14-17).
Most organized fire suppression crews in the United States
carry protective fire shelters42,43,382 as part of their personal protec-
tive equipment (PPE) (Figure 14-19).383 These aluminized “pup
tent” type of structures are intended to protect against radiant
heat.104,394 The USDA Forest Service fire shelter was never designed
to mitigate against sustained, direct flame contact.317 Certain mate-
rials that fail when in direct contact with flames, such as “emer-
gency space blankets,”201 are also not appropriate for use in
wildland fires87 and in fact could cause serious burn injuries.
Similarly, “emergency evacuation smoke hoods,” intended for use
in urban situations or other human-made environments (e.g.,
airplanes), have absolutely no application in a wildland fire
environment despite manufacturers’ suggestions to the contrary.
Spotting is a fire spread or mass-transport heat transfer mecha-
nism by which wind currents carry flaming firebrands or glowing
embers land beyond the main advancing fire front to start new
 CHAPTER 14  Wildland Fires: Dangers and Survival
A
Wind

FIGURE 14-18  Most of the heat felt from a fire is radiant heat, which
B is largely a function of the height, depth, and angle of the flame front.
FIGURE 14-17  Fuels and people upslope (A) or downwind (B) from a Wildland firefighters work far enough from the radiating flames to
fire receive more radiant and convective heat than on the downslope avoid pain to exposed skin (e.g., face and ears). This also limits the
or upwind sides of a spreading fire. (Modified from Barrows JS: Fire amount of radiant heat absorbed through clothing. Wildland firefight-
behavior in Northern Rocky Mountain forests, Station Paper No 29, ers working near an active fire edge with hand tools typically adjust
Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Mountain their distance from the flames so that the radiant heat they receive
Forest and Range Experiment Station.) from the fire is little more than that of direct sunlight. (Courtesy British
Columbia Forest Service.)

fires (Figure 14-20). In this manner, fire spread may accelerate
very quickly, unexpected new fire starts can occur, and fire
intensity and in-draft winds can dramatically increase as spot fires
coalesce (Figure 14-21) and directly increase a fire’s rate of
spread. High-density, short-range spotting up to 100 m (328 feet)
is a common feature of many wildfires, especially when fine fuels
are very dry.39 Low-density, intermediate- to medium-range spot-
ting up to about 1 to 2 km (0.6 to 1.2 miles) is a common occur-
rence with high-intensity crown fires.30 Longer-range spotting
occurs very infrequently in most fuel types. Firebrand material
being transported up to 16 km (10 miles) from its source has
been reported in North America.41 The native eucalyptus forests
of Australia have a notorious reputation when it comes to spot-
ting behavior because of the bark characteristics of many species,
including an authenticated spot fire distance of 30 km (19 miles)
or more.281

A B D
FIGURE 14-19  The personal protective equipment for a firefighter includes hard hat and safety goggles,
fire-resistant shirt and trousers, leather boots and gloves, and an aluminized fire shelter carried in a waist
pouch (A). Firefighters also carry canteens to ensure an adequate water supply in a heat-stressed environ-
ment. The fire shelter (B) is deployed (C) by firefighters as a last resort to provide protection from being
exposed directly to radiant heat and superheated air (D). (Courtesy USDA Forest Service.)

291

FIGURE 14-20  Fires can easily cross narrow canyons. Fuels and people
on the slope opposite a fire in a narrow canyon are subject to intense
radiant heat and spot fires from airborne embers. (Modified from
BURNS, FIRE, AND RADIATION
FUNDAMENTAL WILDLAND FIRE
BEHAVIOR CHARACTERISTICS
One important aspect of fire behavior that distinguishes urban
or structural fires from wildland fires is the latter’s horizontal
spread potential or rate of spread.161 Although urban or structural
fires may exhibit some horizontal as well as vertical fire spread
potential, for practical purposes, they are considered stationary
fire sources. Wildland fires, on the other hand, characteristically
involve moving flame fronts, sometimes advancing with astonish-
ing speed (Figure 14-22). Whereas ground or subsurface fires
may spread very slowly (about 1 m [3 feet] per hour),524 surface
fires in open grown forests can reach rates of about 15 to 25 m/
min (50 to 80 ft/min); conversely, surface fires in closed forest
types typically spread at 5 to 6 m/min (16 to 20 ft/min) before
the onset of crown combustion. Crowning forest fires generally
advance at rates between 30 and 60 m/min (100 to 200 ft/min),
occasionally higher.30,160 Grass fires spread at rates up to about
385 m/min (1263 ft/min) or 23 km/hr (14 miles/hr).129,365 It is thus
quite possible for forest fires to advance up to 80 km (50 miles)
in a single day7,420 and for grass fires to travel correspondingly
even farther.528
The threat to life and property largely depends on a fire’s

Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station
Paper No 29, Missoula, Mont, 1951, USDA Forest Service, Northern
Rocky Mountain Forest and Range Experiment Station.)
PART 3
residence time (Table 14-2). This represents the length of time
any object overrun by a fire will be heated by direct flame
contact. Coupled with the fire’s rate of spread, the residence time
determines the depth of the active or continuous flaming front
(Figure 14-23). The length of time that a fire will continue to
burn by smoldering combustion is much more complicated and
depends on the composition, compaction, moisture content, and
quantity of fuel present.202

A B

C D
FIGURE 14-21  The occurrence of numerous spot fires is a direct indication that the moisture content of
fine fuels has attained a critically dry level and in turn an early-warning signal that the potential for extreme
fire behavior exists or is imminent. This sequence of photos (A to D) spanned a period of just over 100
seconds taken late in the afternoon of July 9, 2005, near Coimbra, Portugal. The fuel type is a blue gum
(Eucalyptus globulus)–maritime pine (Pinus pinaster) stand. (Courtesy Associação para o Desenvolvimento
da Aerodinâmica Industrial; photos by M.G. Cruz.)

292
 CHAPTER 14  Wildland Fires: Dangers and Survival
Finger Head

Left flank

Spot
fire

Pocket
Finger
Right flank
Rear

Unburned island
FIGURE 14-22  A novel approach to reminding people of the capri- Wind direction
cious nature of wildland fire spread. This sign is located at Betty’s Bay
on the South African coast near Cape Town. The vegetation type is FIGURE 14-24  The parts of a fire are described in terms of its left
fynbos—a highly flammable Mediterranean shrubland fuel complex.503 flank, right flank, head, and back or rear. There may also be unburned
(Courtesy CSIR Natural Resources and the Environment, Stellenboch, islands within the fire and spot fires ahead of the fire. The safest travel
South Africa; photo by B.W. van Wilgen.) routes generally involve lateral movement on contours away from the
fire’s flank or movement toward the rear of the fire. Moving in front of
a head fire should be avoided. The burned area inside the fire’s perim-
eter can offer a safe haven provided smoldering or glowing combus-
Flame tion levels are low and the flaming perimeter can be safely penetrated
flashes by an individual; falling trees or snags and rolling rocks could, however,
Prevailing wind still pose a hazard. (Modified from Mobley HE, Moore JE, Ashley RC,
Flame height et al: Planning for initial attack, rev ed, Forestry Report SA-FR-2,
Flame length Atlanta, Ga, 1979, USDA Forest Service, Southeastern Area State and
Private Forestry.)

Flame angle
Ash

Flame depth Compact surface layer

FIGURE 14-23  Cross-sectional view of a stylized free-burning fire in a
grass fuel bed. (From Cheney P, Sullivan A: Grassfires: Fuel, weather
and fire behaviour, ed 2, Collingwood, Victoria, Australia, 2008, CSIRO
Publishing.)

The most basic features of a wildland fire are that (1) it

spreads or moves, (2) it consumes or “eats” fuel, and (3) it pro-
duces heat energy and light in a visible, flaming combustion
reaction.6 Byram105 defined fire intensity as the rate of heat energy
release per unit time per unit length of fire front, regardless of
its depth. Numerically, it is equal to the product of the quantity
of fuel consumed in the flaming front, a fire’s rate of fire spread,
and a fuel heat combustion value. Flame size is its main visual FIGURE 14-25  Elliptical fires resulting from multiple, wind-driven,
manifestation. The fastest-spreading part of a fire is the head; the point-source ignitions associated with a prescribed burning operation
back of the fire is the slowest-spreading part, with the flanks in a southeastern U.S. pine plantation. As indicated by the smoke drift,
being intermediate between the two (Figure 14-24). It is for this the winds are blowing roughly from lower right to the upper left.
reason that the fire intensity, flame length, and flame height (see (Courtesy USDA Forest Service; photo by C.W. Adkins.)
Figure 14-23) are greatest at the front of the fire and least at the
rear113 (Figure 14-25).

TABLE 14-2  Nominal Residence Times for Four Broad Fuel Complexes and Computed Maximum Theoretical Flame
Depths* Associated with Variable Rates of Fire Spread
Rate of Fire Spread
10 m/min (33 ft/ 20 m/min (66 ft/ 40 m/min (131 ft/
Residence Time min) Flame Depth min) Flame Depth min) Flame Depth
Broad Fuel Complex (sec) (min) (m) (ft) (m) (ft) (m) (ft)

Grassland 10 0.17 1.7 5.6 3.4 11.2 6.8 22.3

Shrubland 20 0.33 3.3 10.9 6.6 21.7 13 42.7
Forest stand 45 0.75 7.5 24.6 15 49.2 30 98.4
Logging slash 90 1.5 15 49.2 30 98.4 60 196.8

*Numerically equal to residence time multiplied by the rate of fire spread (in compatible units).

293
 The amount of radiation received from a flame front is deter-
mined by the size and geometry (e.g., height, depth, and tilt
angle) of the flame front. Radiation levels coupled with residence
times determine the nature of burn injuries.87,181
Environmental Factors Influencing Wildland Fire Behavior
A wildland fire behaves according to variations in the fire envi-
ronment (i.e., fuels, weather, and topography). Box 14-4 lists
some of the fire environment factors associated with adverse
burning conditions that can signal the potential or onset for
severe fire behavior. These factors or indicators are subject to
assessment, observation, and measurement.
When a person encounters a wildland fire, the first step
should be to review the principles and indicators of fire behavior,
sizing up the situation in terms of fuel, weather, topographic
BOX 14-4  Early-Warning Signals or Indicators
Associated with Extreme Fire Behavior Potential
Fuel
• Continuous fine fuels, especially fully cured (dead) grasses
• Large quantities of medium and heavy fuels (e.g., deep duff
BURNS, FIRE, AND RADIATION
layers, dead-down logs)
• Abundance of bridge or ladder fuels in forest stands (e.g.,
branches, lichens, suspending needles, flaky or shaggy bark,
small conifer trees, tall shrubs extending from ground surface
upward)
• Tight tree crown spacing in conifer forests
• Presence of numerous snags
• Significant amounts of dead material in elevated, shrubland fuel
complexes
• Seasonal changes in vegetation (e.g., frost kill)
• Fire, meteorologic or insect and disease impacts (e.g.,
preheated canopy or crown scorch; snow-, wind-, or ice-
damaged stands; drought-stressed vegetation; or mountain
pine beetle–killed stands)
Weather
PART 3
• Extended dry spell
• Drought conditions
• High air temperatures
• Low relative humidity
• Moderately strong, sustained winds
• Unstable atmosphere (visual indicators include gusty winds, dust
devils, good visibility, and smoke rising straight up)
• Towering cumulus clouds
• High, fast-moving clouds
• Battling or shifting winds
• Sudden calm
• Virga (i.e., a veil of rain beneath a cloud that does not reach the
ground)
Topography
• Steep slopes
• South- and southwest-facing slopes in the northern hemisphere
• North- and northeast-facing slopes in the southern hemisphere
• Gaps or saddles
• Chutes, chimneys, and narrow or box canyons
Fire Behavior
• Many fires that start simultaneously
• Fire that smolders over a large area
• Rolling and burning pine cones, agaves (a desert plant found in
the southwestern U.S.), logs, hot rocks, and other debris igniting
fuel downslope
• Frequent spot fires developing and coalescing
• Spot fires occurring out ahead of the main fire early on
• Individual trees readily candling or torching out
• Fire whirls that cause spot fires and contribute to erratic burning
• Vigorous surface burning with flame lengths starting to exceed
1 to 2 m (3 to 6 feet)
• Sizable areas of trees or shrubs that begin to readily burn as a
“wall of flame”
• Black or dark, massive smoke columns with rolling, boiling
vertical development
• Lateral movement of fire near the base of a steep slope
294
factors, and observed fire behavior. After the fire’s probable
direction and rate of spread are estimated, travel routes that avoid
hazards to human life can be planned (see Figure 14-24). The
direction of the main body of smoke is often a good indicator
of the direction the fire will take.
Fuel.  Because wildland fuels vary so widely in their distribu-
tion, their physical characteristics or properties (i.e., moisture
content, size and shape, compactness or arrangement, load,
horizontal and vertical continuity, chemical content), and their
effect on fire behavior, some means of classification is needed
for their systematic assessment. Fuels are commonly classified
into four groups or strata (Figure 14-26). Some fuel types may
exhibit only one or two of the strata (e.g., grasslands, shrublands,
and logging slash lack the ladder and crown fuel stratum).
An increase in fuel available for combustion affects fire inten-
sity. In other words, the more fuel that is burning, the greater is
the heat energy released by the fire. As Brown and Davis83 noted:
The ignition, buildup, and behavior of fire depend on fuels more than
any other single factor. It is the fuel that burns, that generates the energy
with which the fire fighter must cope, and that largely determines the
rate and level of intensity of that energy. Other factors that are important
to fire behavior (that is, moisture, wind, etc.) must always be considered
in relation to fuels. In short, no fuel, no fire!
Certain types of fuel, such as chaparral, pine, and eucalyptus,
burn more intensely because their foliage contains flammable oils
and resins (see Figure 14-12). The size and arrangement of fuel
also influence fire behavior. Small, loosely compacted fuel beds,
such as dead grass, long pine needles, and shrubs, burn more
rapidly than does tightly compacted fuel. Large fuels burn best
when they are arranged so that they are closely spaced, such as
logs in a fireplace. Scattered logs with no small or intermediate
fuel nearby seldom burn unless they are decomposed. Seasonal
changes in the moisture content and live-to-dead ratio (e.g.,
degree of curing in grasslands) of conifer tree foliage, shrubs,
grasses, and other herbaceous plants can result in gradual
changes in fuel flammability over the course of a fire season.153,281
Wildland fire research has identified a wind speed threshold
in fuel types with a discontinuous, combustible surface layer
(e.g., caused by the presence of areas of bare, mineral soil).85,89
In these discontinuous fuel types, fire spread is exceedingly
limited until a certain or threshold wind speed level is attained,
and then the rate of advance can be quite unexpectedly rapid207
(Figure 14-27). This type of situation could lead a person into a
false sense of security regarding fire potential, until unfortunately
it is often too late.
Various weather phenomena (e.g., wind, hail, snow, ice, frost)
and insect and disease epidemics can drastically elevate the flam-
mability of a fuel complex, creating decidedly new fire safety
concerns.34 For example, on July 9, 1999, heavy rains and winds
in excess of 145 km/hr (90 miles/hr) blew down about 181,000
hectares (447,000 acres) of sub-boreal forest in northeastern Min-
nesota, resulting in heavy, dead and downed, woody fuel loads.208
Weather.  The greater the wind, the more rapid is the spread
of fire. Thunderstorm downdrafts and winds associated with dry,
cold frontal passages can be especially hazardous.129,427 Low rela-
tive humidity and high ambient air temperatures decrease the
moisture content of fine, dead fuels and thereby increase ignition
ease and rate of spread. Prolonged drought makes more medium
and heavy fuels, such as duff and deep organic layers, available
for combustion, leading to increased intensity levels. When fuels
reach critically dry levels, fires become very responsive to minor
changes in wind and slope. Fires tend to burn more vigorously
under unstable atmospheric conditions.
The North American continent has been classified into 15 fire
climate regions based on geographic and climatic factors427
(Figure 14-28). Major fire seasons, or periods of peak fire activity,
can be used to warn emergency medical personnel and wildland
users of the most probable times for life-threatening situations.
Exceptions occur. For example, rapidly spreading grass and
forest fires can occur during the winter months in the northern
latitudes, as occurred in Alberta, Canada, on December 14, 1997,
under Chinook conditions and no snow cover.223 A wildfire near
the town of Hinton in the mountainous region of the west-central
 CHAPTER 14  Wildland Fires: Dangers and Survival
Crown
fuels

Ladder fuels
Surface
fuels Ground
fuels

Mineral
soil

FIGURE 14-26  Profile of a stylized forest stand showing the location and classification of fuel complex
strata. Wildland fuels contain energy, stored over extended periods through photosynthetic processes, that
is released rapidly, occasionally explosively, in combustion. (Modified from Brown AA, Davis KP: Forest fire:
Control and use, ed 2, New York, 1973, McGraw-Hill.)

part of the province that spread through conifer forests by inter-

mittent crowning posed a significant threat to the community. A
Continuous fuel single grass fire in the southwestern plains region advanced
33 km (20.5 miles) in less than 4 hours for a spread rate of
around 8 km/hr (about 5 miles/hr), seriously threatening the
community of Granum.73 A similar situation was repeated with
grass fires in 2011 and 2012 in southern Alberta.31
Although the fire season for the southern Pacific Coast is
shown in Figure 14-28 as June through September, critical fire
weather can occur year-round in the most southerly portion of
Rate of fire spread

the area. Fire seasons are most active during spring and fall in
the Great Plains, Great Lakes, and North Atlantic regions. The
Discontinuous pattern of seasonal fire occurrence in Australia has also been
fuel
mapped,281 as has the frequency of large fires.119
Topography.  All other environmental factors being the
same, the steeper the slope, the more rapid is the spread of fire.
Fire usually burns uphill, especially during daylight hours.
Changes in topography can cause rapid and violent changes in
fire behavior (Figure 14-29). On steep terrain, rolling firebrands
Wind speed may cause a fire initially to spread downhill, followed by upslope
threshold for runs. Mountainous terrain can modify wind speed and direction
discontinuous and in turn influence fire behavior in exceedingly complex
fuel ways.427 Slope exposure or aspect has a very pronounced diurnal
effect on fine-fuel flammability, a fact directly incorporated into
the Campbell Prediction System of wildland fire behavior predic-
Wind speed tion (www.emxsys.com/cps/default.html).110

FIGURE 14-27  Discontinuous fuel types will not carry a fire until wind Extreme Fire Behavior
speed exceeds a particular threshold value. For example, a wind of Extreme fire behavior is generally, but not conclusively, consid-
12 km/hr (7.5 miles/hr) has been identified from conducting experi- ered a level of fire activity that often precludes any fire suppres-
mental fires as a critical threshold for fire spread in spinifex grasslands sion action by conventional means.313 It usually involves one or
of central Australia. In contrast, fire spread in continuous fuel types is more of the following fire behavior characteristics:
possible even under calm conditions and, predictably, steadily in- 1. High rates of spread and intensity
creases with increasing wind. (Modified from Gill AM, Burrows ND, 2. Active crowning
Bradstock RA: Fire modeling and fire weather in an Australian desert, 3. Prolific spotting
CALMScience Suppl 4:29, 1995.) 4. Presence of large fire whirls
5. Well-established convection column

295
 Fairbanks, AK Cranbrook, BC Prince Albert, SK Churchill, MB Toronto, ON
6 6 6 6 6
Annual Annual Annual Annual Annual
11.7 inches 14.7 inches 19.4 inches 15.4 inches 32.1 inches
4 4 4 4 4

Inches

Inches

Inches

Inches
Inches
2 2 2 2 2

J F MAM J J A S ON D J F MAM J J A S ON D J F MAM J J A S ON D J F MAM J J A S ON D J F MAM J J A S ON D

Month Month Month Month Month

May-Sept. 10 New York City, NY

6
Annual
1 43.9 inches
4

Inches
2
Gull Harbour, BC
10
Annual
J F MAM J J A S ON D
57.1 inches 9

Ju
8 Month

n
July-August
e-S
6
10
Inches

Spring-
ep Fall.
t.
4
June- 2 5 Summer, Decatur, IL
2 6 Annual
Sept. or Combination 37.5 inches
April-Oct. 4

Inches
J F MAM J J A S ON D
4
BURNS, FIRE, AND RADIATION

Month
6 April- 11 13 2
Jun Oct.
Boise, ID e-S Spring- J F MAM J J A S ON D
6
Annual June- 3
e pt. Fall April- Month
13.4 inches Sept. Oct.
4 7 12
Inches

8 Spring-Fall Atlanta, GA
May-June 6
2 Annual
46.5 inches
Sept.-Oct. 14 4

Inches
J F MAM J J A S ON D 15
Month 2
Su
m

Sonora, CA J F MAM J J A S ON D
m

10
Annual Month
er

32.7 inches
8
Lander, WY Prescott, AZ Leon, Mexico North Platte, NE
6 6 6 6 6
Inches

Annual Annual Annual Annual

PART 3

13.6 inches 20.7 inches 15.2 inches 15.7 inches

4 4 4 4 4
Inches

Inches

Inches

Inches
2 2 2 2 2

J F MAM J J A S ON D J F MAM J J A S ON D J F MAM J J A S ON D J F MAM J J A S ON D J F MAM J J A S ON D

Month Month Month Month Month

FIGURE 14-28  Fire climate regions of North America, based on geographic and climatic factors: 1, interior
Alaska and the Yukon; 2, north Pacific Coast; 3, south Pacific Coast; 4, Great Basin; 5, northern Rocky
Mountains; 6, southern Rocky Mountains; 7, Southwest, including adjacent Mexico; 8, Great Plains; 9, central
and northwest Canada; 10, sub-Arctic and tundra; 11, Great Lakes; 12, Central States; 13, North Atlantic;
14, Southern States; and 15, Mexican central plateau. The bar graphs show the monthly and annual pre-
cipitation for a representative station in each of the fire climate regions. Months on the map indicate fire
seasons. The graph for Decatur, Illinois, obscures the provinces of Newfoundland and Prince Edward Island
on the map. (Modified from Schroeder MJ, Buck CC: Fire weather, Agriculture Handbook 360, Washington,
DC, 1970, USDA Forest Service.)

Fires exhibiting such phenomena often behave in an apparent from the fire (e.g., lee side of a ridge).215,228 These fire-induced
erratic, sometimes dangerous manner. tornado-like whirlwinds can travel up to 2.5 km (1.6 miles) from
Fire whirls appear frequently in and around wildland fires.150 the main fire458 and can cause considerable damage and even
Most fire whirls are small and short-lived, but occasionally one lead to injuries and fatalities. On March 7, 1964, a fire whirlwind
becomes large and strong enough to do tornado-like damage that formed on the Polo Fire near Santa Barbara, California, cut
and cause serious injury, such as occurred at Mt Kuki, Japan, in a 1.6-km (1-mile) path, injuring four people and destroying two
1977;189 death is also a distinct possibility. Their occurrence is houses, a barn, four automobiles, and a 100-tree avocado
usually associated with unstable air, moderate winds, and large orchard.387 The fringe of the fire whirl passed over a fire truck
heat sources created by plentiful and dry fuel concentrations and sucked out the rear window. A firefighter standing on the
(Figure 14-30) or terrain configurations that concentrate the heat rear platform of the vehicle was pulled up vertically so that his

296
 CHAPTER 14  Wildland Fires: Dangers and Survival
FIGURE 14-29  Chutes, chimneys, and box canyons created by sharp ridges provide avenues for intense
updrafts (like a fire in a woodstove) and rapid rates of spread. People should avoid being caught above a
fire under these topographic conditions. (Modified from Barrows JS: Fire behavior in Northern Rocky
Mountain forests, Station Paper No 29, Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Moun-
tain Forest and Range Experiment Station.)

feet were pointing to the sky while his hands clasped the safety
bar. A small piece of plywood was rammed 7.6 cm (3 inches)
into an oak tree.
Several years of drought combined with a national forest
health issue that has produced many dead and dying forests set
the stage for extreme fire behavior conditions that threaten
people, property, and natural and cultural resources. Protection
from these conditions requires understanding of the crown fire
process. Crowning involves a fire spreading horizontally as a
“wall of flame” from the ground surface up through and above
the canopies of trees (Figure 14-31) or tall shrubs. The first views
inside a crown fire were documented on videotape during the
International Crown Fire Modelling Experiment near Fort Provi-
dence in Canada’s Northwest Territories in 1997.476 The onset of

FIGURE 14-31  Experimental crown fire in a northern jack pine (Pinus

FIGURE 14-30  Large fire whirl associated with the burning of logging
slash debris near Whitecourt, Alberta. (Courtesy University of Alberta;
photo by M.Y. Ackerman.)
banksiana) and black spruce (Picea mariana) forest near Fort Provi-
dence, Northwest Territories, Canada. The average height of flames
from crowning forest fires is generally one to one and a half times taller
than the tree height. Flame flashes will extend considerably higher into
the fire’s convection column. (Courtesy Canadian Forest Service.)

297
 crowning is significant from both a safety and suppression per-
spective. At a minimum, when a fire crowns, the rate of spread
and intensity doubles, and the area burned quadruples.12
Maclean284 gives an indication of how crown fires were
handled in the early part of the 20th century by the USDA Forest
Service:
By the time they reached the fire, it had spread all over the map, and
had jumped into the crowns of trees, and for a lot of years a prospective
ranger taking his exam had said the last word on crown fires . . . When
asked on his examination, “What do you do when a fire crowns?” he
had answered, “Get out of the way and pray like hell for rain.”
This wisdom seems still valid today. Rothermel417,419 described
the conditions that produce a crown fire:
1. Dry fuels
2. Low humidity and high temperatures
3. Heavy accumulations of dead and downed fuels
4. Small trees in the understory, or “ladder fuels”
5. Steep slope
6. Strong winds
7. Unstable atmosphere
8. Continuous crown layer
The two most prominent behavior patterns of crown fires are
BURNS, FIRE, AND RADIATION
wind driven and plume (or convection) dominated. Each type of
crown fire poses a distinct set of threats to people. Free-burning
wildland fires are seldom uniform and well behaved, so these
descriptions of wind-driven and plume-dominated crown fire
behavior may not be readily apparent. The behavior of these
types of fires can be expected to change rapidly as environmen-
tal, fuel, and topographic conditions change.417
Wind-Driven Crown Fire.  A running crown fire can
develop when winds increase with increasing elevation above
the ground, driving flames from crown to crown (Figure 14-32).
Steep slopes can produce the same effect. Spread rates in conifer
forests can reach up to 12 km/hr (7.5 miles/hr) for brief periods
of time254,444 and are possibly faster in mountainous terrain,417
especially in open forest or nonforested or shrubland fuel
types.98,133 A running crown fire is accompanied by showers of
PART 3
firebrands downwind, fire whirls, smoke, and rapid development
of a tilted convection column. As long as the wind remains fairly
constant from one direction, the flanks of the fire can remain
relatively safe. The greatest threat is to people who are immedi-
Heading fire
1 2
FIGURE 14-32  Cross-sectional view of a wind-driven crown fire, illustrating the various stages of combus-
tion: 1, preignition; 2, ignition and flaming combustion; and 3, glowing or smoldering combustion. People
are most at risk on the downwind side and upper flanks of such a free-burning fire. This type of fire is
caused by winds that increase in velocity with increasing elevation above the ground. (Modified from Cot-
trell WH: The book of fire, ed 2, Missoula, Mont, 2004, Mountain Press Publishing Co.)
298
ately at the head, or downwind side, of the fire, although
medium- and long-distance spot fires can also pose an unex-
pected risk.5,69
Plume-Dominated or Convection-Dominated Crown
Fire.  An alternative form of crown fire develops with relatively
low wind speeds or when wind speed decreases with elevation
above the ground. This type of crown fire is referred to as plume
dominated or convection dominated because it is characterized
by a towering convection column that stands vertically over the
fire (Figure 14-33). This type of fire poses a unique threat to
people because it can produce spot fires in any direction around
its perimeter. It can also spread rapidly as the combustion rate
accelerates.
One form of a plume-dominated crown fire that can be espe-
cially dangerous is when a downburst of wind blows outward
near the ground from the bottom of the convective cell. These
winds can be extremely strong226 and can greatly accelerate a
fire’s spread. This type of wind event occurred during the major
run of the Dude Fire near Payson, Arizona, on June 26, 1990,
when six firefighters were killed.216
Some indicators help signal the onset of a downburst from a
plume-dominated crown fire. The surest indicator is the occur-
rence of precipitation of any amount, even a light sprinkle, or
the appearance of virga (evaporating rain) below the base of a
cloud formation.417,427 Another indicator is rapid development of
a strong convection column above the fire, or nearby thunder
cells. A third and very short warning is the calm that develops
when the in-draft winds stop before the turnabout and outflow
of wind from the cell. This brief period of calm may be accom-
panied by a humming sound just before the reversing wind flow
arrives. If any of these indicators is present, the area should
quickly be evacuated and a safe refuge area sought. The down-
burst may also break or uproot trees, creating an additional
hazard for people.417
Value of Fire Danger Ratings
Forest fire control in the early days before organized protection
was relatively simple. As Williams533 explains:
One tried to keep wild fires out of the settlements and in the woods
where they belonged. There was no planning—fire was fought wherever
it could not be avoided. Later, as forest fire control became organized,
Wind
Backing fire
3 3 2 1
Ignition
point

FIGURE 14-33  Cross-sectional view of a plume-dominated or
convection-dominated crown fire. People are at risk around the com-
plete perimeter of this type of fire, because it has the potential to
spread intensely or spot in any direction around its perimeter with little
or no warning. This form of crown fire develops when wind velocities
are relatively low or when velocities decrease with elevation above the
ground coupled with critically dry and abundant fuel conditions. The
convective plume associated with this type of fire may rise to 7600 to
9100 m (25,000 to 30,000 feet) above the ground. (Modified from
Cottrell WH: The book of fire, ed 2, Missoula, Mont, 2004, Mountain
Press Publishing Co.)
specific plans for fire control action became an obvious necessity. To
form the basis for such plans, a reliable measure of the day-by-day state
of forest flammability was needed.
To help fill that need, full-time research into the systematic
measurement of forest flammability or “fire danger” began in the
United States and Canada in the 1920s and has continued more
or less uninterrupted since that time.22,83
Fire management agencies employ fire danger rating systems
to help them gauge ignition and fire behavior potential based on
fuel characteristics, past and current weather conditions, and
certain topographic variables that encapsulate fire behavior
knowledge garnered from research.23,281,474 Such systems have
been demonstrated to be of value in accurately predicting fire
behavior in the WUI.10 In commenting on the historic fatality fires
around the turn of the 20th century, Brown and Davis83 pointed
out that in general terms, these situations reflected the public’s
indifference to forest fires that had persisted for so many years
and still lingers to some degree today:
The Maine fires of 1947 were a sobering reminder in this respect. They
occurred at a time when fire danger measurement was well understood
and means for mass public dissemination of this information were well
developed. Responsible officials were aware of the mounting fire danger.
Nonetheless, some fifty fires were reported to have been burning in
Maine at the time the major break occurred on October 23. A contributing
circumstance was the general feeling that, as it was late October, the fire
CHAPTER 14  Wildland Fires: Dangers and Survival
season was over.
Fire danger rating outputs are being applied directly to the
task of community fire safety and protection, including early-
warning or alert systems linked to fire weather forecasts that
operate during the fire season, such as those developed for the
Northwest Territories, Canada.40 This information is now com-
monly accessible to the general public on the Internet regarding
countries like the United States (www.wfas.net), Canada (http://
cwfis.cfs.nrcan.gc.ca), New Zealand (www.ffr.co.nz/), the Euro-
pean Union,* and many other countries (www.fire.uni-freiburg
.de). Forecasts of fire weather conditions are by themselves
useful; the information can also be used to forecast fire danger
indexes and potential fire behavior characteristics.63,163,427 In Aus-
tralia, television and radio are relied on extensively to alert the
public of “total fire ban” days (i.e., extreme fire danger) based
on current fine-fuel moisture levels, drought status, and fore-
casted fire weather conditions.127 Fire danger rating and fire
behavior predictions can be used to judge whether evacuations
are required or to assist people with preparing for the eventuality
of a fire arriving.240 Evacuation routes must be established in
advance, and the actual time taken to evacuate to a safe zone
needs to be determined in much the same manner as a wildland
firefighter uses an escape route to reach a safety zone or an
urban dweller evacuates a building fire using preidentified travel
routes and exit locations.
FIRE-RELATED INJURIES
AND FATALITIES
Few would argue that battling wildland fires is physically arduous
work that occurs in austere conditions and includes inherent
dangers. As a result, injuries and death occur infrequently but
regularly. In the United States, statistics for wildland fire–related
serious injuries and deaths have now been maintained for several
decades and have provided useful data in developing protocols
for safe firefighting practices. The nature of these fatalities can
be broadly categorized as deaths directly by fire in burnover or
entrapment situations and deaths resulting from fire suppression
activities.
Most fatalities in wildland fire burnover situations occur on
days of extreme fire danger when people are exposed to abnor-
mally high heat stress caused by weather or proximity to fires.
Loss of life is dramatically highlighted under extreme burning
conditions; however, many more people are injured than are
killed by fires.
One of Australia’s worst bushfire disasters occurred on Febru-
ary 7, 1967, when 62 people died in Tasmania.301,529 Analysis of
the locations and ages of 53 individuals at the time of death are
instructive (Tables 14-3 and 14-4). Most people whose bodies
*www.researchgate.net/profile/Domingos_Viegas/publication/229042984
_Comparative_study_of_various_methods_of_fire_danger_evaluation_in_
Southern_Europe/links/0c96051a8bbd686302000000.pdf.
TABLE 14-3  Location of Bodies of 53 Persons Who
Died in Tasmanian Fires, February 7, 1967
No. of
Location Deaths
Mustering stock 2
Firefighting 11
Traveling in a vehicle 2
Escaping from and found at some distance from houses 11
Within a few meters of houses 10
In houses 17
From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7
February 1967, Hobart, Australia, 1967, Government Printer.
299
 TABLE 14-4  Age Distribution of 53 Persons Who Died
in Tasmanian Fires, February 7, 1967
Age Group (yr) No. in Group Average Age (yr)
1-25 1 23
26-50 13 38
51-75 26 64
76-88 13 82
From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7
February 1967, Hobart, Australia, 1967, Government Printer.
were found within or near houses were old, infirm, or physically
disabled. More than one-half of the houses vacated by the 11
people who traveled some distance before being killed were not
burned. Most of these victims would probably have survived if
they had remained in their homes. Most of the 11 firefighters
who died were inexperienced. Many might have survived if they
had observed fire behavior and safety rules.
Krusel and Petris259 investigated the circumstances surround-
BURNS, FIRE, AND RADIATION
ing the 32 civilian deaths that occurred during the 1983 Ash
Wednesday bushfires in Victoria. As a result, they identified three
categories of victims, suggesting ways to address the deficiencies
in the manner in which individuals respond to the wildfire threat:
• Victims who recognized the real threat to their safety with
enough time to save their lives, but chose an ineffective sur-
vival strategy
• Victims who did not recognize the real threat to their safety
in time to implement an effective survival strategy
• Victims who were physically incapable of implementing an
effective survival strategy
Similar situations have been reported around the world. For
example, during the 1993 fire season in the Tarragona Province
of eastern Spain, five people were killed trying to escape from
their home, built in the woods and surrounded by a fire; four of
PART 3
the victims were older adults who dared not flee until it was
impossible to escape.505
In 2007 the National Wildfire Coordinating Group published
an analysis of 310 wildland firefighter fatalities that occurred in
the United States from 1990 to 2006.295 During this 17-year period,
burnover situations constituted only the fourth most common
cause of death, and the number of these incidents declined
during the surveyed years. A total of 64 deaths, or 20.6%, were
attributed to burnovers during this time period. By comparison,
72 deaths (23.2%) resulted from aircraft accidents, 71 deaths
(22.9%) were caused by vehicle accidents, and 64 wildland fire-
fighters (21.9%) died from heart attacks. The remaining percent-
ages were classified as deaths resulting from falling trees, snags,
or rocks (3.9%), other medical causes (2.9%), and miscellaneous
causes (4.5%). Thus, the three leading causes of deaths related
to wildland firefighting activity were not the result of individuals
being burned over or entrapped by a wildland fire, although five
firefighters were killed at a single location on the 2006 Esperanza
fire in southern California.500 Reports for 2007-2009, in which 49
wildland firefighters died, showed similar trends.297 Interventions
are possible to reduce the number of firefighter fatalities associ-
ated with aircraft and vehicle accidents, as well as those linked
to heart attacks292,296 (Box 14-5).
There have been more than 160 wildland fire suppression–
related fatalities in Canada during the 70-year period between
1941 and 2010.25 The names of many of these wildland firefight-
ers are listed, along with their structural brethren, on the Cana-
dian Fallen Firefighters Foundation website (www.cfff.ca/EN/
index.html). Although the causes for all these firefighter fatalities
are not precisely known, certainly aircraft-related fatalities have
been far more common in recent decades compared with earlier
years of recordkeeping.
It is much more difficult to gather accurate information regard-
ing the incidence of minor to moderate injuries and episodes of
illness among wildland firefighters. These statistics do not exist
for several reasons. First, in general, the field draws individuals
300
with a “can-do” attitude who are willing to work through many
hardships that would cause workers in a general workforce to
take time off for rest. Second, the vast majority of the care
happens informally either on the fire lines as work continues or
at base camps at temporary, low-level medical facilities where
formal records are not maintained. Firefighters will often wait
until they leave a fire to seek treatment from a private provider
for an ongoing problem, and the injury or illness will not be
tracked as a workplace-related incident.
The U.S. Bureau of Land Management has guidelines outlining
the nature of burn injuries that require transport to and evaluation
at a specialized burn center.248 This protocol largely corresponds
to the guidelines of the American Burn Association (www
.ameriburn.org/).
By comparison, other medical protocols are region depen-
dent. Fire suppression crews frequently have one or two medics,
usually trained to the Emergency Medical Technician (EMT)–
Basic level, among their members. The skill set of these medics
depends on whether they are active, professional medical provid-
ers when they are not fighting wildland fires, or if they maintain
the certification solely for the position on the crew. Larger inci-
dents may employ additional medical personnel to survey per-
sonnel on the fire lines or at portable medical tents/trailers in
the base camp. Midlevel providers, such as paramedics, nurse
practitioners, and physician’s assistants, usually staff these facili-
ties. The availability of a medical command physician varies by
region in the United States.
When a firefighter requires evaluation and care outside the
scope of first responders, the patient must be transported from
the incident. The nature of the problem dictates if this transport
requires specialized care at a trauma or burn center or if the local
hospital closest to the incident can provide care. When large fires
require hundreds to thousands of personnel, a small local hos-
pital in a rural area may be overburdened by the temporary
additional population. Transport protocols are determined on a
regional basis and may use ground ambulances or air medical
service (via rotary- or fixed-wing aircraft) depending on the
nature of the incident and availability of resources.
COMMON DENOMINATORS OF FIRE BEHAVIOR
ON FATALITY FIRES
A review of wildland firefighter fatality records between 1926
and 1976 shows that 145 men died in 41 fires from fire-induced
BOX 14-5  21st-Century Common Denominators for
Wildland Fire Fatalities
More than 20% of fatalities during wildand firefighting operations
continue to concur in burnovers and entrapments. Carl Wilson’s
original common denominators536 are just as important in the 21st
as they were in the 20th century. However, as the major causes of
firefighter fatalities shift, it has suggested that additional factors
need to be considered:
• Firefighters are most likely to die in an aircraft accident. Before
every flight, fire managers must ask, “Is this flight essential?”
and “Is everyone onboard essential to the mission?”
• Firefighters are nearly as likely to die in a motor vehicle accident
as in an aircraft accident. Driving too fast for the conditions,
failure to wear seat belts, rushing to a fire, and driving home
while exhausted from firefighting kills firefighters.
• Firefighters can reduce their risk for dying from heart attack on
the job by staying fit, maintaining their ideal body weight, and
having regular medical checkups.
• Unexpected events such as falling snags, rolling rocks, downed
power lines, and lightning strikes cause more than 8% of
fatalities during wildland firefighting operations. Firefighters and
fire managers can reduce fatalities by learning to expect these
unexpected events.
Modified from Mangan R: Wildland firefighter fatalities in the U.S.: 1990-2006,
National Fire Equipment System Publication PMS 841, Boise, Idaho, 2007,
National Interagency Fire Center, National Wildfire Coordinating Group, Safety
and Health Working Team.
injuries.353,354,536 Besides the 1949 Mann Gulch and 1990 Dude
fires, large losses occurred on the 1933 Griffith Park Fire in
California (29 deaths and 150 others injured),182 the Blackwater
Fire in Wyoming in 1937 (15 deaths),78 the Pepper Hill Fire in
Pennsylvania in 1938 (8 deaths),429 the Hauser Canyon fire
in California in 1943 (11 deaths),114,446 the Rattlesnake Fire in
California in 1953 (15 deaths),287 the 1956 Inaja Fire in California
(11 deaths),428,492 the 1966 Loop Fire in California (12 deaths),148
and the 1968 Canyon Fire in California (8 deaths).154 Wilson’s
review536 of people killed by wildfires in areas protected by other
federal, state, county, and private agencies indicated 77 fire-
induced fatalities in 26 fires during this same time period. The
United States is not the only country to have had firefighters
killed by entrapments and burnovers. For example, 25 soldiers
were killed while involved in wildland firefighting operations
near Lisbon, Portugal, on September 6, 1966.245 Australia has
experienced a number of firefighter fatality incidents.119,245 For
example, on December 2, 1998, five volunteer firefighters were
killed near the town of Linton, Victoria, when the tanker they
were traveling in was overrun by fire.145
From his analysis of U.S. incidents from 1926 to 1976, Carl
Wilson536 identified several common features associated with fatal
fires:
1. Most of the incidents occurred on relatively small fires or
isolated sectors of larger fires.
2. Most of the fires were innocent in appearance prior to the
“flare-ups” or “blow-ups.” In some cases, the fatalities occurred
in the “mop-up” stage.
3. Flare-ups occurred in deceptively light fuels.
4. Fires ran uphill in chimneys, gullies, or on steep slopes.
5. Suppression tools, such as helicopters or air tankers, can
adversely modify fire behavior (helicopter and air tanker vor-
tices have been known to cause flare-ups).
Many firefighters were surprised to learn that tragedy and
near-miss incidents occurred in fairly light fuels, on small fires,
or on isolated sectors of large fires, and that the fire behavior
was relatively quiet just before the incident, even in the cases
involving aircraft.154,168,225 Many have been led to believe that it
is the conflagration or large, high-intensity crown fire in timber
and heavy brush that traps and kills firefighters. With some
exceptions, however, most fires were innocuous appearing just
before the fatal moment. Case studies of wildland firefighter
fatality incidents from other regions of the world suggest similar
patterns and circumstances, for example, the 25 fatalities at
Puerto Madryn, Argentina, on January 21, 1994;171 10 fatalities in
the Sabie district of the Mpumalanga Province of South Africa in
1994;172 and five fatalities associated with three different incidents
in Portugal during the 1999 and 2000 fire seasons.508 Wildland
firefighter fatalities have been reported in Italy, Spain, Portugal,
and Croatia in the last decade.507,511
Wilson536 concluded that the hairline difference between fatal
fires and near-fatal fires was determined by the individual’s reac-
tion to a suddenly critical situation. Escapes were the result of
luck, circumstances, advance planning, a person’s ability to avoid
panic, or a combination of these factors. Frequently, poor visibil-
ity and absence of concise fire information threatened survival
opportunities by creating confusion and panic. For many years,
Wilson’s findings were summarized in a popular booklet, pub-
lished initially by the USDA Forest Service and in later years by
the National Wildfire Coordinating Group.352 Beginning in 2010,
this information has now been incorporated into the Incident
Response Pocket Guide, published by the U.S. National Wildfire
Coordinating Group.360
The British Columbia Forest Service found many of the same
factors identified by Wilson in their investigation of a number of
close calls or near misses that occurred during the 1994 fire
season.53 The few wildland firefighter fatalities in Canada caused
by entrapments or burnovers37,480 are also in alignment with Wil-
son’s findings.64
Most fatality fires are the result of a temporary escalation in
fire spread, an increase in flame dimensions, crowning and spot-
ting activity, or the development of large fire whirls, often occur-
ring suddenly and with very little warning. A gentle surface fire
will rapidly develop into a high-intensity fire. This could result,
CHAPTER 14  Wildland Fires: Dangers and Survival
40
Number of deaths
30
20
10
0
90
91
92
93
94
95
96
97
98
19
19
19
19
19
19
19
19
19
Year
FIGURE 14-34  Annual death toll for persons who died from all causes
while involved in fighting wildland fires in the United States from 1990
to 1998 (133 total deaths). (From Mangan R: Wildland fire fatalities in
the U.S.: 1990-1998, Technical Report 9751-2817-MTDC, Missoula,
Mont, 1999, USDA Forest Service, Missoula Technology and Develop-
ment Center.)
for example, from thunderstorm downdraft winds,129,427 a change
in fuel types,53 fire whirl development as the fire reaches a ridge-
line with an opposing gradient wind,150 or a “slope reversal” (e.g.,
fire slowly backs down a northerly aspect, crosses the drainage,
and then rapidly spreads up the south-facing slope),402 such as
documented with time-lapse photography on the 1979 Ship
Island fire in central Idaho.350 As the moisture content of dead
and live fuels decreases, fires become increasingly more respon-
sive to slight changes in wind strength and slope steepness. Once
“critically” dry levels are reached, fire behavior becomes exceed-
ingly unstable.29,88,281
NATURE OF INJURIES AND FATALITIES
Fire-related injuries and fatalities are a direct consequence of
heat, flames, smoke, critical gas levels, or indirect injuries293,330
(Figure 14-34). Injuries and fatalities associated with wildland
fires fall into one of these five categories:
1. Heat: direct thermal injury, inhalation, and heat stress
disorders
2. Flames: direct thermal injury and inhalation
3. Smoke: inhalation and mucous membrane irritation
4. Critical gas levels: oxygen and carbon monoxide (CO)
5. Indirect effects: acute and chronic medical disability and
trauma
Intense fires that produce very high temperatures are gener-
ally brief. The duration of intense heat increases with fuel load,
being greater in a forest fire where heavy fuels471 are burning
than in a grass129 or shrub fire (see Table 14-2). Temperatures
near the ground are lower because radiant heat is offset some-
what by inflow of fresh air, and gases of combustion rise and
are carried away by convection.118 Close to the ground, within a
few meters of flames reaching up to 11 m (36 feet), air tempera-
tures may be less than 15° C (59° F) above ambient levels. The
breathing of heated air can be tolerated for 30 minutes at 93° C
(199° F) and for 3 minutes at 250° C (482° F).281 Death or severe
pulmonary injury occurs when these limits are exceeded. Thermal
injuries of the respiratory tract frequently contribute to the clinical
picture of smoke inhalation. People trapped in a fire may have
no choice but to breathe flame or very hot gases. This usually
injures the tissues of the upper airway and respiratory tract, most
often the nose, nasopharynx, mouth, oropharynx, hypopharynx,
larynx, and upper trachea. These injuries may result in edema
that obstructs the airway and produces asphyxia or that causes
tracheitis and mediastinitis.
Signs of thermal injury to the airway include thermal injuries
to the head, face, and neck; singed facial hair; burns of the nasal,
oral, or pharyngeal mucosa; and stridor or dysphonia.326,467,548
Associated with a history of exposure to flame and hot gases in
a closed space, these clinical findings strongly suggest the pres-
ence of a thermal injury to the airway. With the potential for
acute airway obstruction, there is obvious urgency in establishing
301
 this diagnosis. Most experts who treat thermal injuries of the
tracheobronchial tree advocate early visualization of the vocal
cords by laryngoscopy and bronchoscopy.327 Bronchoscopy is a
useful predictor of the clinical course and urgency of intensive
care unit intervention. In addition, one report shows a signifi-
cantly greater incidence of pneumonia and late mortality in
patients with facial burns than in those without them.544
Burns of the lower trachea are rarely reported. In fact, injuries
to and beyond the carina are difficult to produce when the
trachea is cannulated and hot gases are delivered in the anesthe-
tized dog.324,547 Air has a very low specific heat and is therefore
a poor conductor of thermal energy. In addition, the thermal
exchange systems of the upper airway are quite efficient. The
hot gas or flame is cooled sufficiently in the upper airway so that
it does not burn the bronchi or more distal structures. However,
although water or steam in the hot gas mixture is probably rare,
it is a much more efficient conductor of heat and permits signifi-
cant thermal injury to the lower trachea and bronchi. A delayed
onset (2 to 24 hours after smoke inhalation) of pulmonary edema
and adult respiratory distress syndrome is widely reported and
should be anticipated.
Heat stress177,434 occurs when air temperature, humidity, radiant
heat, and poor air movement combine with strenuous work and
BURNS, FIRE, AND RADIATION

insulative clothing to raise body temperature beyond safe limits.

Sweating cools the body as moisture evaporates. When water
lost through sweating is not replaced, physiologic heat controls
can deregulate, and body temperature may rise, leading to heat
exhaustion or heatstroke (see Chapters 12, 13, and 89).
Direct contact with flames causes thermal injury, and death is
inevitable with exposure for long periods. Burns may be super-
ficial, partial, or full thickness (see Chapter 15). Immediate death
results from hypotension, hyperthermia, respiratory failure, and FIGURE 14-35  USDA Forest Service Ranger Ed Pulaski led 42 men
frank incineration. and two horses to this mine tunnel near Placer Creek in northern Idaho
As mentioned earlier, the common cause of asphyxia in wild- to seek refuge from the 1910 firestorm. One man failed to reach the
land fire is smoke. Danger increases where smoke accumulates tunnel and was burned beyond recognition. All the men in the tunnel
because of poor ventilation, as in caves, box canyons, narrow were evidently unconscious for a time. Five died inside, apparently
valleys, and gullies. Dense, acrid smoke is particularly irritating from suffocation. The remainder of the crew was evacuated to the
to the respiratory system and eyes. Excessive coughing induces hospital in Wallace, where all recovered. (Courtesy USDA Forest
PART 3

pharyngitis and vomiting. Keratitis, conjunctivitis, and chemosis
may make it impossible to keep the eyes open.
The levels of oxygen, CO, and CO2 associated with wildland
fires are a concern. Critical levels readily occur in a closed space
and near burning or smoldering of heavy fuels, but the open
space associated with wildland fires usually contributes to con-
tinual mixing of air. Misconceptions or myths about lack of
oxygen or excessive CO and CO2 in a wildland fire abound in
the popular literature.129
Flaming combustion can be maintained only at oxygen levels
that exceed 12%, a level at which life can also be supported.118,281
With continued in-drafts of air that feed the flames, a fresh
source of oxygen is usually present. Even mass fires, in which
large tracts of land are burning, rarely reduce oxygen to hazard-
ous levels. Low oxygen levels may occur, however, where there
is little air movement, such as in caves or mine shafts (Figure
14-35) or in burned-over land that continues to smoke from
smoldering fuels.
Concentrations of CO exceeding 800 parts per million (ppm)
can cause death within hours. Most fires produce small quantities,
but atmospheric CO concentrations rarely reach lethal levels
because of air movement. High CO concentrations appear to be
associated with smoldering combustion of heavy fuels, such as
accumulations of fallen tree stems or of slash piles, and CO
may also collect in low-lying areas or underground shelters (e.g.,
root cellars).120 Outdoors, the danger lies in continual exposure
to low concentrations that can increase blood carboxyhemoglo-
bin levels. Prolonged exposure affects the central nervous system,
resulting in headache, impaired judgment, progressive lethargy,
decreased vision, and other psychomotor deficits.536
Carbon monoxide levels of 50 ppm were measured close to
a prescribed burn in grass.149 In another estimate, CO concentra-
tions of 30 ppm were found about 61 m (200 feet) from the fire
front. Studies on the 1974 Deadline and Outlaw forest fires in
Idaho showed that firefighters were exposed to CO levels above
the standards proposed by the National Institute of Occupational
Service; photo by J.B. Halm.)
Safety and Health (NIOSH): 35 ppm over an 8-hour period.483
However, more recent measurements of CO levels and particu-
lates made on wildfires between 1992 and 1995408 indicate that
wildland firefighters are seldom exposed to smoke that exceeds
U.S. Occupational Safety and Health Administration (OSHA) per-
missible exposure limits.409
Decreased ambient oxygen may contribute to hypoxia and
the overall picture of smoke inhalation (Table 14-5). This mecha-
nism is at least variably operant. When standing gasoline was
ignited in a closed bunker, the fire self-extinguished, whereas
the ambient oxygen level remained at 14%, a survivable level.324
Injecting burning gasoline or napalm into bunkers produced
nearly complete and prolonged exhaustion of ambient oxygen.
TABLE 14-5  Human Response to Decreased Ambient
Oxygen at Sea Level
Ambient
Oxygen
(%) Human Response
20.9 Normal function
16-18 Decreased stamina and capacity for work
12-15 Dyspnea with walking; impaired coordination; variable
impaired judgment
10-12 Dyspnea at rest; consciousness preserved; impaired
judgment, coordination, and concentration
6-8 Loss of consciousness; death without prompt reversal
<6 Death in 6 to 10 minutes

302
Conflicting data make it difficult to classify definitively situations
in which decreased ambient oxygen and subsequent hypoxia of
exposed individuals contribute to the clinical picture of smoke
inhalation. Studies in which ambient oxygen was measured by
scientists did not show significant depletion at the scene of the
fire.217
Few data are available on CO2 levels around wildland fires.
Although it may be produced in large quantities, CO2 apparently
never reaches hazardous concentrations, even in severe fire
situations.118,281
The quantity of burning fuel and type of topography affect
levels of oxygen and toxic gases. Danger is greater in forest fires
where heavy fuels burn over long periods than in quick-moving
grass and shrub fires. Topography has a major influence: caves,
box canyons, narrow canyons, gulches, and other terrain features
can trap toxic gases or hinder ventilation, thereby preventing an
inflow of fresh air. Although most fatalities result from encounters
with smoke, flames, and heat, critical gas levels can induce
handicaps sufficient to render the victim more vulnerable to other
hazards. Respirators298 are not routinely used on wildland fires
or on WUI fires, but could play a role in the future as a means
of protection against airborne toxic materials.
WILDLAND FIRES, AIR TOXINS,
AND HUMAN HEALTH
In the United States each year, about 80,000 firefighters are
involved with suppression activities on about 70,000 wildland
fires that burn an average of more than 0.8 million hectares (2
million acres). In 1988, more than 2 million hectares (5 million
acres) of land were burned, with a total combined suppression
cost exceeding $600 million. The firefighting effort has another
cost that has not been quantified: the effect of smoke on fire-
fighter health and productivity. Over the 4 months of the 1988
Greater Yellowstone Area fires, about 40% of the 30,000 medical
visits made by wildland firefighters were for respiratory prob-
lems. More than 600 firefighters required subsequent medical
care. In the Happy Camp area during the Klamath fire complex
in California in 1987, ambient CO concentrations measured as
high as 54 ppm on a volume basis.515 A better understanding of
the long-term effects of wildland fire smoke on people is clearly
needed, although “firefighters just keep coming back year after
year,” notes Dr. Brian Sharkey,439 then a wildland firefighter
health and safety specialist with the USDA Forest Service’s
Missoula Technology and Development Center (MTDC), who
coordinated an 8-year study of the health hazards of smoke on
wildland firefighters.435,437
Combustion of wildland fuels produces many by-products in
a variety of concentrations, depending on the type of fuel and
the nature of the fire characteristics.371 The impact of these
byproducts is very difficult to assess. Short-term studies have
been inconclusive, and long-term studies are enormously complex
and essentially absent from the literature. Completion of a
prospective epidemiologic study would be highly informative.
The combustion products of concern include these classes of
materials:
• Particulate matter
• Polynuclear aromatic hydrocarbons
• Carbon monoxide
• Aldehydes
• Organic acids
• Semivolatile and volatile organic compounds
• Free radicals
• Ozone
• Inorganic fraction of particles
Large variances are associated with the development of smoke
combustion products and exposure to the materials of concern.515
Ward and colleagues516 indicated that the toxicity of the combina-
tion of combustion products depends on the relative concentra-
tions of the individual compounds, as well as the overall
concentration and length of exposure. Individual toxicities are
associated with many of the compounds found in smoke. The
combined toxicity of these substances is not known. Detailed
studies will perhaps provide answers so that risk management
options can be exercised. One of these studies suggested that
CHAPTER 14  Wildland Fires: Dangers and Survival
wildland firefighters experience a small, cross-seasonal decline
in pulmonary function and an increase in several respiratory
symptoms.423 Eye irritation, nose irritation, and wheezing were
associated with recent firefighting.
The strenuous work of fighting or escaping a fire magnifies
chronic illnesses, age disabilities, exhaustion, and cardiovascular
instability. Common trauma is induced by falling trees or limbs,
rolling logs or rocks, vehicular accidents, poor visibility, panic,
falling asleep in unburned fuels that later ignite, and leaving the
safety of buildings and vehicles. Cuts, scrapes, scratches, lacera-
tions, fractures, and eye injuries (foreign particles, smoke irrita-
tion, sharp objects) are other common afflictions. Poison oak,
poison ivy, stinging insects, and poisonous snakes are additional
sources of trauma during wildland fires. To avoid fire-related
injuries and fatalities, a person must keep attuned to mental and
physical stress levels and be aware of cumulative effects.434 Igno-
rance of this simple principle is disastrous.
Accurate statistics have not been collected to document the
frequency and nature of injuries and illnesses over the course of
different fire seasons. The common afflictions previously listed
are inherent to completing strenuous work under adverse condi-
tions. Overall, the infrequency of major traumatic injuries speaks
to the success of firefighters’ adhering to established safety
protocols.
A range of occupational and overuse injuries consistently
emerges over the course of the fire season. Blisters and foot
problems occur frequently early in the season, especially if off-
season fitness has fallen by the wayside. As with other soft tissue
injuries, these can be complicated if not promptly addressed with
standard first aid. Muscle strains, back problems, and tendinitis
often follow particularly intense work periods. These maladies
are best prevented by firefighters’ maintaining off-season fitness
regimens to endure the physical rigors of firefighting.276 Research
and development carried out by the MTDC of the USDA Forest
Service have led to invaluable contributions regarding the health
and safety of wildland firefighters, including the following:
• Optimal work-rest patterns
• Firefighter nutrition and hydration requirements and
regimens
• Heat stress and uniform/personal protective equipment
design
• Tool testing to optimize firefighter efficiency
• The relationship between firefighter nutrition and immune
function
These studies have informed U.S. firefighting protocols to
improve productivity and firefighter safety.176,436,438,440,441
The informal surveys conducted of wildland firefighter health
demonstrate a pattern of increasing respiratory symptoms over
the course of the fire season. This pattern has become common
enough that firefighters have coined a term—“camp crud”—to
describe the range of symptoms shared throughout the camps.
The severity and frequency of symptoms can have legitimate
safety and productivity consequences. Smoke exposure has been
considered as one factor contributing to the frequency of respira-
tory illness47 and decreased respiratory function over the course
of the fire season,206 but there is no consensus on how interven-
tions could be feasibly instituted to reduce smoke exposure in
wildland fire suppression. Regular occurrences of the flulike
“camp crud,” especially late in the fire season, suggest a classic
infectious outbreak pattern. Other infectious outbreaks that have
spread through the wildland fire community include a series of
methicillin-resistant Staphylococcus aureus (MRSA) outbreaks in
fire camps during the 2008 and 2009 seasons in the United
States.276,501,502
Infectious illness shared among firefighters is likely promoted
by a variety of factors, including close working and living prox-
imity, challenged immune conditions resulting from strenuous
work and nutritional demands, hygiene conditions dictated to
some degree by the environment, and potentially firefighters’
access to seasonal vaccinations. Identifying possible interventions
to decrease the burden from infectious illness would be benefi-
cial to improving firefighter wellness and productivity. The
epidemiologic data collected for wildland firefighting are very
303
 sparse, either for analysis of short-term outbreak situations or
long-term health and wellness.
WILDLAND-URBAN INTERFACE
FIRE SURVIVAL: PRINCIPLES
AND TECHNIQUES
History has demonstrated repeatedly that individuals simply were
not prepared to make correct choices of survival alternatives
under stressful situations. At least 437 wildland firefighters were
killed in the United States between 1910 and 2009 as a direct
result of a burnover or entrapment by a free-burning wild-
fire.353,295,297 Overconfidence, complacency, ignorance, bad habits,
lack of preparation, poor decision making, and a host of other
human factors quickly lead to improper and unsafe actions
during wildfire emergency situations.370,522,536 “Learning from mis-
takes” in these settings is not a reasonable education strategy
because second chances are frequently unavailable in the wild-
land firefighting profession.
The USDA Forest Service organized a task force in 1957 to
“study how we might strengthen our ways and means of prevent-
ing firefighting fatalities.”323 A major recommendation was to
BURNS, FIRE, AND RADIATION
adopt service-wide standard firefighting orders. Ten standard
firefighting orders300,322 summarize the fundamental principles of
safety on the fire line (Box 14-6). Although these were written
for wildland firefighters, they apply to all people working, living,
or traveling near wildland fires and are adapted here to remind
emergency medical personnel, wildland homeowners, and rec-
reationists of safety precautions to be taken around wildland
fires. Much of this material is summarized in the handy Incident
Response Pocket Guide.360
LCES: THE KEY TO SAFE PROCEDURES IN
WILDLAND FIRE ENVIRONMENTS
LCES stands for lookout(s), communication(s), escape routes, and
safety zone(s).211 These variables are key components in evaluat-
PART 3
ing the threat posed by fire-line hazards and determining the best
course of action to follow (Figure 14-36).
Some fire management agencies have added an “A” to LCES,
thus LACES, for a variety of meanings—attitude, awareness, and
anchor points.262,479 The Australasian Fire Authorities Council, for
BOX 14-6  Ten Standard Firefighting Orders Adapted
for the General Public
1. Keep informed of fire weather conditions, changes, and
forecasts and how they may affect the area where you are
located.
2. Know what the fire is doing at all times through personal
observations, communication systems, or scouts.
3. Base all actions on current and expected behavior of the fire.
4. Determine escape routes and plans for everyone at risk, and
make certain that everyone understands routes and plans.
5. Post lookouts to watch the fire if you think there is any danger
of being trapped, of increased fire activity, or of erratic fire
behavior.
6. Be alert, keep calm, think clearly, and act decisively to avoid
panic reactions.
7. Maintain prompt and clear communication with your group,
firefighting forces, and command and communication centers.
8. Give clear, concise instructions, and be sure that they are
understood.
9. Maintain control of the people in your group at all times.
10. Fight fire aggressively, but provide for safety first.
(Nonqualified or untrained and improperly dressed or
equipped persons should engage in firefighting operations
only when it is absolutely necessary to assist injured persons.
Wildland firefighting is a physically demanding task and
should not be attempted by persons who are not in good
physical condition.)
304
Lookout(s) Hazard
(Fireline hazards such as fire
entrapment or falling or
rolling objects are inherent in
the wildland fire environment)
Communication(s)
X
Firefighters
Escape routes Route 1 Route 2
Safety zone(s)
FIGURE 14-36  Concept of the LCES wildland fire safety system. (From
Gleason P: LCES: The key to safety in the wildland fire environment,
Fire Manage Notes 52:9, 1991.)
example, adopted the LACES wildland fire safety acronym with
the proviso that the “A” stands for awareness.49 Most Canadian
fire management agencies have taken the “A” in LACES to
connote anchor point.38,478 The importance of an anchor point is
quite vividly highlighted in the video A Firefighter’s Return From
a Burnover: The Kelly York Story, which details the severe burn
injuries received by a volunteer firefighter while attempting to
suppress a grass fire in central California during the 1995 fire
season.185 As Australian fire management and research pioneers
Harry Luke and Alan McArthur281 state in their seminal reference
book Bushfires in Australia, fire suppression “must at all times
start from an anchor point.”
The wildland fire environment’s basic hazards are lightning,
volcanoes, falling of fire-weakened trees and snags, rolling rocks
and logs, entrapment by free-burning fires, respirable particu-
lates, air toxins, and heat stress. When these hazards exist, there
are two options: (1) do not enter the environment, or (2) adhere
to safe procedures according to LCES.
LCES should be viewed from a “systems” point of view, stress-
ing their interdependence. For example, the best safety zone is
worthless if the escape route does not offer access at the point
of need. People must be familiar with the LCES plan well before
it is needed. In addition, the nature of wildland fires dictates that
LCES be redefined in pace with changing conditions. The LCES
wildland fire safety system is implemented as follows:
Lookout(s): Fixed lookouts or roving lookouts must be where
both the hazard and the people can be seen. A lookout is
trained to observe the wildland fire environment and to rec-
ognize and anticipate changes in fire behavior. When the
hazard becomes a potential threat or danger, the lookout
relays this information so people can depart for the safety
zone.
Communication(s): Communication refers to alerting people to
the approaching or pending hazard. Promptness and clarity
are essential.
Escape routes: These paths lead from a currently threatened posi-
tion to an area free from danger. More than one escape route
must be available. Escape routes are probably the most elusive
component of LCES because they change continuously. Timely
access to safety zones is the most important component.66
Research on wildland firefighter travel rates28,60,102,424 suggests
that, although civilians could momentarily advance at a rate
in excess of what most wildland fires are capable of achieving,
even the most fit individuals would not be able to sustain
such a pace for more than a few minutes before being burned
 over by an advancing fire, especially on steep slopes—
escaping uphill is thus a very questionable concept, unless a
safety zone is known to be very nearby. Furthermore, some
fire researchers believe there is a common tendency to over-
estimate the distance to a fire when observing through the
forest, which may lull firefighters into thinking there is more
time available for an orderly exit than is actually the case.128
Safety zone(s): In a safety zone, threatened persons find ade-
quate refuge from danger. The size of the safety zone must
be sufficient to provide protection from flames, radiant heat,
convective heat, falling trees and snags, and rolling rocks and
logs. The necessary size varies with changes in fuels, topog-
raphy, wind conditions, and fire intensity. The question of
whether a previously burned area will serve as a safety zone
depends not only on the size of the area, but also on the
degree of completeness in fuel consumption, both vertically
and horizontally.98,380
What constitutes a safety zone varies widely among individu-
als.457 Based on theoretical considerations for radiation emitted
from a “wall of flame” under idealized conditions (e.g., level
terrain, steady-state fire conditions),99 it has been suggested, from
the standpoint of flame radiation, that a safety zone should be
large enough that the distance between the human occupants
and flame front be at least four times the maximum expected
flame height at the edge of the safety zone101 (Table 14-6). It
should be emphasized that in deriving this rule of thumb, several
assumptions had to be made that could ultimately limit the use-
fulness of this simple guide,470 although some field verification
has been accomplished.100 Furthermore, both the modeling and
resultant radiation-based guide do not consider flame impinge-
ment or horizontal reach into a clearing, fire whirls, or any
allowance for convective heat transfer, which will be significant
under windy conditions in sloping terrain.129,416 Obviously, further
study, including field measurements, and development are war-
ranted (e.g., allowance for convective heating on a slope), which
is indeed the case.94,96 Nevertheless, while acknowledging these
limitations, this rule of thumb has been incorporated into existing
operational guidelines,360 training course material,480 and com-
puter programs.44 According to Butler and Forthofer,103 additional
modeling (e.g., radiation on a sloping surface), subsequent
observations, and other field measurements support “four times
flame height” for minimum safety zone size, although research
continues.95
While serving as the ignition boss during the International
Crown Fire Modeling Experiment (ICFME) in the Northwest
TABLE 14-6  Minimum Safety Zone Separation
Distances and Sizes (Circular Shape) in Relation   materials, especially cones and logs, that can roll downhill
to Flame Height*
Separation
Flame Height Distance Area†
Meters Feet Meters Feet Hectares Acres
2 6.5 8 26 0.02 0.05
5 16 20 64 0.13 0.31
10 33 40 132 0.5 1.2
20 66 80 264 2.0 5.0
40 128 160 512 8 20
60 262 240 1048 18 45
*For a single person on flat topography based on the “four-times-flame-height”
rule of thumb for radiant heat only (i.e., no convection) and no allowance for
flame impingement or other fire line hazards.99,101 It is assumed that the person
is standing upright and is properly clothed, including headgear and gloves.
†Assuming the area of a circle is equal to approximately 3.14159 times the
square of the separation distance, where the separation distance is deemed to
be the radius of a circle. For perspective, a typical North American ice hockey
rink is 0.16 hectare (0.39 acre) in size, whereas Canadian and American football
fields are about 0.6 hectare (1.5 acre) and 0.4 hectare (1.1 acres) in size,
respectively. In turn, the maximum sizes of outdoor soccer and rugby fields
would be approximately 0.8 hectare (2.0 acres) and 1.0 hectare (2.5 acres),
respectively. A full-size basketball court is about 0.04 hectare (0.1 acre) in size.
Territories,18,463 one of the authors (MEA) was able to informally
CHAPTER 14  Wildland Fires: Dangers and Survival
evaluate the Butler and Cohen99,101 safety zone guideline. Based
on observations and the experience of being on the backside or
upwind edge of all the ICFME experimental crown fires,464,476 the
four-times-flame-height rule of thumb seems to be reasonably
valid. As Butler and Forthofer103 note, “It’s important to realize
that this should be considered a minimum—meaning that in all
cases larger is better.”
In using Butler and Cohen’s rule of thumb99,101 for safety zones
or in turn, Table 14-6, the logical question is, “How does one go
about estimating flame height in advance of a fire’s occurrence?”
On the basis of various fire behavior observations and various
analyses, we can say with some degree of certainty that the
maximum flame heights in grasslands, shrublands, and hardwood
stands would vary, depending on the burning conditions, from
about 2 to 10 m (7 to 33 feet). Thus, a separation of at least 40 m
(130 feet) should be adequate in most fuel types that do not
contain conifer trees. The average flame height of crown fires in
conifer forests is generally 2 to 2.5 times the stand height.464
Any area smaller than a safety zone should be regarded as a
possible “survival zone” or site. Unfortunately, no quantitative
description of what constitutes a survival zone presently exists.
The FPInnovations Wildland Fire Operations Research Group
(http://wildfire.fpinnovations.ca/index.aspx) and the University
of Alberta are currently engaged in a project to better define the
criteria for survival zones in wildland fires.26,27 Nevertheless, spe-
cific case study examples (e.g., 1937 Blackwater fire in Wyoming,
1958 Wandilo fire in South Australia, 1976 Battlement Creek Fire
in Colorado, 1990 Dude fire in Arizona) suggest that survival is
possible in relatively small areas even when exposed to a highly
hostile thermal environment, provided a person maintains a
prone position and uses every possible protection against radia-
tion, convection, and direct flame contact. Movement within the
survival zone may also be possible and necessary as the flame
front surrounds the survival zone site.
EIGHTEEN “WATCH OUT!” SITUATIONS IN THE
WILDLAND FIRE ENVIRONMENT
The following 18 “Watch Out!” situations, adapted from the
wildland fire community’s safety guidelines,320,325,449 are of particu-
lar relevance to emergency medical personnel and wildland
users:
1. You are moving downhill toward a fire, but must be aware
that fire can move swiftly and suddenly uphill. Constantly
observe fire behavior, fuels, and escape routes, assessing the
fire’s potential to run uphill.
2. You are on a hillside where rolling, burning material can
ignite fuel from below. When below a fire, watch for burning
and ignite a fire beneath you, trapping you between two
coalescing fires.
3. Wind begins to blow, increase, or change direction. Wind
strongly influences fire behavior, so be prepared to respond
to sudden changes.
4. The weather becomes hotter and drier. Fire activity increases,
and its behavior changes more rapidly as ambient tempera-
ture rises and relative humidity decreases.
5. Dense vegetation with unburned fuel is between you and
the fire. The danger in this situation is that unburned fuels
can ignite. If the fire is moving away from you, be alert for
wind changes or spot fires that may ignite fuels near you.
Do not be overconfident if the area has burned once, because
it can reignite if sufficient fuel remains.
6. You are in an unburned area near the fire where terrain and
cover make travel difficult. The combination of fuel and dif-
ficult escape makes this situation dangerous.
7. Travel or work is in an area you have not seen in daylight.
Darkness and unfamiliarity are a dangerous combination.
8. You are unfamiliar with local factors influencing fire behav-
ior. When possible, seek information on what to expect from
knowledgeable people, especially those from the area.
9. By necessity, you have to make a frontal assault on a fire
with tankers. Any encounter with an active line of fire is
305
 dangerous because of proximity to intense heat, smoke, and
flames, along with limited escape opportunities.
10. Spot fires occur frequently across the fire line. Generally,
increased spotting indicates increased fire activity and inten-
sity. The danger is that of entrapment between coalescing
fires.
11. The main fire cannot be seen, and you are not in commu-
nication with anyone who can see it. If you do not know
the location, size, and behavior of the main fire, planning
becomes guesswork, which is an unfavorable response.
12. An unclear assignment or confusing instructions have been
received. Make sure that all assignments and instructions are
fully understood.
13. You are drowsy and feel like resting or sleeping near the
fire line in unburned fuel. This may lead to fire entrapment.
No one should sleep near a wildland fire. If resting is abso-
lutely necessary, choose a burned area that is safe from
rolling material, smoke, reburn, and other dangers, or seek
a wide area of bare ground or rock.
14. Fire has not been scouted and sized up.
15. Safety zones and escape routes have not been identified.
16. You are uninformed on strategy, tactics, and hazards.
17. No communication link with crew members or supervisors
BURNS, FIRE, AND RADIATION
has been established.
18. A line has been constructed without a safe anchor point.
Each of these situations has come about as a result of one or
more wildland firefighter fatalities (http://wlfalwaysremember.
org). Artwork has been developed to help illustrate or visualize
the 10 standard fire orders and 18 “Watch Out!” situations.331
FIFTEEN STRUCTURAL “WATCH
OUT!” SITUATIONS FOR THE
WILDLAND-URBAN INTERFACE
Continuing development creates ever more WUI area; therefore,
fires are tending to occur more often in that interface. These 15
structural “Watch Out!” situations have been defined to increase
awareness of structural fire dangers484:
PART 3
1. Access is poor (e.g., narrow roads, twisting, single lane with
inadequate turning).
2. Load limits of local bridges are light or unknown; the bridges
are narrow.
3. Winds are strong, and erratic fire behavior is occurring.
4. The area contains garages with closed, locked doors.
5. You have an inadequate water supply to attack the fire.
6. Structure windows are black or smoked over.
7. There are septic tanks and leach lines. These are found in
most rural situations.
8. A house or structure is burning with puffing rather than
steady smoke.
9. Inside and outside construction of structures is wood with
shake-shingle roofs.
10. Natural fuels occur within 9 m (30 feet) of the structures.
11. Known or suspected panicked individuals are in the
vicinity.
12. Structure windows are bulging, and the roof has not been
vented.
13. Additional fuels can be found in open crawl spaces beneath
the structures.
14. Firefighting is taking place in or near chimney or canyon
situations.
15. Elevated fuel or propane tanks are present.
These are also known as the “Wildland-Urban Watch
Outs!”360
TAKING REFUGE IN VEHICLES, BUILDINGS,
AND PROTECTIVE FIRE SHELTERS USED BY
WILDLAND FIREFIGHTERS
The radiant energy of a fire, although highly intense at a given
location, typically lasts for only a short time. Because radiant heat
travels in straight lines, does not penetrate solid substances, and
is easily reflected, seeking refuge in vehicles, buildings, or pro-
tective fire shelters should be viewed as a lifesaving solution.
306
Vehicles
Wildland firefighters have survived severe fire storms or the
passage of fire fronts by taking refuge in vehicles.291,302,375,376
Unfortunately, there are reported cases where civilians would
have survived or avoided serious injury had they remained in
their vehicles.245,372 Bereska68 has indicated that he and two
others were forced to drive a 3 4 -ton Dodge 4 × 4 truck at a mod-
erate speed (25 to 30 km/hr [16 to 19 miles/hr]) through the
flame front of a grass fire during a prescribed burning operation
in north-central Alberta in early April 1980. Winds at the time of
the incident were light (<12 km/hr [7 miles/hr]), and the flames,
although high (3 to 4 m [10 to 13 feet]), were not deep (1 to 2 m
[3 to 7 feet]). “It got very hot instantly and as we came out of
the flames we opened the windows and appreciated the cool
fresh air.”68
The following three U.S. case histories serve as examples of
intense burning situations where lives were saved because
people stayed inside vehicles while the fire front passed by their
location.449
• In 1958, a veteran field section fire warden and two young
men were fighting forest fires that burned in heavy fuels near
the Bass River State Forest in southern New Jersey. A 90-degree
wind shift transformed the flank fire into a broad head fire,
with the advancing flames reaching up to 12 m (40 feet) in
height. The men entered their vehicle, a Dodge W300 Power
Wagon, which stood in the middle of a 4-m (13-foot)–wide
sand road. Simultaneously, the engine and radio failed. The
fire warden repeatedly admonished the crewmen, who wanted
to flee, to stay in the truck. Subsequently, the truck was
rocked violently by convection currents and microclimatic
changes generated by the flames. The men could neither see
nor breathe because of smoke, and the cab began to fill with
sparks that ignited the seat. The men stayed with the truck
for only 3 or 4 minutes during passage of the head fire, but
they indicated later that the interval involved seemed more
like 3 or 4 hours. At the first opportunity, all of them left the
vehicle on the upwind side and crouched beside it to escape
the searing heat and burning seats. The warden proceeded to
burn his hand severely while disposing of a flaming gas can
located in the truck bed. Although the young men escaped
virtually unscathed, the older man suffered lung damage and
remained on limited duty for 5 years. He eventually recovered
completely and subsequently retired.
• In a 1962 California Division of Forestry fire in Fresno County,
three men, followed by a flank fire that had turned into a
head fire, raced back to their truck only a few feet ahead of
the flames. The truck would not restart. After the main body
of flames passed over the vehicle, the men jumped out to
breathe because the truck was burning. Almost completely
blinded by smoke and heat, they stumbled headlong into
matted fuels, and two received first- and second-degree burns.
One man was not burned but had to be treated for smoke
inhalation. The truck was a loss.
• In 1976 a firefighter died while fighting a grass fire near the
town of Buhler in Reno County, Kansas. A flashover occurred
from buildup of gases on the lee side of a windbreak. A fire
truck was caught in the flashover, and the firefighter working
from the back of the vehicle ran and was killed. Although the
truck burned, the driver was not seriously hurt.
Sitting in a vehicle during a passing fire front is often perilous,
but when a person is trapped, it is almost certain doom to attempt
escape by running from the fire. The preceding case histories
illustrate the following facts about vehicles and fire, which, if
remembered, may prevent panic-like reactions:
1. The engine may stall and not restart.
2. The vehicle may be rocked by convection currents.
3. Smoke and sparks may enter the cab.
4. The interior, engine, or tires may ignite. (Tires exploded
during the Crank Fire burnover in California in August 1987
involving several wildland fire engines.348 This is obviously
unsettling in an already stressful situation that could lead to
panic-like reactions.)
5. Temperatures increase inside the cab because heat is radiated
through the windows.
6. Metal gas tanks and containers rarely explode.
7. If it is necessary to leave the cab after the fire has passed,
keep the vehicle between you and the fire.
The type of vehicle determines the amount of protection
afforded. Two travelers died in a fire in 1967 in Tasmania, Aus-
tralia, when they were caught in a canvas-topped vehicle.281 A
later fire in Australia led to further research on various vehicles’
protection and the explosiveness of gasoline tanks. In 1969 near
Lara, Victoria, Australia, a fast-moving grass fire crossed a four-
lane expressway.201,281 Several cars stopped in the confusion of
smoke and flames. Seventeen people left the safety of their cars
and perished. Six people stayed inside their vehicles and sur-
vived, even though one car ignited.
Investigations were carried out by the Forest Research Institute
(now the Commonwealth Scientific and Industrial Research Orga-
nization [CSIRO], Division of Forestry and Forest Products) in
Canberra, Australia, to collect accurate data and dispel the mis-
conceptions that make people flee a safe refuge if trapped by
fire.118 Cars were placed between two burning piles of logging
slash to study a car’s ability to shield against radiation.281 The test
was a hotter, longer-duration fire than would normally be
encountered in a wildland setting.
Car bodies halved the external radiation transmitted at the
peak of the fire, but a person inside would have suffered severe
burns to bare skin. Although air temperatures inside the car did
not reach hazardous levels until well after the peak radiation had
passed, smoke from smoldering plastic and rubber materials
would have caused discomfort and made the car uninhabitable.
In this study, metal gasoline tanks did not explode, whether intact
on cars or separated and placed on a burning pile of slash.
Apparently, when tanks are sealed, the space above the liquid
contains a mixture too deficient in oxygen vapor to support an
explosion.
Several years ago, Cheney118,120 offered the following general
advice for survival when in a car and trapped by fire:
• If smoke obstructs visibility, turn on the headlights and drive
to the side of the road away from the leading edge of the
fire. Try to select an area of sparse vegetation offering the
least combustible material.
• Attempt to shield your body from radiant heat energy by
rolling up the windows and covering up with floor mats
or hiding beneath the dashboard. Cover as much skin as
possible.
• Stay in the vehicle as long as possible. Unruptured gas tanks
rarely explode, and vehicles usually take several minutes to
ignite.
• Grass fires create about 30 seconds (maximum) of flame expo-
sure, and chances for survival in a vehicle are good. Forest fires
create higher-intensity flames lasting 3 to 4 minutes (maxi-
mum) and lowering chances for survival. Staying in a vehicle
improves chances for surviving a forest fire. Remain calm.
• A strong, acrid smell usually results from burning paint and
plastic materials, caused by small quantities of hydrogen chlo-
ride released from breakdown of polyvinyl chloride. Hydro-
gen chloride is water soluble, and discomfort can be relieved
by breathing through a damp cloth. Urine is mostly water and
can be used in emergencies.
Subsequent experiences,91 coupled with new research carried
out by the Australian Bushfire Cooperative Research Centre,268
have led to more definitive guidelines (Box 14-7).51
Buildings
The decision to evacuate a house or remain and defend it is not
an easy one. Fire services generally prefer that residents evacuate
the threatened area so that agencies can concentrate on protect-
ing structures. Authorities also agree that evacuation of older
adults and very young, infirm, and fearful people is usually a
good idea.259 People should evacuate only if it can be accom-
plished safely, well in advance of any danger. If not, it is safer
to shelter in place. Several principles should guide the evacuation
decision519:
1. A fire within sight or smell is a fire that endangers you.
2. Occupants are often quite effective in preventing their house
from burning down. The more they understand the dynamics
CHAPTER 14  Wildland Fires: Dangers and Survival
BOX 14-7  Guidance for People in a Vehicle During a
Wildland Fire
Advance Preparation
Always carry woolen blankets, leather gloves, and a supply of
water in the vehicle.
Dress in suitable nonsynthetic clothing and shoes, including a hat.
Encountering Smoke or Flames
If you see a wildland fire in the distance, carefully pull over to the
side of the road to assess the situation. If it is safe to do so, turn
around and drive to safety.
If you have been trapped by a wildland fire, find a suitable place
to park the car and shelter from the fire.
Positioning Your Car
Find a clearing away from dense bush and high ground fuel loads.
Where possible, minimize exposure to radiant heat by parking
behind a natural barrier, such as a rocky outcrop.
Position the car facing toward the oncoming fire front.
Park the car off the roadway to avoid collisions in poor visibility.
Do not park too close to other vehicles.
Inside Your Car
Stay inside your car—it offers the best level of protection from
radiant heat as the fire front passes.
Turn headlights and hazard warning lights on to make the car as
visible as possible.
Tightly close all windows and doors.
Shut all the air vents, and turn the air conditioning off.
Turn the engine off.
Get down below the window level into the foot wells, and shelter
under woolen blankets.
Drink water to minimize the risks of dehydration.
As the Fire Front Passes
Stay in the car until the fire front passes and the temperature has
dropped outside.
Fuel tanks are unlikely to explode.
As the fire front approaches, the intensity of the heat will increase,
along with the amount of smoke and embers.
Smoke gradually gets inside the car, and fumes will be released
from the interior of the car. Stay as close to the floor as possible
to minimize inhalation, and cover your mouth with a moist cloth.
Tires and external plastic body parts may catch on fire. In more
extreme cases, the car interior may catch on fire.
Once the fire front has passed and the temperature has dropped,
cautiously exit the car. (Be careful—internal parts will be
extremely hot.)
Move to a safe area such as a strip of land that has already
burned.
Stay covered in woolen blankets, continue to drink water, and
await assistance.
Modified from Australasian Fire Authorities Council: Guidelines for people in
cars during bushfires, East Melbourne, Victoria, Australia, 2008, AFAC.
of fire behavior and have prepared for a fire occurrence, the
easier and safer this task will be.
3. Evacuation when fire is close is too late; evacuation must only
be done when it is certain that it is safe to do so.
4. More people are injured and killed in the open than in houses.
5. Learn beforehand about community refuges.
6. Evacuate only to a known safe refuge and only when it is
safe to do so.
Whether people can find refuge in buildings depends on
construction materials, house design detail, and proximity of fuels
around the structure. If a home is constructed amid flammable
vegetation, plans and procedures to safeguard the home and its
occupants are essential. A building usually offers protection while
the fire passes, even if it ignites during or after the fire’s passage,
because it shields against radiant heat and smoke. After the fire
passes, it may be necessary to exit if the building is burning.
Attempt to suppress the fire or to move onto burned ground.
Numerous wildfire case histories from Australia, starting with
the 1939 Black Friday fires in Victoria,270 demonstrate that homes
provide safe havens.259,281,372,540 In 1967 in Tasmania, 21 people
307
 left their houses as fire approached. All died, and some were
within a few meters of the buildings. Many houses did not burn
and would have served as safe refuges.
When taking refuge in a building, give people useful jobs,
such as filling vessels with water, blocking cracks with wet blan-
kets, and tightly closing windows and doors. If possible, assign
lookouts to keep watch for spot fires on and within the building
throughout the fire event.
Before fire approaches the house, plan to have taken the fol-
lowing precautions269,449:
• If you plan to stay, evacuate your pets and livestock and all
family members not essential to protecting the home well in
advance of the fire’s arrival.
• Be properly dressed to survive the fire. Wear long pants and
leather boots, and carry for protection a long-sleeved shirt or
jacket made of cotton fabrics or wool. Synthetics should not
be worn because they can ignite and melt. Wear a hat that can
offer protection against radiation to the face, ears, and neck
areas. Wear leather or natural-fiber gloves, and have a hand-
kerchief handy to shield the face, water to wet it, and safety
goggles, if possible.
• Remove combustible items from around the house, including
lawn and poolside furniture, umbrellas, and tarp coverings. If
BURNS, FIRE, AND RADIATION
they catch fire, the added heat could ignite the house.
• Ensure that anything that might be tossed around by strong
fire-induced winds is secured (e.g., sheet metal, lumber,
plywood).
• Ensure that the areas around any external propane tanks are
fuel free for a considerable distance. Ensure that the tanks are
properly restrained and the pressure relief value is directed
away from buildings and access ways.
• Close outside attic, eave, and basement vents to eliminate the
possibility of sparks blowing into hidden areas within the
house. Close window shutters.
• Place large plastic trash cans or buckets around the outside
of the house and fill them with water. Soak burlap sacks, small
rugs, and large rags to use in beating out burning embers or
small fires. Inside the house, fill bathtubs, sinks, and other
PART 3
containers with water. Toilet tanks and water heaters are an
important water reservoir.
• Place garden hoses so that they will reach any place on the
house. Use the spray gun type of nozzle, adjusted to spray.
Avoid laying the hose over or adjacent to combustible
objects.
• If you have portable gasoline-powered pumps to take water
from a swimming pool or tank, make sure they are operat-
ing in place and well protected from nearby combustible
elements.
• Place a ladder against the roof of the house opposite the side
of the approaching fire. If you have a combustible roof, wet
it down or turn on any roof sprinklers. Turn on any special
fire sprinklers installed to add protection. Do not waste water.
Waste can drain the entire water system quickly. Where pos-
sible, divert water from gutters back into the firefighting
supply.
• Back your car into the garage, and roll up the car windows.
Disconnect the automatic garage door opener (otherwise, in
case of power failure, you cannot remove the car). Close all
garage doors, and seal them with wet rags where possible.
Avoid storing combustible elements in a garage that cannot
adequately be sealed from ember attack.
• Place valuable papers and mementos inside the car in the
garage for later departure following passage of the fire, when
it is safe and may become necessary to do so. In addition,
place all pets in the car.
• Close windows and doors to the house to prevent sparks from
blowing inside. Close the damper on the fireplace to prevent
smoke and embers from entering the house. Leave the doors
inside the house open. This will enable occupants to remain
vigilant throughout the exposure. If a room or area in the
house ignites and develops beyond the occupants’ ability to
contain it, doors can be closed in the house to manage smoke
spread. Begin to plan an exit to the outside, bearing in mind
the state of the fire outside the house. The approach should
308
be to retreat to a room with an exit door that opens onto a
region with little fuel. Turn on a light in each room to make
the house more visible in heavy smoke. Have a backup plan
for when the electricity supply fails by having flashlights
handy.
• Turn off the main gas supply to stoves and furnaces.
• If you have time, take down drapes and curtains. Close all
Venetian blinds or noncombustible window coverings to
reduce the amount of heat radiating into the house. This
provides added safety in case the windows give way because
of heat or wind.
• As the fire front approaches, go inside the house. Stay calm;
you are in control of the situation. Continually move around
inside the house, monitoring its state and the progress of the
fire outside. Avoid spending time in the areas that have only
one way of exiting the space. If practical, include monitoring
of the roof cavity. Goggles will prove handy in dealing with
any smoke that enters the house.
• After the fire passes, check the roof immediately. Extinguish
any sparks or embers. Then check the attic for hidden burning
sparks. If you have a fire, enlist your neighbors to help fight
it. For several hours after the fire, recheck for smoke and
sparks throughout the house.
It is worth noting the research in this area by the Australian
Bushfire Cooperative Research Centre is continuing under Project
D1—Building and Occupant Protection under the leadership of
Justin Leonard, CSIRO Land and Water.
If a person expects to take refuge in his or her home and in
turn survive to ensure its defense, it is critical that steps are taken
to reduce the ignition potential of the structure as much as pos-
sible. Recent research on home ignition involving field experi-
ments, coupled with modeling and observations of recent WUI
fire incidents, has provided valuable new insights into the means
of ensuring home survival.134,135,137 The research has shown that
the characteristics of the home (e.g., exterior building materials)
and in an area referred to as the “home ignition zone” located
within 30 to 60 m (100 to 200 feet) of the home (e.g., surface
fuel accumulations immediately adjacent to the structure that
would be receptive to ignition by airborne firebrands) principally
determines its ignition potential and thus its survivability during
exposure to a wildland fire (Figure 14-37); videos that summarize
this research are available from Firewise Communities.136,193,194 For
example, a home could have little or no natural surface fuel
within the immediate vicinity of the dwelling, but because cedar
shake shingles were used in the roof construction, it is vulnerable
to ignition from airborne embers or firebrands from an approach-
ing wildfire. If such a burning structure is not handled soon after
ignition, it can contribute to the demise of neighboring houses
if left unattended,328 or push the limits of fire protection to keep
up effectively if too many structures become involved.138
The use of external sprinkler systems on a home146,363,453
should not be viewed as a panacea for a lack of fuel treatment
in the home ignition zone and beyond or the use of flammable
building materials. There is a perception that sprinklers should
be capable of providing thermal protection from a high-intensity
wildfire assault when in fact their real value is in preventing
ignitions from airborne firebrands,318 direct flame contact, and
radiation. The FPInnovations–Feric Wildland Fire Operations
Research Group has been engaged in a number of research
studies related to the use of sprinkler systems for home and cabin
protection since 2002, including outdoor field trials, using simu-
lated structures, involving both prescribed and experimental
fires.513,514 The group’s leader, Ray Ault,46 maintains that the great-
est use of commercially available Rain Bird types of sprinklers
and small portable pumps for individual home structure protec-
tion is in applying water in sufficient quantities and locations to
inhibit external ignitions from airborne firebrands by an approach-
ing or passing wildfire well in advance. If the presoaking or
application of water for wetting down fuels is applied for too
long, it can lead to other problems (e.g., flooded basements).
Irrigation systems have also been occasionally applied to the
task of WUI protection. Other, more elaborate systems have been
devised. For example, the Saskatchewan Fire Management and
Forest Protection Branch has successfully adapted and applied
 CHAPTER 14  Wildland Fires: Dangers and Survival
Home destruction
Yes No

Yes
High-intensity wildfire
Expected Not expected

No

Not expected Expected

FIGURE 14-37  Expectations of home destruction as a result of exposure to a wildfire. Home survival is
expected if low fire intensities occur (lower right) and unexpected if the home is destroyed (lower left).
Conversely, home survival is not expected if high fire intensities occur (upper left) and unexpected if the
home survives (upper right). (From Cohen JD: Home destruction. In Graham RT, technical editor: Hayman
fire case study: Summary, General Technical Report RMRS-GTR-115, Fort Collins, Colo, 2003, USDA Rocky
Mountain Research Station.)

operationally a manure drag hose transportation system to the
task of creating wet “breaks or belts” in values protection or to
facilitate backfiring or burnout operations.260
PROTECTIVE FIRE SHELTERS USED BY
WILDLAND FIREFIGHTERS
The concept of a protective fire shelter for wildland firefighters
described earlier (see Figure 14-19) was originally conceived by
Australian bushfire researchers in the late 1950s.256,281 The USDA
Forest Service equipment development center in Missoula,
Montana (now the MTDC) initiated research and development of
protective fire shelters about the same time as the Australians,493
and this work has continued to this day,104,394 with a view to
reducing the number of serious burn injuries and fatalities among
firefighters who become entrapped while fighting wildland
fires.42 Shelters designed in the shape of a pup tent protect the
firefighter by reflecting radiant heat. Constructed of an aluminum-
foil and fiberglass cloth laminate, the shelter reflects about 95%
of the radiant heat emanating from a fire. These shelters were
never designed for direct flame contact. Fire shelters were first
introduced operationally on the wildland fire scene in the United
States in the mid- to late 1960s and became a required PPE item
for federal wildland firefighters in 1977. More than 1200 U.S.
wildland firefighters have deployed their fire shelters to date (up
to and including the 2010 fire season).384 The fire shelter is cred-
ited with having saved the lives of more than 320 firefighters and
preventing at least 315 serious burn injuries,384 although it is not
known with any degree of certainty how many would have actu-
ally survived and suffered no burn injuries without the fire
shelter. Some personal accounts of fire shelter deployments have
been published116,411 (Box 14-8).
Why protective fire shelters work well was demonstrated
dramatically on August 29, 1985, when 73 firefighters were forced
to take refuge in their shelters for about 1.5 hours following
passage of a high-intensity, active crown fire that swept over and
around their location.8,340,421 The incident took place during the
Butte Fire in the Salmon National Forest in central Idaho. Observ-
ers described the crown fire that overran the firefighters as a
standing wall of flame that reached about 60 m (about 200 feet)
above the treetops. Within the shelters, firefighters experienced
extreme heat for as long as 10 minutes. Shelters were so hot that
they could be handled only with gloves. After leaving the shel-
ters, some firefighters showed symptoms of possible carbon
monoxide poisoning, including vomiting, disorientation, and dif-
ficulty breathing. Emergency medical technicians administered
oxygen to several individuals before evacuation from the site
after the incident. Five firefighters were hospitalized overnight
for heat exhaustion, smoke inhalation, and dehydration. The
consensus of those interviewed was that without the shelters,
none would have survived.347
It should be emphasized that the fire shelter was intended to
be used as a last resort when it became impossible to escape to
a safety zone before being overrun by a fire. However, despite
the emphasis placed on this basic tenet and extensive training
in entrapment avoidance over the years,320,322,349,355,480 the results
from a study of possible risk taking as a consequence of being
provided with fire shelters77 suggest a possible link to what has
been suspected for many years—that some firefighters are likely
to engage in behavior that neutralizes the gain in safety afforded
by fire shelters. In other words, fire shelters can lead to additional
risk taking426 or what’s called “risk homeostasis.”210
Putnam392 maintains that “you are always better with a fire
shelter in an entrapment situation than not.” This seems fair
advice. Fire shelters are, after all, relatively light to carry—the
current model weighs 1.9 to 2.2 kg (4.2 to 4.8 lb), depending on
the size43,381—and a minor inconvenience. Even when fire shelters
become compromised, they still provide some protection. One
of the entrapment survivors of the 1990 Dude Fire, Dave LaTour,
deployed his fire shelter before the arrival of the fire front and
stayed under his shelter even after a hole was kicked in it by
one of the firefighters who got out of his shelter and attempted
to evade the flames.357 This allowed hot gases to enter his shelter.
Despite this development, LaTour stayed down on the ground
as flat as possible. He did sustain some burn injuries but fully
recovered. LaTour was able to concentrate his attention on his
family to help him through the ordeal of being burned over by
the passage of a high-intensity flame front.
Alexander11 believes that the main issue regarding use of
shelters, beside not knowing what constitutes an adequate
clearing size for a shelter deployment in a particular situation,258
is the time taken for their efficient deployment.67 In trying to
avoid a wildland fire entrapment or burnover, seconds can
mean the difference between life and death.391 Without a regular,

309
 BOX 14-8  What Is It Like to Experience a Wildfire Entrapment in a Protective Fire Shelter?
BURNS, FIRE, AND RADIATION
Shelter deployment on the Shelley fire, Gila National Forest, June
24, 1989. (Photo by Mark Erickson, copyright 2006.)
Mark Erickson, a freelance photographer from Silver City, New
Mexico, was unexpectedly involved along with 40 wildland
firefighters in a fire shelter deployment associated with the major
run of the Shelley fire that took place in the Gila National Forest on
June 24, 1989. He recently recounted the experience190:
Dr Bruce Hayward, a biologist from Silver City, and I had been
putting together a joint effort about the Gila Wilderness, he doing
text and I covering the photography. It was decided that during the
fire season that I should get out and get some images of fire
because of its importance as ecological process in the area.
PART 3
The Shelley fire was started by lightning on June 16, 1989 but I
didn’t visit the fire site until June 23. I initially went out to the Sheep
Corral area toward Goose Lake to photograph the slurry bombers
dropping fire retardant but decided to return the next day and get
on the line. Jim Turner from the Shasta Ranger District in California
was assigned to go with me and we headed up to the Snow Creek
spike camp being manned by the local National Guard. The troops
had a water tender and some miscellaneous stores with which to
resupply the firefighters. We left our vehicle at the spike camp and
headed down the fireline in a northeasterly direction. The fire had
been turned over to a Class I Incident Command Team and an
infrared imaging aircraft had been brought in to determine the
location of hotspots. There was major concern down the valley near
Lake Roberts about the many structures that could conceivably be
in the path of the fire if the current fire suppression efforts were to
fail. I photographed many of the hotshot crew members as they
built fireline and felled snags near the line. It is hot, dirty work,
especially when air temperatures are already high and there is little
or no humidity.
formalized training program, carried out under realistic environ-
mental conditions, the precious time taken to deploy a shelter
might be better spent attempting to evade the fire’s encroachment
on one’s position to reach a safer location.11
The British Columbia Forest Service is the only Canadian fire
management agency to have ever formally included protective
fire shelters as part of a firefighter’s PPE. In 2005, it undertook
an associated risk analysis62 and as a result decided to have its
firefighters no longer carry fire shelters,234 relying instead on situ-
ational awareness and entrapment avoidance. The Australasian
Fire Authorities Council has adopted a similar position on the
grounds that fire shelters cannot guarantee firefighter survival and
may result in firefighters placing themselves at greater risk in the
belief that a fire shelter will protect them.50
310
Working our way along Panther Canyon, we noticed that there
was a large column of smoke in the direction from which we had
just come. Apparently the fire was heading right for the Snow Creek
spike camp where the National Guardsmen were being hurriedly
schooled on the use of fire shelters. A slurry bomber went over just
as the Sacramento Interagency Hotshot Crew came up the fireline
from the south. I took a few photographs of the hotshots with the
“blowout” in the background and we turned and headed back
toward a deployment zone or area on the fireline. The guardsmen
were spared having to deploy as the fire made another turn and
started toward us instead.
Entering the deployment zone, the crew began to take care of
the business of stowing gear such as chainsaws and fuel bottles on
the perimeter of the area. Cubitainers of water were brought to the
center of the deployment zone and personal gear was laid out. Last
minute clearing was taking place as the fire began chugging its way
closer to us.
Even though there was some “good” black between us and
the advancing fire front, the noise created by the crowning was
incredible as it got closer to our location. Someone gave the order
to deploy the fire shelters and all of us retreated underneath.
Located in the center of the deployment zone, I continued to
photograph the fire as it crowned around us. Comments from the
firefighters about the reverberating sounds created by the fire were
prevalent.
The winds created by the fire were truly amazing and I was glad
that the folks at the Technology and Development Center in Fort
Missoula had seen fit to add straps to the fire shelters so that they
wouldn’t fly away. Cinders from the fire were making small pin
holes in the shelter, resulting in a planetarium effect as the flames
surrounded the deployment area. The worst of all was the smoke.
Everyone was chattering back and forth checking on their buddies.
The duff was really burning when the fire decided to come back on
us. We were ordered to move in the opposite direction and ended
up laying in the smoldering pine needles. Thank heavens for Nomex
as we all ended up with lots of holes in our clothing, but nothing
burst into flame. I wish we would have had more time to rake the
area before the fire hit our deployment zone. One could really feel
the radiant heat from the shelters and I was really glad that we had
them. There were many comments about being done on one side
and “could we turn over to the other?”
The fire finally moved on down the canyon, but we stayed in the
shelters for an hour it seems. Finally we stuck our heads out to a
smoke-filled environment where it was difficult to see more than 10
feet. I continued to take photographs as I thought folks wouldn’t
really believe it if I just told them about this. A few of the crew were
having some respiratory problems, but everyone was mobile. The
cubitainers had been stripped of their cardboard casings and cases
of MREs (meals ready to eat) were burnt to the ground. The handles
on the fire tools were history, but the chainsaws and fuel bottles
were intact.
The deployment zone was still smoldering. I’m amazed how small
it felt during the peak period of fire activity. Our shelters were fairly
well spent and we tossed them into a pile—an unwise decision if we
had had to deploy later again that day—and we headed down to
the spike camp.
General observation: cool heads keep a situation from escalation.
EMERGENCY PROCEDURES DURING A WILDLAND
FIRE ENTRAPMENT OR BURNOVER
The danger of being entrapped or burned over and possibly
killed or seriously injured by a wildfire is a very real threat for
people living, working, or visiting498 in rural areas subject to
wildfires. Arnold “Smoke” Elser,188 an accomplished Montana
outfitter, described how he helped guests avoid entrapment by
a forest fire in the mid-1960s:
The fire began at the bottom of the canyon and proceeded up canyon
as fires do. However, the wind currents carried the smoke to the east
and not up the drainage to the north; therefore, we received no warning
of the fire. The Monture Creek trail goes through some very old mature
timber which was not burning as we approached. As my stock, the
guests, and I arrived at the fire site and realized that we were in danger,
we felt we should fall back and try to flank the fire to the east. Starting
back toward this trail, we found a ground fire that made it very hazard-
ous to travel in this direction. Because of my knowledge of the trail and
terrain, I knew that our best bet would be to wet down the stock, guests,
saddles and outer clothing and try to break through the head of the fire.
We successfully did this, receiving only a few minor burns on the horses
and the loss of some apparel tied to the backs of the saddles. Some
lessons that I learned in this experience were that in handling livestock
in a fire situation you must have a very close, firm hand on them. It is
also very important that no one panics or shows any excitement, as this
alarms the livestock and begins the panic run that is so well known. I
found that by talking in very low monotone, keeping the pack stock and
saddle stock very close together (head to tail), and moving on a good
trail, we were able to come through this fire with virtually no harm.
Elser188 had these additional suggestions for wildland
recreationists:
Campers, whether they be livestock-oriented, hikers, or boaters, should
know where to camp to provide adequate fire barriers around campsites.
All campers should consider at least one, and preferably two, safe escape
routes and havens (such as rock piles, rivers, and large green meadows)
away from heavy fuel areas. Campers should be alert to canyon air
current conditions in critical fire seasons. The safety of many recreation-
ists is threatened by nylon and other synthetic fabrics used in the manu-
facture of most backpacking equipment. These materials melt upon
contact with heat. The very nature of good horse packing equipment is
a deterrent to fire; canvas mantles that cover the gear and the canvas
pack saddles are easily wet down. Leather items such as chaps, good
saddle bags, and western hats [that] can shield against heat blasts all
provide important protection for the horse user.
Sometimes there may be no chance to easily escape an
approaching wildfire. Injuries can be minimized or avoided and
possible death averted by adhering to certain fundamental prin-
ciples and procedures (Box 14-9). There are, however, four
simple concepts that one must try to adhere to at all times45,118,125,519:
1. Select an area that will not burn—the bigger the better—or,
failing that, with the least amount of combustible material,
and one that offers the best microclimate (e.g., depression in
the ground).
2. Use every means possible (e.g., boulders, rock outcrops, large
downed logs, trees, snags) to protect yourself from radiant
and convective heat emitted by the flames.
3. Protect your airways from heat at all costs, and try to minimize
smoke exposure.
4. Try to remain as calm as possible.
The first requirement will limit the flame dimensions and in
turn the potential heat energy from flame radiation. It will also
limit the time of exposure, an important factor in thermal injuries.
Radiant heat can kill you long before direct flame contact.147,519
The more exposed skin, the greater is the likelihood of death.
Obviously, the last requirement—to remain as calm as
possible—may seem difficult to establish and maintain. The
expectation that people will panic (i.e., a sudden uncontrollable
fear or alarm leading to unthinking behavior) during an emer-
gency situation such as wildfire entrapment or burnover is very
strong. Admittedly, with the benefit of 20/20 hindsight, it is easy
to point to some decisions that were not optimal and played a
negative role in the outcome of the fire.370 Structural fire research-
ers believe that most people faced with a fire situation react in
a rational manner, considering the ambiguity of the initial cues
about the fire, their limited knowledge about fire development
and fire dynamics, and the restricted time to make a decision
and to take action.452
Panic is viewed as being synonymous with a frightened,
scared, nervous, or anxious response.452 In actual fact, panic in
the form of irrational or crazed behavior (e.g., aimlessly trying
to flee) is rare during fires. Social scientists long ago rejected this
concept to explain human behavior in urban fires.131,389,452 Instead
of panic, what is commonly observed is an increased level of
stress. Stress is not panic. As Dr. Guylene Proulx,389 a human
factors specialist with the National Research Council Canada’s
structural fire research program, suggests, “This stress is not an
CHAPTER 14  Wildland Fires: Dangers and Survival
BOX 14-9  Surviving a Wildland Fire Entrapment
or Burnover
When entrapment or burnover by a wildland fire appears
imminent, injuries or death may be avoided by following these
basic emergency survival principles and procedures.
• Acknowledge the stress you are feeling. Most people are
afraid when trapped by fire. Accept this fear as natural, so that
clear thinking and intelligent decisions are possible. If fear
overwhelms you, judgment is seriously impaired, and survival
becomes more a matter of chance than good decision making.
• Protect yourself against radiation at all costs. Many victims of
forest fires actually die before the flames reach them. Radiated
heat quickly causes heatstroke, a state of complete exhaustion.
Find shielding to reduce heat rays quickly in an area that will
not burn, such as a shallow trench, crevice, large rock, running
stream, large pond, vehicle, building, or the shore water of a
lake. Do not seek refuge in an elevated water tank. Avoid wells
and caves because oxygen may be used up quickly in these
restricted places; consider them a last resort. To protect against
radiation, cover the head and other exposed skin with clothing
or dirt.
• Regulate your breathing. Avoid inhaling dense smoke (which
can impair both your judgment and eyesight). Keep your face
near the ground, where there is usually less smoke. Hold a
dampened handkerchief over the nose. Match your breathing
with the availability of relatively fresh air. If there is a possibility of
breathing superheated air, place a dry, not moist, cloth over the
mouth. The lungs can withstand dry heat better than moist heat.
• Do not run blindly or needlessly. Unless a clear path of
escape is indicated, do not run. Move downhill and away from
the flank of the fire at a 45-degree angle where possible.
Conserve your strength. If you become exhausted, you are
much more prone to heatstroke and may easily overlook a
place of safe refuge.
• Burn out fuels to create a safety zone if possible. If you are
in dead grass or low shrub fuels and the approaching flames
are too high to run through, burn out as large an area as
possible between you and the fire edge. Step into the burned
area and cover as much of your exposed skin as possible. This
requires time for fuels to be consumed and may not be
effective as a last-ditch effort, and does this work well in an
intense forest fire.
• Lie prone on the ground. In a critical situation, lie face-down
in an area that will not burn. Your chance of survival if the fire
overtakes you is greater in this position than standing upright or
kneeling.
• Enter the burned area whenever and wherever possible.
Particularly in grass, low shrubs, or other low fuels, do not delay
if escape means passing through the flame front into the
burned area. Move aggressively and parallel to the advancing
fire front. Choose a place on the fire’s edge where flames are
less than 1 m (3.3 feet) deep and can be seen through clearly,
and where the fuel supply behind the fire has been mostly
consumed. Cover exposed skin and take several breaths, then
move through the flame front as quickly as possible. If
necessary, drop to the ground under the smoke for improved
visibility and to obtain fresh air.
abnormal reaction or a negative response; on the contrary, stress
is regarded as a necessary state to motivate reaction and action,”
and that “Decision-making under stress is often characterized by
a narrowing of attention and focusing on a reduced number of
options. This explains why training is so important because the
person is unlikely to develop new solutions under heightened
stress; a well-run decision plan learned and practiced beforehand
is easier to apply under stress.”
There are four fundamental or basic survival techniques, or
options (see Box 14-9), available to an individual who is caught
out in the “open” and is likely to be entrapped or burned over
by a wildfire and is not able to take refuge in a vehicle or build-
ing201,281,519 or have a protective fire shelter. These four survival
options are as follows19,21,433:
1. Retreat from the fire and reach a safe haven.
2. Burn out a safety area.
311
 3. Hunker in place.
4. Pass through the fire edge into the burned-out area.
These four survival options are presented in no particular
order of priority. Such factors as the size of the fire, fire environ-
ment, size and location of safety areas or zones, prevailing fire
behavior, and location of the person with respect to the head of
fire will ultimately dictate which option or options (should the
first one of these options selected become compromised) should
be selected. Each of these options has its own unique advantages
and disadvantages.
Survival Option 1: Retreat From the Fire and Reach a
Safe Haven
When people are under pressure, they fall back on habitual,
first-learned, and overlearned responses.522 The natural tendency
when a person is threatened by a hazard such as a wildfire is to
try and move away from the danger as quickly as possible to a
place of safe refuge. If the distance between the fire and safe
area is short, the fire’s advance slow, the path to the safe area
easily traversed, and the person able bodied, then selection of
this survival option is appropriate. Bear in mind that a safe refuge
may be nearby, so one should not avoid the most obvious place,
even though it may temporarily be uncomfortable to reach
BURNS, FIRE, AND RADIATION
because of, for example, smoke or low to moderate radiation
levels. In some cases, this might mean just taking a few steps
into the “black” or recently burned-over ground. The question
of whether a previously burned area will serve as a safety zone
will depend not only on the size of the area but also on the
degree of completeness of fuel consumption, both vertically and
horizontally.98,380 Furthermore, a recently burned-over area may
not immediately serve as a safe refuge because of the burnout
time of woody fuels and duff,471 in contrast to grassland fuels,
where a person can enter the recently burned area in a few
seconds.129
Firefighters have escaped injury and death in many cases by
being able to outpace or outmaneuver a spreading fire.380,480
There have also been many well-publicized cases or incidents
during which attempting initially to outpace and then ultimately
PART 3
outrun an advancing flame front have ended in tragedy, includ-
ing several mentioned earlier (e.g., 1938 Pepper Hill Fire, 1949
Mann Gulch Fire, 1953 Rattlesnake Fire, 1956 Inaja Fire, 1966
Loop Fire, 1968 Canyon Fire, 1994 South Canyon Fire). Sadly,
there are many other examples,413 including the 2003 Cramer Fire
in central Idaho involving two firefighter fatalities.133 For informa-
tion on many of these incidents, consult www.fireleadership.gov/
toolbox/staffride/.
Dr. Ted Putnam,393 a retired wildland fire safety specialist with
the USDA Forest Service, considers that many of these fatality
fires were in fact escapable had better decision making been
employed (e.g., dropped tools and packs earlier to maximize rate
of advance, put the fastest pacesetters at the lead, and used fire
shelters as shields against radiant and convective heat).
Incidents similar to those experienced by firefighters involving
civilians have also taken place. For example, on November 30,
1957, four members of a group of nine young hikers perished
while trying to outrun a bushfire in the Blue Mountains of New
South Wales, Australia, as it advanced upslope.201,281 Another
incident occurred on August 26, 1995, near the community of
São Domingos in the district of Sandtarém, Portugal.510 Three
civilians who had been assisting local firefighters in suppression
operations eventually ended up being killed while trying to run
ahead of the fire when it blew up. A fourth individual received
severe burns to his feet, which eventually led to them being
amputated, and he died some months later.
Simulations carried out by the FPInnovations Wildland Fire
Operations Research Group based on their research on firefighter
travel rates,164 coupled with case study information gleaned from
the 1949 Mann Gulch and 1994 South Canyon fires,102 clearly
indicate that a person is not able to sustain a maximum pace for
even a relatively short time without being overrun by a rapidly
advancing flame front, even on a moderately steep slope.28,60 For
example, a fire spreading at 60 m/min (197 ft/min) up a 26%
slope would, depending on the fuel type, overrun someone in
about 6 to 7.5 minutes or after about 360 to 460 m (1200 to 1500
312
feet) once the “race” had started. Chandler and colleagues116 state,
“In most firefighter fatalities . . . the unsuccessful strategy has
been to try and run away from the fire and continue running
until exhaustion or the radiant heat load from the fire front fells
the victim and allows the flame front to pass over him or her.”
Thus, trying to outpace a fire for any significant distance, but
especially uphill, is “courting disaster.”281 For this reason, escape
routes involving travel upslope should generally not be selected.
Survival Option 2: Burn Out a Safety Area
Burning out fuels to create an area of safety or to enlarge an
existing burned area is a viable survival technique or option in
some situations (e.g., light fuels and having sufficient time to
implement). As Luke and McArthur281 have noted, “Carrying a
box of matches is part of survival planning” (in this regard, a
windproof type of matches would be ideal, although a fuse
would be infinitely more reliable and effective than a match).
Undoubtedly the most publicized example of this survival
strategy being used in modern times occurred on the 1949 Mann
Gulch Fire, discussed earlier.285,418 However, the technique was
known to have been used by American Indians in the early
1800s395,494 and undoubtedly by aboriginal peoples in other parts
of the world, as depicted, for example, in the 1989 movie The
Gods Must Be Crazy II. Wag Dodge described his escape fire
during his testimony at the board of review investigation into the
1949 Mann Gulch fire as follows:
After setting a clump of bunch grass on fire, I made an attempt to start
another one, but the match had gone out and upon looking up, I had
an area of 100 feet square that was ablaze. I told the man nearest to me
that we would wait a few seconds to give it a chance to burn out inside,
and then we would cross through the flames into the burned area, where
we could make a good stand and our chances of survival were more
than even.
Interestingly, Dodge’s statement was printed in the letters to
the editors section of the September 1949 issue of Life magazine
after publication of an article on the Mann Gulch Fire entitled
“Smokejumpers Suffer Ordeal by Fire” from the previous issue.
In that letter, the reader stated, “I am sure that there are many
people throughout the country who would appreciate and
perhaps benefit sometime by a more detailed account of how
Foreman Wagner Dodge, who kept calm and did not become
panic-stricken, saved himself.” It has been estimated that Dodge’s
escape fire was about 37 m (121 feet) long and 26 m (85 feet)
wide at the time that his “island” of survival was engulfed by
3-m (10-foot)–tall flames associated with the main fire front.26
Survival Option 3: Hunker in Place
As mentioned previously, when caught in the open, survival may
depend on taking advantage of every possible source of cover
or protection from radiant and convective heat (e.g., depressions
in the ground, large rocks or logs).201 If a cave (see Figure 14-35)
or root cellar538 is used as a refuge, it is important to vacate
into the open at the earliest opportunity because of potential
problems associated with accumulations of smoke and carbon
monoxide.
In selecting this option, the importance of staying as flat as
possible with one’s nose and mouth pressed down into the
ground cannot be overemphasized, because the reduction in
radiation received is considerable.27 Lying prone not only mini-
mizes one’s radiation profile, but cooler, denser air will always
be present at ground level. In selecting this option, also bear in
mind the following advice125:
When a fire passes over a point, the air temperature near the ground is
higher than the air above it and remains higher for longer. So if someone
is sheltering from radiation at ground level, they need to stand up as
soon as possible after the fire passes to breathe cool, fresh air. This is
most apparent in grass fires where air at ground level is hot and smoky
for several minutes whereas at 2 m [6.6 feet] it is cool and breathable
within 10 to 15 seconds of the flames passing.
Although there have been reported cases of firefighters surviv-
ing on large rockslides during a wildfire entrapment or burnover,
most notably two smoke jumpers on the 1949 Mann Gulch
Fire,285,418 there have also been instances in which these appar-
ently safe, fuel-free areas contained enough combustible materi-
als to cause injury or death (e.g., Shephard Mountain Fire in
western Montana on September 4, 1996). Four firefighters died
on a rockslide during the 2001 Thirtymile Fire in north-central
Washington, due in part to the accumulation of duff and rotting
wood lodged in the rock crevices that ignited from airborne
firebrands.81,288,496
In selecting this option, maximum use should be made of any
clothing or other readily nonburnable material to protect exposed
skin. You may have to improvise.495 Synthetics should not be used
because they readily melt when exposed to flame radiation.
During the 1983 Ash Wednesday fires in Victoria, Australia, two
individuals wearing only summer clothing who covered them-
selves with a synthetic blanket perished, while two other indi-
viduals right next to the two victims covered themselves with a
wet woolen blanket and survived the burnover.259
A good example of selecting this option was the Wandilo Fire
that occurred in an exotic pine plantation near Mount Gambier,
South Australia, on April 5, 1958. Eleven firefighters found them-
selves trapped on a narrow firebreak during a “blowup.”281,302
Eight in the group attempted to run back along the firebreak,
but perished after exposure to extreme radiant heat levels and
direct flame contact. Of the three who survived, two remained
in the cab of their firefighting truck to shelter from the worst of
the firestorm and only left this cover when the vehicle was well
alight and the fire’s peak intensity had abated. The remaining
survivor sheltered in a deep wheel rut in the soft sand of the
firebreak with his coat over his face during the peak period of
extreme fire behavior.
Taking refuge in a natural water body such as a pond, lake,
or river must be done with caution, but for other reasons (e.g.,
swimming ability). For example, in 1986, three firefighters in the
province of Quebec, Canada, drowned as a result of being forced
to enter a lake with a steep drop-off when their camp location
was overrun by fire.13 The risk for hypothermia must also be
considered.103 Dion174 described an incident that occurred in
west-central Saskatchewan, Canada, in May 1919 in which 11
Cree Indians perished because they were not able to reach a
nearby lake or find sufficiently deep water to avoid radiation
burns. Of the 12 who survived the ordeal, 11 “bore the marks
of their burns for life.” One adult member of the group “escaped
severe burns by staying under the water” as much as was pos-
sible. It has been suggested that the minimum depth of water
should be 0.45 to 0.6 m (1.5 to 2 feet) deep.358,450
Survival Option 4: Pass Through the Fire Edge Into the
Burned-Out Area
Luke and McArthur281 have suggested that “running through
flames cannot be generally recommended and should certainly
not be attempted when flames are more than 1.5 m [5 feet] in
height or depth.” Nevertheless, a number of firefighters have
done this very thing and survived (e.g., 1991 Tikokino grass fire
in New Zealand406). In fact, the five members of the group of
young hikers that survived the 1957 bushfire in the Blue Moun-
tains of New South Wales mentioned earlier did so successfully
but suffered considerable discomfort. A similar incident occurred
on the Warm Springs Indian Reservation in central Oregon in
June 1985. Wildland fire behavior analyst Jim Roessler415 has
indicated that those individuals who tried to outrun a grass fire
on a moderately steep slope were killed, whereas at least one
person who passed through the flame front survived. In contrast,
during the blowup of the 1937 Blackwater Fire, the “five horse-
men” made the decision to move downhill through the advanc-
ing flames.78 Three did not make it, partly because of the heavy
fuel conditions. Of the two who did survive, one died later of
burn injuries. A group of 41 on another section of the fire rode
out the blowup in a ridgeline clearing as the fire progressed
upslope; three were badly burned and eventually died of their
injuries.
It has been suggested that a person could theoretically survive
passing through flames 3 m (9.8 feet) high and 37 m (121 feet)
in depth and still survive.116 It is presumed that the person would
be immersed in flames for less than 7.5 seconds and would
require ideal running conditions (e.g., good footing, no obstruc-
CHAPTER 14  Wildland Fires: Dangers and Survival
tions) and would be properly clothed to withstand the direct
flame contact. Although it is reasonable to expect a person to be
able to hold his or her breath for this long, the very notion of
attempting such a drastic or draconian116 feat seems unimagina-
ble. Nevertheless, it is worth noting that firefighters have lived,
although while sustaining severe burns as a result, by running
through high-intensity flame fronts. One of the most notable
examples of this involved a prescribed fire (PB-3/79) in heavy
logging slash near Geraldton, Ontario, Canada, on August 22,
1979.36,310,332 As a result of a complex set of unforeseen circum-
stances, eight members of the firing crew found themselves
encircled by fire. One member of the party, a local fire techni-
cian, realizing that there was no other option except to run
through the advancing flame front or face what appeared to be
certain death, tried to get seven seasonal employees to follow
him. They failed to heed his urgings and were eventually engulfed
by the fire, whereas he survived but did sustain serious burn
injuries. This outcome is hauntingly reminiscent of the 1949 Mann
Gulch Fire and Wag Dodge’s escape fire in which 15 firefighters
failed to follow his lead and 13 ended up perishing. In this
regard, Dr. Karl Weick,523 a renowned professor of organizational
behavior and psychology, points out that there is good evidence
to support the notion that when people are threatened, their
thinking becomes much more rigid and difficult to change. Fur-
thermore, they tend to seek out and talk to only those who are
most familiar to them.442
The survival technique or option of moving through the
flame front to previously burned ground would logically be
most suitable in light, discontinuous fuel types that fail to
produce deep, uniform flame fronts, and significant postfrontal
smoldering or isolated flaming, such as that afforded by certain
grasslands (e.g., heavily grazed areas). Furthermore, if one has
the good fortune to take advantage of a lull in the wind, this
would lessen the momentary rate of spread and in turn the
flame depth (see Table 14-2). An area along the flanks of the fire
(see Figure 14-24) would be preferable to the head. One may
only have to travel a relatively short distance before reaching
previously burned ground that has “cooled” down sufficiently to
serve as a safe area.
Having reached the burned area, a person would still have to
be cognizant of the danger posed by fire-weakened trees and
falling snags, hot ash pits and burned-out stump holes, and
rolling rocks or logs.275 This would apply to the other survival
options as well.
It is worth emphasizing that wildland firefighters as well as
members of the general public have been killed and seriously
burned while engaged in using fire as a land management
tool.36,316,458,506,509 Thus, the survival principles and options dis-
cussed earlier are equally applicable to prescribed fires or con-
trolled burns.
Although radiant heat emanating from a wall of flame is
generally viewed as the principal killer in wildland fire entrap-
ments and burnovers,147 under certain conditions, convective
gases or superheated air can have lethal consequences with little
or no warning, most notably upslope of a fire source. Under
strong winds, a fire’s convection column will not lift away from
the surface of a steep slope.129 As slope steepness increases,
flames gradually “attach” themselves (Figure 14-38), thereby
enhancing fire spread by both direct flame contact and convec-
tive heat transfer.416 This is the very reason that fires spread faster
upslope than on level ground given the same fuel and weather
conditions.
WILDLAND FIRES AND
HUMAN BEHAVIOR
As discussed earlier, the reality of human behavior in fires is
somewhat different from the panic scenario “nourished by the
media and movie industry who like to play on strong emotional
images.”389 What is regularly observed in urban fire situations is
a lethargic response to fire alarms or even the initial cues of a
fire (e.g., smoke and visible flame).
313
 Convection
Weak
indraft
Strong
indraft
Flame detached
from slope
A SHALLOW SLOPE
BURNS, FIRE, AND RADIATION
Convection
Indraft
Flame attached
to slope
PART 3
B STEEP SLOPE
FIGURE 14-38  Effect of slope steepness on degree of flame attach-
ment and convective heat transfer for shallow-sloping (A) and steep-
sloping (B) terrains. (Redrawn from Rothermel RC: Fire behavior
considerations of aerial ignition. In Mutch RW, technical coordinator:
Prescribed fire by aerial ignition: Proceedings of a workshop, Missoula,
Mont, 1985, Intermountain Fire Council.)
What has been most troubling to the wildland fire community
in recent years is that the same mistakes seem to be made time
and time again,178 rather than using “the lessons of the past so
we don’t have to keep relearning them the hard way.”354 Since
the mid-1990s, there has been a growing recognition among the
wildland fire community of the role that human factors play in
firefighter fatalities.97,179,391
Morse325 considered the development of a mental “scotoma”
among firefighters to be a major contributing factor in many
wildland fire fatality incidents, noting, “Scotoma is, literally, a
blind spot. In a psychological sense, it is that condition which
occurs when a person tends to block out from his or her con-
sciousness anything considered not important—or critical—to
survival.” In other words, blindness to danger perceived as
routine takes hold and blocks out sensitivity to hazardous events
or conditions present in the wildland fire environment.
The smoke jumpers involved in the 1949 Mann Gulch Fire
would appear to have suffered from a psychological scotoma or
overconfidence.521 By the time they had landed and gathered
their gear together, it was nearly 5:00 PM. At the time, “They did
not feel the fire threatened them then.”418 Less than an hour later,
12 smoke jumpers and a local firefighter were overrun and killed
by the fire. Air temperatures reached a maximum of 36° C (97° F)
314
on the day in question, and in turn, the fully cured grasses were
in a critically dry state.418 It was a day of extreme fire danger.15
One of the survivors, Bob Sallee, commented afterward418:
I took a look at the fire and decided it wasn’t bad. It was burning on
top of the ridge and I thought it would continue on up the ridge. I
thought it probably wouldn’t burn much more that night because it was
the end of the burning period (for that day) and it looked like it would
have to burn down across a little saddle before it went uphill any more.
One crew member was reported to have been taking photo-
graphs of the fire less than 10 minutes before the first fatalities
occurred.285,418 Similarly, photographs were being taken by fire-
fighters on the line just moments before the 1994 South Canyon
fire blowup,98 in which 14 of their fellow firefighters were overrun
and killed (see Figure 14-1).
Even on the major run of the Thirtymile Fire in north-central
Washington on July 10, 2001,81,288 the firefighters behaved more
as spectators than as potential victims until it was too late for
some. A total of 16 people (14 firefighters and 2 civilians) were
entrapped and required to deploy protective fire shelters. Four
firefighters were killed, and two were injured, one with severe
burns. Earlier during the day in question, the feeling was that
the fire was “basically a mop-up show.”81 Some of the firefighters
who were overrun by the fire “spent time taking photos or
making journal entries” just a half hour before the incident.81
Although wildland firefighters may be subject to a host
of human failings or other psychological phenomena,133,369,522
openly acknowledging and constantly being aware of the poten-
tial for entrapment or a burnover, regardless of the situation, is
the initial key step in reducing the risk for injury or death from
wildland fires. Complacency may be the most difficult factor to
overcome.330 The late Paul Gleason,212 a veteran wildland fire-
fighter and accomplished rock climber, noted that three major
causes of climbing accidents are ignorance, casualness, and
distractions.
Although firefighters are expected to engage a wildfire, civil-
ians are not. Nevertheless, the general public could also become
complacent about wildfires and fail to fear the worst, until, unfor-
tunately, it is too late. This may result in part from a fascination
with fire in general (Figure 14-39), denial, indifference, or a
complete ignorance about free-burning fire behavior. In any case,
there is a perception that there is no real sense of urgency until
the threat is imminent. As Proulx389 points out, “People are often
too cool during fires, ignoring or delaying their response to the
initial cues of an actual emergency. Once occupants decide that
the situation requires moving to an area of safety, the time left
could be minimal.” This is probably best exemplified by an urban
fire case study. On May 11, 1985, 56 people burned to death and
more than 200 were injured when a rapidly growing fire, caused
by a cigarette, engulfed the wooden main grandstand at Valley
Parade Stadium in Bradford, England, during a soccer match.
Filmed documentation of the fire indicates that the blaze spread
the entire 88-m (289-foot) length of the stand in less than 5
minutes—a rate of 18 m/min (59 ft/min). Although people in the
immediate vicinity of the developing fire moved toward exits,
“Persons in remote sections of the grandstand continued to watch
the match, apparently unconcerned about (or perhaps unaware
of) the developing fire.”257 One of the seven factors that contrib-
uted to the loss of life was “the failure of patrons to perceive
the danger of the developing fire in the early stages and begin
evacuation.”257
It is sometimes difficult to believe that a wildland fire could
become life threatening, especially if it is far away from the
observer or small in size and is not burning very vigorously at
the time. However, danger is inherent in every wildland fire
occurrence, whether a wildfire or a prescribed fire. Some wild-
land fire situations are simply more hazardous than others and
can catch a person or persons off guard (Figure 14-40), possibly
leading to severe injuries or even death.57,88
Tom Leuschen274 is an experienced fire manager and wildland
fire behavior analyst who worked for many years in north-central
Washington, within sight of the area struck in 2001 by the Thirty­
mile Fire. He was involved in the accident investigation and had
the following to say about the incident:

A preparing for worst-case scenarios.
B an entrapment or burnover at any time given the precarious
FIGURE 14-39  Rural homeowners (A) observing the Haeckel Hill Fire
(B) near the city of Whitehorse, Yukon Territory, Canada, on June 22,
1991. (Courtesy Yukon Wildland Fire Management.)
A intensity flame front approaches (Figure 14-41). This is a poten-
B underwear made of synthetic materials does melt. Wearing exces-
FIGURE 14-40  Fires in fully cured grasslands are very responsive and
can attain exceedingly rapid rates of spread. The flank of a grass fire,
with a change in wind direction, can quite quickly become the head
and catch unwary persons off guard. This scene from the multifire situ-
ation that occurred in the Spokane, Washington, area on October 16,
1991 (A), reinforces the importance of having well-established escape
routes that can be easily navigated (B) to a designated safety zone.
(Courtesy Spokane Statesman Review/WorldPictureNews; photos by
K. King.)
CHAPTER 14  Wildland Fires: Dangers and Survival
BOX 14-10  Envisioning the Worst
Karen Cerulo argues that people have a clear preference,
culturally shaped, for paying attention to best-case scenarios and
casual attention to worst-case scenarios. Whether people render
the worst-case invisible or vague or recast the worst case as
positivity in disguise, the result is that they are unable to envision
the worst case and unprepared to avoid it or deal with it. Thus,
the plaintive phrase provides the title of this work, “we never saw
it coming.”
The reader comes away from this book with a new appreciation
of the need for mindful attention, resilient action, and skills of
improvisation. With these three resources as part of an action
repertoire, we will go a long way toward acknowledging and
Excerpt from Weick KE: Book reviews: Never saw it coming: Cultural changes to
envisioning the worst, Am J Sociol 113:1762, 2008.
When I stand at the deployment site and look at their pictures, knowing
what I know about the fuels, barriers, and interactions between fires, I
honestly do not expect that they will have to shelter either. I am as wrong
as they were. Things got very complex as the fires joined at their loca-
tion. The obvious lesson is that we must prepare for the worst when
trapped, regardless of what we may anticipate. They were entrapped at
1634 and deployed at 1724. They had time to get organized.
Anyone involved in a wildland fire can become a victim of
nature of wildland fires and their environmental influences.
People need to be constantly mindful or conscious of this fact
because, as Weick520,522 says, “Safety is not bankable,” and it is
“an ongoing struggle for alertness.” Plan for and expect the worst
every time out. This may be difficult, because a blatant disregard
for worst-case scenarios is one of the common, yet least studied,
human traits115 (Box 14-10).
PROPER CLOTHING
There are documented cases in which homeowners, who were
seemingly prepared to stay and defend their property, have died
because they were not properly dressed to do so (e.g., clad only
in shorts or a bathing suit and slippers).519 Clothing protects
against radiant heat, embers, and sparks, so it is sensible to
dress appropriately.146,372 The cover of a recent book on the WUI
fire situation in southern California229 depicts a lightly clad
home­owner on the roof of his house presumably attempting to
extinguish sparks or embers with a garden hose as a high-
tial recipe for disaster in many respects. This person is not
properly attired to stay and defend his property, nor is this the
correct approach.
Closely woven material is more resistant to radiation and less
likely to ignite than is open-weave material. Natural fibers are
best. Wool is more flame resistant than cotton, although cotton
can be improved by chemical treatment to retard flammability.
As mentioned earlier, synthetic materials are a poor choice
because they readily absorb heat or, worse, can ignite and melt
onto the skin.385
Closely woven materials that provide protection also restrict
airflow, so clothes should fit loosely so that they do not interfere
with dissipation of body heat. Cotton long johns or undergar-
ments absorb sweat, aid evaporation, and do not melt; however,
sive layers of clothing generally contributes to heat stress.
As little skin as possible should be exposed to fire. Long
trousers and a long-sleeved shirt should be worn. For maximum
protection, the shirt should be kept buttoned with the sleeves
rolled down.
Brightly colored (yellow or orange) coveralls or shirts are
worn by organized firefighting crews. These colors improve
safety and communications because they are visible in smoke,
vegetation, and blackened landscapes.
315

FIGURE 14-41  An inappropriately clad and positioned homeowner
attempting to defend his property from ember attack during a wildfire
in Rancho Penasquitos, San Diego, California, on August 25, 1995. The
fire at the moment appears largely dominated or supported by a
plentiful fuel source. However, given the capricious nature of fire and
winds, this fire could have easily turned into a more wind-dominated
event at any time. Thus, this individual could have been incapacitated
by a momentary blast of superheated air from the convection or
BURNS, FIRE, AND RADIATION
radiant heat produced by the spreading fire. In the absence of any
outside assistance, this would then have left him vulnerable to burning
by direct flame contact along with his home. Fortunately for this indi-
vidual, shortly after the photo was taken, an air tanker dropped a load
of fire retardant near the advancing flames and effectively nullified the
fire’s spread and intensity. (Courtesy California Chaparral Field Insti-
tute; photo by R.W. Halsey.)
Other essential apparel includes a safety helmet (hard hat),
gloves (leather or natural fiber), leather work boots, woolen or
cotton socks, a warm jacket for night wear, goggles, and a hand-
kerchief. Clothing, backpacks, tents, and other camping equip-
ment made of synthetic materials should be discarded when a
person is close to a fire.
PART 3
WATER INTAKE
Sweating is the primary method for body cooling, although
exhaling warm air and inhaling cooler air also decreases body
temperature (see Chapter 89). Because the cooling effect of sweat
evaporation is essential for thermoregulation, fluids lost during
strenuous work must be replaced. In firefighting, water losses of
0.5 L/hr (1 pt/hr) are common, with losses of up to 2 L/hr (2 qt/
hr) under extreme conditions.281 Unless water is restored regu-
larly, dehydration may contribute to heat stress disorders, reluc-
tance to work, irritability, poor judgment, and impatience.
Thirst is not a good indicator of water requirements during
strenuous work, so additional drinking of small quantities of
water at regular intervals is recommended. A useful signal of
dehydration is dark, scanty urine.
An excessive amount of electrolytes may be lost through
sweating, leading to nausea, vomiting, and muscle cramps. When
meals are missed or unseasoned foods are eaten, electrolyte
supplements may be needed to replace lost salts. Sweetened
drinks should be used as a source of energy if solid food is not
available.
PERSONAL GEAR
Some rescue and medical missions take a few days. Therefore,
it is necessary to be prepared for extended periods and changing
conditions in the backcountry (Box 14-11).
HOW TO REPORT A WILDLAND FIRE TO LOCAL
FIRE PROTECTION AUTHORITIES
A caller should be prepared to provide the following information
when reporting a fire:
• Name of person giving the report
• Where the person can be reached immediately
316
• Where the person was at the time the fire was
discovered
• Location of the fire; orient the fire to prominent landmarks,
such as roads, creeks, and mileposts on highways
• Description of the fire: color and volume of the smoke,
estimated size, and flame characteristics, if visible
• Whether anyone is fighting the fire at the time of
the call
The phone number to call varies locally. For example, in
Alberta, Canada, the number for reporting wildland fires is 310-
FIRE or 310-3473 in both the northern and southern halves of
the province, even though they have different area codes. In
other locations, it may simply be 9-1-1. Rural homeowners should
make a point of finding out the number to call before the begin-
ning of fire season.
PORTABLE FIRE EXTINGUISHERS
People should know which extinguisher to select for a specific
hazard in the home or recreational vehicle and be trained in its
use. When a fire is discovered, first evacuate occupants to safety
and promptly report the fire to the appropriate authorities. If the
fire is small and poses no direct threat, an extinguisher should
be used to fight it.
The three major classes of fires are as follows:
Class A fires: Fueled by ordinary combustible materials, such
as wood, paper, cloth, upholstery, and many plastics
Class B fires: Fueled by flammable liquids and gases, such as
kitchen greases, paints, oil, and gasoline
Class C fires: Fueled by live electrical wires or equipment,
such as motors, power tools, and appliances
The right type of extinguisher must be used for each class of
fire. Water extinguishers control class A fires by cooling and
soaking burning materials. Carbon dioxide or dry chemical extin-
guishers are used to control class B fires by smothering flames.
Multipurpose dry chemical or liquefied gas extinguishers control
class A, B, and C fires by a smothering action. Liquefied gas
extinguishers also produce a cooling effect. A dry chemical
or liquefied gas extinguisher is recommended for recreational
vehicles.
BOX 14-11  Personal Gear for a Rescue Mission on a
Wildland Fire Incident
• Boots (leather, high-top, lace-up, nonslip soles, extra leather
laces)
• Socks (cotton or wool, at least two pairs)
• Pants (natural fiber, flameproof, loose fitting, hems lower than
boot tops)
• Belt or suspenders
• Shirt (natural fiber, flameproof, loose fitting, long sleeves)
• Gloves (natural fiber or leather, extra pair)
• Hat (hard hat and possibly a bandanna, stocking cap, or felt hat)
• Jacket
• Handkerchiefs or scarves
• Goggles
• Sleeping bag and ground cover
• Map
• Protective fire shelter
• Food
• Canteen
• Radio (AM radio will receive better in rough terrain; FM is more
line-of-sight; emergency personnel should have a two-way
radio)
• Bolt cutters (carried in vehicles to get through locked gates
during escape from flare-ups or in the rescue of trapped
people)
• Miscellaneous items (mess kit, compass, flashlight, extra
batteries, toilet paper, pencil, notepaper, flagging tape, flares,
matches (windproof), can opener, washcloth, toiletries, insect
repellent, plastic bags, knife, first-aid kit, and lip balm)
BASIC WILDLAND FIRE MATERIALS,
TRAINING COURSES, AND OTHER
INFORMATION RESOURCES
A large number of reference or textbooks on wildland fire sup-
pression currently exist, many of which have been cited or ref-
erenced in this chapter. Wildland Fire Fighting for Structural
Firefighters is a comprehensive text written specifically for fire-
fighters whose primary focus is fighting structure fires, but who
also have wildland and WUI responsibilities.219 The book pro-
vides an excellent overview on wildland fire behavior, fire appa-
ratus and communications equipment for wildland fires, wildland
firefighting tools and PPE, extinguishing agents, wildland incident
management, fire suppression methods, wildland and interface
fire suppression, firefighter safety and survival, fire prevention
and investigation, and fire protection planning. The booklet Plan-
ning for Initial Attack published by the USDA Forest Service is
a handy reference on basic fire behavior and fire suppression
principles.319 Other reference books exist on the basics of wild-
land fire suppression.280 For a good general reference on forest
fires, see the recent contribution by Omi.367 Managing Fire in the
Urban-Wildland Interface is the most comprehensive profes-
sional guide on the WUI fire problem.72
Wildfire magazine, the official publication of the International
Association of Wildland Fire, is an excellent source of information
on current fire management topics (www.iawfonline.org), as is
International Forest Fire News (www.fire.uni-freiburg.de/iffn/
iffn.htm) and Fire Management Today (www.fs.fed.us/fire/fmt).
Other information that would be valuable to emergency
response personnel includes reference materials and materials
associated with the Publications Management System (PMS) and
“S,” or suppression skills, training courses available through the
U.S. National Wildfire Coordinating Group’s National Fire Equip-
ment System (NFES) based at the National Interagency Fire
Center in Boise, Idaho.361 These include “Firefighter Training”
(S-130, 2003), “Look Up, Look Down, Look Around” (PMS 427,
1992),349,350 “Lookouts, Communications, Escape Routes and
Safety Zones (LCES)” (S-134, 2003), “Fire Operations in the
Wildland-Urban Interface” (S-215, 2003), and “Lessons Learned:
Fatality Fire Case Studies” (PMS 490, 1998).354,355 The latter course
uses nine past fatality fires as a learning tool to help fire line
tactical decision makers avoid similar mistakes. It is worth noting
that some NFES publications are available online (www.nwcg
.gov). The WFSTAR (Wildland Fire Safety Training Annual
Refresher) website (www.nifc.gov/wfstar) is an excellent resource
for the latest information on wildland firefighter safety. The
Wildland Fire Staff Ride Library (www.fireleadership.gov/toolbox/
staffride/), developed by the National Wildfire Coordinating
Group, is also a highly useful source of information on past
firefighter fatality incidents.
There are also several CD-ROM–based training courses
available on fire line safety,37,480 fire behavior,481 and fire danger
rating.462 For additional information on introductory to
advanced wildland fire training courses available at the local
area, geographic area, and national levels in the U.S., visit the
Wildland Fire Training website (www.nationalfiretraining.net).
For national wildland fire training courses in Canada, visit the
website of the Canadian Interagency Forest Fire Centre
(www.ciffc.ca).
One of the initiatives of the U.S. National Wildland-Urban
Interface Fire Program was a firefighter safety program in the
WUI series. This training package, which includes three videos,
was developed for small community fire departments to address
the problems faced by structural and wildland firefighters when
fighting fires, especially those threatening structures in the
WUI.267 Copies can be ordered from Firewise Communities online
catalog.
The Wildland Fire Lessons Learned Center (www.wildfire
lessons.net) is a good source for information on almost all aspects
of wildland fire management, including an annotated reading list
and bibliography on wildland firefighter safety management.265
The Fire Research Institute library (www.fireresearchinstitute.org/),
which provides online search capability, is a good source of
scientific and technical wildland fire literature.222
Wildfire Today (www.wildfiretoday.com) and the Global Fire
CHAPTER 14  Wildland Fires: Dangers and Survival
Monitoring Center (www.fire.uni-freiburg.de) are popular web-
sites for the latest news in wildland fire management. Wildland
Fire: Home of the Wildland Firefighter (www.wildlandfire.com)
is another unique website serving the global wildland fire
community.
CONCLUDING REMARKS
Fire suppression efforts in the late 1800s and early 1900s were
largely ineffective because of limited access, absence of trained
firefighting organizations, and lack of a fire detection network.
During these times, many residents and numerous firefighters
died in wildland fires in the United States and Canada. In the
recent past, firefighters were more vulnerable to injuries and
fatalities from wildfires than was the general public. At present,
with many people living and seeking recreation in wildlands, the
odds for serious fire encounters are shifting toward an inexperi-
enced populace. Large property losses and direct injuries are
being reported in increasing numbers in the WUI. It has now
become not a question of “if” a wildfire will come or it “can’t
happen here,” but rather “when and where” the next major WUI
conflagration will take place (Figure 14-42). Emergency medical
personnel will probably have increasing exposure to wildland
fires in the future and will need to know more about fire-related
injuries, fire safety, and fire survival.
Many wildland firefighters are in turn feeling compelled to
save homes,197 in part as a result of the expectations placed on
them by the general public and homeowners in particular,
coupled with a culture derived from more than a century of
wildland fire suppression.61 Not surprisingly, many wildland fire-
fighter fatalities in recent years have been associated with WUI
incidents (e.g., the 2003 Cedar Fire in southern California).107
Given even the best practices,290 there is an overwhelming need
to impress on rural homeowners that no home is worth a fire-
fighter’s life.
Although wildland fires have not yet posed a serious threat
to backcountry recreationists in the United States to any appre-
ciable degree, the prospect for such confrontations is growing.
For example, two recreationists were involved in entrapment and
burnover associated with the major run of the 2001 Thirtymile
Fire.186 Fire investigators concluded they would probably not
FIGURE 14-42  The Strawberry Hill Fire near Kamloops, British Colum-
bia, about 10 minutes after ignition on August 1, 2003. The white
plume in the background is the convection column associated with the
McLure Fire. Although it does seem theoretically possible to com-
pletely eliminate the threat of conflagrations, this is unlikely to happen.
Even with the most highly effective fire prevention, fuel management,
and fire suppression programs, the likelihood that members of the
general public will encounter a high-intensity wildfire event at some
point in their lives is gradually increasing as long as they continue to
live, recreate, and work in fire-prone environments. Coexistence or
living with fire involves taking a proactive stance, including being
prepared for when wildfire arrives in a community. (Photo by D.
Christie.)
317
 have survived, although they did sustain minor injuries, had they
not joined up with the firefighters just before (~14 minutes) their
location was overrun.498
Many years of practical experience with wildland fires allow
us to conclude the following:
• Many indicators show that financial support and programs that
address only emergency responses to wildfires will result in
more damaging and expensive wildfire emergencies in the
future. Public policies and public education that link sustain-
able land use practices with emergency preparedness are
likely to be most successful in the long run.
• Residential shifts to the WUI will increase exposures to life-
threatening situations.
• Expanded use of fire in managing national parks and wilder-
ness areas will increase the likelihood that backcountry rec-
reationists will encounter free-burning fires.
• By and large, the general public tends to underestimate exist-
ing fire hazards and for the most part is usually not experi-
enced in avoiding wildfire threats.
• In some cases, attempted fire exclusion practices have con-
tributed to development of hazardous wildland fuel situations
in terms of quantity and continuity, setting the stage for
extreme fire behavior in some plant communities. The national
BURNS, FIRE, AND RADIATION
ecosystem health issue has compounded this problem by
producing vast expanses of dead and dying forests, increasing
the threat to people from fast-moving, high-intensity fires.
• Knowledge of fire behavior principles and survival guidelines
will prepare people to take appropriate preventive measures
in threatening situations.
The general public must share responsibility with suppression
organizations to minimize fire hazards created by humans. Care
with fire, proper cleanup of debris, fuel reduction efforts on
wildland property, fire-safe construction guidelines, and applica-
tion of survival skills will minimize fire threats. Such precautions
should become as commonplace in the wildland environment as
smoke alarms and fire extinguishers have become in urban set-
tings. Every community should undertake, as part of the risk
management process associated with the wildfire threat, an
PART 3
assessment of their fire environment in terms of potential fire
behavior. A good example of this type of analysis has been
completed for over a hundred communities in northern Saskatch-
ewan, Canada.165
Unfortunately, major disasters are often required for funda-
mental changes to occur. Disasters do not simply happen.488
They usually involve an “incubation period” that involves “the
accumulation of an unnoticed set of events that are at odds with
the accepted beliefs about hazards and the norms for their
avoidance.”487
Wildland fire suppression agencies will continue to provide
fast, safe, and energetic initial attack responses to protect human
life, property, and natural resources.14 Many fires will start and
burn under environmental conditions that permit their control at
a very small size. However, in certain situations (e.g., critically
dry fuels or strong winds), some fires9,32,33 will defy control until
burning conditions ameliorate. The major runs of the 1985 Palm
Coast Fire in south Florida2 and the Millers Reach Fire that
occurred near Anchorage, Alaska, on June 2, 1996,132 are good
examples of this type of fire behavior and associated suppression
problems. No radically new concept of fire suppression for stop-
ping the head of a hot, fast-running wildland fire should be
anticipated in the future.152 In An Introduction to Fire Dynamics,
Drysdale181 states, “Further major advances in combating wildfire
are unlikely to be achieved simply by continued application of
the traditional methods. What is required is a more fundamental
approach which can be applied at the design stage. . . . Such an
approach requires a detailed understanding of fire behavior.”
Strategic fuel management and land use planning could
reduce the total number and size of wildfire occurrences, as well
as influence their geographic distribution, and thereby mitigate
the impacts of too much of the “wrong kind of fire.”400 Science-
based-only solutions221 are considered insufficient; effective wild-
land fire policy must integrate ethics, economics, aesthetics, and
values.400 Furthermore, as Cheney122 points out, if we are to
encourage people to live safely in the wildland environments,
318
they need to be fully aware of the full potential for fire behavior
and what can be done to protect themselves and their assets.
“They must be individually persuaded to recognize what consti-
tutes the fuel for a forest fire and be convinced that, since they
own the fuel, they also own the fire it produces and are respon-
sible for the damage they or others nearby incur.”122 The public
and fire management agencies themselves must fully appreciate
that fuel management is not a panacea for conflagration miti­
gation, but rather a prerequisite to aid in successful fire sup­
pression.20,75,126,490 An excellent source of information on fuel
management is the USDA Forest Service Fuels Synthesis Project
(www.fs.fed.us/rm/pubs/rmrs_rn019.pdf).499
After the 1983 Ash Wednesday fires in southeastern Australia,
the editor of Australian Forestry commented on what could be
learned from studying such wildland fire disasters184:
Advances in technical areas will be of great value. It would be valuable
too to make comparable advances in the areas of public policy. People
forget, community attitudes change and policies erode. Perhaps one of
the greatest challenges, given the realities of southeastern Australia, is to
learn how to ensure the permanence of public interest policies where
permanence is required.
Twenty years later and following the bushfires that engulfed
Canberra, Australia, in 2003 (https://en.wikipedia.org/wiki/2003
_Canberra_bushfires), Cheney124 offered some advice on this
matter:
. . . I believe that there is strong evidence that the policies and institu-
tional arrangements of organizations, both those directly related to fire
management and those completely unrelated, will have the result of
perpetuating major fire disasters. I also believe that the legal framework
in which we’re working is one that [militates against] individuals taking
responsibility for their own actions and lifestyle choices. In this country
wildfire is inevitable but the impact of disastrous fires can be reduced.
But this will only be achieved if policies focus on the physics of fire
spread and foster a climate of awareness where fuel reduction, from the
backyard to beyond, is encouraged and supported by legislation.
At the end of the day, though, what can an individual do to
improve matters when it comes to living with fire? Kaufmann and
colleagues249 offer some very practical advice:
• Get involved in a community-based conservation group
working on local landscape restoration projects.
• Educate yourself about the role of fire in your local
ecosystems.
• Provide feedback on agency land management plans.
• Consult with regional experts on how to safely reintroduce
fire on to your land holding.
• Participate in local workshops (e.g., Firewise Communities) to
learn how to treat fuels around your home and create defen-
sible space.
Their final suggestion: “Start simply. But start.” Local forestry
and fire management agencies are more than willing to offer
technical advice and information. Just give them a call to get
started today, before wildfire comes knocking!191
ACKNOWLEDGMENTS
The authors hereby thank the following individuals for their
candid comments on various sections of the chapter: M. Acker-
man, A. Beaver, K. Brauneis, B. Butler, D. Campbell, P. Cheney,
J. Cohen, M. DeGrosky, T. Greer, M. Heathcott, J. Leonard, T.
Leuschen, S. McCaffrey, J. McLevin, B. Mottus, P. Murphy, S.
Otway, G. Proulx, T. Putnam, D. Quintilio, A. Rhodes, B. Sharkey,
R. Smith, D. Thomas, R. Thorburn, K. Weick, and T. Zimmerman.
The assistance of the following individuals in the preparation
of this chapter is also duly noted: B. Bereska, M. Campbell, M.
Cruz, M. Erickson, J. Handmer, T. Petrilli, G. Pearce, and O.
Spencer.
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318.e9
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BURNS, FIRE, AND RADIATION
PART 3
318.e10
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 CHAPTER 15 
Emergency Care of the
Burned Patient
MICHAEL J. MOSIER, ROBERT L. SHERIDAN, AND DAVID M. HEIMBACH
EPIDEMIOLOGY
In 2013, approximately 486,000 individuals in the United States
were burned seriously enough to seek medical care, and approxi-
mately 40,000 of such burned patients annually require hospital-
ization.73,74 These numbers represent a continued downward
trend in burn injuries. Number of deaths attributable to burns
decreased from 12,000 in 1979 to 3240 in 2013. More than 60%
of U.S. acute hospitalizations for burn injury were patients admit-
ted to 128 burn centers.6 Burn centers average more than 200
annual admissions for burn injury and skin disorders requiring
similar treatment. The other 4500 U.S. acute care hospitals
average less than three burn admissions per year. In the mid-
1970s, patients with more than 20% total body surface area
(TBSA) burns often died.75 Currently, patients with 80% TBSA
burns can survive, although often with permanent impairments.
Although treatment facilities have greatly reduced death rates
from similar-sized burns, the marked decrease in burn incidence
results from better prevention (e.g., burn education, engineering
improvements, widespread use of smoke detectors in public and
private dwellings). It has been estimated that more than 90% of
burns are preventable, and that most are caused by carelessness
or ignorance.
Significant contributions to reduced burn mortality and mor-
bidity are less likely to come from medical scientists than from
improved engineering design and more successful programs to
teach burn prevention to the public.62,66 Legislation to promote
smoke detectors and interior sprinklers saves lives. Developed-
world advances in burn prevention can be applied in the devel-
oping world, where burn rates remain stubbornly high. Steps to
further reduce burn rates in limited-resource settings include
educational campaigns to recognize burn hazards (e.g., keep
children from playing around open flames, do not leave hot
liquids or heaters unattended). School-based burn prevention
programs in rural Malawi (i.e., Africa Burn Relief Program,
www.africaburnrelief.org) and community education programs in
South Africa that focused on safe use of kerosene in the home
are yielding results.89 Effective hazard reduction is neither difficult
nor expensive. Simple steps work, such as encouraging stable
and raised cooking surfaces, separating cooking areas from play
areas, and storing fuels in well-marked, childproof containers.45
As with other forms of trauma, burns frequently affect children
and young adults. Hospital expenses and social costs related to
time away from work or school are staggering. Although most
burns are limited in extent, a significant burn of the hand or foot
may prevent a manual laborer from working for a year or longer
and may permanently prevent return to a former activity. Out-
comes for the burned patient are related to severity of injury,
individual physical characteristics of the patient, quality of treat-
ment of the acute burn, and motivation toward rehabilitation.
Most burns patients seen by U.S. physicians do so by present-
ing to an emergency department (ED). In the ED, judgment in
triage, care plan for small burns, and initial management for
major burns can influence patient survival and eventual cosmetic
and functional results. Because most patients are young (about
one-third are children), they will live with consequences of acute
treatment for an average of 50 years.
Burns are difficult to manage even under ideal conditions. In
austere settings, small burns can be exquisitely painful and debili-
tating. Larger and deeper injuries can be catastrophic. Burn
programs are advanced in most developed countries, with effec-
tive verification programs that ensure a baseline quality of care
and uniform patient experience. This is not the case in most
developing countries, where burns tend to be cohorted with
general surgical patients. In this setting, burns are generally
treated in a nonsurgical manner, with periodic dressing changes
until necrotic material has sloughed. Critical care is less well
developed and integrated into burn care. Sepsis is more common.
Decisions made on initial patient evaluation require answers
to the algorithm shown in Figure 15-1. This chapter describes
first-responder care for major burns, guides assessment of burn
severity and initial management of serious burns, and provides
initial treatment plans for minor burns.
PHYSIOLOGY
For burns other than chemical burns, primary injury occurs
during the period of heat contact. Coagulation necrosis takes
place within cells, and collagen is denatured within dermis.
Blood vessels can be completely destroyed or endothelium
damaged severely enough to cause clotting. This leads to isch-
emic necrosis of remaining viable cells. Burn wounds are not
static. Surrounding the zone of coagulation is a zone of capillary
and small-vessel stasis. Blood cells collect (red cells form into
rouleaux; platelets and white cells form aggregates) and circula-
tion becomes stagnant. In the acute phase (hours to days), the
ultimate fate of the burn wound depends on resolution or pro-
gression of this zone of stasis. Cells and tissue stroma release
mediators (e.g., histamine, serotonin, prostaglandin derivatives,
complement cascade components) and initiate an inflammatory
response. In patients with burns involving less than 10% TBSA,
actions of these mediators are generally limited to the burn site.
Capillary permeability increases, neutrophils marginate, and addi-
tional inflammatory cells (e.g., monocytes, macrophages) are
attracted by chemotaxis to the site of injury and initiate healing.
As burns approach 20% TBSA, responses becomes systemic.
The capillary leak that permits loss of fluid and protein from the
intravascular space into extravascular space becomes general-
ized. Cardiac output falls as a result of markedly increased
peripheral resistance, decreased intravascular fluid volume from
capillary leak, and accompanying increase in blood viscosity.
Decreased blood volume and cardiac output, accompanied by
an intense sympathetic response, lead to decreased perfusion to
skin and viscera. Decreased blood flow to skin can convert the
zone of stasis to one of coagulation. This increases the depth of
burn injury. Capillary leak and depressed cardiac output lead to
depressed central nervous system (CNS) function. In extreme
cases, severe cardiac depression can lead to cardiac failure in
healthy patients or myocardial infarction in patients with preexist-
ing coronary artery disease. The first signs of CNS change are
restlessness, followed by lethargy and finally coma. Without
adequate resuscitation, burns of 30% TBSA frequently lead to
acute renal failure. In a patient with a severe burn, this almost
invariably leads to a fatal outcome.
Cardiovascular changes begin immediately after a burn. The
extent of these changes depends on burn size and to a lesser
extent on burn depth. Most patients with uncomplicated burns
of less than 15% TBSA can undergo oral fluid resuscitation with
salt-containing solution. As burn extent exceeds 20% TBSA,
319
 Burn

<5% TBSA >5% TBSA

Superficial Burn covering Smoke inhalation Smoke inhalation

or >50% of hand without burn with burn
deep but or foot Burn ≤20% TBSA Burn >20% TBSA
very small Eye involvement Electrical burn

FIGURE 15-3  Tar burn of the hand. (Courtesy Paul S. Auerbach, MD.)
First aid First aid Ground transfer Immediate
See MD if See MD by to community transfer to
not healed day 2 hospital burn center
in 3-5 days public hot-water heaters to maximum temperatures well below
60° C (140° F).
FIGURE 15-1  Algorithm for decision making at the scene. TBSA, Total Scald burns from grease or hot oil are generally deep partial
body surface area. thickness or full thickness. Cooking oil and grease, when hot
enough to use for cooking, may be approximately 204.4° C
(400° F). Tar and asphalt burns are a special kind of scald. The
BURNS, FIRE, AND RADIATION

“mother pot” on the back of a roofing truck maintains tar at a

massive shifts of fluid and electrolytes occur from intravascular
into extravascular (i.e., extracellular) spaces. Fluid shifts begin to
reverse during the second postburn day, but normal extracellular
volume is not completely restored until 7 to 10 days after the
burn. Unless intravascular volume is repleted, classic hypovole-
mic shock occurs. Insufficient fluid resuscitation can lead to
irreversible acute tubular necrosis and renal failure. Untreated
patients die of cardiovascular collapse.
TYPES OF BURNS
SCALD BURNS
In civilian practice, scalds, usually caused by hot water, are the
PART 3
temperature of 204.4° to 260° C (400° to 500° F). Burns caused
by tar directly from the mother pot are invariably full thickness.
After tar is spread on the roof, its temperature has decreased
enough that most burns are deep partial thickness (Figure 15-3).
The initial evaluator cannot usually examine these burns because
of adherent tar. Remove tar by applying a petroleum-based oint-
ment (e.g., Vaseline) under a dressing. In the field, mayonnaise
may serve this purpose (Figure 15-4). Remove the dressing and
reapply ointment every 2 to 4 hours until the tar has dissolved.
Only then can the extent of injury and depth of burn be accu-
rately estimated.43,104
FLAME BURNS

most common cause of burns. Water at 60° C (140° F) creates a
deep partial-thickness or full-thickness burn in 3 seconds. At
68.9° C (156° F), the same burn occurs in 1 second. Freshly
brewed coffee from an automatic percolator is generally approxi-
mately 82° C (179.6° F). Boiling water always causes deep burns.
Soups and sauces, which are thicker in consistency, remain in
contact longer with skin and often cause deep burns. Exposed
areas typically tend to be burned less deeply than areas covered
with thin clothing. Clothing retains heat and keeps liquid in
contact with skin for a longer time.
Immersion scalds are deep and severe burns21,31,105 (Figure
15-2). Although water may be cooler than with a spill scald,
duration of contact is longer. These burns frequently occur in
small children or older adult patients with thin skin. Conse-
quently, many states have passed legislation to set home and
Flame burns are the next most common burn injuries after scalds.
Although injuries in house fires have decreased with the advent
of smoke detectors, a significant number of burn injuries still
result from careless smoking, improper use of flammable liquids,
automobile accidents, and clothing ignited from stoves or space
heaters. Patients whose bedding or clothes have been on fire
rarely escape without full-thickness burns. Outdoor misadven-
tures result from spilled hot water while cooking, fuel fires from
cooking stoves and lanterns, fabric fire (e.g., taking lanterns into
tents), smoking in a sleeping bag, tripping and falling into a
campfire, and application of accelerants (e.g., gasoline, charcoal
lighter fluid) to wood or charcoal fires. Most accelerants, whether
gasoline, kerosene, propane, or diesel, have ignition tempera-
tures of 210° to 280° C (410° to 536° F) and cause rapid tissue
injury and full-thickness burns.

FIGURE 15-2  Immersion scald burns are often quite deep. Note pop-
liteal flexor sparing, signifying a tightly flexed position at burning. FIGURE 15-4  Mayonnaise used to dissolve tar off a hand burn.
(Courtesy Rob Sheridan, MD.) (Courtesy Paul S. Auerbach, MD.)

320

FLASH BURNS
Flash burns are next in frequency after scald and flame burns.
Explosions of natural gas, propane, gasoline, and other flam-
mable liquids cause intense heat for a very brief time. Typically,
unignited clothing protects skin from flash burns. Flash burns
generally have a distribution covering all exposed skin, with the
deepest burn areas facing the source of ignition. Flash burns are
partial thickness, with depth dependent on amount and type of
fuel that ignited. Although such burns generally heal without
requiring extensive skin grafts, they may be very large and associ-
ated with significant thermal damage to the upper airway.
CONTACT BURNS
Contact burns result from direct contact with hot materials (e.g.,
metals, plastic, glass, hot coals and rocks). Such burns are usually
limited in extent but are deep. Patients involved in industrial
accidents typically have severe contact burns and crush injuries,
because these accidents are often caused by direct contact with
presses or hot, heavy objects. Toddlers may receive contact burns
by touching wood-burning stoves. They most often receive deep
palmar burns because the child falls with hands outstretched
against the stove. Contact burns, especially in unconscious
persons (e.g., narcotic- or alcohol-intoxicated person falling
against a radiator) or individuals dealing with molten materials,
are frequently fourth degree.19,59,92 In wilderness settings, the most
common contact burns are from hot coals, which are often as
hot as 537.8° C (1000° F). These burns may occur when intoxi-
cated campers dance around and then into campfires, architects
of “river saunas” mishandle hot rocks, children fall into fires, and
beach walkers sustain deep burns when coals are buried in sand
overnight. Coals buried in “extinguished” campfires can remain
dangerously hot for days. Falling into such ashes can cause very
deep burns (Figure 15-5). Even though injured areas may be
small, they can be deep and debilitating when the hiker must
walk a considerable distance on burned feet.27
ELECTRICAL BURNS
Electrical burns are thermal burns from very-high-intensity heat.
As electrical energy encounters body tissue resistance, it is con-
verted to heat. This occurs in direct proportion to current’s
amperage and electrical resistance of body parts through which
it passes. The smaller the body part through which electricity
passes, the more intense the heat and the less it is dissipated.
Therefore, fingers, hands, forearms, feet, and lower legs are
frequently totally destroyed, whereas larger-volume areas (e.g.,
trunk) usually dissipate the current sufficiently to prevent exten-
sive damage to viscera, unless the contact point is on the
FIGURE 15-5  Coals buried in extinguished campfires will stay danger-
ously hot for days. This toddler stumbled into the ashes of a fire
extinguished 24 hours earlier. (Courtesy Rob Sheridan, MD.)
CHAPTER 15  Emergency Care of the Burned Patient
FIGURE 15-6  This patient suffered deep localized burns to fingers
from a 220-volt power source. Electricity passing through smaller body
parts generates more intense heat, so less is dissipated. Fingers,
hands, forearms, feet, and lower legs are frequently destroyed. (Cour-
tesy Rob Sheridan, MD.)
abdomen or chest (Figure 15-6). Although cutaneous manifesta-
tions may appear limited, massive underlying tissue destruction
may be present because muscle, nerves, blood vessels, and
bones can be burned beyond recovery.18,36,37,77
Arc burns occur when current takes the most direct path rather
than the path of least resistance. Arcs create extremely high
temperatures. These deep and destructive wounds occur at joints
that are in close apposition at the time of injury. Most common
are burns from forearm to arm (i.e., when the elbow is flexed)
and from arm to axilla (i.e., current passes from the upper
extremity to trunk) if the shoulder was adducted.
Electrical burns cause a particular set of other injuries and
complications that must be considered during initial evaluation.
Injuries related to a fall are common. Electrical exposure can
cause intense muscle contractions that lead to falls or cause
fractures of lumbar vertebrae, humerus, or femur, and dislocate
shoulders or hips.
Electrical cardiac damage presents with symptoms similar to
those of a myocardial contusion or infarction. The conduction
system may be deranged. There can be rupture of a heart wall
or of a papillary muscle leading to sudden valvular incompetence
and refractory heart failure. Household current (in the U.S., 110
volts) typically causes no damage or induces ventricular fibrilla-
tion. Alternating current (AC) is more likely to induce fibrillation
than is direct current (DC). After exposure to shocks of 110 to
220 volts, if no cardiac abnormalities are present when a patient
is first evaluated, it is very unlikely that cardiac manifestations
will develop.
The nervous system is particularly sensitive to electricity. The
most severe brain damage occurs when current passes through
the head, but spinal cord damage is possible any time current
passes from one side of the body to the other.48,53 Myelin-
producing cells are susceptible. Devastating transverse myelitis
may develop days or weeks after the primary event. Conduction
remains normal through existing myelin, but as myelin ages, it
is not replaced and conduction stops. Peripheral nerves are fre-
quently damaged and may demonstrate severe permanent func-
tional impairment.23,33 Every patient with an electrical injury must
have a thorough neurologic examination as part of initial assess-
ment. Myoglobinuria is a frequent accompaniment of severe
electrical burns (Figure 15-7). Disruption of muscle cells releases
cell fragments and myoglobin into circulation, from where it is
filtered by the kidneys. If untreated, this can lead to permanent
renal failure. Lightning strike is discussed in Chapter 5, and
reviews are available.24,25,28,29,60,77
CHEMICAL BURNS
Chemical burns, usually caused by strong acids or alkalis, most
often result from industrial accidents, use of domestic drain
321
 or neutralized. A full-thickness chemical burn may appear decep-
tively superficial (e.g., only a mild, brownish surface discolor-
ation). Skin may appear intact during the first few days after
exposure and then begin to slough spontaneously. Unless care-
givers can be absolutely certain, chemical burns should be con-
sidered deep partial thickness or full thickness until proved
otherwise.

CLINICAL PRESENTATION
Cutaneous burns are caused by application of heat or caustic
chemicals to skin. When heat is applied to skin, depth of injury
is proportional to temperature applied, duration of contact, and
skin thickness. Burn severity is related to burn size and depth
and body part involved.

ESTIMATION OF BURN SIZE

Burns are a highly quantifiable form of trauma. Burn size in
proportion to the patient’s TBSA is the most important feature to
predict mortality, need for specialized care, and expected com-
plications. Treatment plans, including initial resuscitation and
subsequent nutritional requirements, are derived directly from
BURNS, FIRE, AND RADIATION

FIGURE 15-7  Evidence of myoglobinuria with “cola-colored” urine.
Myoglobin pigment released from damaged muscle by electrical
trauma will cause renal failure if not cleared. Administering intravenous
crystalloid to an end point of 2 to 3 cc/kg/hr urine output reduces risk
of renal failure. Intravenous bicarbonate (1 mEq/kg) may enhance
clearance of these pigments. (Courtesy Rob Sheridan, MD.)
cleaners, improper use of harsh solvents, and assaults.26,38,67,70,84,87,94
Chemical burns cause progressive damage until chemicals are
inactivated by reaction with tissue or by dilution (e.g., flushing
with water). Typically, acid burns tend to be more self-limited
PART 3
burn size.
A reasonably accurate estimate of burn size is provided by
the “rule of nines.” In adults, each upper extremity accounts for
9% TBSA, each lower extremity accounts for 18%, anterior and
posterior trunk each account for 18%, head and neck account
for 9%, and perineum accounts for 1% (Figure 15-8). Although
the rule of nines is rapid and effective, a number of more precise
charts have been developed. To establish TBSA, draw a diagram
of the burn on a chart. Guided by accompanying TBSA estimates,
create a relatively precise calculation of burned area. Children
younger than 4 years have much larger heads and smaller thighs
in proportion to body size than do adults. In an infant, the head
accounts for approximately 18% of TBSA. Body proportions do
not fully reach adult percentages until adolescence. To further
increase accuracy in burn size estimation, especially when burns

than are alkali burns. Acid tends to “tan” skin (i.e., as leather is are in scattered body areas, the observer might calculate the
tanned). This creates an impermeable barrier that limits further unburned areas on a separate diagram. If calculations of burned
acid penetration. In contrast, alkalis combine with cutaneous and unburned areas do not add up to 100%, begin again with a
lipids and saponify skin. This continues until they are removed new diagram to recalculate burned areas. For smaller burns,

9%

9% 9%
1% 18%
9%
9%
9%

A 18%

9%
9%
18%
13.5%
18%

1%

13.5% 9%
18%

B
FIGURE 15-8  “Rule of nines” used for estimating burned surface area. A, Adult. B, Infant.

322
 CHAPTER 15  Emergency Care of the Burned Patient
Epidermis First degree

Partial
Dermis thickness

Subcutaneous
tissue Full
thickness
Muscle
Bone

FIGURE 15-9  Skin anatomy.

accurate assessment of burn size can be made by using the they become erythematous, quite painful, and tender. Erythema
patient’s hand. Skin coverage on the hand amounts to 2.5% TBSA. and pain subside over 2 to 3 days. By day 4, injured epithelium
The dorsal surface accounts for 1%, palmar surface for 1%, and desquamates (“peels.”)
vertical surface for 0.5% (including the fingers).
Superficial Partial-Thickness Burns
Superficial partial-thickness burns include upper layers of dermis
DEPTH OF BURN (Figure 15-10). They characteristically form blisters with fluid
Understanding burn depth requires awareness of skin anatomy collecting at the interface of epidermis and dermis. Blistering may
(Figure 15-9). Epidermis is an intensely active layer of epithelial not occur for some hours after injury. Burns initially thought to
cells under layers of dead keratinized cells. It is superficial to be first degree may therefore be diagnosed as superficial partial
skin’s active structural framework, the dermis. Although metaboli- thickness by day 2. When blisters are removed, the wound is
cally very active, dermis has no regenerative capacity. Epithelial pink and wet, and it is quite painful when contacted by currents
cells must cover the dermal surface before the burn is healed. of air. The wound is hypersensitive to touch and blanches with
Skin appendages (i.e., hair follicles, sebaceous glands, and sweat pressure. Blood flow to dermis is increased compared with that
glands) all contain an epithelial cell lining. When surface epider- of normal skin. If infection does not occur, superficial partial-
mis has been killed, epithelial covering must take place from thickness burns heal spontaneously within 3 weeks without
outward grown of epithelial cells lining skin appendages. As functional impairment. They rarely cause hypertrophic scarring,
these cells reach the surface, they spread laterally and create a
new epithelial surface. As a burn extends deeper into dermis,
fewer and fewer appendages remain, and epithelial remnants
must travel farther to produce a new surface covering, sometimes
taking many weeks to produce coverage. When burns extend
beyond the deepest layer of skin appendages, wounds can heal
only by epithelial ingrowth from the edges, by wound contrac-
tion, or by surgical transplantation of skin from a different site.
Skin thickness varies with age, gender, and body part.
Although thickness of living epidermis is relatively constant,
keratinized epidermal cells can reach a height of 5 mm (0.2 inch)
on palmar and plantar surfaces. Dermal thickness can vary from
less than 1 mm (0.04 inch) on eyelids and genitalia to more than
5 mm (0.2 inch) on the posterior trunk. Although proportional
skin thickness in each body area is similar in children, infant skin
thickness in each specific area may be less than one-half that of
adult skin. Skin does not reach adult thickness until adolescence.
In patients older than 50 years, gradual dermal atrophy causes
skin to thin significantly.
Burn treatment depends on knowledge of burn depth. Burns
are classified by increasing depth as first degree, superficial
partial thickness, deep partial thickness, full thickness, and fourth
degree. These descriptions appear to separate burns into clearly
defined categories, but many burns have a mixture of character-
istics that limit diagnostic precision. Research is being conducted
to devise instruments to allow more precise measurements of
depth of injury.
First-Degree Burns
First-degree burns (e.g., mild sunburn) involve only epidermis. FIGURE 15-10  Superficial partial-thickness burn. Note the pink color
First-degree burns do not blister. Because of dermal vasodilation, and moist surface.

323

FIGURE 15-11  Deep partial-thickness burn. Note the cherry-red color.
but in pigmented individuals, healed burns may never completely
match the color of surrounding normal skin.
BURNS, FIRE, AND RADIATION
Deep Partial-Thickness Burns
Deep partial-thickness burns also blister, but the wound surface
is typically a mottled pink and white color immediately after
injury (Figure 15-11). Alternatively, burned dermis may be dry,
with a cherry-red color. The patient complains of discomfort
rather than frank pain. When pressure is applied to the burn,
capillary refill returns slowly, if at all. The wound is often less
sensitive to touch than is surrounding normal skin. By the second
day, the wound may be white and is usually fairly dry. If infec-
tion is prevented, such burns heal in 3 to 9 weeks, but invariably
do so with considerable scar formation. Unless active physical
therapy is continued throughout the healing process, joint func-
tion may be impaired and hypertrophic scarring, particularly
in children and individuals with pigmented skin, becomes
PART 3
inevitable.
Full-Thickness Burns
Full-thickness burns involve all layers of dermis and can heal
only by wound contracture, epithelialization from the wound
margin, or skin grafting (Figure 15-12). Full-thickness burns are
classically described as leathery, firm, insensitive to light touch
and pinprick, and depressed compared with the adjoining normal
skin. Difference in depth between a deep partial-thickness burn
and a full-thickness burn may be less than 1 mm (0.04 inch).
Full-thickness burns are easily misdiagnosed as deep partial-
thickness burns, because both have many of the same clinical
findings. Both may be mottled in appearance. They rarely blanch
with pressure and may have a dry, white appearance. Burns may
FIGURE 15-12  Full-thickness burn. Note the thick, leathery, white
eschar.
324
be translucent with clotted vessels visible in the depths. Some
full-thickness burns, particularly immersion scalds, have a red
appearance and can be confused with superficial partial-thickness
burns. However, these red, full-thickness burns do not blanch
with pressure. Full-thickness burns develop a classic burn eschar.
An eschar represents structurally intact but dead and denatured
dermis that, over days to weeks, separates spontaneously from
underlying viable tissue.
Fourth-Degree Burns
Fourth-degree burns involve not only all skin layers but also
subcutaneous fat and deeper structures. These burns almost
always have a charred appearance. Frequently, only the cause
of the burn gives a clue to the amount of underlying tissue
destruction.
TREATMENT
CARE AT THE SCENE
Flame Burns
The first responder must remove the injured person from the
source of heat. Because of potential dangers of smoke inhalation
in closed areas, rescuers in a fire must take extreme caution not
to become victims. Persons with burning clothing should be
prevented from running and should be made to lie down (i.e.,
to keep flames and smoke away from the face). If water is not
immediately available, flames can be smothered with a coat or
blanket. If nothing is available to douse or cover flames, the
victim should be rolled slowly on the ground. Once burning has
stopped, clothing should be removed. Some fabrics will continue
to smolder, and synthetic fabrics may melt and leave a hot adher-
ent residue on the victim that will continue thermal injury. Even
flame-retardant cloth burns or smolders when temperatures are
sufficiently high (Figure 15-13).
Scalds and Grease Burns
Remove the victim of a scald or grease burn from the source of
heat. Any wet clothing should be removed, because fabric retains
moist heat and may continue to burn skin that is in contact with
hot material. Accidents resulting from cooking indoors with
grease are particularly hazardous. The startle response to a grease
splatter may cause the victim to drop a pan of grease onto the
fire and so ignite a kitchen fire that can rapidly become a dwell-
ing fire.
Airway
Once flames are extinguished, direct primary attention to the
airway. Any person rescued from a closed space or involved in
a smoky fire should be considered at risk for smoke inhalation
FIGURE 15-13  Even flame-retardant clothing will smolder if tempera-
tures are sufficiently high. It is important to remove burning clothing
promptly while protecting providers from injury. (Courtesy Rob
Sheridan, MD.)
injury. If supplemental oxygen is not available, a patient who is
coughing independently should be encouraged to continue to
do so. If the patient is unconscious or airway status is in ques-
tion, place the patient in a supine position and manipulate the
airway manually using the chin lift or jaw thrust maneuver. When
smoke inhalation is suspected, 100% oxygen should be admin-
istered by a tight-fitting mask. If the patient is unconscious or
airway is compromised, and if capability (i.e., equipment and
training) exists to insert an endotracheal tube, intubate the
patient’s trachea and attach the tube to a source of 100% oxygen.
If the airway is covered with a tight mask, rescuers must be aware
of significant danger of aspiration of gastric contents. Air forced
into the stomach causes distention and may produce vomiting.
Use of a mask prevents expulsion of emesis. The patient can
rapidly aspirate vomitus into the tracheobronchial tree. Never
leave an unconscious supine patient unattended. When possible,
elevate the head to minimize edema.
Other Injuries and Transport
Once an airway is secured, first responders should quickly assess
for other injuries and transport the patient to the nearest hospi-
tal.9,23,77 The patient should be kept flat and warm and should be
given nothing by mouth. After establishing an airway, further
resuscitation is unnecessary if the patient will arrive at a hospital
within 30 minutes. For transport, the patient should be wrapped
in a clean, dry sheet and blanket. Sterility is not required.
Cold Application
Smaller burns, particularly scalds, may be treated with immediate
application of cool water in hopes of limiting the extent of injury.
Application of cold water is controversial. Immediate cooling
decreases pain, possibly by decreasing thromboxane production.
After several minutes have passed, or after arrival in the ED,
further cooling is not likely to alter the pathologic process. Ice
water should not be used except on the smallest burns. Using
ice on larger burns can easily induce systemic hypothermia and
associated cutaneous vasoconstriction that can extend thermal
damage.
Swelling
During transport, remove constricting clothing and jewelry from
burned and distal parts. Local swelling begins almost immedi-
ately. Constricting objects increase swelling and can cause vas-
cular compromise. In addition, it is time-consuming to remove
tight jewelry after distal edema occurs (Figure 15-14).
Electrical Burns
Electrical burns are particularly dangerous to both patient and
rescuer. If patient remains in contact with the source of electric-
ity, the rescuer must avoid touching the patient until the current
can be turned off or wires cut with properly insulated wire
FIGURE 15-14  Jewelry, particularly rings, should be removed promptly
to protect distal circulation. Delay in removal often leads to the need
later to cut away rings. (Courtesy N. Stuart Harris, MD.)
cutters. Once the patient is removed from the source of current,
CHAPTER 15  Emergency Care of the Burned Patient
airway, breathing, and circulation must be checked. Ventricular
fibrillation (VF) or cardiac standstill is a common accompaniment
to a major transthoracic current. If carotid or femoral pulses are
not palpable, institute cardiopulmonary resuscitation (CPR). If
pulses are present but the patient is apneic, mouth-to-mouth
resuscitation alone may be lifesaving. Continue CPR until a
cardiac monitor can be obtained, which will direct treatment for
cardiac standstill or VF. Defibrillate VF as soon as possible.
Follow advanced cardiac life support (ACLS) protocols for man-
agement of cardiac arrhythmias. Once an airway is established
and pulses return, make a careful search for associated life-
threatening injuries. Electrocuted patients frequently fall from
heights and may have serious head or neck injuries. Intense
tetanic muscle contractions associated with electrocution may
fracture vertebrae or cause major joint dislocations. Until frac-
tures can be ruled out, patients with high-voltage electrical inju-
ries should be treated with spinal precautions and splints, if
necessary.
Chemical Burns
Whenever possible, chemical burns should be thoroughly flushed
with copious amounts of water at the accident scene. Chemicals
will continue to burn until removed. Wash for 5 to 10 minutes
under a stream of running water to limit overall burn severity
and remove gross contamination. Remove any contaminated
clothing before moving the patient into the ambulance or ED.
Do not attempt to apply any specific neutralizing agent. Time
delay deepens the burn, and neutralizing agents may themselves
cause burns. The process of neutralizing offending agents fre-
quently generates heat. This adds thermal burn to an already
potentially serious chemical burn.
Hydrofluoric acid is commonly used as a cleaning agent in
the petroleum industry and for glass etching. As an acid, it causes
coagulation necrosis. Fluoride ions (negatively charged) chelate
positively charged ions (e.g., calcium and magnesium), which
causes an efflux of intracellular calcium and results in cellular
death.76 Fluoride ion is also a metabolic poison that inhibits
sodium-potassium adenosine triphosphatase (ATPase), allowing
efflux of potassium.61 Hydrofluoric acid burns are classified by
National Institutes of Health Division of Industrial Hygiene stan-
dards based on the solution’s concentration.108 Concentrations
above 50% cause immediate tissue destruction and pain. Con-
centrations of 20% to 50% create a burn that is apparent within
several hours of exposure. Exposures to concentrations less than
20% may take as long as 24 hours to become apparent. Systemic
symptoms of hypocalcemia or hypomagnesemia are usually
absent, although cardiac dysrhythmias may develop and, once
present, may be difficult to restore to a normal rhythm. QT pro-
longation is the most common abnormal electrocardiogram
(ECG) finding. The goal of treatment for hydrofluoric acid expo-
sure is to neutralize fluoride ion and prevent systemic toxicity.
After wounds are copiously irrigated, apply topical calcium glu-
conate gel as 3.5 g of 2.5% calcium gluconate mixed with 5 oz
of water-soluble lubricant applied to the wound four to six times
a day for 3 to 4 days.64 Pain relief with this approach is often
quite rapid. Return of pain is generally a sign to repeat a dressing
change.
Phosphorus can be found in both military and civilian settings
as an incendiary agent found in hand grenades, artillery shells,
fireworks, fertilizers, and some homemade explosives. White
phosphorus ignites in the presence of air and burns until it is
entirely oxidized or the oxygen source is removed (e.g., by
immersion in water). Irrigate such burns with large amounts of
water. Remove easily identifiable pieces of phosphorus, and
place moist dressings for patient transport. Use ultraviolet light
to identify embedded particles, which phosphoresce, in order
to improve removal. Hypocalcemia, hyperphosphatemia, and
cardiac arrhythmias have been reported.103
First Aid at the Scene for Smaller Burns
Not all burns need immediate medical attention. Burns less than
5% TBSA (excluding deep burns of face, hands, feet, perineum,
or circumferential extremity) can be treated successfully in
325
 austere settings if adequate first-aid supplies are available and
wound care is performed diligently. Except for very shallow
burns that heal within a few days, most burns should be seen
by a physician within 3 to 5 days after injury.
Wash burns thoroughly with ordinary, plain soap and water
and dry with a clean towel. The water used should be suitable
for drinking (e.g., disinfected), but it need not be sterile or
bottled. After gentle cleaning and removal of loose debris, any
obviously dead skin should be peeled off (which may be painful)
or trimmed with sharp manicure scissors (usually painless). Large
(>2.5 cm [1 inch]), thin, fluid-filled blisters should be drained and
dead skin trimmed to prevent potential closed-space infection.
Deep burns, as from a flame, are firm and leathery, usually do
not blister, and do not require immediate debridement. Many
medications are suitable to be placed on the wound before ban-
FIGURE 15-15  Contact burn from stepping on hot coals. Small, flat
daging. These generally have a viscous ointment base to prevent blisters do not require debridement.
dressings from sticking to the wound and often contain an
antibiotic(s). As long as there is no allergy to the contents of the
ointment, they should be useful for most second-degree burns.
Spread a thin layer of silver sulfadiazine cream or antibiotic/
antiseptic ointment (e.g., bacitracin) over the wound and wrap • The dressing should be relatively light and not bulky. It should
it in dry, clean gauze that need not be sterile. Fine gauze mem- not limit the patient’s ability to actively flex and extend all
branes impregnated with antiseptic ointments are useful as burned extremities and digits. Frequent flexion and extension
BURNS, FIRE, AND RADIATION

primary burn dressings in many cases. In austere settings, clean
cotton clothing can be used to improvise many effective burn
dressings. Clean, white cotton T-shirts can be used to good effect.
Oversize clean cotton socks can be used to reinforce dressings
on hands and feet. Simple dressings (i.e., topical cream, plain
gauze) are sufficient. Some patients prefer nonadherent dressings
(e.g., Telfa or Adaptic, the latter sometimes known as “greasy
gauze”), because they are less likely to stick to wounds during
dressing changes. The same effect can be achieved by soaking
(with water) a plain gauze dressing that appears stuck to wound,
waiting a few minutes, and then removing the dressing with
additional water if necessary. Other dressings (e.g., hydrogels,
silver-coated dressings, silicone gel sheets, calcium alginate)
designed to minimize frequency of dressing changes and promote
healing are available but not necessary. To stock first-aid kits,
PART 3
prevents burned skin from tightening and assists with pain
control and prevention of edema.
These principles are much more important than the choice of
topical agent to cover the burn. Commonly used topical agents
that might be carried in first-aid kits include antiseptic and anti-
biotic ointments and creams (e.g., bacitracin, double antibiotic
[Polysporin: polymyxin B, bacitracin], triple antibiotic [Neosporin:
bacitracin/gramicidin, neomycin, polymyxin B], silver sulfadia-
zine) and nonantibacterial ointments (e.g., Aquaphor, Vaseline,
A+D). Any of these agents is acceptable. Using a topical antimi-
crobial is not essential in early postburn care.
Technique of Burn Wound Debridement.  Small, intact
blisters do not need debridement (Figure 15-15). Blisters serve
as sterile biologic dressings to minimize desiccation and pain.
Protect intact blisters from trauma, and observe every few hours

we recommend simple antiseptic/antibiotic ointments (e.g., silver to ensure that the blister has not ruptured. If the blister opens,
sulfadiazine or bacitracin) and plain gauze dressings rather than debridement is usually recommended because leaking blister
“specialty” dressings because they are simple, less expensive, and fluid may lead to crusting that can effectively “seal” the wound
effective. A patient may prefer one dressing over another for over entrapped bacteria, leading to a closed-space infection
various reasons, but no dressing has been shown conclusively (Figure 15-16).
to accelerate burn wound healing. First-aid kits should be stocked Blister debridement is essentially painless as long as blistered
with general-use supplies that are easy to replenish. skin is cut and not peeled or torn. The burn should be washed
Effective burn dressings can be complex and difficult to apply. with soap and water. Forceps are used to grasp blistered skin
Wound area mobility must be actively maintained. Every effort and small (e.g., manicure) scissors can be used to remove the
should be made to avoid dependent positioning, especially when blister roof (Figure 15-17). Remove as much blistered skin as
patient is resting. Focal edema in a small burn wound can be possible, and leave a uniform surface that can be treated with a
painful and alarming and should be prevented with extremity topical agent (Figure 15-18). There should no bleeding during
elevation and active range-of-motion exercises several times a this procedure. To ensure that the procedure will be painless,
day. Wound care should be performed once a day if the outer stabilize the body part to be debrided against a solid surface.
dressing remains dry. A wet, sticky outer dressing needs more This prevents patient motion and optimizes control for the person
frequent wound care to keep up with wound drainage. If only performing the procedure.
the outer dressing is dirty (e.g., soiled from food or dirt), it may
be changed as often as needed to maintain a clean dressing and
aid in patient comfort. For quickest healing of superficial burns,
perform daily wound care to remove all exudates and crust,
because both significantly impair wound healing. Once a wound
has epithelialized or nearly epithelialized, apply moisturizing
lotion to hydrate and decrease scarring. Vitamin E, aloe, and oat
beta glucan are often used for their antiinflammatory and sooth-
ing properties. Melaleuca is a topical antibacterial and antifungal
tea tree oil that Australian aboriginal people have used for a
variety of medicinal purposes. It is the active ingredient in
Burnaid, a popular cream used for superficial partial-thickness
burn injuries.
To determine which type of dressing to apply to a burn
wound, consider the following:
• The dressing should cover the entire burned area (i.e., an
enclosed dressing) and leave no burned skin exposed to air
or air currents.
• The burn wound surface should stay moist. Unburned skin FIGURE 15-16  Contact burn from stepping on hot coals. Leaking
surrounding the burn should not macerate. blisters that have burst should be debrided.

326

A are permeable to both crystalloid and colloid solutions. Capillary
B colloid is given. Rapid administration of crystalloid solution
FIGURE 15-17  Partial-thickness burn to dorsal hand from hot oil while
cooking at camp. A, Blister is debrided 5 days after injury. B, Bacitracin
ointment is applied. (Courtesy Tim Platt-Mills, MD.)
EMERGENCY DEPARTMENT CARE
A reasonable rule for the emergency physician in the initial
assessment of a seriously injured patient is to “forget about the
burn.” Airway management takes priority. Although a burn is
usually readily apparent and may even be a dramatic injury, a
careful search for other life-threatening injuries is critical. Only
after an overall assessment of patient’s condition should attention
be directed to specific burn care. Assessment of the nonthermally
injured patient is presented in Chapter 18. The following para-
graphs consider specific problems encountered in burned
patients.
Resuscitation
Since the 1970s, more than a dozen resuscitation plans have been
suggested. Their common goal is to complete treatment with a
FIGURE 15-18  Burn seen in Figure 15-16, after debridement.
living patient who has normally functioning kidneys and does
CHAPTER 15  Emergency Care of the Burned Patient
not develop cardiac failure or pulmonary edema. Almost all these
plans use a combination of colloid and crystalloid solutions, but
they vary considerably in the ratio of colloid to crystalloid, timing
of colloid administration, sodium concentration of crystalloid
solution, and to a much lesser extent, total volume of fluid
given.16,32,35,41,63,68,71 In recent years, a shift toward earlier admin-
istration of colloid has occurred. Data suggest it reduces overall
volume requirements and morbidity related to edema. Some
protocols require frequent changing of solutions, others require
mixing of solutions, and some require careful monitoring of the
patient’s serum electrolytes. Controversy exists about which
resuscitation plan is best. This need not concern the physician
without a special interest in burn physiology. There is general
agreement on critical facts. A patient with very large burns will
probably need both colloid and crystalloid. Initially, capillaries
leak of albumin and other large molecules repairs itself between
6 and 24 hours after injury.
Choice of formulas for initial resuscitation is of relatively little
consequence as long as the rate of fluid administration is modi-
fied according to the patient’s changing requirements over time.
Because of its simplicity, ease of administration, and need for
little blood chemistry monitoring, the Baxter formula (also known
as the Parkland formula) has been adopted by most experts and
recommended officially by the American College of Surgeons
Committee on Trauma.
According to this formula, crystalloid is given during first 24
hours while capillaries are still permeable to albumin. During the
second 24 hours, when the capillary leak has presumably sealed,
results in early expansion of depleted plasma volume, which will
return cardiac output toward normal. Once the capillary leak has
sealed, colloid (usually in the form of albumin) remains the most
effective solution to maintain plasma volume without further
increasing edema. The Baxter formula was derived to provide
specific replacement of known deficits measured by simultane-
ous determinations of red blood cell volume, plasma volume,
extracellular fluid volume, and cardiac output during burn shock.
Box 15-1 lists first and second 24-hour calculations. The
Baxter formula calls for administration of lactated Ringer’s solu-
tion, 4 mL/kg body weight per percentage of body surface
burned during the first 24 hours after the injury. One-half of this
fluid should be given in the first 8 hours and the second half
during the next 16 hours. Fluid therapy during the next 24 hours
consists of administration of free water in quantity sufficient to
maintain normal serum sodium concentration, as well as plasma
(or other colloid) to maintain normal plasma volume.
Adequacy of resuscitation can best be judged by frequent
measurements of vital signs, central venous pressure, and urine
output and by observing general mental and physical responses.
Despite myriad new monitoring devices, urine output remains
one of the most sensitive and reliable assessments of fluid
BOX 15-1  Baxter (Parkland) Formula
First 24 Hours—Ringer’s Lactate
• 4 mL/kg/% burn in 24 hours
One-half in first 8 hours
One-half in second 16 hours
• Example: 70-kg (154-lb) man with 50% burn
4 mL × 50% × (70 kg) = 14,000 mL in 24 hours
7000 mL in hours 1 to 8
3500 mL in hours 8 to 16
3500 mL in hours 17 to 24
Second 24 Hours—Albumin or Plasma at Maintenance
• Maintain normal vital signs
• Adequate urine output
• Example: 70-kg (154-lb) man with 50% burn
250 to 500 mL plasma
2000 to 2500 mL dextrose 5% in water
327
 resuscitation. In the absence of myoglobinuria, a urine output of
0.5 mL/kg/hr in adults and 1 mL/kg/hr in children weighing less
than 10 kg (22 lb) ensures that renal perfusion is adequate. The
patient’s sensorium gives an indication of state of cerebral perfu-
sion and oxygenation. The patient should be alert and coopera-
tive. Confusion and combativeness are signs of inadequate
resuscitation or warn of other causes of hypoxia. Provide supple-
mental oxygen in addition to fluid resuscitation.
Patients with burns that involve less than 10% TBSA generally
do not require fluid resuscitation. They should stay well hydrated
but should not be encouraged to force fluids. Patients with burns
that involve between 10% and 20% TBSA typically do not require
intravenous (IV) fluid resuscitation. They should be encouraged
to drink fluids that contain electrolytes (e.g., Gatorade) and
should be discouraged from drinking large amounts of plain
water or sodas. Hydration status in these patients should be FIGURE 15-19  Deep full-thickness flame burns to the bilateral lower
monitored by ensuring that oral mucous membranes are moist extremities and buttocks requiring medial and lateral escharotomies.
and urine output is brisk with light-colored urine. Patients with (Courtesy Michael J. Mosier, MD.)
burns that involve more than 20% TBSA should receive IV fluid
resuscitation with crystalloid solution until they reach a facility
where medical professionals can evaluate need for other types
of fluids.
Patients with burns of less than 50% TBSA can usually be
BURNS, FIRE, AND RADIATION

resuscitated with a single large-bore peripheral IV line. Because
of the high incidence of septic thrombophlebitis, lower extremi-
ties should be avoided as IV portals. Upper extremities are
preferable, even if the IV line must pass through burned skin.
Patients with burns larger than 50% TBSA or who have associated
medical problems, are at the extremes of age, or have concomi-
tant smoke inhalation should have additional central venous
pressure monitoring. Because of extreme hemodynamic instabil-
ity in patients with burns over 65% TBSA, these patients should
be monitored in an intensive care unit (ICU) setting with a Swan-
Ganz catheter to measure pulmonary capillary wedge pressure
and cardiac output.
Presence of myoglobinuria alters the resuscitation plan. Myo-
globinuria results from destruction of muscle cells leading to
myoglobin (red muscle pigment) release. This is most often
PART 3
If the abdomen is involved with burn, the inferior margins of
escharotomy may be connected transversely (Figure 15-20).
Fasciotomies are rarely needed in patients with thermal burns.
However, if distal pulses do not return after medial and lateral
escharotomies, fasciotomy should be considered. Fasciotomies
can generally be done through the initial escharotomy incisions
(Figure 15-21). In contrast, patients with electrical injuries fre-
quently need fasciotomies. Careful monitoring is mandatory for
all patients with electrical burns and with burns associated with
soft tissue trauma or fractures. In these circumstances, loss of
pulses is a strong indication for urgent fasciotomy under general
anesthesia in the operating room.
Need for escharotomy in the burned hand is controversial.
Fingers burned severely enough to require escharotomy are
frequently mummified, and lack of muscles in the fingers puts

associated with crush injuries, electrical burns, or extremely deep less tissue at ischemic risk. Escharotomy done in fingers runs the
thermal burns. Characteristic cola-colored urine indicates the risk of exposing interphalangeal joints (Figure 15-22). This can
need to increase the amount of fluid given and to establish lead to subsequent infection that may ultimately require joint
diuresis of 70 to 100 mL of urine per hour (see Figure 15-7). An fusion or finger amputation. Both palmar arch and digital vessels
initial bolus of 25 g of mannitol in adults or 0.5 to 1 g/kg in should be monitored with Doppler ultrasound in any significant
children, with a repeat dose in 15 to 30 minutes, should be hand burn. If the signals disappear over the palmar arch or in
considered. the digital vessels, consider performing a dorsal interosseous
fasciotomy.
Escharotomy
Carefully monitor peripheral circulation in patients with circum-
ferential full-thickness extremity burns. Edema that forms beneath
inelastic eschar can increase tissue pressure beyond that of lym-
phatic pressure, thereby further increasing edema. When edema
exceeds venous pressure and approaches arterial pressure, it can
stop circulation in the extremity distal to the constricted area.
Classic findings of compartment syndrome (e.g., pain, par­
esthesias, pulselessness, tense swelling) may or may not be
present in burned extremities. Carefully monitor distal pulses
with Doppler ultrasound. If any of the classic clinical signs
occur or if Doppler signals disappear, perform an escharotomy
immediately.
Escharotomy performed in the hospital does not require an
anesthetic, because only an insensate full-thickness burn is
incised. Make an incision through eschar into subcutaneous
tissue, first along the lateral aspect of the extremity and, if symp-
toms or signs do not improve, along the medial aspect (Figure
15-19). Incisions need not be as deep as the investing muscle
fascia, and bleeding can usually be easily controlled with elec-
trocautery and topical clotting agents. If arrival to the hospital
will be in less than 6 hours, escharotomies should not be done
in the field because the patient may bleed to death without
proper equipment to control bleeding. FIGURE 15-20  Full-thickness flame burns to the anterior torso and left
In small children, circumferential full-thickness burns of the upper extremity. Escharotomies were performed along the flank,
trunk occasionally demand an escharotomy to improve pulmo- sternum, clavicle, costal margin, and abdomen to release the restrict-
nary function. Chest wall escharotomies are made in the anterior ing eschar and allow improved chest and abdominal wall compliance.
axillary lines bilaterally, extending from clavicle to costal margin. (Courtesy Michael J. Mosier, MD.)

328

FIGURE 15-21  Fasciotomies are indicated in deeply burned extremi-
ties if escharotomies fail to reduce tissue tension and restore perfusion.
They can generally be performed through the initial escharotomy inci-
sions, as illustrated in this patient with deep flame burns to the leg.
(Courtesy Rob Sheridan, MD.)
FIGURE 15-22  Full-thickness flame burns to the right hand with escha-
rotomies in a fan pattern between metacarpals to adequately release
pressure from edema formation. (Courtesy Michael J. Mosier, MD.)
Burn Wound Management
Clean burn wounds initially with a surgical detergent. All loose,
nonviable skin should be trimmed (Figure 15-23). Debridement
should be done gently. Small doses of IV narcotic are usually
sufficient analgesia for this procedure. Unless other surgical pro-
FIGURE 15-23  Initial debridement to remove loose necrotic material
should generate almost no bleeding. This can generally be done with
light analgesia. (Courtesy Rob Sheridan, MD.)
cedures are necessary, general anesthesia and operating room
CHAPTER 15  Emergency Care of the Burned Patient
debridement should be avoided until resuscitation is complete.
Once the wound is cleansed, apply a topical chemotherapeu-
tic agent. Agents most often used in the United States and other
industrialized countries contain silver sulfadiazine. It comes as
a white cream, is soothing to the wound, has a good antimicro-
bial spectrum, and has almost no systemic absorption or toxic-
ity.7,40,88,97 Carefully question the patient about allergy to sulfa
drugs before using silver sulfadiazine. Allergic reactions are en-
countered in approximately 3% of patients. These reactions may
be manifested clinically as pain after application rather than the
soothing feeling that silver sulfadiazine typically provides. If an
allergy is suspected by history, a small patch (10 by 10 cm [4 by
4 inches]) of silver sulfadiazine should be applied as a test dose.
The remainder of the wound can be dressed using bacitracin. If
no local reaction occurs after 2 to 4 hours, an allergy is unlikely,
and silver sulfadiazine is the dressing of choice. If an allergy is
confirmed, refer the patient to a burn center, where the next
choice of topical antimicrobial would probably be silver nitrate
solution.
OUTPATIENT BURNS
The vast majority of patients with burns do not require hospital-
ization. In many cases, the burn, if merely kept clean, heals
spontaneously in less than 3 weeks with acceptable cosmetic
results and no functional impairment. Unfortunately, good results
in treating superficial minor burns may entice the unwary physi-
cian to treat more complex burns by the same methods. For the
patient, the consequences of such a mistake can include subse-
quent hospitalization, joint dysfunction, and hypertrophic scar-
ring that may be difficult to correct, as well as considerable loss
of time from work or school.
First-Degree Burns
Although first-degree burns are very painful, patients rarely seek
medical attention unless the burned area is extensive. These
patients do not require hospitalization, but pain control is
extremely important. Aspirin or codeine may be adequate for
small injuries, but for large burns, liberal use of a more potent
narcotic for 2 to 3 days is indicated.
For topical medication, we recommend one of the many
proprietary compounds containing extracts of the Aloe vera plant
in concentrations of at least 60%. Aloe vera has antimicrobial
properties and is an effective analgesic.51,85 Anecdotal evidence
suggests that it may decrease subsequent pruritus and peeling.
Burns from ultraviolet rays (e.g., sunlight, sunlamp) may ini-
tially appear to be only epidermal, but the injury may in fact be
a superficial partial-thickness burn with blistering apparent only
after 12 to 24 hours (Figure 15-24). Patients with such a burn
should be cautioned about blisters and be asked to return if
FIGURE 15-24  Patients with apparently severe first-degree sunburn
will often slough to a painful superficial second-degree burn in the
ensuing 12 to 24 hours. This compromises their mobility and ability to
carry gear. (Courtesy Rob Sheridan, MD.)
329
 blisters form, because wound management then becomes more
important because of potential for infection and subsequent
scarring.
Superficial Partial-Thickness Burns
Treatment of superficial partial-thickness burns presents little
problem. If the wound is kept clean, patient kept comfortable,
and joints kept active, these wounds heal in less than 3 weeks
with minimal scarring and no joint impairment.
First, clean and debride the wound as described previously.
Small blisters may be left intact. Biochemical analysis using poly-
acrylamide gel electrophoresis of burn blister fluid has shown it
to be similar to that of serum.101 We suggest that blister fluid is
an exudate mainly from the vascular system, provides a good
environment for fibroblasts in the damaged site, and facilitates
healing. Larger blisters are difficult to protect, however, and
blister fluid is a rich culture medium for bacteria that live in skin
appendages. Therefore, large blisters and small blisters in large
burns should usually be totally removed with forceps and scis-
sors. In some instances, blister fluid can be aspirated with a
large-bore needle, allowing blistered epidermis to remain on the
wound as a biologic dressing. This dead epidermis is fragile,
tends to contract, and rarely stays intact except over small areas.
BURNS, FIRE, AND RADIATION
After debridement, the most common treatment is wound
coverage with silver sulfadiazine and application of a light dress-
ing to promote active range of motion. Some wounds can be
managed with synthetic dressings that contain elemental silver
(e.g., Aquacel Ag, Acticoat, Mepilex Ag). These can be applied
and left in place for 1 week or until the burn is healed at approxi-
mately 2 weeks (Figure 15-25). Some very small burns do not
require topical agents. For small facial burns, bacitracin ointment
may be a better choice than silver sulfadiazine cream because it
is less drying.
Pain is managed as for first-degree burns. Patient usually
should return every 2 to 3 days until the wound heals or the
patient has demonstrated ability to manage the wound without
supervision.
If silver sulfadiazine is used, an appropriate home treatment
PART 3
regimen is to have the patient cleanse the wound once daily with
FIGURE 15-25  Many new silver-releasing membranes are available
that provide antiseptic coverage of wounds for several days. They need
to be monitored for development of submembrane infection. (Cour-
tesy Rob Sheridan, MD.)
330
tap water and reapply a topical agent and light dressing. During
dressing changes, and as often as possible, put all involved joints
through a full range of motion. The dressing may be unnecessary
while the patient is at home, but he or she should dress the
wound before leaving the house. This method is highly success-
ful, but is inconvenient, may be fairly painful, and requires good
patient cooperation.
The “exposure” method has little to recommend it. This
method involves leaving the wound open, allowing wound drain-
age to desiccate and form a scab. Controlled studies in animals
have shown that desiccation and crust formation interfere with
wound healing. Our experience has also shown that crusts
crack over joints, cause considerable discomfort, and can hide
infection.
Deep Partial-Thickness and Full-Thickness Burns
Treatment of deep partial-thickness and full-thickness burns is a
matter of grave concern. Full-thickness burns heal only by con-
traction and epithelialization from the periphery. Epithelium
does not begin to migrate until eschar is removed, and the
growth rate is only approximately 1 mm (0.04 inch) per day.
Healing of even a small full-thickness burn may involve many
weeks of discomfort and disability. Deep partial-thickness burns
may take 4 to 8 weeks to heal and then leave an unacceptable
scar. If a joint is involved, some loss of joint function is the rule.
We have adopted a policy of early excision and grafting for such
wounds.
Initial outpatient treatment can be followed by elective surgery
as soon as it can be scheduled. Small wounds can be treated
through day surgery. Larger wounds located over dynamically
important areas can be closed with only 1 or 2 days of hospital-
ization. Excision and grafting procedures should be done by a
surgeon experienced in tangential wound excision. Advantages
of this aggressive approach are a pain-free patient with normal
joint function, better cosmetic result, and a rapid return to work
or school. These more than compensate for the brief hospitaliza-
tion and very small risk associated with minor surgery.
Should excision and grafting be unacceptable to the patient
or treating physician, use the standard method of daily cleansing
and application of silver sulfadiazine cream. Most full-thickness
burns need grafting at about 3 to 4 weeks after injury. Deep
dermal burns should be seen by the physician frequently during
healing. Active physical therapy is crucial to ensure a successful
outcome.
REHABILITATION
Physicians who regularly care for burn-injured patients recog-
nize that treatment goals extend far beyond survival of the
patient and healing of wounds. The aim is to return patients at
least to their preburn functional status physically and to ensure
smooth and timely reentry into family and social situations.
Recovery from burn injury is a team effort and depends on mul-
tiple nonphysician health care workers. Depending on burn
severity and associated social situation, participation is usually
required of nurses, nutritionists, occupational therapists, physical
therapists, recreational therapists, social workers, vocational
rehabilitation counselors, psychologists, pain management spe-
cialists, and clergy.
Burn rehabilitation should be initiated by the first physician
to see the patient. Once all systemic and wound issues have been
addressed, proper positioning of wounded extremities or digits
should be assessed by an occupational therapist specially trained
in burn management. If deemed appropriate, splints should be
made immediately. Range-of-motion exercises should be started
on the day of injury, and frequent follow-up by a physical thera-
pist is essential. Best functional outcomes result from meticulous
attention to early mobility. Patients almost universally choose not
to move a burned body part. An active ancillary burn staff team
is essential for satisfactory results. Burn scars require approxi-
mately 1 year to fade, soften, and mature. Physical therapy may
be required throughout this period or longer. Pressure garment
therapy may be used in certain cases in an attempt to prevent
hypertrophic scar formation. The reader is referred to books
dealing with acute burn care, reconstructive plastic surgery, and
burn rehabilitation.1,8,12
INHALATION INJURY
Of the almost 40,000 fire-injured patients admitted to U.S. hos-
pitals each year, smoke or thermal damage to the respiratory tree
may occur in as many as 30%.79 Carbon monoxide poisoning,
smoke poisoning, and thermal injury are three distinctly separate
aspects of clinical inhalation injury. Inhalation injury rarely occurs
in an outdoor setting unless the victim is trapped in a conducive
enclosed space.
CARBON MONOXIDE POISONING
Pathophysiology
Carbon monoxide (CO) is a colorless, odorless, and tasteless gas
with an affinity for hemoglobin 200 times greater than that of
oxygen. The simplest explanation for the mechanism of action
of CO poisoning is that it reversibly displaces oxygen on hemo-
globin. Although worsening hypoxia is critical and percentage
of blood carboxyhemoglobin (COHb) indicates significance of
hypoxia, this simple mechanism cannot account for all experi-
mental and clinical findings seen with exposure to CO. For
example, an experimental group of dogs exchange-transfused
with blood containing 80% COHb showed no symptoms. In a
control group with COHb levels of 80% produced by inhalation
of CO, all animals died. Furthermore, degree of enzyme and
muscle impairment may not correlate accurately with levels of
blood COHb.13,20,30,52
In vitro, CO combines reversibly with cardiac muscle myoglo-
bin and heme-containing enzymes, such as cytochrome oxidase
(a3).13 Despite its intense affinity, CO readily dissociates according
to the laws of mass action. The half-life of COHb in humans
breathing room air is 4 to 5 hours. Breathing 100% oxygen, the
half-life is reduced to 45 to 60 minutes.56 In a hyperbaric oxygen
chamber at 2 atmospheres (atm), the half-life is 30 minutes, and
at 3 atm, it is reduced to 15 to 20 minutes.100
Clinical Presentation
Blood levels of COHb provide a laboratory measure to correlate
with associated symptoms of CO poisoning. Levels less than 10%
do not cause symptoms, although patients with exercise-induced
angina may show decreased exercise tolerance. At levels of 20%,
healthy persons complain of headache, nausea, vomiting, and
loss of manual dexterity. At 30%, they become confused and
lethargic and may show depressed ST segments on ECG. In a
fire situation, this level may lead to death because victims experi-
ence diminished volition and ability to flee smoke. At levels
between 40% and 60%, victims lapse into unconsciousness.
Levels much above 60% are often fatal.
Therapy
Nonpregnant patients who have not lost consciousness and who
have a normal neurologic examination on admission typically
recover completely without treatment beyond administration of
100% oxygen. Patients who remain comatose once COHb levels
have returned to normal have a poor prognosis. Hyperbaric
oxygen treatment (HBOT; see Chapter 72) remains controversial
for asymptomatic, moderate CO poisoning.2,3,54,65,80,86 In one study,
patients with elevated COHb levels and symptoms (e.g., loss of
consciousness, confusion, headache, malaise, fatigue, forgetful-
ness, dizziness, visual disturbances, nausea, vomiting, cardiac
ischemia, or metabolic acidosis) treated with three HBOTs in a
24-hour period appeared to have reduced risk of cognitive
sequelae at 6 weeks and 12 months.107 A follow-up meta-analysis
found insufficient evidence to establish whether HBOT for CO
poisoning reduces the incidence of adverse neurologic out-
comes.14 When associated with a major burn, transport to a
chamber delays definitive care and is associated with numerous
complications (e.g., emesis, seizures, eustachian tube occlusion,
aspiration, hypocalcemia, agitation requiring restraints or seda-
tion, arterial hypotension, tension pneumothorax, cardiac arrhyth-
mia or arrest).34,95 A large, multicenter trial of sufficient size to
CHAPTER 15  Emergency Care of the Burned Patient
address HBOT’s efficacy for CO poisoning is needed.
THERMAL AIRWAY INJURY
Pathophysiology
The term pulmonary burn is a misnomer. True thermal damage
to the lower respiratory tract and lung parenchyma is extremely
rare unless live steam or exploding gases are inhaled. Air tem-
perature near the ceiling of a burning room may reach 540° C
(1004° F) or more, but air has such poor heat-carrying capacity
that most heat is dissipated in the nasopharynx and upper airway.
Heat dissipation in the upper airway, however, may cause sig-
nificant local thermal injury.
Clinical Presentation
Patients who have been in explosions (e.g., propane, natural gas,
gasoline) and have burns of the hands, face, and upper torso are
particularly at risk for pharyngeal edema (Figure 15-26).
Therapy
Maintenance of the airway is the main concern if thermal airway
injury possibly occurred. Patients injured in explosions should
be examined for oropharyngeal erythema and edema. Seek evi-
dence of voice change, stridor, or singed nasal hairs. If these are
present, early, empirical endotracheal intubation is prudent.
Patient should be intubated for 24 to 72 hours until edema sub-
sides. A simple test to determine if extubation should occur is to
deflate the cuff to see if the patient can breathe around the
endotracheal tube (ETT). If so, airway edema has probably
resolved, and extubation should be safe. If doubt exists, extuba-
tion should be performed over a fiberoptic bronchoscope or
nasogastric tube, which allows easy replacement of an ETT if
necessary. Because there is no pulmonary parenchymal injury,
the purpose of endotracheal intubation is to protect the airway
and not necessarily to assist with ventilation. Ventilator settings
should be adjusted accordingly and vigorous pulmonary toilet
should be instituted to prevent the pulmonary problems (atelec-
tasis and pneumonia) frequently seen in intubated patients.
SMOKE POISONING
Pathophysiology
More than 280 toxic products have been identified in wood
smoke. Modern petrochemical and building industries have
produced a multitude of plastic materials in homes and automo-
biles that when burned, produce almost all these and many
other toxins not yet characterized.46,72,93,109 Prominent byproducts
of incomplete combustion are oxides of sulfur, nitrogen, and
many aldehydes. One such aldehyde, acrolein, causes severe
FIGURE 15-26  Deep full-thickness flame burns to the face and neck
with emergent cricothyroidotomy secondary to the inability to perform
oropharyngeal intubation. (Courtesy Michael J. Mosier, MD.)
331
 pulmonary irritation and edema in concentrations as low as
10 ppm. Although chemical mechanisms of injury may be differ-
ent with different toxic products, overall end-organ response is
reasonably well defined.* There is immediate loss of bronchial-
epithelial cilia and decreased alveolar surfactant. Microatelecta-
sis, and sometimes macroatelectasis, results in and is then
compounded by mucosal edema in small airways. Wheezing and
air hunger are common symptoms. After a few hours, tracheal
and bronchial epithelia begin to slough, and hemorrhagic
tracheobron­chitis develops. In severe cases, interstitial edema
becomes prominent, resulting in a typical picture of adult respi-
ratory distress syndrome (ARDS). Pulmonary alveolar macro-
phages are poisoned, causing severe impairment of chemotaxis,
which undoubtedly contributes to high incidence of late pneu-
monia seen in patients with associated cutaneous burns. Acti-
vated neutrophils release superoxides and free radicals of
oxygen. This, together with other inflammatory mediators, aggra-
vates alveolocapillary damage and leads to increased interstitial
edema and impaired oxygenation.
Clinical Presentation
Any patient who has been indoors or in an enclosed space with
a smoky fire and has a flame burn should be assumed to have
BURNS, FIRE, AND RADIATION
smoke poisoning until proved otherwise. Acrid smell of smoke
on the patient’s clothes should raise suspicion. Rescuers are
often the most important historians and should be carefully
questioned.
Perform early, careful inspection of the mouth and pharynx.
Hoarseness and expiratory wheezes are signs of potentially
serious airway edema or smoke poisoning. Copious mucus pro-
duction and carbonaceous sputum are sure signs, but their
absence should not raise false hopes that injury is absent. COHb
levels should be obtained. Elevated COHb or any clinical symp-
toms of CO poisoning are presumptive evidence of associated
smoke poisoning. In very smoky fires, COHb levels of 40% to
50% may be reached after only 2 to 3 minutes of exposure.100
Arterial blood gases (ABGs) are drawn from patients with
suspected smoke poisoning. One of the earliest indicators of
PART 3
smoke poisoning is an improper ratio of arterial partial pressure
of oxygen (PaO2) to fraction of inspired oxygen (FIO2). This P/F
ratio is typically 400 to 500. Patients with impending pulmonary
problems have a ratio of less than 300 (e.g., PaO2 <120 mm Hg
with FIO2 of 0.40). A ratio less than 250 is an indication for vigor-
ous pulmonary therapy, not for merely increasing inspired
oxygen concentrations.
A number of authorities suggest routine use of fiberoptic
bronchoscopy for airway assessment11,57,82,88 (Figure 15-27). It is
inexpensive, quickly performed by an experienced clinician, and
useful for accurately assessing edema of the upper airway. Aside
from establishing evidence of tracheal erythema, it may not
materially influence treatment for smoke poisoning.
We have conducted a multivariate analysis of a constellation
of history, signs, and symptoms with bronchoscopic findings in
100 consecutive patients admitted with suspected smoke inhala-
tion. If the patient had the combination of history of exposure
to closed-space fire, carbonaceous sputum, and COHb level
greater than 10%, there was a 96% correlation with positive
bronchoscopy. Presence of two of the above features dropped
correlation to 70%, and if only one was present, to 36%. As
discussed previously, upper airway edema was best correlated
with an explosion (i.e., flash burn) that involved the face and
upper torso. Almost 50% of such patients had significant upper
airway edema and underwent prophylactic airway intubation.
Therapy
All patients burned in an enclosed space or having any sugges-
tion of neurologic symptoms should be given 100% oxygen while
awaiting measurement of COHb levels. This should be adminis-
tered through a tight-fitting mask in the field. If the patient
demonstrates labored breathing, or if a prolonged transport time
*References 10, 17, 39, 42, 55, 56, 83, 91, 106, 109.
332
FIGURE 15-27  View of the proximal airway on bronchoscopy, demon-
strating moderate erythema and carbonaceous debris, consistent with
a grade 2 inhalation injury by bronchoscopic criteria. (From Kim CH,
Wool H, Hyun IG, et al. Pulmonary function assessment in the early
phase of patients with smoke inhalation injury from fire. J Thorac Dis
2014;6(6):617-624.)
is anticipated, endotracheal intubation should be performed.
Oxygen at 100% can then be administered by ventilator.
Mucosal burns of mouth, nasopharynx, and larynx respond
with edema formation and may lead to upper airway obstruction
at any time during the first 24 hours after the burn. Red or dry
mucosa or small mucosal blisters should alert the observer to the
possibility of subsequent airway obstruction. These signs also
should raise suspicion that significant smoke inhalation may have
occurred. Carefully inspect the mouth and pharynx of any patient
with facial burns. If abnormalities are found, the larynx should
be examined immediately on arrival at the hospital. Presence of
significant intraoral and pharyngeal burns is a clear indication for
emergency endotracheal intubation. Progressive edema may
make later intubation extremely hazardous, if not impossible.
Mucosal burns are rarely full thickness and can be successfully
managed with good oral hygiene.
Pulmonary functions early in the course of smoke poisoning
may be variably affected. Typical findings include decreased lung
volume (i.e., functional residual capacity) and vital capacity,
evidence of obstructive disease with reduction in flow rates,
increased dead space, and rapid decrease in compliance. Much
of the variability in pulmonary response appears to correlate with
severity of the associated cutaneous burn.12 Without associated
burns, mortality from smoke poisoning is low, disease rarely
progresses to ARDS, and symptomatic treatment usually leads to
complete resolution of symptoms in a few days. In the presence
of burns of any size, smoke poisoning appears approximately to
double the mortality rate. Pulmonary symptoms (e.g., hypoxia,
rales, rhonchi, wheezes) are seldom present on admission but
may appear 12 to 48 hours after exposure. In general, earlier
onset of symptoms is associated with more severe disease.98
No standard treatment has evolved to ensure survival after
smoke poisoning. Each recommended treatment modality is tem-
pered by the opinion and individual experience of the treating
physician. In the presence of increasing laryngeal edema, naso-
tracheal or orotracheal intubation is indicated. A tracheostomy is
never an emergency procedure and certainly should be avoided
as initial airway management in patients with burns to the face
and neck. A cuffed ETT should be left in place for 3 to 5 days
until generalized oropharyngeal edema subsides.
Mild cases of smoke poisoning are treated with highly humidi-
fied air, vigorous pulmonary toilet, and bronchodilators as
needed. ABGs are drawn at least every 4 hours, and the P/F ratio
is calculated. Worsening symptoms, difficulty in handling secre-
tions, and falling P/F ratio are indications for intubation and
respiratory assistance with a volume ventilator. If oxygenation
is impaired (P/F ratio ≤250), positive end-expiratory pressure
(PEEP) or continuous positive airway pressure (CPAP) is initiated
and increased by increments of 3 to 5 cm H2O until no further
improvement in P/F ratio occurs or there is evidence of decreased
cardiac output.
Carefully search for other mechanical causes of poor ventila-
tion (e.g., restricted chest wall motion from full-thickness burns,
pneumothorax from high ventilator pressures, or mechanical
difficulties with ETT). Prophylactic antibiotics have no role in
treatment of chemical pneumonitis. Early use of antibiotics
can encourage development of resistant organisms and compli-
cate subsequent burn management and treatment of bacterial
pneumonia.
Corticosteroids are often used in patients with severe asthma.
Clinicians dealing with smoke poisoning often use them for their
spasmolytic and antiinflammatory actions. Several authors have
studied use of corticosteroids, but a most convincing study comes
from Moylan,69 who showed in a prospective blinded study of
patients with smoke poisoning and associated major burns that
rates of mortality and infectious complications were higher in
corticosteroid-treated patients. In patients with associated burns,
corticosteroids did not alter the hospital course of patients admit-
ted after the MGM Grand and Hilton Hotel fires in Las Vegas
in 1981.84
To decide whether to admit smoke inhalation patients to the
hospital for specialized care, consider severity of symptoms from
smoke and presence and magnitude of associated burns. Any
patient who shows symptoms of smoke inhalation and has more
than trivial burns should be admitted. If the burns are greater
than 15% TBSA, the patient should be referred to a special care
unit. In the absence of burns, the decision to admit depends on
severity of symptoms, presence of preexisting medical problems,
and the patient’s social circumstances. Otherwise healthy patients
with mild symptoms (e.g., only a few expiratory wheezes,
minimal sputum production, COHb <10%, normal ABGs) can be
observed in the ED and then discharged if they have a place to
go and someone to observe them. Patients with preexisting car-
diovascular or pulmonary disease should be admitted for obser-
vation if they have any symptoms related to the smoke. Patients
with moderate symptoms (e.g., generalized wheezing, mild
hoarseness, moderate sputum production, COHb levels 5% to
10%, normal ABG levels) may be admitted for close observation
and treated as for asthma. Patients with severe symptoms (e.g.,
air hunger, severe wheezing, copious and usually carbonaceous
sputum) require prompt endotracheal intubation and ventilatory
support in an ICU setting.
OTHER CONSIDERATIONS
Burns are tetanus-prone wounds. The need for tetanus prophy-
laxis is determined by the patient’s current immunization status.
If there is any doubt about the date of most recent vaccination,
or time since last vaccination is more than 5 years and significant
burns have occurred, update tetanus immunization.
Patients undergoing IV resuscitation should have an indwell-
ing urinary catheter placed for hourly monitoring of urine output.
Arterial lines are useful in patients who need frequent ABG
determinations or who will need repeated blood sampling for
other reasons. Necessary laboratory work during resuscitation
phase is relatively minimal. Blood should be drawn for baseline
blood chemistries. If major operative procedures, such as fasci-
otomy or multiple escharotomies, are expected, blood should be
sent for type and crossmatching in anticipation of potential need
to transfuse several units of whole blood. Determine ABG levels
in any patient with a suspected inhalation injury. Arterial pH
measurement is useful to help assess overall treatment of shock.
If the Baxter formula is used for resuscitation, frequent electrolyte
determinations are not necessary, because levels will remain in
the normal range. By 48 hours, however, careful monitoring of
serum sodium and potassium levels becomes important. High
CHAPTER 15  Emergency Care of the Burned Patient
levels of circulating aldosterone result in an increase in renal
potassium excretion. Evaporative water loss through eschar dra-
matically increases free-water requirements of burned patients.
Hemoglobin and hematocrit levels are initially high and tend to
remain high to normal until the third or fourth postburn day.
Blood glucose level is typically elevated because of glycogeno-
lytic effect of elevated catecholamines, gluconeogenetic effect
of elevated glucocorticoid and glucagon levels, and relative
insulin resistance.44,90,102,110 This well-described “stress diabetes”
can become a problem in normal patients if glucose-containing
solutions are given during resuscitation. It is frequently a serious
problem in patients with preexisting diabetes. All diabetic patients
require careful monitoring of blood and urine glucose levels, and
most require supplemental insulin during resuscitation.
All medications during the shock phase of burn care should
be given intravenously. Subcutaneous and intramuscular injec-
tions are unreliably systemically absorbed, so their use should
be avoided. Pain control is best managed with small IV doses of
morphine or another suitable narcotic analgesic until pain control
is adequate without affecting blood pressure.
Before the modern antibiotic era, 30% of burn patients died
during the first week after their injury from overwhelming β-
hemolytic streptococcal sepsis. Availability of penicillin decreased
streptococcal infections but had no influence on mortality or
incidence of bacterial sepsis. Patients survived the first postburn
week only to die of gram-negative penicillin-resistant bacterial
sepsis during the second or third week. The advent of effective
topical chemotherapeutic agents applied directly to burn wounds
made possible control of streptococcal infection, obviating the
need for prophylactic penicillin. Use of prophylactic antibiotics
in outpatient burns has not been carefully evaluated, but is un-
likely to improve outcomes in patients without evidence of
infection.
Stress ulceration of the stomach and duodenum was once a
dreaded complication, occurring in approximately 30% of patients
with burns. Protection of gastric mucosa with immediate feeding
by nasogastric tube and decreasing gastric acidity (e.g., histamine-2
[H2]) receptor antagonists, proton pump inhibitors) or coating
the gastric mucosa (e.g., sucralfate) have made stress ulcers
rare.50,65,78,81,96
Psychosocial care should begin immediately. Patient and
family must be comforted, and a realistic outlook regarding
prognosis of burns should be given, at least to the patient’s
family. In house fires, the patient’s loved ones, pets, and posses-
sions may have been destroyed. If family is not available, a
member of the burn team (e.g., social worker), should find out
the extent of damage in hopes of comforting the patient. If the
patient is a child and circumstances suggest that the burn may
have been deliberately inflicted or resulted from negligence,
physicians in most states are required by law to report their
suspicion of child abuse to local authorities.
BURN SEVERITY AND CATEGORIZATION
Severity of injury is proportionate to size of total burn, depth of
burn, age of patient, and associated medical problems or injuries.
Burns have been classified by the American Burn Association
and American College of Surgeons Committee on Trauma into
categories of minor, moderate, and severe.5 Moderate burns are
defined as partial-thickness burns of 15% to 25% TBSA in adults
(10% to 20% in children), full-thickness burns of less than 10%
TBSA, and burns that do not involve eyes, ears, face, hands, feet,
or genitals/perineum. Because of the significant cosmetic and
functional risk, all but very superficial burns of face, hands, feet,
and genitals/ perineum should be treated by a physician with
special interest in burn care in a facility that is accustomed to
dealing with such problems (Box 15-2). Major burns (previously
described), most full-thickness burns in infants and older adults,
and burns combined with diseases or injuries should also be
treated in a burn center. Moderate burns can be treated in a
community hospital by a knowledgeable physician provided
other members of the health care team have resources and
333
 BOX 15-2  Burn Center Referral Criteria
A burn center may treat adults, children, or both.
Burn injuries that should be referred to a burn center include the
following:
1. Partial-thickness burns of greater than 10% of the total body
surface area
2. Burns that involve the face, hands, feet, genitalia, perineum,
or major joints
3. Third-degree burns in any age group
4. Electrical burns, including lightning injury
5. Chemical burns
6. Inhalation injury
7. Burn injury in patients with preexisting medical disorders
that could complicate management, prolong recovery, or
affect mortality
8. Any patients with burns and concomitant trauma (such as
fractures) in which the burn injury poses the greatest risk of
morbidity or mortality. In such cases, if the trauma poses
the greater immediate risk, the patient’s condition may be
stabilized initially in a trauma center before transfer to a
burn center. Physician judgment will be necessary in such
situations and should be in concert with the regional
medical control plan and triage protocols.
BURNS, FIRE, AND RADIATION
9. Burned children in hospitals without qualified personnel or
equipment for the care of children
10. Burn injury in patients who will require special social,
emotional, or rehabilitative intervention
Excerpted from Guidelines for the Operation of Burn Centers (pp 79-86),
Resources for Optimal Care of the Injured Patient 2006, Committee on Trauma,
American College of Surgeons.
knowledge to ensure a good result. Adoption of early excision
and grafting or creative use of local tissue rearrangement to
achieve early wound closure have made burn care more complex.
An increasing number of patients with small but significant burns
PART 3
are being referred to specialized burn care centers to take advan-
tage of these concepts.
Criteria for admission to the hospital of patients with minor
and moderate burns vary according to physician preference, the
patient’s social circumstances, and ability to provide close
follow-up. In some circumstances, superficial burns as large as
15% TBSA can be successfully managed on an outpatient basis.
In other circumstances, burns as small as 1% may require admis-
sion because of patient’s inability or unwillingness to care for the
wound. In general, threshold for admission of older adults and
infants should be low. Any patient (child or adult) whom the
physician suspects has been abused must be admitted.
TRANSPORT AND TRANSFER PROTOCOLS
Once an airway is established and resuscitation is underway,
burn patients are eminently suitable for transport.9,22,47 Resuscita-
tion can continue en route, because patients tend to remain stable
for several days. To facilitate a safe transport, stable vascular
access should be ensured. If venous access is difficult or lost en
route, intraosseous access is generally adequate for several hours
of resuscitation (Figure 15-28). This was well proved during the
Vietnam War, when burn patients were transported from Vietnam
to Japan and then from Japan to the military burn center in San
Antonio, Texas. The transport was generally accomplished during
the first 2 weeks after the burn. Few complications occurred.
More recent U.S. Army combat support hospital experience in
Iraq reports that complex, definitive care was successfully pro-
vided to burned patients in austere environments.99,58 Evacuations
when more advanced care was indicated were successful.15
Hospitals without specialized burn care facilities should decide
where they will refer patients and work out transfer agreements
and treatment protocols with the chosen burn center well in
advance of need. If this is done, definitive care can begin at the
initial hospital and continue without interruption during transport
and at the burn center. Mode of transport depends on vehicle
334
availability, local terrain, weather, and distances involved. For
distances of less than 80 km (50 miles), a ground ambulance is
typically satisfactory. For distances between 80 and 241 km (50
and 150 miles), helicopter transport may be preferred. Monitor-
ing, airway management, and changes in therapy are more dif-
ficult to achieve in a helicopter. All patients transported by air
should have a nasogastric tube inserted and be placed on depen-
dent drainage, because nausea and vomiting usually result during
the flight. Two large-bore IV lines should be established in case
one stops working. For distances greater than 241 km (150
miles), fixed-wing aircraft are usually satisfactory. Air ambulances
may function as well-equipped, flying ICUs, and personnel are
typically trained for both critical care and peculiarities of advanced
burn care during a flight (see Chapter 58).
The referring physicians must ensure that patient’s condition
is suitable for a long transport and prepare the patient for flight.
Secure the patient’s airway. At 9144 m (30,000 feet), planes
can be pressurized to an altitude of about 1676 m (5500 feet).
Although supplemental oxygen can be administered during flight,
if the patient’s oxygenation is marginal, performing endotracheal
intubation and initiating mechanical ventilation before transport
is preferred. In-flight endotracheal intubation is difficult. If there
is any question of upper airway edema, intubate the patient
before transport from the referring hospital. Wrap patients to
keep them warm because burned patients have difficulty main-
taining body temperature. Bulky dressings, blankets, and a Mylar
sheet (usually available from the flight team) can help maintain
body temperature. If the patient has any cardiac irregularities,
advanced cardiac monitoring must be available. In-flight noise
and vibrations make clinical monitoring difficult.
Only after all other assessments are complete should attention
be directed to the burn. If the patient is to be transferred from
the initial hospital to a definitive care center during the first
postburn day, personnel at the referring hospital can leave the
burn wounds alone. They should calculate burn size for resuscita-
tion purposes and monitor pulses distal to circumferential full-
thickness burns. Wrap the patient in a clean sheet and keep him
warm until arrival at the definitive care center.
INTERNATIONAL RESOURCES
Outside the United States, advanced burn care can be found at
many large academic medical centers. Box 15-3 lists American
Burn Association/American College of Surgeons–verified burn
centers outside the United States. Dedicated burn centers are still
uncommon in the developing world. Most are in large cities and
therefore inaccessible to the majority of the indigenous popula-
tion. Many smaller hospitals lack basic medical supplies and the
FIGURE 15-28  Intraosseous access is generally sufficient to support
several hours of burn resuscitation when needed. Devices should 
be placed in unburned areas if possible. If placed through burned 
skin, they should be removed as soon as is practical. (Courtesy Rob
Sheridan, MD.)
 BOX 15-3  Burn Centers Outside the United States
clinical training needed to treat burns successfully.49 In patients
with severe burn injury, if circumstances allow, medical evacua-
Verified by American Burn Association and American tion to a developed country or large, local city burn center will
College of Surgeons* likely yield the best results. An example of a burn center in a
developing country is the Nepal Cleft and Burn Center in Kath-
Australia mandu, Nepal, a 501(c)3 Non-Profit Charitable Organization
Royal Adelaide Hospital Adult Burn Center, Adelaide organized to deliver quality, deformity-correcting reconstructive
Canada surgery to the poorest patients of Nepal through a permanent,
University of Alberta, Toronto sustainable health care infrastructure.
Firefighters Burn Treatment Unit
The Hospital for Sick Children
Pediatric Burn Center REFERENCES
Sunnybrook Health Sciences Centre
Ross Tilley Burn Centre Complete references used in this text are available
Adult Burn Center
online at expertconsult.inkling.com.
*These burn centers have resources required for provision of optimal care to
burn patients from the time of injury through rehabilitation.
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PART 3
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CHAPTER 16 
Exposure to Radiation from the Sun
ANDREW C. KRAKOWSKI AND ALINA GOLDENBERG
Adverse effects of sunlight overexposure are well documented.84,139
Public attention is increasingly focused on the adverse effects of
sun exposure, but sun-protective strategies are still debated.
These issues are of particular concern to wilderness enthusiasts.
Salutary effects of sun protection against acute phototrauma (e.g.,
sunburn) are more easily judged than are sequelae of chronic
phototrauma (e.g., cataracts, photoaging, photocarcinogenesis).
These chronic effects are increasingly relevant given the state of
demographically aging populations. Economic concerns are stag-
gering; billions of dollars are spent annually in the cosmetic and
medical industries to prevent and repair photodamage, photoag-
ing, and skin cancer. With improvements in sunscreens and
photoprotective clothing, limiting skin damage while remaining
active outdoors is increasingly simpler.
SOLAR RADIATION
ELECTROMAGNETIC SPECTRUM
The sun produces a continuous spectrum of electromagnetic
radiation (Figure 16-1). The most energetic rays are those with
wavelengths that are shorter than 10 nm: cosmic rays, gamma
rays, and x-rays. These do not penetrate the atmosphere to reach
Earth’s surface. Phototrauma is primarily the result of ultraviolet
radiation (UVR). UVR (10 to 400 nm) accounts for approximately
10% of the incident radiation at Earth’s surface; visible light (400
to 760 nm) approximately 50%; and infrared (IR; 760 to 1700 nm)
approximately 40%.84 Longer-wavelength visible light and IR
may also cause cutaneous phototrauma. Solar urticaria has been
reported to occur with exposure to visible wavelengths. IR may
produce epidermal and dermal alterations.145
Ultraviolet radiation has four components. Vacuum UVR (10
to 200 nm) is readily absorbed by air and does not penetrate
Earth’s atmosphere. Ultraviolet C (UVC; 200 to 290 nm) is almost
entirely absorbed in the stratosphere 15 to 50 km (9.3 to 31.1
miles) above Earth’s surface by oxygen and ozone. Man-made
sources of UVC (e.g., germicidal lamps, arc-welding devices) are
rarely medically relevant.
Ultraviolet B (UVB; 290 to 320 nm) is biologically active
and principally responsible for tanning, burning, and nonmela-
CHAPTER 16  Exposure to Radiation from the Sun
noma skin cancer formation.139 Beneficial effects of UVB in-
clude vitamin D production from a cutaneous precursor, 7-
dehydrocholesterol, to form previtamin D3, which is quickly
converted to vitamin D3 (cholecalciferol). Cholecalciferol is first
hydroxylated in the liver into 25-hydroxyvitamin D3, then in the
kidneys into the active metabolite 1,25-dihydroxyvitamin D3,
which stimulates calcium absorption from the gut.122 Approxi-
mately 90% of 25-hydroxyvitamin D3 is formed in this manner.234
At Earth’s surface, approximately 10% of UVR is UVB and 90%
is ultraviolet A (UVA; 320 to 400 nm). This ratio can vary with
season and time of day. UVA is divided into “near UVA,” or UVA
II (320 to 340 nm), and “far UVA,” or UVA I (340 to 400 nm).
These categories are based on photobiologic responses. UVA
contributes to tanning, burning, photoaging, and carcinogenesis.
It is the principal trigger for photo-drug reactions. UVA penetrates
skin more deeply than does UVB, with less energy lost in the
stratum corneum and epidermis.
ENVIRONMENTAL INFLUENCES ON ULTRAVIOLET
RADIATION EXPOSURE
Exposure to UVR varies substantially by latitude, altitude, season,
time of day, solar zenith angle, albedo (reflectivity), clouds,
atmospheric pollution, ozone levels, and individual factors (e.g.,
occupation and personal behaviors). Most UVR reaches Earth
around midday when the sun is at its zenith: 80% between 9 AM
and 3 PM and 65% between 10 AM and 2 PM.84 UVB peaks at
midday.176 UVB is absorbed, reflected, and scattered by the atmo-
sphere. During early morning and late afternoon, when the sun
nears the horizon, UVB decreases considerably. Latitude and
season have similar effect; peak UVB exposure is approximately
100 times greater in June than in December.176 For each degree
of latitude away from the equator, UVB intensity decreases an
average of 3%. UVA varies considerably less than does UVB with
latitude, time of day, and season, as predicted by Rayleigh’s law:
Atmospheric light scattering ∝ 1 λ
where λ is the wavelength. A shorter wavelength results in
greater atmospheric scattering. UVB is scattered much more
readily than is UVA. UVA (but not UVB) is transmitted through
335
 0 10 400 760 103 1011
nm
= 10–9 m

toag is

toal ty
y
nes
ing

lerg
ci
= 10 Å

n
zing

tan
bur

t
x

t
ge

Ligh

Hea
toto
Sun
o
Sun
Ioni

rcin
Pho

Pho
Pho
Ca
Gamma rays
Cosmic rays

X- rays
Ultraviolet Visible Infrared Microwaves Radiowaves

Does not reach Reaches

Earth’s surface Earth’s surface

Vacuum
UVR UVC UVB UVA

UVA II UVA I
BURNS, FIRE, AND RADIATION

nm = 10 200 290 320 340 400

FIGURE 16-1  The electromagnetic spectrum.

window glass. Reflection increases UVR exposure. Water is a bons. CFCs may reside in the stratosphere for 50 to 200 years.
relatively poor reflector. UVR at midday penetrates water up to CFCs rise into the stratosphere. Catalyzed by solar radiation, they
60 cm (23.6 inches). Submerged skin is not well protected.176 Ice release chlorine ions (Cl−) and chlorine monoxide (ClO−), which
and snow are considerably better reflectors. Clean snow may degrade ozone117:
reflect up to 85% of UVR.176 Grass, sand, metal, concrete, salt
Cl − + O3 → ClO− + O2
flats, and other surfaces reflect UVR to varying degrees. A 2010
study demonstrated the importance of surface reflection; while a O3 + UVR → O + O2
canvas beach umbrella blocked direct UV radiation at the umbrel- ClO− + O → Cl − + O2
PART 3

la’s base, 34% of UV was present because of reflection.289

Clouds absorb 10% to 80% of UVR, but typically less than Net reaction:
40%.139 Polluted clouds containing the greatest concentration of 2O3 + UVR → 3O2
hydrocarbons are the most effective at absorbing UVR. Clouds
more effectively absorb heat (i.e., IR), making excessive midday Note that Cl is preserved in this reaction. The half-life of Cl− is
−

UVR exposures a risk.
Wind augments sunburn. In mice, exposure to wind plus UVR
results in more erythema than does exposure to UVR alone.223 In
humans, wind reduces heat perception and encourages longer
exposure. Altitude profoundly influences UVB exposure. Until
recently, UVB exposure was thought to rise 4% for each 305-m
(1000-foot) rise above sea level. However, recent research dem-
onstrated an 8% to 10% increase in UVB for each 305-m (1000-
foot) rise above sea level.240 This study found that UVB exposure
readings in Vail, Colorado (latitude 39 degrees North) at 2591 m
(8500 feet) approximated readings at Orlando, Florida (latitude
28 degrees North, elevation 18 m [60 feet]), 772 miles nearer the
equator.
OZONE DEPLETION AND ULTRAVIOLET
RADIATION EXPOSURE
Stratospheric ozone, which lies 15 to 50 km (9.3 to 31.1 miles)
above Earth’s surface, provides a thin and fragile shield against
UVR. Ozone attenuates UVB and modestly reduces UVA II, but
allows transmission of all UVA I.313 Natural physicochemical
processes continuously create and remove ozone from the strato-
sphere. Man-made pollution accelerates ozone degradation.
Molina and Rowland206 first suggested that chlorofluorocarbons
(CFCs) could cause ozone depletion. Developed during the 1970s
as refrigerants, CFCs contain carbon, chlorine, and fluorine. CFCs
have been used in air-conditioning systems, insulation, cleaning
solvents, degreasing agents, and metered-dose inhalers. Halons,
related compounds containing bromine, also deplete strato-
spheric ozone. Halons arise from seawater, fire extinguishers,
and various industrial processes.117 CFCs and halons are halocar-
approximately 75 years.302 Each Cl− ion may destroy 100,000
molecules of ozone.302 Above Antarctica, molecular halogens coat
the surface of ice clouds, making them even more reactive and
able to degrade ozone.117
Ozone losses were first reported in 198574 by the British Ant-
arctic survey. Ozone above Antarctica showed large declines in
the austral springtime (September/October), and decreased 35%
during the springs from 1975 to 1984.117 Ozone depletion is now
documented at all latitudes except the equator. This depletion is
uneven, with more loss at the poles and less at the middle lati-
tudes.302 Waxing and waning occurs with the seasons. Docu-
mented ozone depletion exists over continental Europe, North
and South America, South Africa, New Zealand, and Australia.160
Significant increases in UVB caused by ozone depletion have
been documented, even near the middle latitudes. In Toronto
from 1989 to 1993, Kerr and McElroy144 documented surface UVB
increases of 35% per year in winter and 7% per year in summer,
corresponding with ozone decreases of 4% per year and 1.8%
per year, respectively. In Scotland, similar increases in ground-
level UVB caused by decreased stratospheric ozone have been
documented.208 In the northern hemisphere’s middle latitudes,
ozone losses are greater during winter (~6% per decade) than
summer (~3% per decade).117 Pollution (e.g., smog, particulates)
may mitigate UVR increases by absorbing UVB.302
Ozone depletion affects the biosphere and human skin cancer
rates. Data suggest that every 1% decrease in ozone causes an
increased incidence of skin cancer: 1% for melanoma, 2% for
basal cell carcinoma, and 3% for squamous cell cancer.59,302 Given
the paucity of direct sunlight, even if UVB triples near the poles,
as suggested in worst-case scenarios, polar areas will still receive
less UVB than current equatorial levels.302 Ozone depletion may

336
have its greatest effects on nonhuman biosystems. Plant and
plankton yields may be diminished significantly, with severe
detriment to terrestrial and marine life.313
To prevent ecologic disturbances and restore ozone levels,
international agreements have been negotiated. The Vienna Con-
vention (1985) was among the first. The Montreal Protocol (1987),
ratified by all 196 countries,291 agreed to limit and then reduce
CFC production, leading to a 50% reduction by 1998.117 The
London Amendment (1990) required complete phaseout of halo-
carbon production. The Copenhagen Amendment (1992) acceler-
ated the timetable for complete phaseout of CFC production,
including hydrochlorofluorocarbons, by 1996 in developed
countries and 2002 in undeveloped nations. Further amendments
were made in Vienna (1995), Montreal (1997, 2007), and Beijing
(1999).257 The 2007 Adjustment to the Protocol calls for phaseout
of hydrofluorocarbons (HFCs) by 2030. Although HFCs do not
directly contribute to ozone depletion, they are considered active
gases that contribute to climate change and are regulated by the
Kyoto Protocol.159
Total atmospheric chlorine peaked in 1990 and has since
declined, although only two-thirds as fast as expected.257 This is
thought to result from CFCs being released from existing, unregu-
lated sources such as air conditioners, insulating foams, and
increased production in East Asian developing countries. Because
of the high cost of CFC substitutes,40 a “black market” of illegal
importation of CFCs into the United States from Mexico has
emerged.83
Between 1988 and 2010, total ozone-depleting emissions from
human activities have decreased by more than 80%. It is projected
that global ozone will continue to increase and will return to
pre-1980 levels by 2050.257 Total UVB levels are expected to
decrease below 1960 values by the year 2100.
ACUTE EFFECTS OF ULTRAVIOLET
RADIATION ON SKIN: SUNBURN
AND TANNING
The effect of UVR on skin depends primarily on wavelength, an
individual’s age and genetic factors, and the exposure’s duration,
intensity, frequency, and anatomic location. To have a biologic
effect, UVR must be absorbed by molecules in the skin known
as chromophores. Different UVR wavelengths are absorbed by
different chromophores, including nucleic acids (especially
pyrimidine bases), amino acids in cutaneous proteins, and lipo-
proteins in cell membranes. Chromophores exist at various skin
depths, resulting in differing photobiologic responses to UVR.
There is imprecise knowledge of how a given photochemical
reaction results in a specific biochemical product and leads to
an observable clinical change.
ULTRAVIOLET C RADIATION
UVC is effectively screened from Earth’s surface by stratospheric
ozone and oxygen. It has no known appreciable impact on
human health. Even with continued ozone depletion, levels of
UVC are not expected to rise. Man-made sources of UVC (e.g.,
germicidal lamps, arc-welding devices) are rarely associated with
cutaneous pathology, because UVC is effectively absorbed by the
outermost cutaneous layer, the stratum corneum.84
ULTRAVIOLET B RADIATION
UVB acutely induces a cutaneous inflammatory response.127 Clini-
cally, erythema (i.e., sunburn) is the hallmark of acute overex-
posure to UVB. UVB is considered to be 1000-fold more effective
than UVA for induction of erythema. In a human model, 300-nm
UVB is 1280-fold more effective at inducing erythema than is
360-nm UVA.316
Erythemogenic doses are defined as multiples of the minimal
erythema dose (MED). MED is the lowest dose that elicits
perceptible erythema. In a typical fair-skinned individual, the
MED might range from 15 to 70 millijoules (mJ)/cm2 for UVB
and from 20 to 80 joules (J)/cm2 for UVA. For a typical fair-
skinned individual in San Diego, 1 MED of UVB would require
CHAPTER 16  Exposure to Radiation from the Sun
20 minutes of midsummer exposure; 1 MED of UVA would
require 2 to 3 hours of exposure. A person can receive 15 MEDs
of UVB in a day, but only 2 to 4 MEDs of UVA.196 Although
people are exposed to 10 to 100 times more UVA than UVB,
more than 90% of sunlight-induced erythema can be attributed
to UVB. The erythema action spectrum is remarkably similar to
the absorption spectrum of DNA213 and peaks in the UVB range.
This suggests that DNA is a principal target chromophore for
UVB-induced erythema315 and pyrimidine dimer formation.106
ULTRAVIOLET A RADIATION
UVA penetrates the skin more deeply than does UVB; 95% of
incident UVB is reflected or absorbed by the epidermis, whereas
approximately 50% of UVA reaches the dermis.73 UVA contributes
modestly to sunburn and clinical erythema. Prolonged daily UVA
exposure can approach 125 J/cm2, which significantly exceeds
the threshold erythema dose of 20 to 80 J/cm2.273 UVA-induced
erythema has onset within 4 to 6 hours, peaks after 8 to 12 hours,
and fades after 24 to 48 hours.127,139 UVA-induced erythema may
have a distinct pathophysiologic mechanism caused by keratino-
cyte cytotoxicity.127 Histologically, UVA-induced erythema dis-
plays more epidermal spongiosis, fewer sunburn cells, and more
dermal changes than does UVB-induced erythema, which dis-
plays a denser, deeper mononuclear cell infiltrate and more
vascular damage.127
INFRARED RADIATION
Infrared radiation plays a less well-defined role in photodamage.
Near-IR preirradiation prevents UVR-induced cytotoxicity196 and
suggests a possible evolutionary protective mechanism for IR by
preparing skin cells to resist UVR-induced damage. No data
indicate whether IR protects against UVR’s mutagenic and carci-
nogenic effects.
PHOTOTRAUMA
NATURAL DEFENSES AND SKIN TYPE
Exposure to UVR causes insidious, cumulative biologic and clini-
cal changes. UVA and UVB have distinct effects on the epidermis,
dermis, extracellular matrix, cytokines, and immune response.304
In response to UVB, the stratum corneum thickens99 and melanin
increases, mitigating further UVB photodamage. The stratum
corneum (outermost layer of skin) is composed of flattened
anucleate keratinocytes. Depending on its thickness, it reflects,
scatters, or absorbs up to 95% of incident UVB.112 In response to
UVB, the stratum corneum can increase its thickness up to
sixfold84 and serves as the main photoprotective factor in white
persons.99 Repeated UVA exposures cause thickening to a much
lesser degree.174 UVA tans are less photoprotective than UVB tans.
Melanin reflects, scatters, and absorbs throughout the UVR
spectrum. It acts as an antioxidant and reduces UVR-induced
photoproducts.148 Consequently, constitutive (racial) skin color is
a principal determinant of an individual’s erythema response to
UVR. Although blacks and whites have similar numbers of mela-
nocytes, these cells are differently melanized and distributed.
Increased melanin in blacks can decrease dermal penetration of
UVR up to fivefold53 and increase the MED up to 30-fold. Tanning
is much less protective. After an entire summer of tanning, the
MED in whites increased only 2.3-fold.53 These racial differences
in melanization are reflected in lower rates of burning, photoag-
ing, and skin cancer in blacks.
Susceptibility to photodamage is typically defined by six dis-
tinct skin types (Box 16-1). Racial pigmentation alone does not
account for differences in skin type; some redheads tan easily,
and some blacks burn readily. Skin type correlates well with
MED. Age and anatomic site influence MED, with lower MEDs
recorded in very young and very old persons.139 Differences in
stratum corneum thickness and melanocyte concentration may
account for body site–specific differences in MED (e.g., the MED
of the back is typically less than the MED of the lower leg).
337
 BOX 16-1  Skin Types
I. Always burns; never tans
II. Often burns; tans minimally
III. Sometimes burns; tans moderately
IV. Burns minimally; tans well
V. Rarely burns; tans deeply; moderately pigmented (brown)
VI. Never burns; deeply pigmented (black)
Chronic suberythemal UVA exposures also cause photodam-
age. Repetitive low-dose exposures to UVA result in histologic
changes174: thickening of the stratum corneum, granular and
stratified cell layers; decreased elastin, vascular dilation, and
inflammation.
Intrinsic mechanisms of photoprotection include antioxidants
(e.g., glutathione peroxidase-reductase system mitigates damage
from UVR-induced reactive oxygen species), DNA repair enzymes
(correct most UVR-induced mutations), and carotenoids (stabilize
biologic membranes from singlet oxygen attack).
SUNBURN
BURNS, FIRE, AND RADIATION
Sunburn reflects a local vascular reaction. The causes are multi-
factorial; DNA damage, prostaglandin activation, cytotoxicity, and
other mechanisms are implicated. Onset of UVB erythema occurs
2 to 6 hours after exposure, peaks at 12 to 36 hours, and fades
after 72 to 120 hours.84,127,139 Acute histologic changes accompany-
ing UVB exposure include edema with vasodilation of the upper
dermal vasculature127 and endothelial cell swelling, most likely
caused by release of vasoactive mediators.102 Delayed histologic
changes include appearance of sunburn cells within 30 minutes
after exposure. These dyskeratotic cells have enlarged nuclei and
vacuolated cytoplasm. Initially, sunburn cells localize in the epi-
dermis’s lower half; after 24 hours, they are also found in the
upper half. Sunburn cells may represent proliferating basal cells
that cannot adequately repair UVR-induced DNA lysosomal
PART 3
damage.55 Stainable Langerhans cells (i.e., cutaneous antigen-
presenting cells) decrease rapidly: at 1 hour by 25% and at 72
hours by 90%.127 In mice exposed to repetitive suberythemogenic
doses of UVB, normal numbers of Langerhans cells return by 8
days. Vacuolization of melanocytes is seen after 1 hour and
returns to normal 4 to 24 hours after exposure. Mast cells decrease
in number and granularity within 1 hour, returning to normal
after 12 to 72 hours.127 By 24 to 48 hours after exposure, there
are increases in melanin synthesis, epidermal proliferation, and
thickening of stratum corneum.
Biochemical changes that accompany sunburn include in-
creased levels of histamine,127 which return to normal within 74
hours. Histamine is unlikely to be the principal mediator of
vasodilation and erythema, because antihistamines are ineffective
at preventing sunburn. UVR increases phospholipase activity,
with accompanying increases in prostaglandins (PGs). PGD2,
PGE2, PGF, and 12-hydroxyeicosatetraenoic acid are increased in
blister aspirates immediately after UVB exposure, and peak after
18 to 24 hours.127 Topical and intradermal indomethacin (a pros-
taglandin inhibitor) blocks UVB-induced erythema for 24 hours
after exposure,268 supporting the thesis that eicosanoids (PGs
and leukotrienes) are significant mediators of UVR-induced
inflammation.151
SUNBURN TREATMENT
Sunburn is self-limited. Treatment is largely symptomatic and
involves local skin care, pain control, and antiinflammatory
agents (Box 16-2). Studies of sunburn therapies include agents
used immediately after UV exposure (i.e., before symptoms
have manifested) and agents for treatment of acute sunburn
reactions.110
Cool-water soaks or compresses may provide immediate relief
from sunburn. Topical anesthetics are sometimes useful; use
nonsensitizing anesthetics (e.g., menthol, camphor, pramoxine,
lidocaine) rather than potentially sensitizing anesthetics (e.g.,
338
benzocaine, diphenhydramine). Refrigerating topical anesthetics
before application provides added relief. Topical remedies
include aloe, baking soda, and oatmeal, but controlled studies
are lacking. Topical corticosteroids, with their vasoconstrictive
effects, are often considered “first-line” treatment for acute
sunburn; however, their efficacy remains controversial. A trial
comparing erythema reactions in skin treated with either topical
moderate-potency corticosteroid (hydrocortisone-17-butyrate) or
high-potency corticosteroid (clobetasol propionate) 30 minutes
before or 6 or 23 hours after exposure to UVB, found decreased
erythema only in areas pretreated with high-potency corticoste-
roid 30 minutes before UVB exposure.76 When applied after
exposure, diclofenac gel, a topical nonsteroidal antiinflammatory
drug (NSAID), alleviates pain, erythema, and edema for up to 48
hours.145 Oral NSAIDs provide analgesia and may reduce sunburn
erythema.84 Combined use of topical corticosteroids and oral
NSAIDs slightly decreases erythema during the first 24 hours if
administered before sunburn becomes clinically apparent.235 A
recent metastudy found no therapy to be consistently effective,
and no consensus could be made regarding treatment of
sunburn.110
TANNING
As with sunburn, tanning is caused by UVR. Persons who seek
a tan risk sunburn. Tanning is biphasic. There is immediate
pigment darkening within minutes (caused by UVA), followed
by delayed pigment darkening (DPD) in 3 days (primarily a re-
sponse to UVB). Immediate pigment darkening results from
action of UVA on preformed melanin precursors and occurs as
soon as 5 minutes after exposure, peaks in 60 to 90 minutes, and
then fades quickly. DPD represents new melanin synthesis within
melanocytes and subsequent spread of richly melanized melano-
somes into surrounding keratinocytes. DPD is notable by 72
hours after UVB exposure, peaks after 5 to 10 days, then slowly
fades. Most tanning studies have been performed with erythemal
doses of UVR. Multiple suberythemal UVA exposures are signifi-
cantly more melanogenic than is similarly dosed UVB.17 The
mechanism of DPD is multifactorial. UVB stimulates tyrosinase
release and arachidonic acid metabolites, and releases α-
melanocyte-stimulating hormone from keratinocytes.8 UVB in-
creases binding affinity of melanocytes for melanocyte-stimulating
hormone, resulting in increased melanocyte proliferation, mela-
nization, and arborization.24 UVB increases melanocytes in both
exposed and protected skin,276 suggesting a UVR-stimulated cir-
culating factor that promotes melanocyte proliferation.
PHOTOAGING
Repetitive long-term exposures to sunlight result in photoaging.80
The process termed dermatoheliosis is clinically and histologically
BOX 16-2  Sunburn Treatments
Pain Control
Acetylsalicylic acid
Nonsteroidal antiinflammatory drugs
Skin Care
Cool soaks and compresses
Nonmedicated moisturizers
Topical anesthetics
Pramoxine (Prax) lotion
Menthol plus camphor (Sarna) anti-itch lotion
Anti-itch concentrated lotion (pramoxine) plus camphor plus
calamine (Aveeno)
Lidocaine plus camphor (Neutrogena Norwegian Formula)
soothing relief moisturizer
Corticosteroids
Topical agents (e.g., triamcinolone 0.1% cream applied twice daily
when erythema first appears)
Systemic agents

A B
C D
FIGURE 16-2  Phototrauma. A, Tan and peeling after sunburn. B to
D, Dry, mottled, wrinkled, and pebbled skin with photoaging.
different from chronologic aging and does not merely represent
accelerated chronoaging. Photoaged skin is characterized by
dryness, roughness, mottling, wrinkling, atrophy, and pebbling
and may be studded with precancers (actinic keratoses) or
cancers (Figure 16-2). Photoaging contributes more to “old-
looking” skin than does chronoaging. Age can be estimated
from observing sun-exposed sites, but not from photoprotected
sites.300 The action spectrum for photoaging includes UVB, UVA,
and IR.174
Chronically sun-exposed sites have fewer Langerhans cells. In
culture, keratinocytes and fibroblasts from sun-damaged skin
have diminished life span.95 Chronic UVB exposure leads to
deposition of thickened, amorphous elastic fibers high in the
dermis, demonstrable in photoexposed white skin by age 30. In
a transgenic mouse model, UVB produces this solar elastosis;
UVA does not.283 Another mouse model suggests the action spec-
trum for “photosagging” peaks in UVA at 340 nm,111 and this
action spectrum is remarkably similar to generation of singlet
oxygen by excitation of transurocanic acid. Antioxidants may
reduce free radicals. Ascorbic acid (vitamin C) stimulates collagen
production in culture229 and reduces wrinkling in UVB-treated
hairless mice.21 Vitamin E reduces wrinkling in mice and humans
exposed to UVR.21
Tropoelastin and fibrillin synthesis diminish with chronic UVB
exposure.303 Transcription of other extracellular matrix genes is
enhanced. Photoaged skin demonstrates increased matrix metal-
loproteinases (MMPs), which are potent mediators of connective
tissue damage.80 MMPs arise within hours of UVB exposure, even
after suberythemal exposure.78 Tretinoin inhibits induction of
UVB-induced proteinases,78,80 perhaps explaining its clinical use-
fulness against photoaging.301 Tretinoin normalizes photoaltered
epidermal differentiation and deposits new type I collagen in the
upper dermis.105
There is increased demand for treatments to manage photoag-
CHAPTER 16  Exposure to Radiation from the Sun
ing. Ablative fractional laser resurfacing vaporizes ablated micro-
channels through the skin, stimulates neocollagenesis within the
dermis, and leads to rapid healing with minimal side effects.129,184
Photoaging treatment pales in comparison to simple prevention.
Sun-protective behaviors remain the most effective management
approach.
SUN AND SKIN CANCER
MOLECULAR BASIS OF PHOTOCARCINOGENESIS
Photobiology
Nonmelanoma skin cancer (NMSC) refers to cutaneous basal cell
carcinoma (BCCa) and squamous cell carcinoma (SCCa). Several
photomolecular events are associated with NMSC. UVR causes
characteristic changes of adjacent pyrimidines on DNA.32,316 The
5-5 double bonds absorb UVR photons, creating 6-4 (pyrimidine-
pyrimidone) photoproducts (if a single bond opens) and cyclobu-
tane dimers (if both bonds open).32 Cyclobutane dimers
predominate 3 : 1, with thymine (T-T) dimers being the most
common.151 Even suberythemal doses of UVR can induce T-T
dimers.315 High-performance liquid chromatography can quanti-
tatively measure these UVB photoproducts38 and reveal 30-fold
interindividual variations.38
Resultant UVR-induced mutations have a distinctive signature,
which is that two-thirds of the mutations display cytosine →
thymine (C → T) substitutions at dipyrimidine sites, and 10%
show CC → TT substitutions.32 These mutations are unique and
allow UVR-induced mutations to be distinguished from chemical
mutations.32
Data suggest that cyclobutane dimers and 6-4 photoproducts
are primarily responsible for the mutagenic162 and carcinogenic151
properties of UVR. Many genes, including those involved in
tumor suppression and promotion, may be targets for UVR muta-
tions. Tumor suppressor genes (TSGs) that play a role in photo-
carcinogenesis include p53, p16, and protein patched homolog
1 gene (PTCH).31,123 A mutation of p53, the most common genetic
alteration identified in human cancers, is found in approximately
50% of BCCa, 60% of actinic keratoses, and 90% of SCCa.32,123,151,317
Although p53 mutations may be found in non–sun-damaged skin
at a low frequency, mutations are much more common in sun-
exposed sites.32
The p53 protein is a transcription factor that regulates the
cell cycle. DNA damage stimulates p53 protein production. This
leads to cell cycle arrest in G1 (a premitotic phase), allowing
time for DNA repair.32 Irreparable damage leads to apoptosis.
Sunburn cells are examples of apoptotic cells.317 Cells with
mutated p53 are more resistant to apoptosis with subsequent
UVR exposures.
Within the p53 gene, there are “hot spots” where mutations
frequently occur.32,40 Most p53 mutations result in a single amino
acid substitution, typically cytosine to thymine (C → T).317 Normal
wild-type p53 has a short half-life and is generally unstable and
unstainable. Mutated p53 is more stable and so stainable by
immunohistochemical techniques.40,240 Both UVA and UVB upreg-
ulate p53 expression in human skin.43 After a single UVR expo-
sure to the forearms, p53 protein expression peaks in 24 hours
and returns to baseline after 360 hours.107
Mutations in p53 occur as an early initiating event in photo-
carcinogenesis.151 Unique p53 mutations are present in actinic
keratosis.317 Different actinic keratoses display different p53 muta-
tions, supporting the role of p53 mutations as initial causative
events, followed by clonal expansion of mutated cells to form
clinically visible lesions (e.g., precancerous actinic keratosis).317
Altered p53 provides a survival advantage to mutated cells. In
response to chronic UVR, neighboring nonmutated cells become
apoptotic and die, allowing space for further expansion of the
mutated clone and ultimately resulting in development of actinic
keratosis or SCCa.32
The p53 mutations alone may be insufficient to produce
NMSC. Patients with Li-Fraumeni syndrome inherit a mutated
form of the p53 gene and have increased incidence of sarcomas,
adenocarcinomas, and melanomas, but not NMSC.151 Other factors
339
 (e.g., decreased DNA repair, UVR-induced immunosuppression)
likely play a permissive role. Patients with xeroderma pigmento-
sum (XP) have increased numbers of p53 mutations,32 defective
gene repair mechanisms, and greatly increased NMSC incidence.
Cutaneous lymphomas show a higher frequency of UVR signature
p53 mutations.193 In mycosis fungoides, mutations are found in
the tumor stage but not the plaque stage,193 suggesting that UVR
promotes clinical progression of this lymphoma. Epidemiologic
data demonstrate increased incidence of non-Hodgkin’s lym-
phoma among persons who live closer to the equator.1
Other TSGs are less well studied but have increasingly defined
roles in photocarcinogenesis. In melanoma, p16 is frequently
inactivated130 and increasingly downregulated as melanoma pro-
gresses.271 Another TSG, PTCH, which is also located on chromo-
some 9, is frequently mutated in both familial and sporadic BCCa.
Mutations of PTCH are especially notable in patients with XP and
multiple BCCa130
In addition to downregulating TSGs, UVR can activate proto-
oncogenes (e.g., bcl-2, c-fos, and ras) to form functional onco-
genes.130 In response to UVR, bcl-2 protein is overexpressed,
suppressing apoptosis and permitting expansion of malignant
clones. UVR alters c-fos, disrupting transcription of nuclear pro-
teins involved in cell proliferation. UVB causes mutations in ras,
BURNS, FIRE, AND RADIATION
disrupting mitogenic signaling pathways. Mutations in BRAF, a
critical component of the ras protein kinase pathway, are found
in a large percentage of nevi158 and melanomas,227 especially
melanomas that arise on intermittently sun-exposed skin.182 BRAF
mutations occur only rarely in melanomas arising in chronically
sun-exposed or completely sun-protected skin,182 suggesting mul-
tiple genetic pathways for melanoma induction. Mutations of
BRAF and p53 may interact to form melanoma.227
UVR-related oxidative damage is another mechanism contrib-
uting to photocarcinogenesis. Although UVA causes fewer direct
mutations than does UVB, it is a more potent cause of cellular
oxidative damage, producing reactive molecular oxygen and
nitrogen species. Oxidative damage to DNA, proteins, and lipids
contributes to carcinogenesis through inflammation, immunosup-
pression, and ultimately mutation.109 The MMPs, a group of zinc-
PART 3
dependent enzymes, increase in response to UVR to favor tumor
invasion and spread.34,130
Photoimmunology
Ultraviolet radiation produces local and systemic immunosup-
pression.216 UVB depletes immunocompetent antigen-processing
cells (Langerhans cells) for up to 2 weeks after exposure.204 UVB
alters Langerhans cells by interfering with their ability to present
antigens to T cells.101 UVB diminishes type 1 helper T cell
responses (which promote contact hypersensitivity) while pre-
serving type 2 helper T cell responses (which suppress contact
hypersensitivity), converting Langerhans cells from immunogenic
to tolerogenic. As a consequence, UVR exposure diminishes
contact hypersensitivity and mixed-lymphocyte reactions. This
may explain why UVR-induced skin cancers, which are antigenic,
progress to clinical lesions. UVR-induced immunosuppression
can be transferred in mice with irradiated T lymphocytes.216
Immunoregulatory failure contributes to formation of skin
cancer.156 In immunosuppressed patients, skin cancer is often
more aggressive and occurs at an earlier age.71 In kidney trans-
plant patients in Australia, 45% develop skin cancer within 11
years and 70% within 20 years.28 For heart transplant patients in
Australia, the incidence of skin cancer is 31% at 5 years and 43%
at 10 years. In immunosuppressed patients, the ratio of SCCa to
BCCa is 4 : 1, the opposite of the ratio in immunocompetent
patients.72 Of note, although kidney transplant patients are taking
higher doses of immunosuppressive drugs than are heart trans-
plant patients, skin cancer rates appear higher in heart transplant
patients. Chronic sun exposure and fair complexion further
increase risk of skin cancer in transplant patients, possibly as a
result of overexpression of p53.93
NONMELANOMA SKIN CANCER
Americans240 have a 20% lifetime risk of developing NMSC. The
incidence continues to rise.98 Factors that play a role include a
340
“sun-worshiping” lifestyle (sunbathing, tanning), poor preventive
behaviors (e.g., insufficient use of sunscreen, hats, and covering
bathing suits), aging population, and depletion of the ozone
layer.
Exposure to UVR causes the majority of precancerous actinic
keratoses and true skin cancers (Figure 16-3). Laboratory data
confirm UVR induces and promotes NMSC in mammalian animal
models.139 Ninety percent of all NMSC are attributed to sunlight
exposure alone.251 NMSC has a much greater incidence in whites
than in blacks and occurs primarily on sun-exposed areas. Risk
for NMSC increases with increasing sun exposure. Repeated
sunburn is an independent risk factor.155 Patients with XP have
impaired ability to repair UVR-induced DNA damage and
1000-fold greater risk of developing NMSC, typically at a very
early age.151
Development of NMSC in humans is related to time and
intensity of UVR exposure. British immigrants to Australia assume
the much higher Australian risk of NMSC only if they emigrate
before age 18 years; after that time, immigrants retain the lower
British risk.187 Another study suggests NMSC risk decreases for
UVR exposure after age 10 years.154
Basal Cell Carcinoma
Basal cell carcinoma is associated with sun exposure up to the
age of 19 years but is not associated with mean annual cumula-
tive summer sun exposure.87 Risk for BCCa is associated with fair
complexion and freckling. Intermittent (rather than continuous)
sun exposure in poor tanners may be the most important factor
in development of BCCa.155
Basal cell carcinoma includes a heterogeneous group of low-
grade malignant cutaneous tumors characterized by markers
associated with hair follicle development. BCCa is the most
common cancer in the United States and is most often found on
the head and neck (Figure 16-4). In contrast with SCCa, BCCa is
relatively uncommon on the dorsal surface of the hand, where
solar radiation exposure is high. While locally aggressive, BCCa
is rarely metastatic. Several clinical morphologies of BCCa exist;
diagnosis depends on the astute clinician. Nodular BCCa, the
most common form, manifests as one or a few small, pearly
papules with a central depression. Telangiectasias may be seen.
Lesions are usually friable and frequently bleed when rubbed
vigorously with a cotton-tipped swab. Pigmented BCCa is similar
to nodular BCCa but appears brown or black because of pig-
mentation. Cystic BCCa manifests as bluish gray, dome-shaped
cystic papules or nodules similar in appearance to hidrocystomas.
Morpheaform BCCa manifests as a white sclerotic plaque, usually
without the characteristic findings of a pearly border, leading to
this morphologic lesion often being overlooked or misdiagnosed
as a benign scar. Superficial BCCa, the most common pattern in
patients with human immunodeficiency virus (HIV), favors the
trunk and distal extremities. It typically manifests as superficial,
dry, scaly lesions that may resemble patches of slow-growing
eczema or psoriasis; close examination typically reveals the char-
acteristic raised border. “Rodent ulcer” is a neglected BCCa that
has ulcerated; consequently, the “rolled” border of the lesion may
not be present or recognizable (Figure 16-5).
Squamous Cell Carcinoma
Both UVC and UVB are effective inducers of SCCa in mice.127
SCC may begin as an actinic keratosis, appearing clinically as an
irregularly bordered, pink, rough papule or plaque. Actinic kera-
toses may be successfully treated with cryotherapy, topical
imiquimod, topical 5-fluorouracil (5-FU), and surgical removal.
True SCCa, the second most common form of skin cancer,
may manifest clinically as dull-red, superficial, indurated, well-
demarcated papules and plaques arising on sun-exposed areas
(i.e., the face and dorsal surfaces of the hands). Lower-lip lesions
may develop with actinic cheilitis; a history of repeated sunburns
and tobacco use are predisposing factors. As the lesions grow
over the course of months, they become deeply nodular and
ulcerated (Figure 16-6). The ulcer may be hidden by an overlying
crust that, when removed, reveals a discrete, indurated, and
elevated base. Careful examination of regional lymph nodes is
warranted in suspected cases. Rate of metastasis ranges from
 CHAPTER 16  Exposure to Radiation from the Sun
A
B

C D
FIGURE 16-3  A, Actinic keratoses: thin, vague, and scaly papules. B, Basal cell carcinoma: smooth, pearly
papule. C, Squamous cell carcinoma: keratotic red and tan papule. D, Melanoma: note the asymmetry,
border irregularity, color variegation, and diameter of more than 6 mm (0.24 inch).

0.5% to about 5%; risk factors for metastasis include location on
the temple, scalp, ear, or lip; recurrence after prior treatment;
size and depth of the primary lesion; aggressive histologic find-
ings; and host immunosuppression.
The relationship of photoexposure and SCCa is different than
that between photoexposure and BCCa. SCCa and cumulative
lifetime photoexposure do not appear to be associated, but SCCa
risk increases with chronic occupational exposure, especially
during the 10 years before diagnosis.87 SCCa risk factors include
periodic recreational exposure, pale complexion, and red hair.
In select mouse models, suberythemal UVR has caused SCCa,
and gradual suberythemal exposures may be more carcinogenic
than erythemal doses.86,213 This may explain why persons with
no prior sunburns may develop SCCa. In SCCa exposed to in
vitro UVR, a gene segment (KNSTRN) was the target of point
mutations in 19% of reviewed SCCs. The presence of such a
mutation may predispose to aggressive tumor behavior; mutated
KNSTRN drives cells toward aneuploidy and tumor development.
UV-activated mutations and their lasting tumorigenesis effects
may be prevented with UV blockers, such as sunscreen.163

FIGURE 16-4  Pink, pearly papule with a rolled border and overlying
telangiectasias located on the right pectoral area of a 55-year-old FIGURE 16-5  Basal cell carcinoma demonstrating characteristic
surfer from San Diego; biopsy revealed a basal cell carcinoma. “rolled” borders and central ulceration.

341
 A B
FIGURE 16-6  Squamous cell carcinoma. A, Neglected squamous cell carcinoma on lateral and posterior
shoulder. B, Closer image of the same carcinoma.
MELANOMA
BURNS, FIRE, AND RADIATION
Melanoma is a skin cancer derived from melanocytes, cells found
within the basement membrane of epidermis. It results from
environmental and genetic factors. In the United States, incidence
of melanoma has increased since records were first kept in the
1930s, rising 121% in the 20 years between 1973 and 1994.108
Between 2002 and 2011, incidence of melanoma has been rising
on average 1.8% each year.4 Melanoma is the most common
cancer for persons 25 to 29 years old and the second most
common for those 15 to 29 years old.23 Approximately 76,100
Americans were diagnosed with new cases of invasive cutaneous
melanoma in 2014.4 Large increases in melanoma incidence have
been noted in Europe, Australia, and even Japan.142 Melanoma
mortality rates show signs of stabilizing, possibly as a result of
improved sun-protective behaviors. Survival with melanoma
PART 3
increased to 92% in 2003, from 49% in the 1950s.238 The total
estimated cost of treating melanoma was $2.36 billion in 2010.280
Melanoma includes different clinicopathologic types. Nodular
melanomas are typically smooth, dome-shaped, and friable
lesions occurring most frequently on sun-exposed areas of the
head, neck, and trunk. They are twice as common in men as in
women. Lentigo maligna manifests as a tan macule on sun-
damaged skin that may darken and spread so slowly that patients
are often unaware of changes (Figure 16-7). It typically occurs
among older patients who live in sunny climates. Superficial
spreading melanoma has no preference for sun-damaged skin
and affects adults of all ages. Color variegation (i.e., dark brown,
black, red, white, blue) is common (Figure 16-8). Lesions may
arise de novo or in association with preexisting nevus. A new
FIGURE 16-7  Melanoma on the posterior helix, which made early self-
detection difficult.
342
papule or nodule may develop as the vertical growth phase
develops. Acral lentiginous melanoma, the most common type
of melanoma in dark-skinned and Asian populations, may begin
as a light brown, uniformly pigmented macule that gradually
darkens, thickens, and ulcerates. Subungual or plantar lesions are
often present, and Hutchinson’s sign (i.e., black discoloration of
the proximal nailfold at the end of a hyperpigmented linear
streak) portends melanoma in the matrix of the nail. Amelanotic
melanoma is difficult to discern clinically. It lacks pigment and
mimics pyogenic granuloma or BCCa.
Ultraviolet radiation contributes significantly to melanoma and
is believed to be the only modifiable risk factor.7,103 The UV action
spectrum for melanoma remains uncertain. The 1000-fold
increased incidence of melanoma in humans with XP strongly
supports UVB as a causative agent.152 UVB induces melanocytic
hyperplasia, atypia, and melanoma in newborn human foreskin
xenografts on RAG-1 (immunodeficient) mice.8
Melanoma incidence increases with proximity to the equator
in white populations142 in the United States, Australia, Scandina-
via, and the nonwhite population of India.157 Intermittent intense
exposures pose a particularly high risk for melanoma.69 A 2005
meta-analysis of 57 studies associates increased risk of melanoma
with a history of intermittent sun exposure and sunburn.89 There
is only a small increased risk for total sun exposure, and a
decreased risk with heavy occupational exposure.70,89 Patients
with melanoma are twice as likely to relate a history of prior
sunburn than are age-matched controls, and are three times as
FIGURE 16-8  “Yin-yang”–shaped melanoma on back demonstrating
asymmetry, color variegation, and a diameter of more than 6 mm 
(0.24 inch). The location made early self-detection difficult.
likely to relate a history of multiple prior sunburns.70 Persons

CHAPTER 16  Exposure to Radiation from the Sun

who tan poorly and burn readily are at higher risk for mela-
noma.178 Distribution of melanomas on the trunk (in both genders)
and the lower legs (in women) is consistent with the hypothesis
that intermittent sun exposure is provocative. Melanomas also
arise in sun-protected sites, especially in nonwhite populations,
suggesting an additional cause.
Occupational UVR exposure likely plays a role in melanoma
incidence. Servicemen who served in the Pacific theater during
World War II have a higher risk of melanoma than do those who
served in Europe.36 A meta-analysis of 19 studies and 266,431
participants found airline pilots and cabin crew had an almost
twofold higher incidence of melanoma than the general popula-
tion (standardized incidence ratio [SIR] for pilots 1.83 and cabin
crew 2.09).248 Pilots and air crew had a 42% higher mortality rate
compared with the general population. Although cosmic radia-
tion exposure for air crews was not found to be above the
allowed limit, the total amount of UVR exposure has not been
FIGURE 16-9  Melanoma on the back demonstrating the ABCDEs:
quantified and may be a factor in their rising melanoma rates. asymmetry, border irregularity, color variegation, diameter of more
Glass windshield materials allow 54% of UVA radiation to pass than 6 mm (0.24 inch), and evolving features (i.e., the patient’s wife
through, and for every 900 m (2970 feet) of altitude increase, the had noticed that the area at 9 o’clock was “growing out from the rest
level of UVR increases by 15%. Cumulative UVR exposure for of it”).
pilots and cabin crew may be staggeringly high.210 Pilots have
higher rates of cataracts than the general population214 The
Federal Aviation Association has not issued any special regula- of their components: organic (i.e., chemical) and inorganic (i.e.,
tions for sun protection for pilots and crew. physical) UV filters. Both absorb UVR; inorganic filters can also
Sunburns in childhood may be particularly relevant to the later reflect and scatter UVR.183
development of melanoma. Celtic migrants to Australia who Organic sunscreens were first discovered in 1926. By 1928,
arrived before age 10 years assume the high melanoma risk of the first commercial sunscreen, which contained benzyl salicylate
native Australians; migrants more than 15 years old on arrival and benzyl cinnamate (organic filters), was marketed in the
have only one-fourth that risk.246 Europeans who live more than United States.82 Subsequent sunscreen evolution focused on UVB
1 year in a sunny climate have an increased relative risk (2.7) of protection to mitigate against development of sunburn.
melanoma. Risk increases substantially (4.3 times) if they arrive Table 16-1 lists current sunscreening ingredients approved by
before age 10.11 One study suggests childhood sun exposure the U.S. Food and Drug Administration (FDA). Two names are
contributes a serious risk only if there is subsequent and signifi- sometimes given for the same agent, because the U.S. Pharma-
cant sun exposure as an adult.9 copeia changed the names of several sunscreening agents (effec-
Association of increased melanoma risk with sun exposure tive September 1, 2002) to conform better to international
during youth may be attributable to the effect of sun on the standards.289
development of melanocytic nevi (moles) in children. The most Paraaminobenzoic acid (PABA) was patented in 1943 and
important risk factors for melanoma are number of nevi and the became commercially available in 1960. PABA is an effective UVB
number of atypical nevi.90 Numbers of benign acquired nevi
increase with increasing acute and chronic sun exposure.33,90,113,294
In Australia, the number of nevi (up to 12 years old) increases TABLE 16-1  Sunscreening Agents Approved in the
with increasing proximity to the equator.143 Sun-related increased United States
nevus counts are demonstrable at early ages. In Queensland
preschoolers less than 36 months old, increased nevus counts Maximal Ultraviolet
are associated with more time spent outdoors and a history of Sunscreen Screen (%) Radiation
sunburn.113 Established nevi may develop histologic changes
transiently, simulating melanoma after a single UVR exposure.281 Organic
Data suggest sunburn can induce malignant transformation in Aminobenzoic acid 15 UVB
benign nevi.44 Avobenzone 3 UVA I
Efforts have been made to educate and protect populations Cinoxate 3 UVB
at risk; improved photoprotection and early detection have been Dioxybenzone 3 UVB, UVA II
widely promoted. In Australia, sunscreen sales are tax free, hats Ecamsule* 2 UVB, UVA
are typically required for children when they are playing outdoor Homosalate 15 UVB
sports, and public parks increasingly feature artificial shade. The Menthyl anthranilate (meradimate) 5 UVA II
Skin Cancer Foundation encourages monthly self-examinations, Octocrylene 10 UVB, UVA II
with special attention to pigmented lesions that display atypical Octyl methoxycinnamate 7.5 UVB
clinical features: the ABCDEs of melanoma232: asymmetry; border (octinoxate)
irregularity; color variegation; diameter of more than 6 mm (0.24 Octyl salicylate (octisalate) 5 UVB
inch); and evolving features (Figure 16-9). Nevi with these clinical Oxybenzone 6 UVB, UVA II
features, symptomatic nevi, or nevi that bleed or ulcerate should Padimate O 8 UVB
be evaluated by a dermatologist. Notably, conventional ABCDEs
Phenylbenzimidazole sulfonic acid 4 UVB
may fail to detect a majority of pediatric melanomas, especially
(ensulizole)
in prepubertal children. For this reason, any de novo, amelanotic,
bleeding, or rapidly enlarging “bump” should be treated as highly Trolamine salicylate 12 UVB
suspicious in this uniquely vulnerable population.52 Inorganic
Titanium dioxide 25 UVB, UVA
Zinc oxide 25 UVB, UVA
PHOTOPROTECTION
Modified from US Food and Drug Administration: Sunscreen drug products for
SUNSCREENS over-the-counter human use [stayed indefinitely]. 21 CFR 352. www.gpo.gov/
fdsys/pkg/CFR-2002-title21-vol5/pdf/CFR-2002-title21-vol5-sec352.10.pdf.
Sunscreens are topical temporary protectants against UVR. They Revised April 1, 2013. Effective June 4, 2004.
are classified into two distinct types based on the chemical nature *Approved by the U.S. Food and Drug Administration on July 21, 2006.

343
 absorber but provokes contact and photocontact dermatitis in
approximately 4% of exposed persons and can permanently stain
fabrics a dull-yellow color. PABA has been largely replaced by
PABA esters (e.g., amyl dimethyl PABA [padimate A] and octyl
dimethyl PABA [padimate O]). These absorb UVB well and are
less staining and less allergenic.
Cinnamates are the next most potent class of UVB absorbers,
often replacing PABA in PABA-free sunscreens. Octyl methoxy-
cinnamate (octinoxate; Parsol MCX) is an order of magnitude less
potent than padimate O.167 Octocrylene, which is a cinnamate
derivative, is a weak UVB absorber that also absorbs UVA mod-
estly up to 360 nm. Cinnamates may cause contact dermatitis.
Cinoxate is the most frequent contact sensitizer, with cross-
sensitization to related cinnamates in coca leaves, balsam of Peru,
and cinnamon oil.64
Salicylates (e.g., homosalate, octyl salicylate [octisalate]) are
relatively weak absorbers of UVB. They are most often used in
combination with other sunscreening agents. Salicylates are non-
sensitizing and water insoluble and help to solubilize benzophe-
nones in commercial products.84
Anthranilates (e.g., methyl anthranilate [meradimate]) are simi-
larly weak UVB absorbers, which also filter UVA. They display
peak absorption at 340 nm.167
BURNS, FIRE, AND RADIATION
Phenylbenzimidazole sulfonic acid (ensulizole) is a unique
UVB absorber, in that it is water soluble. It is increasing used in
oil-free cosmetic sunscreens.167
Benzophenones (e.g., oxybenzone, dioxybenzone, sulisoben-
zone) are broader-spectrum sunscreening agents, with good
absorption in the UVB and UVA ranges up to 360 nm.167
As UVA photodamage is increasingly appreciated, UVA-
blocking agents (e.g., avobenzone, ecamsule) have been
introduced. Avobenzone (Parsol 1789, butyl methoxydibenzoyl-
methane) is a potent UVA absorber and the only organic filter
approved as a long-range UVA protectant.167 Its absorption
peak at 358 nm falls almost to zero at 400 nm.243 Photodeg­
radation may limit its effectiveness. Under simulated solar
light, avobenzone can be degraded 36% within 15 minutes,250
but a patented complex known as Helioplex, a combination
PART 3
of avobenzone, oxybenzone, and diethyl 2,6-naphthalate, is
remarkably photostable.50 Select stabilizing compounds (e.g.,
vitamin C, vitamin E, iron chelators) may additionally retard
photodegradation.194
Ecamsule (Mexoryl SX) is the newest sunscreening agent to
be approved by the FDA. It has been available in Europe for
several years. It is an excellent UVA filter and modest UVB filter.
Ecamsule is highly photostable and thermostable. It protects skin
from repeated UVA exposures and prevents histologic changes
associated with photoaging.258
Inorganic filters, historically known as inorganic sunscreens,
are opaque agents that include calamine, ichthammol, iron oxide,
kaolin, red veterinary petroleum, starch, talc, titanium dioxide
(TiO2), and zinc oxide (ZnO). Of these, only TiO2 and ZnO are
FDA approved. Inorganic filters protect throughout the UVR and
visible spectra and may even protect against IR-induced ery-
thema.224 Classic inorganic blockers tend to be messy, uncomfort-
able, and cosmetically undesirable.
Preparations of TiO2 and ZnO with a submicron (i.e., nano)
particle size are now widely available. Classic TiO2 and ZnO
particle size ranges (150 to 300 nm for TiO2 and 200 to 400 nm
for ZnO) permit light to be reflected and scattered. Submicron
dimensions (20 to 150 nm for TiO2 and 40 to 100 nm for ZnO)
make these particles more soluble and minimally reflective of
visible light. This makes them nearly transparent in thin coats.
ZnO’s lower refractive index in the visible range makes it more
transparent than TiO2.203 Submicron-sized preparations signifi-
cantly absorb UVR, providing broad-spectrum protection from
UVB and UVA, and blur the distinction between organic and
inorganic sunscreens.63,167,249 TiO2 and ZnO are sometimes
marketed as “chemical-free” sunscreens, which is clearly a
misnomer.
No studies have shown percutaneous penetration of the
nanoparticles into human adult skin or any cellular damage.39,217
The ecologic impact of large amounts of metal oxide nanopar-
ticles in the environment is unknown.222
344
Eight different UV filters (e.g., quinolone derivatives and novel
UVA filters) are currently in the FDA application process. Already
in use in Australia and Asia, these filters will greatly broaden the
U.S. sunscreen market if approved.37,231,287,298
Sunscreen Vehicles
Sunscreen vehicles affect efficacy and acceptability. The ideal
vehicle spreads easily, maximizes skin adherence, minimizes
interaction with active sunscreening agent, and is noncomedo-
genic, nonstinging, nonstaining, and inexpensive. The best
vehicle is highly dependent on personal preference. Creams
and lotions (emulsions) are most popular. Lipid-soluble sun-
screening agents result in an objectionable greasy feel. “Dry
lotions” minimize the lipid component(s) and often include
water-soluble sunscreening agents to reduce oiliness.167 Sun-
screen oils contain only a lipid phase and are cosmetically less
acceptable.
Gels tend to be nongreasy but wash or sweat off easily. Gels
produce more stinging and irritation. Sticks typically incorporate
sunscreening agents into wax bases but are difficult to apply to
larger areas. Aerosols cover large areas quickly but tend to dis-
perse spray into the air and form an uneven film.167 Aerosols
need to be rubbed in to provide uniform protection.14 Sunscreens
are increasingly being incorporated into cosmetics (e.g., founda-
tions, lipsticks, moisturizers).
Sun Protection Factor
A sunscreen’s ability to protect skin from UVR-induced erythema
is measured by the sun protection factor (SPF). SPF is defined
as the ratio of UVR required to produce minimal erythema (1
MED) in sunscreen-protected versus unprotected skin.139,284 Mul-
tiplying the time required to burn an individual’s unprotected
skin by the sunscreen’s SPF factor provides the time skin would
be protected from burning with sunscreen. It can be represented
by the following formula:
MED of sunscreen-protected skin
SPF =
MED of unprotected skin
Testing conditions are standardized by the FDA.284 The
agent to be tested is applied at a standard concentration of
2 mg/cm2. Testing is performed indoors with a solar simulator
on the back between the beltline and the scapulae. SPF is typ-
ically determined on a panel of 20 (or a maximum of 25) indi-
viduals with skin types I, II, or III (see Box 16-1). The mean
determines the sunscreen’s SPF. Although indoor testing with a
solar simulator is more reproducible than outdoor natural sun
exposure, it may yield a falsely high SPF value. In outdoor
testing of more than 30 sunscreens labeled SPF 15, none was
found actually to have an SPF of more than 12.226 Factors
responsible for lower SPF values with outdoor testing include
sweating, clothing, toweling off, sand abrasion, and application
variability. Solar simulators generally have less UVA output
than does sunlight.250
Determinations of SPF use erythema as the measurable end
point. Erythema is predominantly a result of UVB and not UVA
exposure. Consequently, SPF is primarily a measure of UVB
protection. Tables 16-2 shows the relationship of SPF to UVB
absorption.
How high an SPF is necessary? Given that SPF 15 blocks 93%
of UVB, some argue SPF 15 is sufficient,185 and that higher label-
ing claims are misleading and costly for consumers. In several
studies, higher SPF sunscreens conferred clinical and histologic
benefits. In one study, a single application of SPF 25 sunscreen
protected just as well as did multiple applications of SPF 15 for
up to 6 hours of exposure.220 Histologically, an SPF 30 sunscreen
provides better protection against sunburn cell formation than
does an SPF 15 sunscreen.137
Sunscreen Application
Sunscreen underapplication, uneven application, and de-
layed application result in unnecessary photoexposure and
photodamage.

TABLE 16-2  Skin Protection Factor and Ultraviolet B
Radiation Absorption
Sun Protection Factor Ultraviolet B Radiation Absorption (%)
2 50.0
4 75.0
8 87.5
15 93.3
30 96.7
50 98.0
The most persuasive argument favoring higher-SPF sunscreens
is that there are variations in application technique. Protection
provided by sunscreen is related to amount of product applied.253
Typically, sunscreens are applied at much lower concentrations
(0.5 to 1 mg/cm2) than they are tested (2 mg/cm2).252 Resultant
SPF is thereby reduced to as low as 20% to 50% of the labeled
value SPF for organic sunscreens.35,277 Inorganic sunscreens tend
to be applied even more thinly, most likely because of their
cosmetic visibility.32 For TiO2 products, application concentra-
tions of 0.65 mg/cm2 result in SPF values of only 20% to 30% of
labeled value.277 Persons who burn more easily tend to apply
thicker concentrations of sunscreen.61
Uneven application further reduces sunscreen protection.
Individuals typically cover the forehead adequately, but temples,
ears, and posterior neck are often undertreated or missed
entirely.172 Sunscreens containing disappearing colorants are
popular because they provide visible assurance of complete
coverage. Adequate coverage of only chronically exposed areas
(face, ears, dorsal surfaces of hands) requires 2 to 3 g (0.07 to
0.11 oz) of product per day.167 This requires using an 8-oz bottle
of sunscreen every 80 to 120 days.
Application delay imposes a further decrease in protective-
ness. In one study,241 sunscreen was applied only after arriving
at the beach in 98% of families. Median delay from arrival at the
beach to sunscreen application to the entire family was 51
minutes.
Ultraviolet A Radiation Protection Factors
With increased understanding of UVA-induced photodamage and
the recent addition of better UVA-blocking agents (e.g., avoben-
zone, ecamsule, micronized TiO2 and ZnO), more attention has
been focused on measuring UVA protection. Several measures
of UVA protectiveness (e.g., the UVA protection factor) have
been suggested. None has been widely accepted.244
Sunscreen Regulation
In the United States, sunscreens are regulated over-the-counter
(OTC) drugs. The FDA’s Final Over-the-Counter Drug Products
Monograph on Sunscreens (1999) established allowable sun-
screening agents, testing procedures, and labeling claims for
efficacy, water resistance, and safety.284 In 2011 the FDA updated
labeling claims and testing procedures.285 The final rule estab-
lishes labeling and effectiveness testing for OTC sunscreen prod-
ucts marketed without an approved application under Section
505 of the Federal Food, Drug, and Cosmetic Act. It does not
address determinations for substances generally recognized as
safe and effective (GRASE) in sunscreen products. The new rule
provides the following services to the public:
• Helps ensure products will be appropriately labeled and
tested for both UVA and UVB protection
• Promotes proper use of sunscreens and greater consumer
protection from damaging effects of UVR
• Identifies claims that render a product “misbranded” or claims
that are not allowed on any OTC sunscreen drug product
marketed without an approved application (e.g., “sunblock,”
“sweatproof,” and “waterproof” have been deemed misleading
and are no longer permitted)
The final regulations reduce the number of individuals
required in SPF testing from 20 to 10 and require only a single
in vitro test to demonstrate broad-spectrum protection. Perfor-
CHAPTER 16  Exposure to Radiation from the Sun
mance is on a pass/fail basis using a critical wavelength of
370 nm. Critical wavelength is defined by FDA as the wavelength
at which the integral of the spectral absorbance curve for a par-
ticular sunscreen product reaches 90% of the integral over the
UV spectrum from 290 to 400 nm:
λc 400
∫ A ( λ ) d λ = 0. 9 ∫ A ( λ )d λ
290 290
where λc = critical wavelength, A(λ) = mean absorbance at
each wavelength, and dλ = wavelength interval between
measurements.289
Labeling.  Products that pass testing (i.e., possess a mean
critical wavelength ≥370 nm) will be labeled broad spectrum and
SPF 15 (or higher), and demonstrate protection against both UVB
and UVA radiation. New labeling will also inform consumers that
these sunscreens not only protect against sunburn, but also can
reduce risk of skin cancer and early skin aging. For these broad-
spectrum products, higher SPF values also indicate higher levels
of overall protection.
Sunscreen products that are not broad spectrum, or that are
broad spectrum with SPF values from 2 to 14, will be labeled
with a warning such as, “Unlike broad-spectrum products and
those higher SPF values, this product has been shown only to
help prevent sunburn, not skin cancer or early skin aging.”
The FDA requires labels to include a new “direction
statement”:
Sun Protection Measures: Spending time in the sun increases your risk
of skin cancer and early skin aging. To decrease this risk, regularly use
a sunscreen with a Broad Spectrum SPF of 15 or higher and other sun
protection measures including:
• Limit time in the sun, especially from 10 a.m.-2 p.m.
• Wear long-sleeved shirts, pants, hats, and sunglasses.
Required warnings on all covered OTC products will also
include the following (Figure 16-10):
• “Do not use on damaged or broken skin.”
• “When using this product, keep out of eyes. Rinse with
water to remove.”
• “Stop use and ask a doctor if rash occurs.”
Issues Not Finalized.  Products containing inorganic sun-
screen agents can no longer be marketed as “sunblocks,”284 but
other marketing issues remain. The “Advance Notice of Proposed
Rulemaking (ANPR): Sunscreen Drug Products for Over-The-
Counter Human Use; Request for Data and Information Regard-
ing Dosage Forms” has approved gels, oils, lotions, creams,
butters, pastes, and ointments, but not powders, body washes,
shampoos, or wipes, which no longer may be able to be mar-
keted in the United States.288 Sprays continue to be marketed and
are not mentioned in the regulations.
Proposed FDA rules would limit maximum SPF value on
sunscreen labels to “50+,” because data are insufficient to show
that products with SPF values higher than 50 provide greater
protection.
Substantivity
Substantivity is the ability of sunscreens to resist being washed
off by water. The FDA’s 2011 final rule changed testing and
labeling requirements to make it easier for consumers to under-
stand water resistance.285 Data indicate that individuals at the
beach or pool spend an average of 21 minutes in the water and
go into the water an average of 3.6 times per outing.285
Sunscreens newly labeled “water resistant (40 minutes)” or
“water resistant (80 minutes)” will have passed testing require-
ments that include water immersion (with moderate activity) for
20 minutes with 15-minute drying times (no towel drying),
repeated once or thrice, respectively.285
Substantivity testing is an imperfect science. Numerous
factors (e.g., relative humidity, amount applied, immersion time,
activity level) must be considered. MED for skin in salt water is
less than the MED for skin in fresh water; both are lower than
the MED of dry skin.88 Cold churning water, sand abrasion, and
toweling add to sunscreen loss. It is not clear if water-resistant
345
 sunscreens are truly surf resistant. The concerns about saltwater
substantivity have led to marketing of “surf shop” sunscreens.
Few published data indicate whether these products are more
substantive.
The PABA and PABA esters are intrinsically substantive as a
result of bonding to stratum corneum proteins. Other sunscreens
must be incorporated into vehicles that confer substantivity.
Substantivity can be increased by applying sunscreen 15 to 30
minutes before water exposure. Reapplication after swimming
or sweating increases protection. Affordable UVA- and UVB-
protective water-resistant sunscreens are widely available
(Table 16-3).
Stability
Photostability is a sunscreen’s ability to remain intact and
effective after sun exposure. Questions regarding photostability
have been raised about avobenzone, octyl dimethyl PABA, and
octyl methoxycinnamate. Photodegradation of octyl methoxycin-
namate allows histologic and enzymatic injury to the skin.188
Failure of a photolabile sunscreen may result in genotoxicity.189
In a study of 27 photoprotective lipsticks, 14 became partially
photoinactive after moderate UVR exposure.181 Twelve were pho-
tolabile in the UVA range, one in the UVB range, and one in
BURNS, FIRE, AND RADIATION
both UVA and UVB ranges.
Photostability can be improved by using combinations of
sunscreening agents. Octocrylene stabilizes avobenzone in a
number of sunscreen formulations; 4-methylbenzylidene camphor
stabilizes octyl methoxycinnamate.25 Vehicle formulations also
affect stability.25
PART 3
FIGURE 16-10  Sunscreen labeling according to 2011 final rule. (From US Food and Drug Administration:
Sunscreen drug products for over-the-counter human use: Final rule, Fed Reg 76:35620, 2011.)
346
There are few published data regarding packaging, storage,
and shelf life of sunscreens. Packaging may affect sunscreen
acceptability and stability. Shelf life of at least 1 year is presumed
for most commercially available sunscreens. Sunscreens exposed
to extremes of temperature for long periods (e.g., glove compart-
ments) may be degraded.
Sunscreen Prevention of Chronic Photodamage
Sunscreens prevent sunburns and mitigate UVR-induced histo-
logic damage, UVR-induced immunosuppression, photoaging,
and photocarcinogenesis. Sunscreens reduce UVR-induced DNA
damage,41 decreasing pyrimidine photoproducts in humans41 and
UVR-induced p53 mutations and skin cancer in mice.5 Sunscreen
nearly eliminates overexpression of p53 in mice after acute233 and
chronic88 UVR exposure. In humans, an SPF 15 sunscreen reduces
p53+ cells by 33% after chronic UVR exposure.18
Published effects of sunscreen on immunosuppression are
contradictory, largely resulting from the complex relationships of
UVR dosing and sensitivity in different experimental models.
Overall, sunscreens mitigate UVR-induced immunosuppression.
SPF is not a reliable measure of a sunscreen’s ability to block
UVR-induced immunosuppression; two sunscreens with identical
SPF values may vary considerably in their immunoprotectant
effects.16,237,314 A broad-spectrum SPF 15 sunscreen prevents the
UVR-induced suppression of contact hypersensitivity to dinitro-
chlorobenzene, a potent topical allergen, in humans.259 In suscep-
tible mice injected with melanoma, sunscreens fail to adequately
suppress UVB enhancement of melanoma growth.305 This finding
has been used to support a peculiar antisunscreen stance. A

FIGURE 16-10, cont’d
reasonable interpretation is that sunscreens by themselves are not
sufficient to prevent all immunosuppressive sequelae of UVR
exposure.
Sunscreens reduce sunburn cell formation and solar elastosis29
in humans. Histologic changes of photoaging in mice are pre-
vented by pretreatment with SPF 15 sunscreen.146,147 Higher-SPF
sunscreens provide increasing protection against UVB-induced
wrinkling in mice.22 Histologic and clinical signs of UVA-induced
photoaging are prevented by broad-spectrum sunscreens.114
Sunscreens and Nonmelanoma Skin Cancer
Daily sunscreen use is associated with prevention of AKs, SCC,
and melanoma.103,56
Actinic Keratoses and Squamous Cell Carcinoma.  Sun-
screen use reduces formation of precancerous actinic keratosis
and promotes resolution of preexisting lesions.48,212 In a 2-year
trial of sunscreens, persons who benefited most had the greatest
number of keratoses at enrollment,212 underscoring the value of
continuing sunscreen use in adults. A trial in Australia comparing
an SPF 16 sunscreen (2% avobenzone and 8% octinoxate) against
a sunscreen of the participants choosing, found a 24% reduction
in actinic keratosis development and acquisition at 4.5 years and
a 38% reduction in SCCa.104 Liquid-base makeup provides an
approximate SPF 4 because of pigments used in the founda-
tion.167 Women who use lipstick have a lower incidence of SCCa
than those who do not use lipstick.120,167
Basal Cell Carcinoma.  Daily use of SPF 15 sunscreen in
adults reduces the incidence of SCCa but not of BCCa.104 One
study estimated that using an SPF 15 sunscreen from birth until
CHAPTER 16  Exposure to Radiation from the Sun
age 18 years would reduce the lifetime risk of NMSC by 78%,
but did not show a significant decline in BCCa.275
Sunscreens and Melanoma
Controversy exists regarding the effects of sunscreen use on
melanoma incidence. Previous epidemiologic studies have failed
to demonstrate conclusive evidence of decreased melanoma inci-
dence with sunscreen use. Several studies have suggested an
increased risk of melanoma with sunscreen use.12,62 A 1996 meta-
analysis evaluated melanoma risk in sunscreen users;62 one study
showed decreased risk,124 and seven showed increased risk.
Subsequent studies have continued to show contradictory results.
Confounding these studies are the following:
• Persons at the highest risk for melanoma (i.e., those with fair
complexions who burn easily) may be the same persons who
use sunscreens.
• Prior sunscreen products were inferior (e.g., lower SPFs and
narrower spectra). Modern sunscreens are more substantive,
with higher SPFs and substantially broader and better UVA
protection.
• Because sun exposure during childhood appears to be the
most provocative for melanoma, surveying adults about their
current sunscreen habits may be irrelevant and misleading.
A large, community-based 2011 study in Australia provides
strong evidence that daily application of sunscreen may directly
reduce melanoma risk.103 During 15 years of follow-up, in persons
provided with broad-spectrum (SPF 16) sunscreen for daily
use, risk for any first primary melanoma was reduced by 50%
(p = 0.051) and for invasive melanoma by 73% (p = 0.045).
347
 TABLE 16-3  Select Sunscreen Products

Product Sun Protection Factor Active Ingredients

High Sun Protection Factor Waterproof Broad-Spectrum Creams and Lotions

Banana Boat Sport 50 30 B, C, OC, S
Banana Boat Sunscreen Sport Family Size Broad 50 A, S, B, C
Spectrum Sun Care Sunscreen Lotion
Blue Lizard Australian Sunscreen Lotion 30+ B, C, OC, ZO
Blue Lizard Australian Sunscreen, Sensitive 30+ ZO, TI
Coppertone Sport Sunscreen 30 B, C, S
Coppertone Water Babies Sunscreen Lotion 45 B, C, S
Dermatone Sunscreen Lotion 36 C, PBSA, ZO
EltaMD UV Clear 46 ZO, C
EltaMD UV Physical 41 ZO, TI
Hawaiian Tropic Sunscreen Silk Hydration 30 A, B, C
Kiss My Face Sensitive Side 30 ZO, C
Neutrogena Ultra Sheer Dry-Touch Sunscreen 55 A, B, OC, S
Neutrogena Age Shield Face Lotion Sunscreen 110 A, C, S, B
Ocean Potion Broad Spectrum, Anti-Aging Lotion 50 A, B, C, S
Ombrelle Complete Extreme Lotion 50 A, B, OC, S
Panama Jack Sunscreen Lotion 50 B, C, OC, S
BURNS, FIRE, AND RADIATION

SolBar PF Cream 50 B, C, OC, S

High Sun Protection Factor Gels

Bullfrog Land Sport With Breathable Sweat TECH 50 B, C, OC, S
Quik Gel

High Sun Protection Factor Sprays

Banana Boat Sunscreen Sport Performance Quik 30 A, S, B, C
Dri Broad Spectrum Suncare Sunscreen Spray
Banana Boat Sunscreen Sport Performance 30 A, OC, B
CoolZone Broad Spectrum Suncare Sunscreen
Spray
Coppertone Sport Continuous Sunscreen Spray 30 B, C, S

High Sun Protection Factor Sticks

PART 3

Neutrogena Sunscreen Ultra Sheer Stick 70 A, S, OC, B

Shade Stick 30+ B, C, S

Specialty Sunscreens
Australian Gold Spray with Bronzer 30 A, S, B, C
Babyganics Mineral-Based Baby Sunscreen Lotion 50 S, ZO, TI
Loreal Paris Sublime Sun Advanced Sunscreen 30 A, S, C
Crystal Clear Mist

Lip Screens
Dermatone Medicated Lip Balm 23 B, PB
Neutrogena Lip Moisturizer 15 B, C

Inorganic (Physical) Sunscreens

Neutrogena Sensitive Skin Sunscreen Lotion 30 TI
Vanicream Sunscreen 30 TI, ZO

Moisturizers Containing Higher-SPF Sunscreens

Anthelios SX Daily Moisturizing Cream 15 A, E, OC
Aveeno Positively Radiant Daily Moisturizer Broad 15 A, C, S
Spectrum SPF
Eucerin Daily Protection Moisturizing Face Lotion 30 ZO, TI, S, PBSA
Lubriderm Daily Moisture Lotion with Sunscreen 15 B, C, S
Broad Spectrum SPF
Neutrogena Healthy Defense Daily Moisturizer 30 C, OC, PBSA, ZO
Broad Spectrum SPF
Neutrogena Oil-Free Moisture 35 OC, S, A, B
Purpose Dual Treatment Moisture Lotion 15 C, MA, TI

Data from Shuai X, Kwa M, Agarwal A, et al: Sunscreen product performance and other determinants of consumer preferences. JAMA Dermatol 2016;152(8):920-927.
A, Avobenzone; B, benzophenones; C, cinnamates; E, ecamsule; MA, methyl anthranilate (meradimate); OC, octocrylene; PB, paraaminobenzoic acid or
paraaminobenzoic acid ester; PBSA, phenylbenzimidazole sulfonic acid (ensulizole); S, salicylates; TI, titanium dioxide; ZO, zinc oxide.

348
Limitations of the study include borderline significance of the risk
reduction.97 Results of this study support sunscreen use to help
reduce risk of melanoma.
The effect of sunscreens and clothing protection on numbers
of nevi in children and adolescents (a prominent risk factor for
melanoma)90 is uncertain. In one study of children younger than
36 months, sunscreen use is associated with decreased nevus
counts,113 whereas in another, sunscreen increased benign nevi
in adolescents.294 Protective clothing had no effect.165 It is not
clear why intermittent sun exposure, especially during childhood,
is associated with increased risk of melanoma, whereas chronic
occupational exposure may be partially protective.89
Sunscreen Side Effects
Sunscreen side effects are generally mild and limited. In one
study, participants applied SPF 15 sunscreen or vehicle control;81
19% of both groups had adverse reactions. Most were irritant in
nature, fewer than 10% were allergic, and more than 50% of
persons who developed irritation were atopic. Allergic reactions
to sunscreens are more often the result of preservatives and
fragrances than of active sunscreening agents.64,261
While uncommon, most sunscreening agents may cause aller-
gic or photoallergic contact dermatitis.139 Benzophenone-3 and
octyl methoxycinnamate are leading UV filters triggering allergic
responses.116 In children with allergic contact dermatitis with a
photodistribution, patch testing to evaluate their sunscreens may
be helpful to determine the allergic trigger. PABA is now rarely
used because it sensitizes approximately 4% of exposed persons.
After an individual is sensitized, cross-sensitization with thiazides,
sulfonamides, benzocaine, and hair dyes that contain paraphenyl-
enediamine may occur.239
Stinging or burning without accompanying erythema, scaling,
or dermatitis is common, especially in periocular areas and in
patients with rosacea. Addition of skin protectants (e.g., cyclo-
methicone) to the sunscreen vehicle can mitigate this.215 Certain
vehicles (e.g., alcoholic gels) may be more stinging. Even when
periocular application is avoided, perspiration, water immersion,
and rubbing may cause sunscreen to migrate, thus producing
symptoms.
Comedogenicity is primarily related to ingredients in the
vehicle base. Certain common excipients (e.g., almond oil, cocoa
butter, isopropyl myristate, isopropyl palmitate, olive oil) are
possible comedogens.
Both TiO2 and ZnO can generate reactive molecular species,
called free radicals, with sun exposure.63 TiO2 is more photoac-
tive than is ZnO.203 Photoactivated TiO2 can damage DNA in
vitro.119 In vivo, it is unlikely that TiO2 particles penetrate the
stratum corneum to reach underlying epidermal cells that contain
DNA. Transmission electron microscopy fails to demonstrate TiO2
penetration of the stratum corneum.65 Data demonstrate that ZnO
is not absorbed and Zn levels are unchanged after application.92
Coating TiO2 or ZnO with silicone halts photoproduction of reac-
tive species.63 Concerns have been raised regarding use of these
agents on broken skin.
Some sunscreening agents may have weak estrogenic or anti-
androgenic activity.256 Benzophenone-3, octyl-methoxycinnamate,
and 3-(4-methylbenzylidene) camphor may have estrogenic
effects on human breast cancer cells in culture.255 In one study,
whole-body application of these three sunscreening agents was
tested. Plasma and urine levels of these agents were detectable
in men and postmenopausal women; luteinizing hormone and
follicle-stimulating hormone were unchanged, and there were
only minor changes in testosterone and estradiol (in men only).
The authors concluded that these endocrinologic alterations are
clinically insignificant, and that these sunscreen products are safe
for use in adults. With chronic use, oxybenzone may have estro-
genic and antiandrogenic activity.118,177,255,297 Oxybenzone is not
concentrated in plasma after use and does not have high affinity
for estrogen receptors.133
ROLE OF VITAMIN D
The relationship among sun exposure, skin cancer, and vitamin
D has garnered media attention. Skeletal effects of vitamin D are
well established in the literature.138 Extraskeletal effects of vitamin
CHAPTER 16  Exposure to Radiation from the Sun
D began to be studied after discovery of vitamin D receptor
(VDR) within skin, pancreas, breast, prostate, and colon cancer
cells.138 Additionally, VDR has been found on immune system
cells.47,263,290 A 2001 Institute of Medicine report stated evidence
was insufficient to provide recommendations on vitamin D for
extraskeletal disease prevention.131 A 2011 meta-analysis by the
U.S. Preventive Services Task Force (including 19 randomized
controlled trials and 28 observational studies) found no signifi-
cant benefits of vitamin D in prevention of cancer.48
Other studies show a possible protective effect of vitamin D
against systemic malignancies. Mortality rates of several common
cancers in the United States (e.g., breast, colon, prostate) increase
with increasing latitude, and thus with decreasing sun exposure.68
Sunlight reduces the risk of non-Hodgkin’s lymphoma.267 Among
men in the U.S. Navy, regular sun exposure reduces melanoma
risk.91 In patients with melanoma,19 sun exposure is associated
with increased survival. Melanoma may be among the tumors for
which vitamin D has a salutary effect. Supporting this hypothesis
are laboratory data demonstrating VDRs on melanoma cells and
growth inhibition in response to vitamin D.51 A case-control study
found that diets rich in vitamin D and carotenoids were associ-
ated with reduced melanoma risk.198 Long-term studies of vitamin
D assessing causation and dose-response in skin cancer preven-
tion are necessary.
Sunscreen’s role in reduction of systemic vitamin D levels
has been extensively studied. Although regular sunscreen use
can decrease cutaneous synthesis of vitamin D3191 and circulat-
ing levels of measurable 25-hydroxyvitamin D,192 even the
most conscientious sunscreen users appear to maintain normal
levels of vitamin D.186 Individuals using SPF 15 sunscreen for
2 years maintained normal parathyroid hormone levels and
normal bone metabolic markers.75 Patients with XP maintained
normal vitamin D levels over 6 years, despite rigorous photo-
protection with sunscreens, clothing, and sun avoidance.270
The NHANES 2003-2006 questionnaires showed that frequent
sunscreen use was not associated with lower vitamin D levels
in Caucasians.170
Controversy surrounding vitamin D and sunscreen may stem
from inadequacies in sunscreen application in real-life settings.
Appropriately thick application of sunscreen allows for 1/SPF%
of UVR to be absorbed, providing a source of vitamin D produc-
tion. Most adults do not apply sufficient sunscreen (at 0.5 mg/
cm2 instead of the recommended 2 mg/cm2). This can decrease
the labeled SPF by a factor of 8. Sunscreen alone is not sufficient
to be the sole predictor of vitamin D insufficiency in the general
population.219
The recommended dietary allowance (RDA) has varied. Amer-
ican Academy of Pediatrics 2008 guidelines recommending a
daily intake of vitamin D of 400 international units (IU) per day
effectively doubled the dose recommended in the 2003 guide-
lines.295 Some authors advocate for more aggressive supplementa-
tion to meet physiologic need, particularly for individuals who
are deprived of sun exposure.254 Given that only brief sun expo-
sures are needed to synthesize vitamin D,121 Holick122 suggests
an approach of sensible sun exposure, which involves 5 to 10
minutes of exposure two or three times weekly in conjunction
with the dietary intake of vitamin D and vitamin supplements.
This recommendation has raised considerable controversy and
concern in the dermatologic community.213
In 2010, the Institute of Medicine concluded that bone health
was the only outcome for which causality and sufficient dose-
response evidence are established. Vitamin D’s role in cancer
prevention was not found to be conclusively demonstrated. The
new RDA for vitamin D assumes minimal sun exposure and
suggests the following:
• 1 to 70 years, 600 IU per day
• 71 years or older, 800 IU per day
The committee continued to recommend 400 IU per day as
adequate intake (AI) for infants up to 12 months of age. The
group also established tolerable upper intake levels (UL) for
vitamin D, taking into account emerging evidence of U-shaped
associations (i.e., increased risk at both low and high levels and
lowest risk at moderate levels of serum 25-hydroxyvitamin D)
349
 for all-cause mortality, cardiovascular disease, vascular calcifica-
tion, pancreatic cancer, falls, frailty, and fractures. The recom-
mended UL for vitamin D follows131:
• 9 years and older, 4000 IU per day
• 4 to 8 years, 3000 IU per day
• 1 to 3 years, 2500 IU per day
• 6 to 12 months, 1500 IU per day
• 0 to 6 months, 1000 IU per day
These recommendations have been upheld by the U.S. Pre-
ventive Services Task Force Unit in its 2013 recommendations,
with a goal of 800 IU for asymptomatic adults older than 65.209
OTHER SOURCES OF SUN PROTECTION
Clothing Protection
Clothing provides substantial sun protection to broad surface
areas. The United States has the most stringent UV-protective
clothing standards in the world and assesses fabrics using the
ultraviolet protection factor (UPF). UPF measures both UVB and
UVA radiation blocked. Approved fabrics must undergo 40 simu-
lated launderings, must be exposed to 100 fading units of simu-
lated sunlight (equivalent to 2 years of sun exposure), and must
be exposed to chlorinated water if marketed for water use.272
BURNS, FIRE, AND RADIATION
Although the FDA was initially involved, the Federal Trade Com-
mission now reviews clothing applications.
Several manufacturing strategies are used to achieve high
SPFs. Solumbra is made of tightly woven nylon with an SPF of
30 or more (Figure 16-11). In hairless mice, this fabric is signifi-
cantly better than cotton for reducing formation of UVR-induced
SCCa.197 SolarKnit uses chemically treated cotton and cotton-
synthetic blends to achieve an SPF of 30 or more. Rayosan, a
UVR-absorbing agent, bonds to various fabrics and increases the
SPF by up to 300%.176 Tinosorb FD, a unique organic UVR pro-
tectant, may be incorporated into detergents to increase the SPF
of clothing with each wash.
Unregulated clothing varies considerably in ability to block
UVR. The SPF fabrics range from 2 (polyester blouse) to 1000
(cotton twill jeans).242 A typical dry white cotton T-shirt has SPF
PART 3
of 5 to 9.242 The most important factors for determining SPF are
tightness of the weave176,242 and the actual fabric. Lycra is an
extreme example of this; it blocks almost 100% of UVR when lax
and only 2% when maximally stretched.176 Other determinants
include wetness and color. Dry and dark fabrics have a higher
SPF than do wet and white fabrics.
Clothing prevents chronic photodamage and is associated
with fewer nevi.10 Blue denim reduces UVR-induced p53+ cells
twice as effectively as does an SPF 15 sunscreen.18 Denim greatly
A B
FIGURE 16-11  Photoprotective clothing. A, Solumbra hiking apparel.
B, Coolibar swimwear. (A courtesy Sun Precautions; B courtesy
Coolibar.)
350
reduces formation of skin cancers in patients with XP.17 Wearing
long sleeves was associated with lower 25(OH)D levels.169
However, 100% cotton clothing transmits 15% of UVR. Adequate
vitamin D levels can be achieved even if only the face and palms
are exposed.269
Ladies’ hosiery provides surprisingly low SPF: black hose have
SPF of 1.5 to 3, and beige hose SPF of less than 2.262 Hat protec-
tion varies as a function of brim diameter and style. Small-
brimmed (<2.5 cm [1 inch]) hats adequately protect the forehead
and the upper nose; medium-brimmed (2.5 to 7.5 cm [1 to 3
inches]) and wide-brimmed (>7.5 cm [3 inches]) hats protect
proportions of the nose, cheeks, chin, and neck.60 Wide-brimmed
hats provide SPF of 7 for the nose, 3 for the cheeks, and 2 for
the chin. Baseball-style caps are especially useful for children.
They protect the forehead well, allowing sunscreen application
below the cheekbones, thus mitigating the risk of stinging from
application near the eyes.
Glasses, contact lenses, and sunglasses protect the corneas
from most UVB and from variable amounts of UVA.247 A complete
discussion of this is provided in Chapter 48.
SUN AVOIDANCE
An indoor lifestyle is undesirable for most persons. More practical
is avoidance of excessive midday sun (i.e., 10 AM to 3 PM), which
significantly reduces UVB exposure.172 Shade provides variable
protection. In one study, shade beneath leafy trees provided SPF
of less than 4.225 Shade cloths allow significantly more UVB
exposure than does clothing of the same fabrics, largely because
of atmospheric scattering and surface reflection.306
Automobile windshields block UVB and some UVA. Side
windows typically block only UVB.282 This may explain why
photodamage is more prominent on the left side of the face of
Americans (and on the right side of the face of Australians) who
drive a great deal.58 Factors that affect UV-protective properties
of glass include color, type, coating, and interlayers between
layers of glass. Transparent plastic films that meet legal require-
ments in all 50 states can be applied to block more than 99% of
UVR (e.g., LLumar UV Shield).
SUNLESS TANNING
Bronzers
Most artificial tanners and bronzers contain dihydroxyacetone
(DHA). DHA reacts with amino groups of keratin proteins by the
Maillard reaction to form brown-pigmented products known as
melanoidins.166 With DHA, bronzing can occur within 1 hour. It
often requires multiple applications to achieve the desired depth
of color. Maintaining this bronzed look requires reapplication
every few days, because stained stratum corneum is shed from
the skin surface. Depth of color is related to thickness of the
stratum corneum and amount and frequency of application.167
Cosmetic complaints include difficulty with obtaining an “even”
tan and yellowing of the palms.
Dihydroxyacetone alone is an inadequate sunscreen. It does
not absorb UVB; rather, DHA absorbs higher-wavelength UVA I
and lower-wavelength visible light,85 which makes it useful for
certain photosensitivity disorders, such as porphyrias and poly-
morphous light eruption. Some commercial bronzing products
now contain sunscreen in addition to DHA. Although the artificial
tan produced by these combination products lasts for days, pho-
toprotection lasts for only hours. The FDA requires bronzers
without sunscreens to display a warning that they do not protect
against sunburn.
Other products to promote indoor tanning have been used.
Few are safe and effective. Tan accelerators containing melanin
precursors (e.g., tyrosine) that have no discernible benefit.134
Sunscreen preparations that containing psoralens (most often
5-methoxypsoralen [oil of bergamot]) are available in Europe.
These stimulate melanin synthesis, but are tumorigenic in mice.45
Psoriasis patients treated with psoralen plus UVA (PUVA) have
a higher incidence of SCCa275 and melanoma.274 Psoralen-
containing sunscreen is associated with increased risk of subse-
quent melanoma.12 Oral carotenoids (e.g., canthaxanthin) are
potentially toxic and consequently not approved in the United
States.
Spray Tan
Spray tanning consists of topical application of DHA by a spray
applicator. Literature on the adverse effects of spray tanning are
lacking.153 Oral or ophthalmic absorption of DHA by the spray
technique warrants further review.
Tanning Booth
Ultraviolet radiation from artificial sunbeds is a human carcino-
gen.211 Approximately 30 million North Americans (including 2.3
million adolescents) use tanning salons each year.79 Caucasian
women (18 to 21 and 22 to 25 years old) have the highest use
(31.8% and 29.6%, respectively).150 A 2011 Youth Risk Behavior
Surveillance System report found 29% of high school girls have
used indoor tanning.66 A recent study found daily doses of UVR
increased serum levels of β-endorphins that act in the same brain
pathways as opioid drugs. When this stimulus was removed, the
mice showed signs of withdrawal. This mechanism suggests
“tanning addiction” may play a role in tanning bed use.96
Damage from tanning salons is insidious. Links between
indoor tanning and melanoma risk have been reported (relative
risk [RR] 1.20). First use of sunbeds before age 35 was associated
with 1.87 times the risk of melanoma.27,49 In adults 18 to 29 years
old, 76% of all melanoma cases can be attributed to tanning bed
use alone.54 Approximately 25% of BCC can be attributed to
indoor tanning.77 Relative risk of squamous carcinoma is 2.5 times
higher among tanning bed users.140 An estimated 170,000 yearly
cases of NMSC can be attributed to indoor tanning alone.299
The dangers of indoor tanning prompted the World Health
Organization, American Academy of Dermatology, and American
Medical Association to recommend legislation to ban indoor
tanning for minors under 18 years old. A number of states have
banned indoor tanning for minors. In 2014, the FDA reclassified
UV tanning devices from class I (moderate risk) to class II (mod-
erate to high risk), which allows for more regulatory control.221
Indoor tanning lamps are now required to include a black-box
warning stating that use should be avoided in persons less than
18 years old, if skin lesions or open wounds are present, or if
there is a personal or family history of skin cancer. Users should
receive regular evaluations for skin cancer.286 As of 2015, only
Brazil and Australia have banned tanning salons (“commercial
solariums”).126
Until 1980, most sunlamps emitted mostly UVB.12 Current
tanning salons make use of high-output UVA tanning beds and
market their services as a way to tan without burning, with a
subtle but incorrect message that such tans are safe. Chronic
suberythemal UVA contributes to photoaging, immunosuppres-
sion, and carcinogenesis. There is significant variation in radia-
tion output of tanning beds. In one study,307 UVA output varied
by a factor of 3, and UVB output by a factor of 60. Typical tanning
bed outputs are contaminated with 2% to 10% UVB,296 more
than the average UVB content of natural sunlight. In another
study in Scotland, 10 minutes of exposure yielded the same
carcinogenic risk as did 30 minutes of peak summer sun at the
same latitude.208
UNIQUE PHOTOPROTECTANTS
Antioxidants
Exposure to UVR creates reactive oxygen species (ROS) that
contribute to DNA damage228 and peroxidative destruction of
membrane lipids.127 Various natural antioxidants (e.g., vitamins
A, C, and E; reduced glutathione; urocanic acid; melanin) and
enzymatic systems (e.g., catalase, superoxide dismutase) protect
skin from ROS.127 Chronic exposure to UVR depletes the skin of
these antioxidants.179
Animal studies have found applying antioxidants (e.g., tocoph-
erol sorbate and vitamins C and E) before UVR exposure delays
skin damage.58,136,164,213 Although vitamin C does not act as a
sunscreen (it does not absorb UVR), it protects against erythema
and sunburn cell formation by quenching free radicals that are
at least partially causative.57 Routine use of antioxidants (e.g.,
topical vitamin E) may provoke contact sensitization and serve
CHAPTER 16  Exposure to Radiation from the Sun
as a tumor promoter.202
Oral antioxidants may also be of value for preventing photo-
damage.67 A combination of oral vitamins C and E decreased
clinical signs of sunburn and thymine dimer formation after UVB
irradiation.230
Botanicals
Botanical sunscreens are gaining attention due to potential pho-
toprotective, photoabsorbant, antioxidative, antimutagenic, anti-
inflammatory, and anticarcinogenic properties.171
Camellia sinesis (i.e., green tea) contains polyphenols that are
potent antioxidants. Polyphenols remove UVR-produced ROS
and protect skin from further damage.161 Green tea can be used
orally and topically. Green tea polyphenol’s antiphotocarcino-
genic effects are believed to be mediated through interleukin-12
(IL-12). The use of the phenol in IL-12 knockout mice did not
result in photocarcinogenic protection, but it did in IL-12 intact
mice.3,195
Resveratrol, which is a potent antioxidant found in grapes,
nuts, and red wine, mitigates the UVB-associated damage in
mouse skin. It reduces UVB-induced edema, inhibits lipid per-
oxidation, and decreases production of enzymes associated with
tumor promotion.2
Silmarin, which is a flavonoid derived from milk thistle, also
has antioxidant, antiinflammatory, and salutary immunomodula-
tory effects when applied topically.141 Topical applications of aloe
and tamarind xyloglucan protect against UVR-induced immuno-
suppression by acting as antioxidants rather than sunscreens.278
Cucuma longa (i.e., turmeric containing curcumin) possesses
rich antiinflammatory and antioxidant properties.132 Curcumin
induces apoptosis of BCCa cells.135 Curcumin is noted for its
chemopreventive and chemotherapeutic effects in various cancer
types, including the skin, lung, breast, gastrointestinal, and geni-
tourinary areas.173
Flowers of Spathodea campanulata, a tree endemic to road-
sides of tropical Africa, possess flavonoids that strongly absorb
in the 205 to 252 nm range and moderately in the 280 to 330 nm
range.293 Topical application may help avoid sunburn and UVR
skin damage.
Ferulic acid is found in grains, fruits, and vegetables. Combin-
ing ferulic acid with vitamin C and E antioxidants in a topical
solution doubled its photoprotective properties and was found
to inhibit thymine dimer formation.168
Capparis spinosa (i.e., caper bush, Flinders rose), endemic to
the Mediterranean countries, contains ferulic acid, cinnamic acid,
and other derivatives with significant antioxidative and photo-
protective effects. It reduces UVB-induced erythema, suggesting
it may be a potential sunscreen additive.26
Root and flowers of Pongamia pinnata (i.e., Indian beech nut
tree, Karanja), a tree found along the coast or rivers in India,
contain a bioflavonoid that possesses many differing properties,
including antiinflammatory and antisolar effects. Aqueous extract
was most absorbent in the UVB range of 300 to 320 nm and UVA
range of 335 to 400 nm. Acetone extract exclusively absorbed
within the UVA region, with the maximum wavelength of absor-
bance at 337.9 nm.260 This additive could also serve as a potential
sunscreen ingredient.
Synthetic Molecular Structures
Postexposure therapy for sunburn with topical application of the
DNA repair enzyme T4 endonuclease V (T4N5) is of interest.
When applied in liposomes, T4N5 localizes in the epidermis and
epidermal appendages,309 and it enhances repair of UVR-induced
DNA damage in mice and humans.311 T4N5 prevents UVR-induced
immunosuppression156 and reduces UVR-induced skin cancer in
mice.308 In a study of patients with XP, T4N5 in a liposomal base
significantly reduced the incidence of new actinic keratoses and
BCCa after 1 year.310
ATTITUDES TOWARD PHOTOPROTECTION
During the 20th century, a tan was equated with health, wealth,
and stylishness. Coco Chanel’s 1929 pronouncement that “a golden
351
 tan is the index of chic” characterized the times. This attitude led
to dangerous behaviors and created cultural norms that remain
challenging to overcome. Numerous recent studies document
continued skepticism toward photoprotection.15,149,194,318
Even patients with sun-related problems often do not adopt
adequate sun protection habits. One study documented that
patients with dysplastic nevus syndrome, at high risk for mela-
noma, do not avoid sunburning.30 Among patients 1 year after
treatment for BCCa, only 49% wore hats or long sleeves in the
summer, and 62% used less than two bottles of sunscreen per
year.115 Studies found that organ transplant recipients did not
considerably improve sun-protective behaviors after their
transplant,197a,265 and only 40% reported using sunscreen.279
Sunscreen use correlates with knowledge of the harmful
effects of sun exposure and understanding of SPF values.20 In a
survey of American adults, 42% were aware of the term mela-
noma, and 34% knew it was a type of skin cancer.199 Some use
sunscreens in the belief that sunscreens will promote tanning.
More education is needed. In college students in Southern Cali-
fornia, a 12-minute videotape about photoaging in conjunction
with UV facial photography resulted in improved sun-protective
behaviors 1 month after the education.180 In Australia, where
there are significant educational efforts about UV-related skin
BURNS, FIRE, AND RADIATION
BOX 16-3  Common Oral Photosensitizing Medications
Antihistamines
Fluoroquinolones
Nonsteroidal antiinflammatory drugs
Oral contraceptives
Phenothiazines
Sulfonamides
Sulfonylureas
Tetracyclines
Thiazides
Tricyclic antidepressants
identifying the specific causative agent is crucial, and discontinu-
ation or substitution should be considered.
Treatment for polymorphous light eruption includes super- or
high-potency topical corticosteroids for several daily to weekly
pulses, frequently in combination with systemic antihistamines
(e.g., diphenhydramine, hydroxyzine, doxepin). Hardening of
the skin in the spring with UVB, narrow-band UVB, or PUVA
can be very effective. Systemic antimalarials (e.g., 200 to 400 mg/
day of hydroxychloroquine sulfate, started in late winter) are

injury, three-fourths of adults visiting family physicians reported generally less effective than phototherapy. For patients with
using sunscreens.190 Australian state-sponsored and privately severe issues, azathioprine, cyclosporine, thalidomide, and myco-
sponsored programs stress sun avoidance and clothing protection phenolate mofetil may be considered.
over sunscreens, and Australian fashion magazines feature more
hats and models who are less tan.46 For information regarding
sun protection, patients rely on the Internet as much as on their BOX 16-4  Topical Phototoxins and Photoallergens
physicians. Utilizing electronic media and social networking tools
to promote sun-protective behaviors is an option for policy Topical Phototoxic Compounds
makers, public health officials, and medical professionals.100 Dyes
Photoprotection education needs to begin during childhood. Eosin
Considerable sun exposure occurs by the age of 18 years, and Methylene blue
childhood exposure may be more significant than lifetime expo- Medications
sure for determining subsequent risks of BCCa and melanoma. Phenothiazines
Sulfonamides
Children who use sunscreens at an early age are more likely to
Psoralens
use sunscreens as adolescents.13 Sun protection policies in U.S. Methoxypsoralen
PART 3

schools are lacking. In one study, only 10% of 484 secondary Trimethylpsoralen
schools in 27 cities surveyed had a formal policy in place.38 Tars
Education of parents is required to alter parental behavior, Creosote
beginning with the first well-baby visit. Sun avoidance and cloth- Pitch
ing protection should be advocated for infants who are less than
Topical Phototoxic Plants
6 months old, and sunscreen should be added to the photopro-
Angelica
tective regimen for older toddlers and children.
Carrot
Advertisers and the fashion industry continue to glorify tanning Celery
and offer an oxymoronic message: you can get a “healthy tan” Cow parsley
while protecting your skin.236 In a review of American fashion Dill
magazine models, there was a trend toward lighter tans, more Fennel
sunscreens, and more articles about sun awareness. Men’s maga- Fig
zines did not demonstrate this trend.94 Gas plant
Giant hogweed
Lemon
PHOTOSENSITIVITY DISORDERS Lime
Meadow grass
ENDOGENOUS PHOTOSENSITIVITY DISORDERS Parsnip
Sun protection is especially important for persons with endog- Stinking mayweed
enous photosensitizing disorders, who take photosensitizing Yarrow
medications (Box 16-3), and who are exposed to topical photo- Topical Photoallergenic Compounds
sensitizers (Box 16-4). For each of these conditions, use of broad- Antiseptics
spectrum sunscreens, sun avoidance, and clothing protection Chlorhexidine
provide appropriate prophylaxis. Hexachlorophene
The most common endogenous photodermatosis is polymor- Fragrances
phous light eruption, affecting 10% to 14% of whites, predomi- Methylcoumarin
nantly females less than 30 years old. This manifests with pruritus, Musk ambrette
erythema, macules, papules, or vesicles on sun-exposed skin Phenothiazines
arising 1 to 2 days after exposure and resolving spontaneously Salicylanilides
over the next 7 to 10 days. It is most common with initial sun Sulfonamides
exposures during the spring or early summer. “Hardening” of the Sunscreens
Benzophenones
skin may occur with subsequent exposures. Patient education is
Cinnamates
very important. Sun avoidance and protective clothing are critical. Dibenzoylmethanes
Liberally applied sunscreens are helpful; a broad-spectrum sun- Paraaminobenzoic acid
screen that contained padimate O and avobenzone was quite Paraaminobenzoic acid esters
effective.85 For medication-related photosensitization disorders,

352
 Sunlight may exacerbate lupus erythematosus. UVB is typi-
cally causative; UVA can contribute. Broad-spectrum sunscreens,
sun avoidance, and clothing protection are appropriate. A broad-
spectrum sunscreen diminished clinical severity in a 4-week
study.42 Systemic antimalarials may be used in more serious cases.
Porphyrias are caused by inherited abnormalities in heme
synthesis. Clinical manifestations vary with genetic subtype, but
photosensitivity is common. Sunscreens other than inorganic
blockers are generally inadequate. Topical DHA and oral beta-
carotene may be useful adjuncts to sun avoidance.
Chronic actinic dermatitis manifests as persistent macules and
plaques that are often infiltrated and lichenified on chronically
sun-exposed sites on older men. Patients may demonstrate der-
matitic flares with even modest exposure to UVR and shorter-
wavelength visible light. The disorder can progress from dermatitis
to T cell lymphoma. Broad-spectrum sunscreens, sun avoidance,
and clothing protection (including wearing brimmed hats) are
essential. For advanced cases, therapy with azathioprine, cyclo-
sporine, PUVA, and retinoids has been used.
Persistent light reaction is a peculiar and persistent overreac-
tion to sun exposure resulting from prior topical photoallergy.
Musk ambrette, found in many perfumes, may provoke persistent
light reaction.239 UVB is most often causative.
For disorders in which melanocytes are defective or absent
(e.g., albinism, vitiligo) and for disorders in which DNA repair
mechanisms are deficient (e.g., XP), the protective triad of sun-
screens, sun avoidance, and clothing protection is required.
PHOTOTOXICITY
Most oral photodrug eruptions are phototoxic and clinically
manifest as exaggerated sunburn on exposed skin with sharp
cutoffs at the neck and short-sleeve line. Less common is photo-
onycholysis, in which the distal fingernails separate from their
underlying beds. Photodrug eruptions are usually triggered by
UVA. The most common offending drugs are listed in Box 16-3.
Topical photosensitizers may cause phototoxicity, photoal-
lergy, or both. Phototoxicity results in exaggerated sunburn,
typically followed by postinflammatory pigmentation. Phototox-
icity is nonimmunologic and typically caused by UVR.
Many plants can produce phototoxic reactions in exposed
skin (see Box 16-4), resulting in phytophotodermatitis. Common
chemical precipitants are furocoumarins, especially psoralens,
which are found in limes, lemons, and certain other plants
(Figure 16-12). Phytophotodermatitis is common among farm-
workers, bartenders, cannery packers, and vacationers to sunny
climates. Oil of bergamot, which contains 5-methoxypsoralen, is
a frequent cause of phototoxicity related to perfumes (berloque
dermatitis). This eruption manifests as streaks of erythema and
subsequent pigmentation on exposed skin of the face, neck,
and wrists. Meadow-grass dermatitis among hikers is caused by
contact with various common weeds (e.g., meadow parsnip)
containing furocoumarins. This leads to whip-like erythematous
FIGURE 16-12  Phytophotodermatitis on a teenager after a “lime
fight” that took place during an outdoor summer picnic.
streaks and postinflammatory hyperpigmentation after exposure
CHAPTER 16  Exposure to Radiation from the Sun
to sunlight.
Psoralens have been incorporated into sunscreens in Europe
to promote tanning, although their use is associated with increas-
ing risk of burns and carcinogenicity.45 PUVA is used therapeuti-
cally for psoriasis and other select dermatoses.
PHOTOALLERGY
Photoallergic reactions occur only in previously sensitized indi-
viduals and are uncommon. Provoked by interaction of UVA with
a topical proallergen, they result in contact dermatitis within 48
hours. Unlike phototoxic reactions, which are limited to exposed
skin, photoallergic reactions can spread to adjacent sun-protected
sites. Sunscreens are paradoxically the current leading cause of
photoallergy.125 Prevention requires excellent UVA protection,
including use of broad-spectrum sunscreens.
TIPS FOR THE WILDERNESS
ENTHUSIAST
Moist skin (e.g., swimmers and hikers in humid environments)
reflects less UVR, resulting in greater absorption of UVB.84 Snow,
wind, and altitude augment UVB exposure for skiers and climb-
ers. One study reported 36% of climbers (24 of 67) developed
significant sunburns during expeditions up to 7000 m (23,400
feet) despite application of sunscreen.264 A year-long study
using continuous dosimetry monitoring of professional alpine
mountain guides confirmed exceedingly high cumulative UVR
exposure.205
Acute UVB overexposure may cause photokeratitis (snow-
blindness) in skiers and climbers.312 Chronic exposure to UVR
may cause or contribute to pterygia, cataracts, and macular
degeneration (see Chapter 48).
To prevent cutaneous manifestations of toxic sun exposure,
use a broad-spectrum sunscreen. Ointments and waxes may be
desirable for climbers and winter campers because these reduce
the risk of chapping and frostbite. Concomitant use of sunscreen
and insect repellent containing diethyltoluamide (DEET) lowers
the effective SPF by 34%.207 If no commercial sunscreen can be
obtained, extemporaneous inorganic blockers can be made from
ashes, mud, and leaves. Clothing, such as long sleeves, pants,
hats, and polarized sunglasses, grant significant UVR protection
without need for topical sunscreens.
Sunburn treatments can include application of cold teabags,
especially green tea, on the involved areas; temperature, antioxi-
dative, and antiinflammatory properties help soothe and decrease
erythema. Cool compresses with cotton material and oatmeal
soaks can help relieve pain associated with sunburns. Topical
analgesics such as Hamamelis (witch hazel), as well as the
botanicals discussed earlier, may be used.128
UVB is a potent stimulus for reactivation of herpes labialis in
outdoor enthusiasts.266 Sun exposure leads to immune system
depression. UVR suppresses herpes simplex virus (HSV) antigen
presentation by the epidermal cells and decreases immune detec-
tion of the virus. Ample viral replication allows for a recur-
rence.292 UVB induces HSV recurrence in animal models218 and
humans.245 A recent study found spending 8 or more hours per
week outdoors without eye UVR protection resulted in increased
risk of ocular HSV recurrence.175 Sunscreen is ineffective for
preventing recurrences in outdoor skiers,200 but it effectively
prevents recurrences in the laboratory.245 This may reflect a dif-
ference in application techniques. Zinc oxide inhibits the first
step of HSV-2 pathogenesis, entry into target cells, spread among
infected cells, and ability to neutralize virions of both HSV-2 and
HSV-1.6,201
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353
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 CHAPTER 17 
Volcanic Eruptions, Hazards,
and Mitigation
JOANNE FELDMAN AND ROBERT I. TILLING
Volcanic eruptions are spectacular, violent, and often quite dan-
gerous expressions of Earth’s dynamic internal processes (Figure
17-1). More than 80% of the earth’s surface above and below sea
level is of volcanic origin, and gaseous emissions from volcanoes
helped form Earth’s oceans and atmosphere.24 On average, about
60 to 70 eruptions occur worldwide each year; half of these are
continuations of previously erupting volcanoes, and the others
are new eruptions.70,79 There are approximately 600 active volca-
noes in the world and probably another 800 that have erupted
at least once during the past 10,000 years.79 Some volcanoes erupt
only once in their lifetime, whereas others erupt repeatedly or
even continuously. The largest explosive eruptions occur infre-
quently; in general, the longer the time interval between erup-
tions, the larger the next eruption tends to be. Some of the worst
volcanic catastrophes in history have occurred at volcanoes
believed to be extinct, including the famous eruption of Vesuvius
in AD 79, which destroyed the cities of Pompeii and Herculaneum
(see later).79 In fact, in the past two centuries, 12 of the 17 largest
eruptions were the first eruptions known in historical times.66,70
Table 17-1 lists some notable historical eruptions, including the
one at Chaitén Volcano in southern Chile, coming back to life
after being inactive for 9400 years.43 The Chaitén eruption, which
began in May 2008, continued nonexplosively through 2009
before ending in early January 2010, constructing a new lava
dome (0.8 km3).49 This eruption has special volcanologic signifi-
cance because it is the world’s first major rhyolitic eruption since
the 1912 eruption of Novarupta, Alaska—the largest of the 20th
century (Figure 17-2; see Table 17-1).
Volcanic eruptions have been responsible for the deaths of
approximately 300,000 people in the past 400 years. In recent
FIGURE 17-1  Eruption of Mt St Helens on May 18, 1980. (Courtesy
Robert M. Krimmel, U.S. Geological Survey.)
354
years, the average is two to four fatal volcanic events per year.
Causes of death and number of fatalities are not well docu-
mented.73 As the most deadly volcano hazards, pyroclastic flows
have claimed the most lives, whereas tephra is the most common
killer (Box 17-1). Long after the eruption, famine and disease
epidemics are responsible for up to one-third of the total fatalities
attributed to explosive eruptions73 (Tables 17-2 and 17-3).
Compared with other natural disasters, volcanic eruptions
occur infrequently, affect few people, and are responsible for
only a small percentage of fatalities. Only about 2% of all natural
disasters are from volcanic activity.38,74 The deadliest volcanic
eruption in history, Tambora, Indonesia in 1815, killed approxi-
mately 60,000 people, whereas 1 million people were killed in
the worst hurricane (Ganges Delta in Bangladesh, 1970) and
830,000 were killed in the worst earthquake (Shaanxi earthquake
in China, 1556).41,71,79 Nevertheless, volcanoes have the potential
to unleash one of the most destructive forces on Earth. Approxi-
mately 74,000 years ago, an Indonesian volcano named Toba
B
FIGURE 17-2  A, Satellite view of an ash plume produced during the
explosive phase of the 2008-2010 eruption of Chaitén Volcano, south-
ern Chile; plume is drifting downwind across Argentina and dissipating
over the Atlantic Ocean. B, Aerial oblique view in January 2010 of the
new lava dome constructed within Chaitén’s 3-km (1.9-mile)–wide
summit caldera. (A, MODIS/NASA image, May 3, 2008; B courtesy
John Pallister, U.S. Geological Survey.)
 CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
TABLE 17-1  Some Notable Historical Volcanic Eruptions

Volcano Country Year Significance

Santorini Greece 1650 BC One of the largest explosive eruptions on Earth; may have contributed to the decline of
Minoan civilizations
Mt Vesuvius Italy AD 79 First major historical eruption to occur within range of major cities; first eruption to be well
documented by an eyewitness (Pliny the Younger)
Laki Iceland 1783 Largest historical lava flow eruption on Earth; catastrophic impact on Iceland’s population
from famine caused by loss of livestock from poisoning by hydrogen fluoride emissions
Mt Tambora Indonesia 1815 Largest historical volcanic eruption on Earth; highest estimated eruption column (43 km [27
miles]); largest known death toll of over 60,000 (12,000 directly by pyroclastic flows* and
tephra*; 48,000 indirectly from starvation and disease); global sulfuric acid aerosols caused
worldwide climate change resulting in the “Year Without a Summer” in 1816; abnormally
low temperatures in the northern hemisphere caused famine from widespread crop failure
Krakatau Indonesia 1883 First large eruption of the modern age; two-thirds of the island destroyed; tsunami* killed
36,000 people living in adjacent coastal areas
Montagne Pelée Martinique 1902 Classic example of a moderate-sized eruption causing severe loss of life: 29,000 people died
Novarupta U.S. 1912 Largest eruption in the world in the 20th century; occurred in uninhabited part of Alaska; no
fatalities
Mt St Helens U.S. 1980 First major explosive eruption to be monitored intensively with modern technology; worst
volcanic disaster in U.S. history; $1 billion worth of damage but only 57 people died
because timely forecasting prompted evacuation
El Chichón Mexico 1982 Erupted violently three times; first eruption came as a complete surprise; pyroclastic flows
killed 2000; worst volcanic disaster in Mexican history
Nevado del Ruiz Colombia 1985 Example of small eruption causing severe loss of life; lahar* caused 23,000 deaths and $212
million of damage; worst volcanic disaster in Colombian history; disaster demonstrates that
in densely populated areas, even very small eruptions can cause widespread devastation
and kill thousands
Mt Pinatubo Philippines 1991 Second-largest eruption of the 20th century; major societal impact in Philippines; important
but temporary global atmospheric effects; despite its huge size, eruption directly caused
only 300 deaths because of timely evacuations prompted by precise forecasts by scientists
Chaitén Chile 2008 Largest eruption in the 21st century to date; volcano had been dormant for 9400 years
before abrupt onset of eruption in May 2008; activity is continuing nonexplosively through
mid-June 2010; lahars and ashfalls caused relatively few deaths but severe socioeconomic
impacts in southern Chile and downwind neighboring Argentina
Eyjafjallajökull Iceland 2010 Major flight disruptions across northern Europe; the ash cloud both drifted over the Atlantic
and for considerable intervals passed directly over Europe, halting flights of most
commercial aircraft for almost a week in a controversial shutdown with economic impacts
in the billions of dollars
Mt Merapi Indonesia 2010 Over 350,000 people were evacuated from the affected area due to ash plumes, pyroclastic
flows, and lahars; ash plumes caused major disruption to aviation across Java; 353 deaths
Bardarbunga Iceland 2014 Subglacial stratovolcano beneath Vatnajökull ice cap has erupted continuously since late
August 2014 and was ongoing as of early February 2015; the lava flow field formed to date
is the largest in Iceland since that of the Laki eruption in 1783-1784
Mt Ontake Japan 2014 A phreatic eruption occurred with no warning at this volcano; pyroclastic flows, ashfall, and
ballistic ejecta killed more than 56 hikers and visitors; Japan’s deadliest eruption since
1926 at Tokachi Volcano

Data from Sigurdsson H: The history of volcanology. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000, Academic
Press; Tilling RI: Volcanic hazards and their mitigation: Progress and problems, Rev Geophys 27:237, 1989; Clemens JA: Volcano! Evacuation and military medical
implications, ADF Health 3:25, 2002; Major JJ, Lara LE: Overview of Chaitén Volcano, Chile, and its 2008-2009 eruption, Andean Geology 40:196, 2013; and
Smithsonian Institution Global Volcanism Program http://www.volcano.si.edu/.
*See definitions in Box 17-1.

BOX 17-1  Glossary of Volcano-Related Terms

exploded and ejected 2800 km3 (672 cubic miles) of ash, dust,
and volcanic gases high into the stratosphere, where it was car-
Lahar Volcanic mudflow ried around the world by high-altitude winds. The particulate
Lava Magma that has erupted at the earth’s surface matter interfered with solar radiation and is thought to have led
Magma Molten rock inside the earth to a 10° C (22° F) temporary global cooling of the earth’s sur-
Pumice Lightweight solidified fragments of magma face.71,88 Such a degree of cooling today would be catastrophic
ejected explosively from an eruption on a global scale.
Pyroclastic flow Ground-hugging ash and rock clouds that We can expect more fatalities from volcanic eruptions as
sweep down slopes at hurricane speeds human settlements inexorably encroach on areas with high-risk
Tephra Explosively erupted airborne volcanic material volcanoes.4 Current estimates suggest that about 500 million
such as ash, pumice, and rocks people, or 10% of the world’s population, live within 100 km (62
Tsunami Seismic sea wave generated by an earthquake miles) of a volcano that has been active in the historical record.4,60
or eruption Auckland, New Zealand, occupies an area of young volcanoes.
Volcanologist Scientist who studies volcanoes Seattle-Tacoma, Washington, is on land that could be devastated
by mudflows from an eruption of Mt Rainier. Naples, Italy, is
built on the flanks of Mt Vesuvius, where in the first minutes of

355
 TABLE 17-2  Causes of Fatalities from Notable Volcanic Disasters Since 1000 AD

Number of Deaths According to Primary Cause

Volcano Country Year Pyroclastic Flow Lahar Tsunami Lava Flow Posteruption Starvation

Mt Merapi Indonesia 1006 1000 — — — —

Kelut Indonesia 1586 — 10,000 — — —
Mt Vesuvius Italy 1631 — — — 18,000 —
Mt Etna Italy 1669 — — — 10,000 —
Mt Merapi Indonesia 1672 300 — — — —
Mt Awu Indonesia 1711 — 3200 — — —
Oshima Japan 1741 — — 1480 — —
Cotopaxi Ecuador 1741 — 1000 — — —
Makian Indonesia 1760 — 3000 — — —
Mt Papadayan Indonesia 1772 2960 — — — —
Laki Iceland 1783 — — — — 9340
Mt Asama Japan 1783 1150 — — — —
Mt Unzen Japan 1792 — — 15,190 — —
Mayon Philippines 1814 1200 — — — —
Mt Tambora Indonesia 1815 12,000 — — — 48,000
Mt Galunggung Indonesia 1822 — 4000 — — —
Nevado del Ruiz Colombia 1845 — 1000 — — —
BURNS, FIRE, AND RADIATION

Mt Awu Indonesia 1856 — 3000 — — —

Cotopaxi Ecuador 1877 — 1000 — — —
Krakatau Indonesia 1883 — — 36,420 — —
Mt Awu Indonesia 1892 — 1530 — — —
La Soufrière St Vincent 1902 1560 — — — —
Montagne Pelée Martinique 1902 29,000 — — — —
Santa María Guatemala 1902 6000 — — — —
Taal Philippines 1911 1330 — — — —
Kelut Indonesia 1919 — 5110 — — —
Mt Merapi Indonesia 1951 1300 — — — —
Mt Lamington Papua New 1951 2940 — — — —
Guinea
Mt Hibok-Hibok Philippines 1951 500 — — — —
Mt Agung Indonesia 1963 1900 — — — —
PART 3

Mt St Helens United States 1980 57 — — — —

El Chichón Mexico 1982 >2000 — — — —
Nevado del Ruiz Colombia 1985 — >25,000 — — —
Mt Merapi Indonesia 2010 353
Mt Ontake Japan 2014 >56
Totals: >65,606 >57,840 53,090 28,000 >57,340
GRAND TOTAL >261,876

Modified from Tilling RI: Volcanic hazards and their mitigation: Progress and problems, Rev Geophys 27:237, 1989; and Tanguy J-C, Ribière C, Scarth A, et al: Victims
from volcanic eruptions: A revised database, Bull Volcanol 60:137, 1998; and Smithsonian Institution Global Volcanism Program http://www.volcano.si.edu/.

TABLE 17-3  Fatalities from Volcanic Eruptions,

a major eruption, more than 100,000 people could be killed4,10,66
(Figure 17-3). Latin America and the Caribbean are areas of par-
1783-2000 ticularly high risk because of population density. During the 20th
century, 76% of all fatalities from volcanic eruptions and one-half
Fatalities
of the most powerful eruptions occurred in this region. To date,
Volcanic Hazard Number % eruptions during the 21st century have been moderate in size,
occurred in diverse locales, and luckily caused relatively few
Posteruption famine and disease epidemics 75,000 30 deaths. In general, most fatalities occur in densely populated,
Pyroclastic flows 67,500 27 less developed countries60 (Table 17-4).
Lahars 42,500 17 Although volcanic eruptions constitute a significant natural
Volcanogenic tsunamis 42,500 17 hazard, other processes and products of volcanism can be highly
Debris avalanches 10,000 4 beneficial to society, explaining in part why so many people live
Volcanic ash 10,000 4 on or near volcanoes.71 Volcanic ash rejuvenates soil and can
Volcanic gases 1750 <1 prevent loss of phosphorus, resulting in highly productive agri-
Lava flows 750 0.3 cultural land (Figure 17-4). Volcanic ore deposits supply dia-
TOTAL 250,000 —
monds, copper, gold, silver, lead, and zinc. Products of volcanic
activity are used as building materials, as abrasive and cleaning
Modified from Baxter PJ: Impact of eruptions on human health. In Sigurdsson agents, and for many chemical and industrial uses.24 Geothermal
H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San heat and steam can drive turbines to generate electricity, heat
Diego, 2000, Academic Press. homes and industries directly, and be enjoyed by people at hot-
spring resorts (Figure 17-5). The beauty of volcanoes and volca-
nic activity also generates income for communities through
tourism.

356
 CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
A

FIGURE 17-4  Farmer plowing a lush rice paddy in central Java, Indo-
nesia. Sundoro Volcano looms in the background. The most highly
prized rice-growing areas have fertile soils formed from breakdown of
young volcanic deposits. (Courtesy Robert I. Tilling, U.S. Geological
Survey.)

planted on the slopes and human settlements on the mountain’s

B flanks. Unlike the nearby often-erupting volcanoes Mt Etna and
C The town of Herculaneum, lying at the foot of Mt Vesuvius
FIGURE 17-3  A, Mt Eden, one of 50 geologically young but dormant
volcanoes in the Auckland Volcanic Field, within the city of Auckland,
New Zealand. B, Mt Rainier sits just 137 km (85 miles) southeast of
Seattle-Tacoma, Washington. C, Bay of Naples, Italy, with Mt Vesuvius
in the background. (A courtesy Lloyd Holmer, Institute of Geological
and Nuclear Sciences, New Zealand; B courtesy Lyn Topinka, U.S.
Geological Survey; C courtesy Robert I. Tilling, U.S. Geological Survey.)
Stromboli, Mt Vesuvius was not considered volcanic. Even a
series of pre-eruption earthquakes, as typically occurs before an
eruption, did little to raise concern that Mt Vesuvius was an active
volcano. The eruption was witnessed and documented by Pliny
the Younger. In two letters to the Roman historian Tacitus, Pliny
wrote that the first explosion began in the early afternoon and
ended the evening of the following day. At first, Vesuvius pro-
duced an enormous eruption cloud that ejected ash, pumice, and
volcanic gases vertically up to 30 km (19 miles) high. Then, from
a darkened sky, ash and pumice rained down on the towns of
Pompeii and Straide, causing roofs to collapse under the weight
of the ashfall and burying the towns (Figure 17-6).
on a cliff overlooking the sea, was initially spared from burial.
The prevailing wind blew away from the town and toward
Pompeii. In the early hours of August 25, however, Vesuvius
exploded again, this time ejecting hot gases, ash, and pumice
down the mountain’s slopes as a pyroclastic flow. Herculaneum
was destroyed, buried beneath more than 20 m (66 feet) of
pumice and ash. Whatever remained of Pompeii was also

MT VESUVIUS, AD 79
The best-known volcanic eruption was Mt Vesuvius on August
24, AD 79. This eruption killed thousands of people, devastated
the surrounding countryside, and destroyed at least eight towns,
most notably Pompeii and Herculaneum. Before this eruption,
Mt Vesuvius was seen as a benign mountain with lush vineyards

TABLE 17-4  Fatalities From Volcanic Eruptions by

Region, 1600-1982
Fatalities
Region Number %

Indonesia 161,000 67
Caribbean 31,000 13
Japan 19,000 8
Iceland 9400 4 FIGURE 17-5  Blue lagoon in Iceland, with Svartsengi power plant in
Everywhere else 19,000 8 the background. Clean geothermal energy heats 87% of the homes in
TOTAL 239,400 100 Iceland, including the entire capital city, Reykjavík. Excess geothermal
water (which is absolutely clean) is ejected into the lagoon, and where
Modified from Blong RJ: Volcanic hazards: A sourcebook on the effects of there is swimming, the temperature averages about 40° C (104° F). The
eruptions, Orlando, Fla, 1984, Academic Press. lagoon is a very popular tourist destination. (Courtesy Mary Dagold.)

357
 FIGURE 17-6  View from the main square of the well-preserved ruins
of Pompeii, with Vesuvius in the background. (Courtesy Harvey E.
Belkin, U.S. Geological Survey.)

destroyed at that time.65 Pliny the Younger wrote of the death of

his uncle, Pliny the Elder, who probably died of asphyxiation
BURNS, FIRE, AND RADIATION

from being caught too close to a pyroclastic flow.4

The remains of more than 2000 people found amid the ruins
offer clues as to the causes of death. People unwilling or unable
to flee their homes were instantaneously suffocated as hot vol-
canic ash and gases entered buildings. Others had multisystem
trauma as the force of the explosion and pyroclastic flows
scooped up rocks and building materials and smashed them into
anything in their path. Skeletons recently uncovered in beach
caves in Herculaneum suggest that the cause of death was the
intense heat, about 500° C (932° F)13,51,77 (Figure 17-7).
VOLCANOES AND THEIR
GLOBAL DISTRIBUTION
PART 3
FIGURE 17-7  The “Garden of the Fugitives,” in Pompeii, Italy, reveals
13 adults and children huddled together in a futile attempt to shield
themselves from pyroclastic flows from the eruption of Vesuvius in AD
79. The human casts are obtained by filling cavities left in hardened
ash with liquid chalk. (Courtesy Lancevortex.)
snow-capped Volcán Villarrica in Chile, or rivers of lava flowing
down the flanks of Kilauea Volcano in Hawaii (Figure 17-8).
Volcano also means the opening, or vent, in the earth’s crust
through which molten rock, ash, and gases are ejected. Molten
rock, while underground, is called magma. It becomes lava once
it reaches the surface. Whether a volcano erupts explosively (e.g.,
Vesuvius, Mt St Helens) or nonexplosively (e.g., lava flows of

Different images are associated with the word volcano—for Kilauea) depends on the magma: its composition, temperature,
example, a violently erupting Mt St Helens, a peaceful-looking gas content, viscosity, and crystal content.71 Magma that is fluid

B C
FIGURE 17-8  A, Violently erupting Mt St Helens on May 18, 1980. B, Villarrica Volcano, Chile, looks peace-
ful and even has a ski lift on its flanks, but the mountain is actually the most active volcano in Chile. C, A
long river of lava flowing downhill from Kilauea Volcano in 1983. It ultimately enters the ocean 12 km (7.5
miles) away. (A courtesy Keith Ronnholm; B courtesy Robert I. Tilling, U.S. Geological Survey; C courtesy
J. D. Griggs, U.S. Geological Survey.)

358
 layer is broken into a number of rigid plates that move relative

CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation

to one another as they float atop the hotter, semisolid, and more
mobile material of the mantle. The nature and distribution of
volcanic activity depend on formation, movement, and destruc-
Aleutian tion of these plates at their margins (Figure 17-10).
Kurile trench trench
Japan trench
When two tectonic plates move away from each other, or
Izu Bonin trench
diverge, new crust is created as molten rock pushes up from the
Ryukyu trench
Puerto Rico
mantle and oozes out onto the earth’s surface or the seafloor.
Philippine
trench
Marianas trench
trench One well-known, mostly oceanic, divergent boundary, the Mid-
Challenger Deep
Middle America Atlantic Ridge, is a submerged mountain range in the Atlantic
trench
Bougainville trench
Equator Ocean that extends from the Arctic Ocean to beyond the south-
ern tip of Africa. Along the Mid-Atlantic Ridge are numerous
Java (Sunda)
trench
Peru-Chile trench
volcanoes, including those that rise above sea level in Iceland
Tonga trench
(Figure 17-11). Another prominent divergent boundary, entirely
Kermadec trench
continental, is the 11,000-km-long (6835-mile-long) Great African
Rift. About 75% of Earth’s volcanism occurs unseen along diver-
South
Sandwich gent boundaries, deep on the ocean floor.
trench
Two plates can also move toward one another, or converge.
How two converging plates interact depends on the type of
crust—continental or oceanic. Continental parts of plates, com-
FIGURE 17-9  The Ring of Fire, a zone of frequent earthquakes and posed largely of granitic rocks, are relatively lightweight com-
volcanic eruptions encircling the Pacific Ocean. Where the plates come pared with the much denser and heavier oceanic parts of plates,
together, they form deep oceanic trenches (green). (From Kious WJ, which are composed of basalt. When two continental plates
Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, collide, both buckle upward to form a mountain range. The
DC, 1996, US Government Printing Office.) Himalaya Mountains are the result of the Indian plate colliding
against the Eurasian plate (Figure 17-12). Few volcanoes are
located in zones of continental collisions.
Many of the world’s volcanoes are located at the convergent
and hot tends to erupt frequently (every few years) and generally boundary between a continental plate and an oceanic plate.
nonexplosively. This type of volcano most commonly produces When these plates converge, the heavier oceanic plate dives, or
fountains or rivers of red-hot lava.83 In contrast, magma that is subducts, below the lighter continental plate. This produces
less fluid and cooler, and that contains trapped gases, tends to tremendous pressure and heat, melting the rock deep in the
rise sluggishly and can plug up the volcanic vent. If enough mantle. This molten rock, or magma, traps gases, such as carbon
pressure builds up as trapped gases expand during ascent, the dioxide (CO2) and sulfur dioxide (SO2), making it buoyant in the
pent-up pressure can blow the plug, abruptly unleashing the surrounding denser, solid rock, and it begins to rise through the
expanding gases and producing a violent eruption.40 surrounding solid rock. Magma movement causes earthquakes
The most volcanically and seismically active zone in the that can be recorded with sensitive volcano-monitoring equip-
world, called the Ring of Fire, coincides roughly with the borders ment. If the rising magma finds an area of weakness at the earth’s
of the Pacific Ocean (Figure 17-9).40 The volcanically active surface, a volcano is created either just inland from the coast—for
countries in this zone include Russia, Japan, the Philippines, example, the volcanoes in eastern Russia, the Cascades in North
Indonesia, Papua New Guinea, New Zealand, and the countries America, and the Andes in South America—or just off the coast,
on the Pacific coasts of North, Central, and South America. Vol- such as the volcanic island arcs of the Aleutian Islands in Alaska,
canoes are also scattered in the Atlantic and Pacific Oceans—in and Indonesia (Figure 17-13). Because of their proximity to a
Hawaii, Iceland, and the Galápagos. continent’s coastline or to an island, subduction volcanoes are
often near populated regions and thus can have a significant
human impact. Eruptions tend to be violent and explosive, such
THEORY OF PLATE TECTONICS as the 1980 eruption of Mt St Helens or the 1991 eruption of Mt
The global distribution of volcanoes, as well as the origin and Pinatubo in the Philippines.71
distribution of mountain ranges and earthquakes, are explained Some volcanoes are found far from plate boundaries. The
by plate tectonics.63,79 This theory states that the earth’s outermost Hawaiian volcanoes are more than 3200 km (1988 miles) from

Convergent Transform Divergent Convergent Continental rift zone

t ial

plate boundary plate boundary plate boundary

ob rrestr

plate boundary (young divergent plate boundary)

jec
te
tra
Ex

Oc
Isl ea
an nic
Tre
d
ar Tr Shield rid spre nc
c ge ad h
volcano ing
en

Strato-
ch

volcano Continental crust

Lithosphere
Moho Ma
tle

Asthenosphere Oceanic crust Sub

duc ntl Moho
an

te Hotspot ting e
M

pla plat
e
ting
uc
bd Mantle
Su
Mantle plume ?

Not to scale Schematic cross section of plate tectonics

FIGURE 17-10  Cross section of the main types of plate boundaries. (From “This Dynamic Planet,” a wall
map produced jointly by the U.S. Geological Survey, the Smithsonian Institution, and the U.S. Naval
Research Laboratory.)

359
 the nearest plate boundary, and Yellowstone, with more than
10,000 geysers, hot springs, and boiling mud pools, is located in
Divergent boundary the interior of the North American plate. At both these locations,
an inferred hot spot below the plate melts overriding rock to
produce magma that can rise toward the surface and ultimately
Oc erupt onto the seafloor or land. It has been assumed that the hot
ea
ni Tre spot is stationary, whereas the tectonic plate above it moves.
c
rid spr nch However, recent studies have questioned the fixedness of hot
ge ead spots, prompting substantial debate among Earth scientists.
i ng
Examination of oceanic hot spots shows that in a series of
islands created by plate movement, the islands farthest from the
hot spot are the oldest. For example, a 6000-km (3728-mile) chain
of volcanoes stretches from the older Emperor Seamounts (under-
Lithosphere water sea mountains) off Alaska to the younger Hawaiian Islands.
Oceanic crust These were all created by passage of the Pacific Plate over the
Asthenosphere Hawaiian hot spot. This hot spot, currently located under the Big
Island of Hawaii, has remained stationary for about 45 million
A years, whereas the Pacific Plate has been slowly moving to the
northwest. According to the stationary-hot-spot model, as the
plate continues to move over the hot spot, a new Hawaiian island
will eventually emerge above sea level. In fact, just 35 km (22
miles) southeast of the Big Island there is an underwater volcano,
Loihi, that has risen 3 km (1.9 miles) above the seafloor and is
BURNS, FIRE, AND RADIATION

within 1 km (0.6 mile) of the ocean surface (Figure 17-14). At

hot-spot volcanoes, eruptions tend to be nonexplosive and are
rarely life threatening.40 Huge volumes of fluid lava pour out,
often creating large volcanic mountains, such as Mauna Loa, the
largest single volcano in the world, standing 8851 m (5.5 miles)
above the sea floor.

TYPES OF VOLCANOES
As erupted material accumulates around a volcanic vent, a
volcano is formed and progressively grows. Classified by struc-
ture, the most common types of volcanoes are composite volca-
noes, calderas, shield volcanoes, subglacial volcanoes, and flood
basalts. These can be roughly grouped as either explosive or
nonexplosive volcanoes. However, volcanoes can show both
PART 3

explosive and nonexplosive behavior during their life span. For

B C
FIGURE 17-11  A, Cross section of an oceanic divergent boundary.
B, Map of the Mid-Atlantic Ridge, along which the Eurasian and African
plates are pulling away from the North American and South American
plates. Note the ridge rising above sea level in Iceland. C, Exposed
segment of the Mid-Atlantic Ridge at Thingvellir, Iceland. Left of the
fissure, the North American Plate is pulling westward away from the
Eurasian Plate (right of the fissure). (A from “This Dynamic Planet,” a
wall map produced jointly by the U.S. Geological Survey, the Smithson-
ian Institution, and the U.S. Naval Research Laboratory; B and C from
Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics,
Washington, DC, 1996, US Government Printing Office.)
example, in recorded history, Kilauea typically has erupted non-
explosively, spewing out fountains and rivers of lava, yet its 1790
and 1924 eruptions were spectacularly explosive. New studies
show that if activity in the geologic past is taken into account,
Kilauea’s explosive eruptions are as frequent as those of Mt St
Helens.
GENERALLY EXPLOSIVE VOLCANOES
Composite Volcanoes
Composite volcanoes, or stratovolcanoes, have steep sides and
are typically associated with subduction zones at converging
plate boundaries. Mt Fuji in Japan, Mt Pinatubo in the Philippines,
and Mt Rainier in the United States are classic examples. However,

e
au

ng
ra
late

ain
nt
hp

ou
Hig

Continental crust
Continental crust

Lithosphere Lithosphere

Asthenosphere Ancient oceanic crust

A B
FIGURE 17-12  A, Cross section of two continental parts of plates converging, resulting in formation of a
mountain range. B, The snow-capped Himalayas and the Tibetan Plateau are produced by collision of the
Indian-Australian Plate (left) against the Eurasian Plate (right). (A from Kious WJ, Tilling RI: This dynamic
Earth: The story of plate tectonics, Washington, DC, 1996, US Government Printing Office; B courtesy
NASA, photo STS41G-120-22.)

360
 CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
arc
anic
ch
en

Volc
Tr
Oceanic crust Kronotsky
Continental crust Volcano

Lithosphere Lithosphere

Asthenosphere

Ocean
A

Pacific
rc
h

da
nc
e

an
Tr

Isl
Oceanic crust
Continental B
crust
Lithosphere
Lithosphere

Asthenosphere

D
FIGURE 17-13  A, Cross section showing subduction of an oceanic plate resulting in formation of continental
volcanoes and mountains. B, Kronotsky Volcano, at 3525 m (11,570 feet) above sea level, lies at the margin
of the Pacific Ocean on the Kamchatka Peninsula of Russia. It was formed from subduction of the Pacific
Plate (right) under the Eurasian Plate (left). C, Cross section illustrating subduction of an oceanic plate with
formation of volcanic island arcs. D, View of steep-sided, symmetric Carlisle volcano on Carlisle Island in
the central Aleutian Islands. The 1620-m (5315-foot)–high stratovolcano has erupted several times since the
late 1700s. (A and C from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington,
DC, 1996, US Government Printing Office; B modified from NASA, photo STS61A-45-0098; D courtesy M.
Harbin, University of Alaska Fairbanks, U.S. Geological Survey.)

composite volcanoes can also be formed at divergent plate
boundaries (e.g., Hekla in Iceland, Mt Kilimanjaro in Tanzania)
or at hot spots (e.g., Mt Erebus in Antarctica, Tenerife of the
Spanish Canary Islands).65,66 The steep-sided shape results from
deposition of viscous lava flows alternating with pyroclastic flows
and ashfall deposits. The explosive nature of composite volca-
noes comes from high viscosity and volatility of the magma
(Figure 17-15).
Calderas
Formed by collapse of a volcanic structure, calderas are circular
or elliptical depressions, generally more than 1 km (0.62 mile)
in diameter. Crater Lake in the U.S. Cascade Range is a large,
partially filled caldera 10 km (6.2 miles) in diameter and 600 m
(1970 feet) deep, formed when Mt Mazama exploded 7700 years
ago. Krakatau, in Indonesia, was created by an 1883 eruption
that involved rapid emptying of the magma chamber and subse-
quent collapse of the volcano.65 Kilauea Crater is another well-
known caldera (Figure 17-16).
Very large calderas fed by huge active magma chambers have
been called supervolcanoes and are capable of producing enor-
mously explosive eruptions. Yellowstone Caldera, 85 km (53
miles) long by 45 km (28 miles) wide, the largest and most wor-
risome in the United States, has a magma chamber that is 40 km
(25 miles) long, 20 km (12 miles) wide, and 10 km (6 miles)
deep.66 Yellowstone has produced explosive eruptions 1000
times larger than the 1980 Mt St Helens eruption. Two other
geologically young, large calderas located in the United States
are Long Valley Caldera in California and Valles Caldera in New
Mexico. Outside the United States, very large calderas include
Campi Flegrei in Italy, Kamari Caldera on the island of Kos in
the eastern Aegean Sea, and Rabaul Caldera in Papua New
Guinea. Fortunately, very large caldera-forming eruptions were
rare events, occurring approximately once in hundreds of thou-
sands of years (Figure 17-17).66
GENERALLY NONEXPLOSIVE VOLCANOES
Shield Volcanoes
Shield volcanoes have gentle slopes and are formed almost ex-
clusively of layers of lava that have often flowed great distances
from the eruptive vents. The magma, unlike that of explosive
volcanoes, is predominantly of low viscosity and low volatility.
Shield volcanoes are mostly formed at hot spots, although some
are located at convergent or divergent plate boundaries—for
example, Erta Ale in Ethiopia and Mt Etna in Italy. The largest
volcanoes on Earth, Mauna Loa and Mauna Kea of Hawaii, are
classic examples of shield volcanoes (Figure 17-18).
Subglacial Volcanoes
Historically active volcanoes located under glaciers, called sub-
glacial volcanoes, are known only in Iceland and Antarctica. They
can erupt explosively, but thick glacial ice cover generally inhib-
its material from being ejected high into the atmosphere. Instead,
lava generally is erupted effusively, forming flows that often melt
ice to create subglacial lakes and rivers. If this subglacial water

361
 southern rim of the 6- by 8-km (3.7- by 5-mile) caldera is exposed
(Figure 17-19).66 Its most recent eruption was in May 2011, which
was the largest in Iceland in 50 years and included an explosive
TE ua
i
PLA Ka est)
phase that produced a high ash plume that impacted air travel
FIC
P ACI (ol
d in Europe. Eyjafjallajökull, another subglacial volcano 120 km (75
hu miles) from Reykjavik, Iceland, began to erupt on March 20, 2010,
Oa after being dormant since 1823. During the eruption, hot lava
ui
Ma melted the overlying glacial ice and generated jökulhlaups (see
aii Figure 17-19C) that caused destructive flooding and prompted
Haw est)
n g evacuation of more than 800 inhabitants. Then, on April 14, the
(you
eruption entered a much more explosive phase and propelled
an enormous ash plume more than 8 km (5 miles) into the
atmosphere.72 This plume drifted easterly over northern Europe
So for the next several weeks, causing massive disruption of inter-
lid
de national air travel. This drifting Eyjafjallajökull ash cloud in 2010
nse
roc Zone of and the one from the more powerful, but shorter-lived, 2011
k
magma Grimsvötn eruption provide illustrative examples of the potential
formation hazards of volcanic ash for aviation safety (see Volcanic Ash,
later). The Eyjafjallajökull eruption ended in October 2010.
Fixed
A "Hot Spot" Flood-Basalt Plateaus
Flood-basalt plateaus are massive areas of hardened lava pro-
duced from the largest volcanic events known on Earth.34 Found
BURNS, FIRE, AND RADIATION

on all continents and ocean floors, flood-basalt plateaus are

created when basaltic magma erupts rapidly from fissures to form
sheets of lava flows, typically tens of meters thick and covering
tens of thousands of square kilometers.34 Good examples are the
Columbia River Plateau (Figure 17-20) and the Deccan Plateau
of India. The rate of erupting lava can be 20 times the average
eruption rate of a hot-spot volcano, and the eruption is on
average 1000 times larger than that of a supervolcano.66 Not
surprisingly, the copious release of volcanic gases during the
eruptions of flood basalts can severely affect the climate, and
there is strong correlation between mass extinction on Earth and
eruption of flood basalts.66
Undersea Volcanoes
Most undersea volcanoes are found at oceanic divergent plate
PART 3

boundaries. Others are found at undersea hot spots or near

B island arcs at convergent plate boundaries. Where two plates
FIGURE 17-14  A, Cross section of the Hawaiian hot spot. B, Map of
the 6000-km (3728-mile)–long Emperor Seamount–Hawaiian Ridge
formed by passage of the Pacific Plate over the Hawaiian hot spot over
a span of 70 million years. (A from Kious WJ, Tilling RI: This dynamic
Earth: The story of plate tectonics, Washington, DC, 1996, US Govern-
ment Printing Office; B from “This Dynamic Planet,” a wall map pro-
duced jointly by the U.S. Geological Survey, the Smithsonian Institution,
and the U.S. Naval Research Laboratory.)
suddenly escapes onto the glacier’s surface (a glacial burst, or
jökulhlaup), a huge river can form and destroy anything in its
path. Grímsvötn, historically the most active volcano in Iceland,
lies largely beneath the vast Vatnajökull icecap. The caldera lake
is covered by an ice shelf 200 m (656 feet) thick, and only the
Central vent
diverge, magma is injected along the space created. If magma
reaches the seafloor, pillow lava (from slow effusions) or sheets
of lava (from more rapid effusions) form. Sometimes, if the
magma supply to a single point is sufficiently large and persis-
tent, a cone-shaped volcano, called a seamount, rises from the
seafloor. Seamounts found at undersea hot spots become island
shield volcanoes, such as the Hawaiian volcanoes, if they rise
above sea level. Seamounts at subduction zones become island-
arc volcanoes, such as the volcanoes of Indonesia, above sea
level. Hot-spot seamounts can emerge above sea level and then
later sink as the seamount moves away from the hot spot and
the seafloor subsides under the weight of the lava. Atolls, found
in equatorial regions, are the coral reefs around drowning island
volcanoes, after they become inactive and sink below sea level
(Figure 17-21).66

Pyroclastic layers

Lava flows

B
A
FIGURE 17-15  A, Cross section of a composite volcano (stratovolcano). B, Mt Fuji, Japan, is a perfect
example of a composite volcano. (Courtesy Thomas C. Pierson, U.S. Geological Survey.)

362
 CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
B

C
II

III
Lake

D
IV
A
FIGURE 17-16  A, Cross section of formation of a caldera. B, Crater Lake, Oregon, was formed by the
caldera-forming eruption of Mt Mazama 7700 years ago. C, When that mountain erupted cataclysmically,
the summit collapsed, forming a caldera that eventually filled with water to form Crater Lake. D, Kilauea
Caldera, Hawaii, in 1954 after an eruption within the caldera (dark area is the new lava). (B courtesy Peter
Dartnell, U.S. Geological Survey; C courtesy Crater Lake Natural History Association; D courtesy U.S. Geo-
logical Survey.)

VOLCANO HAZARDS
Some volcanic eruptions cause injury, death, and destruction
within minutes to hours. Others produce hazards that pose risks
to human life, livestock, and the environment for months to years
after the eruption. Explosive and nonexplosive volcanoes gener-
ate unique hazards, but explosive eruptions are usually associ-
ated with much larger numbers of deaths.
HAZARDS FROM EXPLOSIVE VOLCANOES
Volcanoes with explosive characteristics are extremely danger-
ous. They can cause thermal injury from hot gases and ash;
mechanical injury from mudflows, debris avalanches, and falling
tephra; chemical injury from toxic gases; and rarely, electrical
injury from lightning or ionizing radiation injury from radon gas
(Figure 17-22).4 Most volcano-related deaths, injuries, and psy-
chosocial effects occur because the volcano erupts violently and
rapidly, leaving little or no time for people to escape or take
shelter.57 However, significant fatalities have been associated with
mudflows and release of toxic gases during noneruption periods.
Unfortunately, global distribution of explosive volcanoes, mostly
along convergent plate boundaries, places them in densely popu-
lated areas.7 Fortunately, explosive eruptions occur infrequently,
and technologic advances have increased the ability of volcanolo-
gists to predict an eruption. Before the 1980 and 2004 eruptions
of Mt St Helens, 1991 eruption of Mt Pinatubo, and 2010 eruption
of Mt Merapi, high-risk zones around the volcanoes were evacu-
ated because of timely warnings by scientists. These actions

363
 A B
BURNS, FIRE, AND RADIATION

FIGURE 17-17  A, Map of Yellowstone National Park and the 650,000-year-old caldera (outlined in red)
that is 45 km (28 miles) wide and 85 km (53 miles) long. B, View from space of Rabaul Caldera, Papua New
Guinea. The caldera is 9 km (5.6 miles) wide by 14 km (8.7 miles) long and filled by the sea. (A courtesy
U.S. Geological Survey; B courtesy NASA.)

greatly minimized the loss of life, especially in the case of Pina-
tubo, which was the largest eruption in the world in the 20th
century.
Pyroclastic Flows and Surges
Typically, when an explosive volcano erupts, a volcanic cloud
of gas, ash, and lava fragments rises vertically into the atmo-
sphere. If this rising eruption cloud becomes denser than the
PART 3
surrounding air, it collapses and falls back toward the ground.
Such gravitational collapse of the cloud leads to formation of a
hot, high-speed avalanche of ash, volcanic gases, lava fragments,
and heated air, called a pyroclastic flow.65 Pyroclastic surges are
similar to flows but are more dilute and less dense and can travel
farther4 (Figure 17-23).
There is little chance for survival in the direct path of a pyro-
clastic flow or surge traveling at 300 km/hr (186 miles/hr) or

even greater, with temperatures of 600° to 900° C (1112° to

Central vent
Summit caldera
Magma reservoir
A Some of the most famous volcanic disasters have involved
B 752° F).81 Gophers were the only animals to survive, because they
FIGURE 17-18  A, Cross section of a shield volcano. B, Snow-capped
Mauna Loa as seen from the Hawaiian Volcano Observatory on the Big
Island of Hawaii. (B courtesy Robert I. Tilling, U.S. Geological Survey.)
1652° F).66 Everything living is carbonized by the extreme tem-
peratures and swept away by the hurricane force of gas, ash,
and rock sweeping downhill. Most human victims die as a result
of asphyxiation (from breathing overwhelming amounts of ash
or from oxygen deprivation), exposure to the intense heat, or
burial under volcanic debris. Moreover, fatal traumatic injuries
can result from associated devastating winds that can flatten trees
and throw rocks. Survivors might have severe and extensive
burns to their skin and respiratory tracts, or blunt trauma inju-
ries.60 Although the main impact only lasts a few minutes, pyro-
clastic deposits can remain extremely hot for weeks and pose a
lingering danger.4 Subsequent fires could cause further injury and
death.
pyroclastic flows and surges. The AD 79 eruption of Vesuvius
sent pyroclastic flows down the volcano flanks, killing thousands
in nearby towns. The 1980 eruption of Mt St Helens created a
pyroclastic surge cloud that enveloped more than 100 people as
it moved at locally supersonic speeds. The 57 people closest to
the crater died. Many were buried by volcanic debris, and others
died from exposure to intense heat or from asphyxia. One man
was killed by a falling tree and another by a rock that flew
through his car windshield. Two men died in the hospital from
lung injury (acute respiratory distress syndrome) caused by inhal-
ing fine ash.4 Two others, near the edge of the pyroclastic surge,
survived with minimal injury. More people would have died, but
the area surrounding Mt St Helens had been evacuated after
swarms of earthquakes and changes in the shape of the mountain
signaled an impending eruption. Two weeks after the eruption,
ash deposits on the volcano were still 300° to 400° C (572° to
were below ground.
The most devastating eruption of the 20th century occurred
on May 8, 1902, when Montagne Pelée, on the Caribbean island
of Martinique, sent pyroclastic flows moving greater than 100 km/

364
 Ice cap Subglacial lake Skin should be completely covered, the head swathed in cloth,

CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation

and to prevent severe lung damage, the breath should be held
during the seconds to minutes when the hot cloud passes. Emer-
gency medical personnel should be prepared to treat burns and
blunt trauma injuries.
Lahars (Volcanic Mudflows)
Lahars, the Indonesian term for volcanic mudflows, can accom-
A pany most active, explosive volcanoes (particularly those with
snow or ice cover). Historically, lahars have been almost as
devastating as pyroclastic flows.60 Mudflows occur when hot or
cold volcanic debris mixes with water. Because the mixture has
a high proportion of sediment, lahars behave like liquid cement
and may cover 20 times the area of equivalent rock avalanches.40
The mass of rock, mud, ash, and water sweeps down valleys,
and when it reaches lowland plains, slows down and spreads
out to cover hundreds of square kilometers. Lahars destroy build-
ings, bridges, and other structures and leave thick deposits
behind (Figure 17-25). Most fatalities occur when victims are
caught in the flow and are killed by trauma resulting from this
destruction, flying debris, or burial.4 More deaths occur later from
famine and disease as people are displaced from their homes
and local water sources become contaminated.
Lahars are especially dangerous because they come unher-
alded. They can form during or after an eruption, or they may
be completely unrelated to eruptive activity.4 Water is the key
B ingredient. Lahars need at least 10% water by weight to become
mobile.66 During an eruption, hot pyroclastic material can melt
glacial ice or snow, producing water that mixes with ash on the
volcano’s flank. The water may come from a crater lake drained
during an eruption or from the volcano’s own subsurface geo-
thermal system. A subglacial eruption can form a subglacial lake
that subsequently breaks out to the surface and mixes with glacial
debris. Heavy rainfall occurring during an eruption can initiate
lahar formation. Shortly after an eruption, when new volcanic
material is on the volcano’s flank and there is no ground cover,
rainfall can mix with the ash to create a lahar. Even long after
an eruption, under circumstances such as a sustained intense

0 150
C Kilometers
BC
FIGURE 17-19  A, Cross section of a subglacial volcano. B, Subglacial
volcano Grímsvötn in Iceland lies largely beneath the vast Vatnajökull WA ID
icecap. The caldera lake is covered by a 200-m (656-foot)–thick ice
shelf. A volcanic plume rises, during the November 2004 eruption,
from the exposed southern rim of the 6- by 8-km (3.7- by 5-mile) Mount Spokane
caldera. C, Aerial view of jökulhlaups from the 2010-to-present erup- St. Helens
Seattle Columbia Plateau
tion at Eyjafjallajökull, Iceland (see text). (B courtesy Freysteinn Sig-
Vantage
mundsson, Nordic Volcanological Center.)
Yakima
Pasco

Portland Pendleton
hr (62 miles/hr) down the mountainside. Within minutes, the city
of Saint-Pierre, 6 km (3.7 miles) away, was annihilated and
Pacific Ocean

29,000 people were killed. Only two survived in the town. At

sea, ships were capsized and demasted, and people were burned
by hot-air fall.66 Since then, Montagne Pelée has been relatively
quiet. Saint-Pierre has been rebuilt, but the population now is
only 5000, much below the 1902 level (Figure 17-24). Pliocene–Quaternary
Mitigation.  Mitigation of future disasters from pyroclastic Major Quaternary
flows depends on evacuation before an impending eruption. Volcanoes
Failure for any reason to evacuate in time will result in many Cascade Range
deaths. Unfortunately, many countries with human settlements Columbia River
OR Basalt Group
close to active volcanoes do not have the resources to monitor
volcanic activity closely, as the United States did for Mt St Helens. CA
Oligocene–Miocene
In Latin America and the Caribbean alone, almost 60% of all Intrusions
deaths from volcanic eruptions are caused by pyroclastic flows.60
Survival is possible without evacuation far from the volcano if FIGURE 17-20  The Columbia River Flood-Basalt Plateau (green)
there is adequate shelter to protect against high temperatures, covers approximately 163,000 km2 (63,000 square miles) of the Pacific
asphyxiating gases, falling trees, and projectiles. Once persons Northwest. In some areas, it is up to 1800 m (5900 feet) thick. (Cour-
are sheltered, windows, doors, and dampers should be closed. tesy U.S. Geological Survey.)

365
 Fringing

Barrier

Atoll
BURNS, FIRE, AND RADIATION

C
B
FIGURE 17-21  A, Scuba divers filming undersea volcanic activity offshore of Kilauea Volcano. B, Formation
of an atoll. C, Bora Bora (top right), Society Islands, French Polynesia. The island of Bora Bora includes
remnants of an extinct volcano surrounded by a barrier coral reef. Tupai Atoll (bottom left) is all that
remains of a sunken volcano. (A from Doug Perrine / SeaPics.com; C courtesy NASA, photo STS068-
258-042.)
PART 3

rainfall, water may mix with ash, and a lahar (now called a sec-
Eruption cloud
ondary lahar) can start to flow. Posteruption secondary lahars
(volcanic ash cloud) Prevailing wind caused more fatalities than occurred during the catastrophic erup-
tion of Mt Pinatubo, in the Philippines, on June 15, 1991.
Tephra (ash) fall Eruption column Lahars can flow far from the site of the eruption. It is not
Ballistic projectiles
Debris avalanche necessarily the largest mudflows that produce the highest fatality
Acid rain (landslide) rate; other factors include the victims’ proximity to the hazard
(bombs, blocks)
Vent
Pyroclastic flow and the efficacy of a warning system. The greatest volcano
Lava dome collapse tragedy of recent times began late at night on November 13,
Lava dome Pyroclastic
Pyroclastic flow surge 1985, with a small eruption of the Colombian volcano Nevado
Mud or debris flow Fumaroles del Ruiz. Small pyroclastic flows melted the snow cap and glacial
(lahar) ice on the mountain at 1656 m (5433 feet). The water mixed with
Lava flow

Ground
water

Crack

Magma

(After Myers et al., 1998)

FIGURE 17-22  Common volcanic hazards. (Modified from Bobbie

Meyers, U.S. Geological Survey.) FIGURE 17-23  Pyroclastic flow sweeping rapidly downslope from
Unzen Volcano, Japan, in 1991. (Courtesy Shigeru Suto, Geological
Survey of Japan.)

366
 CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
A

B C
FIGURE 17-24  A, City of Saint-Pierre, Martinique, with Montagne Pelée in the background, before the
1902 eruption. B, City of Saint-Pierre showing destruction from pyroclastic flows from Montagne Pelée,
May 8, 1902. C, Seven months later, another, smaller pyroclastic flow sweeps down the flank of Montagne
Pelée on December 16, 1902. (A from an anonymous source; B and C courtesy Academy of Sciences,
France.)

volcanic ash, forming lahars that swept down the steep valleys
July 23, 1991 and destroyed the town of Armero 50 km (31 miles) away, killing
23,000 inhabitants (Figure 17-26). Around midnight, the first lahar
struck the town, which was completely unaware of the danger,
and covered it with 3 to 4 m (10 to 13 feet) of mud, burying
three-quarters of the population.4 Causes of death included suf-
focation from mud aspiration, trauma, hypovolemic shock, and
later, gangrene. Of the 834 survivors, 578 (69.3%) had lacerations,
343 (41.1%) had penetrating injuries, 312 (37.4%) had fractures,
and 272 (32.6%) had eye injuries; many had multiple injuries.87
Armero had been rebuilt on the site of previous settlements
destroyed by similar lahars in 1595 and 1845. Local officials were
warned of the risk by an on-site scientific team, but failed to act.
Another devastating lahar occurred in 1953 when Ruapehu
volcano in New Zealand claimed 151 lives after an ash and ice
A dam retaining its crater lake collapsed. The resultant lahar swept
away the Tangiwai railway bridge just minutes before the arrival
August 15, 1991

B
FIGURE 17-25  Structure buried by mudflows (lahars) along the
Sacobia-Bamban River during eruption of Mt Pinatubo. (Courtesy R.S.
Punongbayan, Philippine Institute of Volcanology and Seismology.)

FIGURE 17-26  Armero, Colombia, after devastating lahars from

Nevado del Ruiz swept down the steep-sided valley (top center) on
November 13, 1985. (Courtesy Richard Janda, U.S. Geological Survey.)

367
 of the Wellington-Auckland express, and five train cars plunged
into the river.66,83
Mitigation.  For communities at risk for being struck by a
lahar, evacuation is as important as when the threat is a pyro-
clastic flow. Early-warning systems include using trip wires
stretched across lahar channels, seismic instrumentation (e.g.,
acoustic flow monitors), video cameras, automated rain gauges,
and human observers. Also, lahars might be partly diverted or
contained by creating channels, and they might be held back by
dams and retention basins.66 To reduce the water source, reser-
voirs or crater lakes can be lowered in level. Survival is possible
without complete evacuation if the population at risk can be
quickly moved to higher ground. Caution should be taken when
crossing bridges. Emergency medical personnel in high-risk
areas need to be prepared to treat blunt and penetrating trauma
(crush injuries, lacerations, fractures, eye injuries), hypovolemic
shock, and wounds with gangrene complications. Access to
victims buried in the thick, cement-like mud can be difficult and
prolonged.
Tsunamis
Tsunami, the Japanese term for harbor wave, is a seismic sea
wave triggered by an earthquake or by volcanic activity. Specific
BURNS, FIRE, AND RADIATION
triggers include major earthquakes along subduction zones, sub-
marine landslides, underwater explosions, eruptions of island
volcanoes, and avalanches on the flanks of a volcano.40 Waves
can move at speeds of more than 800 km/hr (497 miles/hr) and
travel hundreds or even thousands of kilometers away from the
source. In deep water, a tsunami is generally less than 1 m (3.3
feet) high and of no threat, but as the wave approaches the
shore, its speed falls and height increases until it becomes a
steep-breaking wave or an enormous surging wall of water.
Although relatively infrequent, tsunamis pose a severe risk
that cannot be ignored, as was illustrated by the 2004 Indian
Ocean Banda Aceh undersea earthquake, magnitude 9.0, which
generated a tsunami that devastated the shores of Indonesia, Sri
Lanka, India, Thailand, and other countries, with waves of up to
15 m (49 feet) high, killing approximately 228,000 people,
PART 3
although it is difficult to know the exact figure (Figure 17-27).
FIGURE 17-27  Hundreds of dead bodies and debris are piled along
the coast, a dramatic demonstration of devastation caused by tsunamis
affecting the Indian Ocean basin, this one triggered by the Banda Aceh
earthquake, December 26, 2004. (Photographer unknown.)
368
FIGURE 17-28  Early in the morning on April 1, 1946, an earthquake
(magnitude 7.1) in the Aleutian Islands off Alaska sent large, destruc-
tive waves toward the Hawaiian Islands. Five hours later, the waves
struck the Big Island, killing 159 people, including many curious school-
children who ventured into the exposed reef area, not knowing the
receding water was a sign of an approaching tsunami. Pictured are
people fleeing the approaching tsunami (seen in background) in Hilo,
Hawaii. (Courtesy the Pacific Tsunami Museum Archives; photo by
Cecilio Licos.)
Tsunamis caused by volcanic activity have directly killed more
than 42,500 people, which is as many as have been killed by
lahars. Tsunamis, as with lahars, can come unheralded to settle-
ments close to the source but can also affect distant coastal
regions. Fortunately, many of these distant communities can now
receive forewarning from the Pacific Tsunami Warning System
and the newly established Indian Ocean Tsunami Warning Sys-
tem. Death and destruction occur when a tsunami slams ashore
and destroys low-lying coastal communities (Figure 17-28).
Fatalities associated with volcanogenic tsunamis include those
triggered by Mt Unzen, Japan, in 1792 and Krakatau, Indonesia,
in 1883. Mt Unzen, on the Japanese island of Kyushu, is an
island-arc volcano created above a subduction zone. In 1792,
part of the volcano collapsed, probably as a result of seismic
activity. The subsequent debris avalanche swept 6 km (3.7 miles)
down the volcano to devastate the city of Shimabara, killing more
than 9500 people. Most of the debris then emptied into the sea
and triggered a tsunami that struck much of the seacoast of
Ariake, killing another 5000 people in villages and on farms, even
those as high as 30 m (98 feet) above sea level, along nearly
100 km (62 miles) of coastline.65 The famous eruption of Krakatau
in 1883, involving volcano collapse and sending pyroclastic flows
into the sea, set off a series of tsunamis that washed away 165
coastal villages on Java and Sumatra, killing 36,000 people.40,66
Mitigation.  Volcanic islands at risk for being hit by a
tsunami include the islands of Hawaii, the Marquesas, the Canar-
ies, Tristan da Cunha, and Réunion.66 Other low-lying coastal
regions are at risk. Key to mitigation is a worldwide tsunami
warning system similar to the Pacific Tsunami Warning System,
which was created in 1965 to warn of impending tsunamis in the
Pacific Basin. In Hawaii, the warning system consists of sirens
throughout the islands. Lobbies of coastal high-rise buildings are
designed to allow water to pass through them without causing
structural damage.66 In addition, tsunami-warning-system buoys
are scattered throughout the Pacific Ocean, and many coastal
communities are educated to flee to high ground in case of
earthquake or volcanic eruption (Figure 17-29). As a result of the
2004 Indian Ocean Banda Aceh undersea earthquake and
tsunami, three more tsunami warning systems have been pro-
posed. The Indian Ocean Tsunami Warning System became
active in June 2006, whereas the other two—the Caribbean
Sea and Adjacent Regions Tsunami Warning System and the
Northeastern Atlantic, the Mediterranean and Connected Seas
Tsunami Warning System—have been established but are still in
the planning stages and not yet fully operational. The United
Nations Intergovernmental Oceanographic Commission, through

A B
FIGURE 17-29  A, Tsunami buoy contains pressure sensors for determining a wave’s size by gauging the
weight of the water column passing over it. B, “TsunamiReady” sign. (Courtesy National Oceanic and
Atmospheric Administration.)
the International Tsunami Information Center, coordinates the
four systems.
Evacuation to higher ground is essential to reduce morbidity
and mortality associated with tsunamis, and effective evacuation
depends on public education of the officials and inhabitants of
coastal communities. Emergency medical personnel need to be
prepared to treat drowning victims, the effects of trauma, and
disease epidemics.
Debris Avalanches
Volcanoes, especially steep-sided composite volcanoes, can be
the site of catastrophic debris avalanches at any time.65 In 1792
at Mt Unzen, mentioned previously, it was a debris avalanche
that swept down the side of the volcano, killing thousands before
emptying into the sea and setting off a devastating tsunami. Also
in Japan, in 1888 an avalanche from the north flank of Bandai
volcano sent 1.5 km3 (0.36 cubic mile) of debris down the moun-
tainside, killing 400 people below.65,66 A debris avalanche also
contributed to the eruption of Mt St Helens in 1980. Triggered
by an earthquake, a debris avalanche on the north flank of the
mountain removed rock overlying a shallow magma chamber.
Pent-up volatile gases in the magma, no longer contained by the
overlying pressure of the rock, quickly expanded, causing explo-
sive fragmentation of the magma and the first eruption.
Mitigation.  Mitigating danger from debris avalanches in-
cludes mapping the zones of potential slope collapse and avoid-
ing travel to and high-density development within those areas.
Fatalities and injuries are associated with blunt trauma and burial
beneath rock debris. A victim caught in a rock fall should im-
mediately seek some sort of shelter and roll into a ball to protect
the head. Health care professionals need to be prepared for
victims of blunt trauma.
Tephra
Tephra is the general term for fragmented rock of any size (vol-
canic blocks, glass shards, pumice, ash) ejected into the air by
volcanic explosions. Tephra can range in size from large ballistic
ejecta (>1 m [3.3 feet]) to ash (<2 mm). The largest tephra fall
back to the ground at high speeds in the immediate vicinity of
the volcano. Smaller fragments stay airborne longer, and the
smallest are carried away by prevailing winds before ultimately
being deposited, even at distances of many hundreds of kilome-
ters from the volcano.
CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
Ballistic Ejecta.  An erupting volcano can eject huge ballistic
fragments at high velocities (Figure 17-30). These can travel
kilometers away from the volcanic vent and can cause significant
damage (skull injuries, lacerations, blunt trauma of the chest and
abdomen) to humans on impact.4,66 The zone of damage from
volcanic ballistics is generally limited to about 5 km (3 miles)—
the maximum recorded range—so this is rarely a major human
health hazard.4 However, in Italy in 1944, three men were killed
at Terzigno by falling volcanic rocks from Mt Vesuvius 5 km (3
miles) away. In 1924, an explosive eruption at Kilauea knocked
a photographer down with flying stones and severed his leg. He
died later that day, probably from toxic gas exposure.10 Fire is a
more common hazard, because hot flying ejecta can set fire to
wooden structures, forests, or grassland.
Volcanic Ash.  Smaller-sized tephra, especially ash, pose a
much greater danger than do blocks and bombs. Drifting volcanic
ash can be deposited hundreds to thousands of kilometers down-
wind from a volcano. Heavy accumulations of ashfall can col-
lapse roofs, interfere with driving, clog machinery, and damage
vegetation (Figure 17-31).
A layer of ash only 10 cm (4 inches) thick is enough to col-
lapse a flat roof, especially if it is wet with rainfall.60,66 Approxi-
mately 10,000 fatalities have been directly associated with ashfall,
and the majority of these are from collapsed roofs. In 1991, Mt
Pinatubo in the Philippines erupted during an untimely typhoon.
Subsequent ash mixed with rain collapsed roofs and killed at
least 300 people.66
Decreased visibility from airborne ash and slippery ash-coated
roads pose danger to drivers of motor vehicles. During and after
an eruption, the incidence rises of motor vehicle crashes and
associated injuries. Moderate amounts of ashfall can also directly
damage motors and other machinery, because fine ash clogs
engine filters and lubrication systems.66 Damaged machinery is
rarely a risk to human health, except in the case of jet engines.
Volcanic ash clouds contain a combination of fine rock and
glass particles. If a jet aircraft flies into a volcanic ash cloud, even
thousands of kilometers away from the eruption site, the ash can
damage engines, avionics, and airframes. Ash particles can block
fuel nozzles, air filters, and external navigational equipment.
Abrasion damage can severely scratch cockpit windows, landing
lights, and turbine blades. Volcanic glass sucked into the engine
will melt in the heat, accumulate, and solidify into a glassy layer
that chokes fuel nozzles, coats turbine engines, and interferes
369
BURNS, FIRE, AND RADIATION

A B
FIGURE 17-30  A, Spectacular explosive spray of ballistic ejecta when hot lava from Kilauea Volcano entered
the ocean in 2008 in Hawaii; observers (left corner) give scale. B, Large ballistic block thrown up onto the
shore from a previous lava entry into the ocean in the 1980s. (A courtesy Michael Poland, U.S. Geological
PART 3

Survey; B courtesy Christina Heliker, U.S. Geological Survey.)

with sensors, leading to reduced engine performance and ulti-
mately total engine failure. High levels of static electricity in
volcanic material can also interfere with radio communication.
Comprehensive summaries of the damage and impacts of volca-
nic ash on aircraft operating and support systems have been
described.14,53
Since the mid-1950s, more than 80 commercial aircraft have
accidentally flown into eruption clouds, and seven of these
encounters caused in-flight loss of jet engine power.28,55 In 1982,
two jetliners flew into the eruption cloud from Galunggung
volcano on Java. The first, a British Airways jumbo jet carrying
240 people, lost all four engines and plummeted 7500 m (24,600
feet) in 16 minutes before cold air chilled and shattered the
volcanic glass and the engines could be restarted. The jet made
an emergency landing at Jakarta airport with three functioning
engines and flying blind because the windshield was opaque
from ash abrasion. A few weeks later, a Singapore Airline jumbo
jet flew into a volcanic ash cloud from the same volcano, lost
three engines and dropped 2400 m (7874 feet) before one engine
restarted, and the aircraft was able to make an emergency landing
(Figure 17-32).10 Fortunately, to date no lives have been lost from
aircraft–volcanic ash encounters. However, in mid-April 2010, the
high eruption cloud from the Eyjafjallajökull eruption (Figure
17-33A) and its easterly drift over northern Europe (Figure
17-33B) raised serious concerns of possible damaging encounters
between commercial aircraft and volcanic ash. As a precautionary
measure, aviation officials closed many airports and grounded
flights in the United Kingdom, France, Germany, Norway,
Sweden, Finland, and Spain; many Europe-bound flights from
the United States were also cancelled. The many airport closures
and flight cancellations (>107,000) resulted in the largest disrup-
tion in commercial aviation since that caused by the September
11, 2001, terrorist attacks on the United States. An ash cloud from
the 2011 eruption of Grimsvötn caused a similar crisis for com-
mercial aviation. This time, however, even though the Grimsvötn
plume was very large, it lasted for a relatively short time. Equally
important, the international civil aviation agencies had learned
valuable lessons from the Eyjafjallajökull experience in how to
better manage a volcanic ash crisis. These two factors combined
to greatly reduce the impact of the Grimsvötn eruption on global
air travel.76
Heavy ash can strip vegetation from plants and coat surviving
leaves. Destroyed vegetation and crops result in starvation of
animals and can ultimately lead to famine in areas dependent on
agriculture for subsistence. Famine from ash-related destruction
of crops was the number-one cause of fatalities associated with
volcanic eruptions before the 20th century. With global com-
munication and world relief organizations, famine is now less
common.
Most volcanic ash poses little direct danger to humans. Eye
irritation may cause conjunctivitis and corneal abrasion, espe-
cially in persons wearing contact lenses.39,60 Nose and throat irrita-
tion are common in persons not wearing a mask. Inhalation of
ash, typically thought to be a significant health hazard, is for the
most part benign, except for people with preexisting lung disease
and heavily exposed workers, such as gardeners, road workers,
and police.6,8,11,15,26,50,67,86 Most ash particles are too large to be
respired, high dust concentrations are of brief duration, and ash
is biologically inert.60,83
However, fine ash particles less than 10 µm in diameter can
irritate the lungs. This is especially dangerous for people with
asthma and chronic bronchitis and results in increased visits to
emergency departments (EDs) for exacerbation of chronic lung
disease.54,68 For example, after Mt St Helens erupted in 1980,

370

A ties formerly were advised to keep flat roofs clear of ash buildup,
C
FIGURE 17-31  A, Enormous ash cloud from the 1980 eruption of Mt
St Helens passing over the small town of Ephrata, Washington, 233 km
(145 miles) to the west. B, Ash-covered village of Parentas, Java, after
one of the eruptions of Galunggung Volcano in 1982. C, In the city of
Yakima, central Washington, ash made roads slippery and decreased
visibility after the 1980 eruption of Mt St Helens. (A courtesy Douglas
Miller; B courtesy Maurice Kraft; C courtesy U.S. Geological Survey.)
there was a fourfold increase in the number of asthma patients
and a twofold increase in the number of bronchitis patients visit-
ing EDs in two large hospitals.6 However, except for a single
recent study,31 no other studies have suggested significant long-
term consequences of regularly breathing ash, even in the
densely populated regions around Mt Sakurajima in Kyushu,
Japan, where eruptions occur hundreds of times each year.86
Some studies have shown certain types of ash, especially ash
with a high content of the mineral cristobalite, can cause lung
inflammation, but there is no evidence of any fibrogenic lung
changes.36,44,69
Mitigation.  To prevent injury from large-size tephra, danger
CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
zones around the volcano should be mapped, and these zones
should be closed when eruption is a possibility. If closure is not
possible, concrete shelters can be built in danger zones for the
public to access in case of sudden onset of tephra fall. Hard hats
should be worn at all times, and anyone unprotected caught in
the open should watch for falling fragments and try to dodge
them.4 Emergency medical personnel need to be prepared for
blunt trauma to the head and torso, and for burn victims.
To minimize injury from ash, drive slowly, minimize engine
use, and wear eye protection and a dust mask. All vehicles and
machinery should be put inside a garage or barn. Animals and
livestock should be brought into closed shelters. Consider evacu-
ating children and high-risk individuals (e.g., with asthma or
chronic bronchitis) until ash levels are lower. Although communi-
this is not recommended now, because people have been injured
or killed from falling off roofs while removing ash (Figure 17-34).
Health care professionals should be ready for an increase in
emergency visits from motor vehicle collisions, eye injuries, and
respiratory problems.
To mitigate the dangers associated with aircraft possibly
encountering volcanic ash clouds, air traffic is routed away from
eruption clouds based on the analyses of a global system of
Volcanic Ash Advisory Centers. Working with volcanic observa-
tories, these centers disseminate information on atmospheric
volcanic ash clouds that may endanger aircraft. In addition, if
aircraft accidentally fly into an ash cloud, pilots are now trained
in what to do at the first sign of engine failure. Pilots will turn
around the plane to fly out of the eruption cloud and try to cool
the engines by idling. With engine cooling, the glassy coating
will break off, thus preventing total engine failure.
A
B
FIGURE 17-32  A, Eruption cloud from Rabaul Volcano, New Britain
Island, Papua New Guinea, September 1994. Note the difference in
appearance between the eruption cloud and ordinary meteorologic
clouds. B, Aircraft damage after flying into an eruption cloud from
Redoubt Volcano in Alaska, December 1989. (A courtesy NASA, photo
STS064-116-47; B courtesy Joyce Warren.)
371

A asphyxiant, and at concentrations higher than 20%, even a few
BURNS, FIRE, AND RADIATION
B Only 2 years earlier, at nearby Lake Monoun, a similar but smaller
FIGURE 17-33  A, High-rising eruption cloud from the explosive phase
of the ongoing eruption of the subglacial volcano Eyjafjallajökull in
Iceland. B, The airspace of northern Europe affected by the drifting
eruption ash cloud from Eyjafjallajökull Volcano (arrow, red dot). (Cour-
tesy UK Met Office.)
PART 3
FIGURE 17-34  Ash removal in Moses Lake, eastern Washington, after
1980 eruption of Mt St Helens. Keeping roofs clear of ash is not
advised because of the risk of falling. (Photographer unknown.)
372
Volcanic Gases
Gases dissolved in magma can separate explosively or passively
from the molten rock and can be discharged into the atmo-
sphere. During an explosive eruption, 10 million to 1 billion tons
of volcanic gases can be released into the atmosphere over a
few hours to a few days. During noneruptive periods, gas can
also escape continuously from fissures, geysers, and other sites
of volcanic activity. The most abundant gas released from magma
is water (H2O) vapor. Second is CO2, closely followed by SO2.
Carbon monoxide, hydrochloric acid, hydrogen, and hydrogen
sulfide (H2S) are other common gases released in appreciable
quantities.65 CO2 and H2S are by far the most dangerous. Because
both are denser than air, they collect in low-lying areas and
cause harm if inhaled by unsuspecting individuals.60 CO2 is an
breaths can very quickly lead to unconsciousness and death
from acute hypoxia, severe acidosis, and respiratory paralysis.
H2S, the colorless gas that smells like rotten eggs, is so toxic that
a high-level exposure can kill a human after a single breath.66
H2S, similar to cyanide, arrests cellular respiration and thus
aerobic metabolism.
There are numerous accounts of fatalities associated with CO2
emissions from volcanic activity. Perhaps the most lethal tragedy
occurred in 1986 at Lake Nyos, Cameroon, when dangerous
amounts of dissolved CO2, once trapped in the lower levels of
this volcanic crater lake, suddenly rose to the surface and were
abruptly released, like champagne suddenly uncorked.33 The gas
rose 80 m (262 feet) before the CO2 settled to the ground and
rolled down valleys and into villages up to 20 km (12 miles)
away, instantly suffocating 1746 people and 3000 livestock. Sur-
vivors suffered transiently from burns, headache, nausea, vomit-
ing, cough, dyspnea, hemoptysis, and chest pain (Figure 17-35).1
cloud of CO2 welled up from the lake, flowed downhill, and
killed 39 people.33 In Indonesia in 1979, a release of CO2-rich
volcanic gas from Sinila Crater (Dieng Plateau) killed 142 local
inhabitants as they evacuated the area via a low-lying valley.45
Less dramatically, CO2 leaking from underground volcanic
systems in Italy has been linked to the deaths of animals and
two children. In the Mammoth Lakes region in eastern central
California, accumulation of volcanic CO2 trapped under snow
may have contributed to the death of a cross-country skier as
well as three ski patrol members.12,32
There are a few reports of H2S-associated fatalities. Six down-
hill skiers on Kusatsu-Shirane volcano in Japan died in 1971, and
four hikers who wandered into the lowest part of the summit
crater on Adatara volcano in Japan died in 1997. Neither volcano
Lake
Nyos
w
flo
gas
2
CO
FIGURE 17-35  Village of Fulani downslope from Lake Nyos in
Cameroon, Africa, where 25 people died from CO2 poisoning in 1986.
Clusters of white dots (in rectangles) on slope are dead cattle, also
killed by the CO2. (Courtesy John P. Lockwood, U.S. Geological
Survey.)
was erupting at the time.35,66 Chronic low-level H2S exposure may
also have deleterious health effects. In Rotorua, New Zealand,
where 30% of the city’s population lives downwind of an actively
degassing geothermal field, preliminary findings indicated a
spatial relationship between exposure and an increase in respira-
tory symptoms, especially in individuals with chronic obstructive
pulmonary disease.23
An irritant to mucous membranes, SO2 can induce respiratory
distress and can adversely affect pulse rate and blood pressure,
but it has never been proved to directly cause death.2,46-48,66
However, in Japan, SO2 emissions from Mt Oyama on the island
of Miyake forced evacuation of Miyake’s 3900 residents to the
mainland from September 2000 to February 2005.17 Since the
return of residents to Miyake, despite ongoing SO2 emissions,
research has showed a relationship between SO2 concentrations
and acute respiratory symptoms such as cough, sore throat, and
shortness of breath.37 Similarly, there are no fatalities associated
with hydrogen fluoride (HF), but indirectly, HF was responsible
for the death of 10,000 Icelanders in 1783. HF from the prolonged
Laki fissure eruption poisoned much of the pastureland and
crops, causing the death of half the livestock and crop failure,
which ultimately led to famine and death.64-66
Mitigation.  Mitigating the danger associated with toxic vol-
canic gases depends on the type of gas and how it is released.
Since the Lake Nyos disaster, scientists have placed 12 pipes into
the lake at different depths to allow CO2 to escape continuously
rather than accumulating to dangerously high levels. Danger
zones can be mapped and warnings signs posted. Equipment
can be stationed to monitor gas emissions. Recreationists should
be educated to avoid certain activities at times of gas release or
buildup under snow. Low-lying areas where poisonous gases can
collect should be avoided. Emergency medical personnel should
remove victims from the source of toxic gases, place them on
high-flow oxygen, and treat other injuries accordingly.
HAZARDS FROM NONEXPLOSIVE VOLCANOES
In general, nonexplosive volcanoes pose little direct danger to
humans. Few fatalities are associated with them because lava
usually flows slowly enough for people to avoid it.4,5 Generally,
those who have died either lingered to watch the lava or returned
to their homes too early. On the other hand, rivers of lava can
cause significant property damage as they set fire to, knock
down, or bury buildings and roads. On rare occasions, flows of
low-viscosity lava have been witnessed to travel down steep
slopes at speeds as high as 100 km/hr (62 miles/hr).
Lava Flows
Fatalities associated with lava flows account for only about 0.3%
of total deaths from volcanic activity. The most deadly lava flow
took place at Mt Nyiragongo, Congo.4 Nyiragongo is among the
few volcanoes with an active lava lake inside its summit crater,
and during an eruption in 1977, this lake suddenly drained
through fissures in the crater wall. A very fluid lava flow, esti-
mated to be traveling at 100 km/hr (62 mph), swiftly engulfed
small towns, killing hundreds of people.4,58,65,66 In 1947, a scientist
filming a lava flow at Mt Hekla in Iceland was killed by a glowing
lava block rolling downslope.10 Other hazards include methane-
fueled explosions when lava overruns vegetation, and explosions
or scalding steam when lava flows over ice or snow or into water
(Figure 17-36).66
Mitigation.  Because lava flows rarely pose a significant
health hazard during volcanic activity, they are not a high priority
for health planning.60 However, to limit property damage, lava
flow diversion is a possibility. In 1973, after 6000 years of inactiv-
ity, Eldfell volcano on the island of Heimaey in Iceland reawak-
ened and lava poured out, threatening the most important port
of the Icelandic fishing industry. To stop or divert the lava flow,
cold seawater was sprayed onto the advancing lava front, and
after 2 weeks of nonstop work, the port was saved.65,66 Other
attempts at diversion, including building rock and dirt barriers,
and aerial bombings,79 have not been successful. Health care
professionals should be prepared to treat burns from contact with
lava or scalding steam.
CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation
2:58 PM, July 2, 1983
A
3:11 PM, July 2, 1983
B
FIGURE 17-36  A rapidly advancing lava flow from Puu Oo vent,
Kilauea Volcano, Hawaii, engulfs vehicles. (Courtesy Robert W. Decker,
U.S. Geological Survey.)
Jökulhlaups
A jökulhlaup is a large outburst flood associated with eruption
of a subglacial volcano. The heat from the volcano melts overly-
ing ice, forming a subglacial lake. As the lake rises, the overlying
glacier is lifted and begins to melt, forming a subglacial river. If
this river bursts to the surface, disastrous flooding can occur.
When this happened in 1996 from a subglacial eruption at Gríms-
vötn in Iceland, water escaped from a 3.5-km (2.2-mile) crevice
at a maximum rate of 45,000 m3/sec (12 million gal/sec) to form,
temporarily, the second-largest river on Earth.66 Miles of road and
bridges were destroyed. A smaller jökulhlaup emerged in Novem-
ber 2004 from volcanic activity at Grímsvötn, with a peak dis-
charge of up to 4000 m3/sec (1 million gal/sec), but this time no
roads or bridges were destroyed.75 In 2010, jökulhlaups of the
Eyjafjallajökull eruption (see Figure 17-19C) caused substantial
destruction of roads and infrastructure locally, but fortunately no
deaths or injuries.
POSTERUPTION HAZARDS
Major eruptions can be hazardous long after the eruption is over.
Large quantities of gas released into the atmosphere can cause
air pollution, produce acid rain, and deplete ozone, possibly
affecting global climate for a few years.4 Water supplies can be
contaminated and crops destroyed, leading to disease epidemics
and famine.3 Moreover, overcrowding and poor sanitation condi-
tions, commonly associated with temporary evacuation camps,
pose health hazards and sometimes lead to disease epidemics.
After the eruption of Mt Pinatubo in June 1991, a measles out-
break, diarrhea, and respiratory infections resulted in the death
of hundreds of children from an isolated tribe forced to live in
evacuation centers.25 Ongoing smaller eruptions, such as the
continuing (since 1983) nonexplosive activity at Kilauea Volcano,
can also cause problems related to sustained volcanic gas emis-
sions80 (Figure 17-37). In Italy, Mt Etna is the largest continuous
source of volcanic SO2 globally, and Stromboli is probably the
second largest in Europe.22
During the 8 months that the Laki fissure in Iceland was erupt-
ing in 1783, at least 122 million metric tons (MT) of SO2, 7 MT
373

Vog free
A the lymphatic system, causing inflammation, lymphatic fibrosis,
Heavy vog
BURNS, FIRE, AND RADIATION
B radiation.
FIGURE 17-37  The ongoing eruption of Kilauea’s east rift zone (which
began in 1983) has put a huge amount of natural pollutants, including
sulfur oxides, into the air. Introduced vegetation, such as Kona coffee
plants, can be scorched, and downwind of Kilauea, only native species
PART 3
tolerant of the natural acid rain survive. The two images compare
atmospheric clarity between a volcanic-smog (vog)–free day (A) and a
heavy-vog day (B). (Courtesy Jeff Sutton, U.S. Geological Survey.)
of hydrogen chloride, and 15 MT of HF were released into the
atmosphere.84 HF poisoned most of Icelandic sheep and destroyed
crops, contributing to the death of nearly a quarter of Iceland’s
entire population from famine.64 In addition, the Laki eruptions
were probably responsible for the death of more than 10,000
people in England during summer 1783 and winter 1784. Noting
that the mortality rate was 16.7% above normal for this time
period, experts in the United Kingdom suggest that a cloud of
volcanic gases and particles swept south from Laki into England
and was responsible for the very hot 1783 summer and subse-
quent severe winter.64,84 Climatic data, burial records, and written
accounts describe a summertime “volcanic haze” or “dry fog” that
shrouded the moon and sun, reduced visibility, withered vegeta-
tion, and caused health problems.22,64 As with smog, the dry fog
caused headache and eye irritation, exacerbated lung disease,
and irritated mucous membranes. Wintertime deaths were associ-
ated with unusually cold temperatures. Benjamin Franklin, U.S.
ambassador to France in Paris at the time, was the first to link
the effect of Laki’s eruption on climate and presented a scientific
paper on the topic.
Eruption clouds that penetrate the upper atmosphere can
spread volcanic particles and gases across an entire hemisphere.66
During the 3 months it can take fine ash particles to settle out,
solar heating is reduced and the lower atmosphere is cooled.
The 1991 eruption of Mt Pinatubo in the Philippines created a
large volcanic cloud that drifted around the world and caused a
temporary average global temperature drop of 0.5° C (0.9° F).40
The largest eruption in recorded history in 1815 at Tambora,
Indonesia, reduced the average global temperature by 3° C
(5.4° F) for several years.40 This eruption directly or indirectly
374
caused the death of an estimated 60,000 people in Indonesia and
was responsible for a typhus epidemic in Great Britain, cholera
in India, and mass migration from northern Europe and Russia.
It ruined farms in New England and spurred westward migra-
tion.66 The greatest eruption since humans evolved was that of
Toba in Indonesia, about 74,000 years ago. The global tempera-
ture dropped 5° C (9° F) for many years, causing a global envi-
ronmental catastrophe. It may have resulted in an estimated
decrease in the population of Homo sapiens from over 100,000
to less than 2000.66
Some volcanic soils may also pose a health risk. Nonfilarial
elephantiasis, otherwise known as podoconiosis or mossy foot,
appears to be caused by chronic exposure of unprotected feet
to irritant alkalic red-clay soils rich in volcanic particles. Micro-
scopic particles absorbed through abrasions in the feet penetrate
and ultimately blockage. As the lymphatics are obstructed, the
lower extremities swell, resulting in elephantiasis. Podoconiosis
is predominantly found in high-altitude areas (>1250 m [4101
feet]) of tropical Africa, Central America, and North India.18-20,56,82,85
Fluoride leached from volcanic rocks into drinking water can also
cause disease. In eastern Turkey near Tendurek Volcano, mottled
enamel from high levels of fluoride, called endemic dental fluo-
rosis, has been observed in humans and livestock since the
1950s.59
Several studies have suggested people living near volcanoes
may be at increased risk for developing thyroid cancer.9,21,27,42,61,62
Epidemiologic surveys conducted in Italy, Iceland, Hawaii,
and the Philippines report increased incidence of thyroid cancer
in volcanic areas. However, the specific carcinogenic agent has
yet to be identified; suspects include toxic air pollutants, a pol-
lutant in volcanic soil or volcanic aquifers, and volcanogenic
RISK REDUCTION FROM
VOLCANIC HAZARDS
Humans are vulnerable to severe, unpreventable volcanic erup-
tions. Risk reduction starts with comprehending the seriousness
of volcanic hazards and being prepared for the associated
dangers. Almost 99% of fatalities associated with volcanic erup-
tions are from pyroclastic flows and lahars, yet one-tenth of the
world’s population lives in cities and homes near volcanoes,
sometimes on the volcano slopes or on the remains of a previ-
ous pyroclastic flow, lahar, or debris avalanche.60,66 Fortunately,
most volcanic eruptions are preceded by premonitory events,
such as earthquakes and other measurable phenomena, far
enough in advance to enable scientists and emergency workers
to plan for disaster. However, a few of the most severe erup-
tions have occurred with little or no warning, and most of the
world’s dangerous volcanoes are in densely populated coun-
tries that lack the resources or political interest to monitor
them.5,79
Nevertheless, emergency planning for an eruption, including
creation of hazard-zone maps and hazard evaluation, should be
routine for all populated areas near volcanoes, regardless of their
location or apparent state of activity.5 Risk reduction includes
volcano monitoring, eruption prediction, and effective coordina-
tion between volcanologists, scientists, health care professionals,
and the community at risk. In addition, with tourism increasing
to volcanic destinations, the tourist industry, practitioners of
travel medicine, and adventure travelers need to educate them-
selves and others about the potential health hazards of volcanic
environments.29
VOLCANO MONITORING
Scientists monitor volcanoes for seismic activity (earthquakes),
changes in volcano shape (ground deformation), surface tem-
perature, magma level, gas emissions, and other chemical and
physical attributes (Figure 17-38).57 Earthquakes and ground
deformations are the most reliable diagnostic observations for
helping scientists predict when a volcano might erupt or when
 Additional eruptions took place over the next 2 days. On June

CHAPTER 17  Volcanic Eruptions, Hazards, and Mitigation

15, a cataclysmic eruption took place during a typhoon. The
eruption cloud rose 12 km (7.5 miles) into the atmosphere and
spread out like an umbrella more than 200 km (124 miles) in all
directions. Wet ash covered a 4000-km2 (1544-square-mile) area,
burying crops and collapsing roofs, and many destructive lahars
were generated.16 Ash fell as far away as the Indian Ocean. The
warning saved at least 5000 lives and prevented extensive
property damage.

COORDINATION BETWEEN VOLCANOLOGISTS

FIGURE 17-38  U.S. Geological Survey scientists sampling volcanic
gases within the Mt St Helens crater. (Courtesy Kathy Cashman, Uni-
versity of Oregon.)
it is no longer likely to erupt.52,78 The importance of monitoring
cannot be overstated. During the last half of the 20th century,
most eruptions from monitored volcanoes were anticipated
weeks or months in advance. These include the eruptions of Mt
St Helens in 1980 and 2004 and Mt Pinatubo in 1991 (see next).
Often, the problem is not predicting when the volcano will
erupt but convincing government officials to act on the warning.
Before 1985, authorities in Armero, Colombia, were warned that
lahars could devastate their town, but the warning was disre-
garded, and the eruption at Nevado del Ruiz and the subse-
quent lahars destroyed the town and killed more than 25,000
people.66
AND HEALTH CARE PROFESSIONALS
Coordination among geologists, other scientists, and health care
professionals is essential to prepare communities for volcanic
emergencies. Planning for future eruptions requires determining
the history of a volcano’s past eruptions and their impact, devel-
oping a hazard-zone map, anticipating when a volcano might
erupt, and describing the types of hazards to be expected and
their potential effects on health (Figure 17-40). Furthermore,
health care professionals need to identify high-risk populations,
prepare for disaster victims, and help volcanologists educate
the community about potential health effects for each volcanic
hazard.57 Evacuation of communities, especially in low-lying
areas and river valley regions, is of utmost importance. Goggles
and masks should be distributed, especially to individuals who
must work in dusty conditions.

ERUPTION PREDICTION AND MT PINATUBO:

EFFECTIVE VOLCANIC-EMERGENCY RESPONSE
In April 1991, the Philippine volcano Mt Pinatubo began to erupt,
weakly, for the first time in recorded history. Ultimately, the
activity escalated into the world’s largest eruption in the preced-
ing eight decades. However, only 300 people were killed, even
though at least 600,000 people lived in cities, villages, and mili-
tary bases around the volcano. The larger tragedy was prevented
by effective cooperation between local authorities and scientists
of the Philippine Institute of Volcanology and Seismology (PHI- FIGURE 17-39  Volcano Disaster Assistance Program “SWAT” team
VOLCS) and the U.S. Geological Survey (USGS). lands near Rabaul Volcano, Papua New Guinea, in 1994. (Courtesy
Two months before the climactic eruption on June 15, PHI- Elliot Endo, U.S. Geological Survey.)
VOLCS consulted the USGS’s Volcano Disaster Assistance Program
(VDAP), a mobile volcano-response team (i.e., an eruption SWAT
[special weapons and tactics] team) of experienced volcanologists
and other scientists who rapidly respond to a developing volcanic
crisis with state-of-the-art portable monitoring equipment (Figure
17-39). The request for assistance came after an increase in the
number of earthquakes (up to 500 per day), explosions, and new
cracks opening in the volcano. The VDAP team set up a base
camp at Clark Air Force Base and began to monitor and interpret
seismic activity, ground deformation, and gas emissions. They
also gathered data about Pinatubo’s previous eruptions to predict
the types of hazards that could be expected and to create a map
of the area, delineating zones at risk during an eruption. Finally,
the PHIVOLCS-USGS team worked with local authorities to
develop an evacuation plan and educate people. A 30-minute
video, Understanding Volcanic Hazards, produced after the
tragedy of Armero, Colombia, in 1985, was shown to local offi-
cials and populations to raise awareness of hazardous volcanic
processes.
On June 7, a month and a half after the USGS team arrived,
a warning was sent out about a possible major eruption within
24 hours. Villages and cities were evacuated. Five days later, the FIGURE 17-40  First of a series of powerful explosions beginning on
first in a series of powerful explosive eruptions began. An erup- June 12, 1991, Pinatubo Volcano, Philippines (see text); note within
tion cloud rose 19 km (12 miles) into the air, and small the yellow oval a farmer and buffalo plowing. (Courtesy David Harlow,
pyroclastic flows started down to the north and northwest. U.S. Geological Survey.)

375
 TABLE 17-5  Casualties Caused by Pyroclastic Flows in 20th-Century Explosive Eruptions

Eruption Year Deaths (N) Ratio of Dead to Injured Survivors after Treatment

Montagne Pelée, Martinique 1902 28,000 230 : 1 163 treated, 123 survived
La Soufrière, St Vincent 1902 1565 11 : 1 194 treated, 120 survived
Taal, Philippines 1911 1335 10 : 1 Not known
Lamington, Papua New Guinea 1958 2942 44 : 1 70 treated, 67 survived
Mt St Helens, United States 1980 58 16 : 1 130 airlifted, 9 treated, 7 survived
Unzen, Japan 1991 43 5 : 1 17 treated, 4 survived (minor burns)
Mt Merapi, Indonesia 1994 63 3 : 1 86 treated, 11 dead on arrival
Soufrière Hills, Montserrat 1997 19 4 : 1 7 treated, all survived

From Baxter PJ: Impact of eruptions on human health. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000,
Academic Press.

EMERGENCY MEDICAL RESPONSE BOX 17-2  Summary of Health Effects from

Emergency medical care plays a small role in severe volcanic Volcanic Eruptions
eruptions. The number of injured who could benefit from treat-
ment is much smaller than the number of victims killed within Physical
BURNS, FIRE, AND RADIATION

minutes of a catastrophic eruption (Table 17-5).5 Therefore, pre- Blunt trauma from pyroclastic material, lahars, debris avalanches,
vention is of utmost importance, and evacuation is the key to tsunamis, and tephra
decreasing morbidity and mortality.5 Health care professionals Burns, wounds, and gangrene complications
should be prepared to treat a variety of medical problems in Asphyxiation from lack of oxygen or inhaled ash
persons who survive (Box 17-2), and they must be aware that Acute irritation of the respiratory tract caused by ash
access to victims will be limited by high-level ash conditions, Exacerbation of prior respiratory disease caused by inhaled particles
burial beneath volcanic debris, and ongoing hazards. Transient Respiratory tract and lung burns caused by inhalation of hot steam
increases in ED visits and hospital admissions will require addi- Conjunctivitis and corneal abrasions
Toxic effects of gases such as CO2, H2S, SO2, HF, CO, and radon
tional resources.8
Gastroenteritis
Skin irritation from acid water
GEOTOURISM Drowning in lahars or tsunamis
With the increased interest in visiting volcanic environments, the Psychological
numbers of injuries and illnesses are increasing. Areas such as Depression
Hawaii Volcanoes National Park have experienced a high rate of Anxiety
Nightmares
PART 3

injuries and illness because of inexperienced hikers entering

Psychomotor disorders
high-risk environments and disregarding warning signs.30 People
Irritability
working or traveling near an active volcano or volcanic environ- Insomnia
ment should heed these safety recommendations: Confusion
• Read about the volcanic environment, including past erup- Neurosis
tions and accidents. Stress
• Know the current volcano warning level, and obey local
authorities. Modified from Zeballos JL, Meli R, Vilchis A, et al: The effects of volcanoes on
• Travel with a guide experienced in local conditions. health: Preparedness in Mexico, World Health Stat Q 49:204, 1996.
• Leave travel details with a responsible person. CO2, Carbon dioxide; CO, carbon monoxide; HF, hydrogen fluoride;
H2S, hydrogen sulfide; SO2, sulfur dioxide.
• Wear a hard hat and carry a gas mask, if appropriate.
• Beware of the sources of danger on a volcano:
Rock falls
Avalanches REFERENCES
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• Look for warning signs of an eruption. Complete references used in this text are available
• Immediately leave the area if it becomes dangerous. online at expertconsult.inkling.com.
• Do not approach lava flowing through vegetation.

376
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PART 4

Trauma
 CHAPTER 18 
Wilderness Trauma and
Surgical Emergencies*
MICHAEL J. KRZYZANIAK, TIMOTHY C. NUNEZ, AND RICHARD S. MILLER
This chapter has been written primarily to provide physicians
and health care workers with a logical approach to management
of trauma and surgical emergencies that may be encountered in
the wilderness environment. The focus is on health care profes-
sionals who will be responsible for the urgent management of
such emergencies for all expedition members.
Wilderness expedition health care providers have varied expe-
riences and capabilities. In this environment, the location, dis-
tance from medical facilities, conditions, and available resources
are the most influential factors in patient outcome. It is often
impractical to perform complex interventions in the field, but it
remains clear that simple, basic processes, such as identifying
injuries, establishing an airway, keeping the patient warm, and
expediting evacuation, strongly influence the patient’s chances
of survival.40,104 The key to successful management of wilderness
emergencies is preparedness. Advanced Trauma Life Support
(ATLS) protocols can provide a template for preparation for
wilderness travel. The principles embodied in ATLS concepts are
well suited to management of wilderness emergencies, especially
in circumstances where scant resources are available and, thus,
a prompt response is essential for the victim’s survival. The
American College of Surgeons has formulated the Rural Trauma
Team Development Course, which emphasizes the ATLS princi-
ples in situations where a small trauma team, typically two
or three rescuers, is in charge. The course is applicable to the
wilderness environment.135
When team members are planning an expedition, the role for
each member should be explained clearly. Teamwork is essential
for solving problems, communicating, executing procedures,
transporting a patient, and continually improving the skills of
team members. The medical director (director) of an expedition
takes on significant responsibility during preparation. The direc-
tor must screen participants to make sure they can tolerate the
expedition and must tell the expedition leader of the findings. It
is important to know the medical and surgical history of each
expedition member. The director must also know wilderness
medical protocols. For lengthy expeditions, the director should
consider carrying diagnostic modalities such as a portable ultra-
sound unit and point-of-care testing equipment. Communication
with appropriate rescue facilities prior to starting the trip is
essential. The director should also have a plan for transfer of
information to the next level of care. When an emergency occurs,
the director will likely be placed in a position of authority, so it
is essential to clarify the command structure and role of each
member. The specifics of wilderness preparation, equipment, and
medical supplies are presented in Chapter 102.
*Disclaimer: The views expressed in this article are those of the author(s)
and do not necessarily reflect the official policies or positions of the U.S.
Department of the Navy or Department of Defense or the U.S. Govern-
ment. LCDR Krzyzaniak is a military service member (or employee of the
U.S. Government). This work was prepared as part of my official duties.
Title 17, USC, §105 provides that “Copyright protection under this title is
not available for any work of the U.S. Government.” Title 17, USC, §101
defines a U.S. Government work as a work prepared by a military service
member or employee of the U.S. Government as part of that person’s
official duties.
378
WILDERNESS TRAUMA
EMERGENCIES OVERVIEW
All classic mechanisms of trauma (penetrating, blunt, and thermal)
occur in the wilderness environment and are discussed in this
chapter. Blast injury is also mentioned briefly because its treat-
ment in combat situations has led to some important advances
in wilderness medicine. Blunt trauma remains the most common
cause of injury in an austere environment; it can often be difficult
to definitively diagnose. Delays in diagnosis in the wilderness
can substantially increase complications and deaths.
HISTORY OF WILDERNESS MEDICINE
The medical literature is limited regarding the incidence of injury
during wilderness-related activities. It is estimated that more
than 10 million Americans participate in wilderness backpacking
and camping activities annually. A study by Gentile and col-
leagues57 documented the injury and evacuation patterns
recorded by the National Outdoor Leadership School over a
5-year period. Injuries occurred at a rate of 2.3 per 1000 person-
days of exposure, with orthopedic and soft tissue injuries most
frequent. Montalvo95 analyzed case incident report files from
eight California National Park Service parks and found an injury
incidence of 9.2 nonfatal events per 100,000 visits, with 78 fatali-
ties reported in a 3-year period. In a prospective surveillance
study evaluating 38,940 days of wilderness exposure on the
Appalachian Trail,18 foot blisters and diarrhea were the most
common reasons for premature discontinuation of hikes. Leemon
and Schimelpfenig89 showed that more than 50% of evacuated
participants in the National Outdoor Leadership School were
able to return and finish their courses. The Rocky Mountain
Rescue Group reported on their rescue experiences from 1998
to 2011 in Boulder County, Colorado, where they had a total of
2198 rescues over that time period.83 These studies document a
low risk for injury but highlight the possible morbidity resulting
from wilderness injury or illness and the need for rapid, uniform
intervention.
A 2001 study from the University of Arizona61 highlighted
wilderness deaths over 13 years. Alcohol was the most common
causative factor, involved in 40% of the 59 unintentional trauma
deaths. In addition, 80% of these victims died immediately or
before evacuation could be completed. This emphasizes the
importance of sound judgment and preparedness of rescuers
and expedition members in maximizing care. A recent study
of emergency medical services (EMSs) in the California state
parks emphasizes the difficulty of providing care to wilderness
participants.65
ESTABLISHING PRIORITIES IN THE WILDERNESS
There are three immediate priorities in managing wilderness
trauma:
1. Control oneself. It is normal to feel anxious when con-
fronted with an injured victim. However, anxiety must not
be transmitted to the victim or other members of the expe-
ditionary team. One must be in control of oneself to take
control of the situation.
 2. Control the situation. The first priority in controlling the
situation is ensuring the safety of uninjured members of
the party. Expeditious evacuation of a victim requires that
all expedition members function at maximal efficiency;
even minor injuries to other members in the group can
jeopardize physical strength, functional manpower, and
success of the evacuation. Although the physician member
of the team may not be the expedition leader, his or her
position is automatically elevated during a medical crisis.
However, this does not mean that the physician should
dominate the evacuation process. Although the expedition
leader must rely on the medical assessment provided by
the physician, the leader is best prepared to plan the
evacuation.
3. Obtain an overview of the situation. The victim’s general
condition should be evaluated. Is the victim in immediate
distress from a condition that requires relatively straight-
forward management, such as airway control? Is the victim
in such a precarious environmental situation that he or she
needs to be moved prior to any attempt at resuscitation?
Scene security may be integral to the safety of the injured
person and caregiver. Is the victim properly protected from
the elements, including sun, wind, cold, and water?
There are several key principles paramount to treatment of
injuries in an austere environment: ensure scene and provider
safety, use primary and secondary surveys, provide cervical spine
immobilization, control external hemorrhage, keep the patient
warm and use warm intravenous (IV) resuscitation fluid if pos-
sible, initiate early transport, and, above all, do no further harm.
After the victim has been placed in the most stable and
safest environment possible, the examining physician is ready
to implement the ATLS-based five steps of wilderness trauma
management:135
1. Primary survey
2. Resuscitation
3. Secondary survey
4. Definitive plan
5. Packaging and transfer preparation
The purpose of the primary survey is to identify and begin
initial management of life-threatening conditions by assessing the
ABCDEs of trauma care:
Airway maintenance and cervical spine stabilization
Breathing
Circulation, with control of significant external hemorrhage
Disability: neurologic status
Exposure/environmental control: completely undress the vic-
tim with careful attention to prevention of hypothermia
After the primary survey has been performed, resuscitation
efforts are initiated. The level of resuscitation depends on the
equipment and expertise available. At a minimum, resuscitation
consists of control of external hemorrhage and administration of
oxygen and warm IV fluids when they are available.
The third step is the secondary survey, a head-to-toe evalua-
tion of the trauma victim that uses inspection, percussion, and
palpation techniques to evaluate each of the body’s five regions:
head and face, thorax, abdomen, skeleton, and skin. A history
should be taken while the secondary survey is being done. The
specifics of the mechanism of injury may be of vital importance
(i.e., loss of consciousness, head injury, height of a fall, or species
of attacking animal may influence treatment and evacuation plans
and also affect the stability of the scene). After this survey, the
examining physician should formulate a definitive plan. It is
useful to document all observations if circumstances permit. Such
data may be critically important for field evacuation or hospital
personnel.
The first step in formulating a plan is to compile a list of
injuries. The next step is to determine if any injury warrants
evacuation. The route of evacuation, whether air, land, or water,
must be chosen. Aeromedical evacuation is expensive and,
depending on the environment, may pose its own risk to both
victim and medical evacuation team; it should be considered only
for victims with potentially life- or limb-threatening injuries
where the terrain and environment allow safe access, for the
purpose of evacuation, to the patient.
Packaging the victim for evacuation is the final step. The
CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
evacuation effort requires organization, coordination, and great
effort on the part of the expedition team.
The most effective means of managing the injured patient in
the wilderness setting is to take the approach of the old adage
“the best offense is a good defense.” Preparation for wilderness
patient care should address the challenges associated with
varying levels of personnel help, minimal medical resources,
prolonged prehospital care, and difficult evacuation proceedings.
With ATLS knowledge, improvisation, and an organized effort,
the patient’s outcome can be maximized.
UNIVERSAL (BODY FLUIDS) PRECAUTIONS
IN THE WILDERNESS
A number of life-threatening viruses are transmitted through
contact with bodily fluids. The Centers for Disease Control and
Prevention have established a set of standard precautions to be
applied in all cases of contact with human body fluids:
Goggles
Gloves
Fluid-impervious gowns
Shoe covers and fluid-impervious leggings
Mask
Head covering
Multiple types of body fluids (blood, semen, vaginal secre-
tions, and cerebrospinal, pleural, synovial, pericardial, peritoneal,
and pericardial fluids) can place a caregiver at risk. In the wilder-
ness setting, the materials necessary for universal precautions are
rarely available. Every victim in the wilderness must be assumed
to carry a communicable disease, and every effort should there-
fore be made to approximate universal precautions, particularly
protection of the hands and eyes.
PRIMARY SURVEY
Persons injured in the wilderness should be assessed and their
treatment priorities established based on the mechanism of
injury, vital signs, and specific injuries. The vital signs must be
assessed quickly and efficiently, with restoration of life-preserving
vital functions.
AIRWAY
Rapid airway assessment should include inspection for signs of
obstruction, including foreign bodies, and signs of facial or tra-
cheal fractures. A chin lift or jaw thrust may be helpful to estab-
lish an airway, can be lifesaving, and may be all that is necessary.
If the victim can speak, the airway is likely not jeopardized, but
this is not an absolute rule.
Specific attention should be directed toward the possibility of
cervical spine injury. The victim’s head or neck should never be
hyperextended, hyperflexed, or rotated to establish or maintain
an airway. A cervical spine injury should be assumed to exist in
any person with a significant injury above the level of the
clavicle. If a situation requires removal of immobilizing devices,
in-line stabilization, not traction, must be maintained.
BREATHING AND VENTILATION
The victim’s chest should be exposed and chest wall movement
observed. Establishment of an airway during the primary survey,
although critical to patient survival, does not ensure adequate
oxygenation or ventilation. All trauma victims must be continu-
ously monitored for signs and symptoms of hypoxemia and
hypercarbia.
Auscultation, observation, and palpation of the chest after
establishment of the airway are integral parts of the primary
survey. Diminished breath sounds or asymmetric chest wall
movement can occur with pneumothorax (simple or tension),
hemothorax, tracheobronchial obstruction, or main-stem intuba-
tion. Observation and palpation of the chest may identify thoracic
injuries such as rib fractures, fractures with flail segments, or
pneumothorax (by the presence of subcutaneous emphysema).
379
 CIRCULATION
Circulation is evaluated by assessing the cardiac output and
controlling any major external hemorrhage. Manometric blood
pressure measurement is not easily performed in the field,
although it may provide useful data. Important information
regarding perfusion and oxygenation can be obtained rapidly by
determining level of consciousness, assessing peripheral and
central pulses, looking at skin color, and evaluating capillary refill
time.
Pulses should be assessed first. Although the following are
only general estimates and carry some inaccuracy, approxima-
tions of the minimum systolic blood pressure can be used if a
palpable pulse is present:
Radial artery: 80 mm Hg
Femoral artery: 70 mm Hg
Carotid artery: 60 mm Hg
If hypovolemia is suspected on the basis of absent pulses or
prolonged capillary refill, the examiner should immediately
assess the neck veins. Distended neck veins, although a nonspe-
cific sign, may suggest tension pneumothorax or pericardial
tamponade in the context of hypotension. Flat neck veins may
suggest hypovolemia and hemorrhagic shock.
Major hemorrhage can occur in five anatomic areas:
Chest
Abdomen
Retroperitoneum
Thigh
External environment
Exsanguinating external hemorrhage should be identified and
controlled during the primary survey. Control of blood loss is
addressed specifically in later sections; it basically involves using
direct pressure or a tourniquet. Proper stabilization of long bone
TRAUMA
Hypoxia, hypovolemia, and hypothermia should be promptly
corrected.
EXPOSURE AND ENVIRONMENTAL CONTROL
The victim should be fully undressed and exposed, if possible
in a protected environment. Garments and gear should be
removed if necessary by cutting them away, unless the garments
can be dried and are essential for future protection from the
environment. Wet clothing must be removed early to prevent
hypothermia. It is mandatory to visualize the entire victim to
document and assess injury. However, this step of the primary
survey should be performed with caution. First, it is imperative
to cover the victim immediately after removal of clothing. Hypo-
thermia and its effects on mental status, cardiovascular function,
and coagulation are among the most underappreciated entities
in care of the trauma victim. The possibility of hypothermia
should be entertained in all environments. A victim with hypo-
thermia may not be able to use stored energy to carry on normal
metabolic processes. A severely injured patient may become
hypothermic in any ambient environment. Second, clothing and
gear should not be removed unless complete immobilization of
injuries can be achieved. Assessment of an area of injury should
be performed, but clothing should be left to cover the patient to
ensure that the body temperature is maintained. A patient may
be wearing a variety of gear and clothing, including a helmet for
biking, skiing, or climbing; the helmet should be removed, with
in-line stabilization of the cervical spine.
SECONDARY SURVEY
The secondary survey is an extension of the primary survey and

(femur) fractures minimizes blood loss into soft tissues. In the
wilderness, little can be done about significant intrathoracic or
intraabdominal hemorrhage. Survival of patients with significant
blunt injuries is likely if basic ATLS principles are followed.
DISABILITY AND NEUROLOGIC ASSESSMENT
PART 4
should not be undertaken until the primary survey is complete
and the victim has been stabilized. In addition, resuscitative regi-
mens, if available, should have been initiated. The secondary
survey is a head-to-toe assessment of the victim, including history
taking and a physical examination. The face, neck, chest,
abdomen, pelvis, extremities, and skin should be examined in

sequence. A more detailed neurologic examination should be

Neurologic assessment during the primary survey should be rapid completed, including reassessment of the GCS. The neck should
and efficient. The level of consciousness should be established, be examined independently of the thoracolumbar spinal cord.
and pupillary size and reactivity should be assessed. Level of Examination of the pelvis should not include the traditional
consciousness assessment uses the Glasgow Coma Scale (GCS) “rocking” to determine stability, because if pelvic fracture has
(Box 18-1). It is critical that the neurologic assessment be repeated occurred, this action may exacerbate existing comminution.
hourly, particularly if evacuation is delayed. Deterioration in The detailed secondary survey should not delay evacuation
mental status portends a poor prognosis, although a variety of packaging. As in the nonwilderness setting, it is imperative to
conditions other than intracranial injury can affect mental status. repeat the primary survey as the victim’s condition warrants.
Specific examinations are discussed in the sections covering
regional injuries.
BOX 18-1  Glasgow Coma Scale
HISTORY
The Glasgow Coma Scale evaluates the degree of coma by
determining the best motor, verbal, and eye-opening responses to The victim’s history should be assessed during the secondary
standardized stimuli. survey. Knowledge of the mechanism of injury and any comorbid
Eye Opening medical conditions or allergies may enhance understanding the
Spontaneous 4
victim’s physiologic state.
To voice 3 The ATLS “AMPLE” history is a useful and rapid mnemonic
To pain 2 for this purpose:
None 1 Allergies
Medications currently used
Verbal Response
Past medical history/Pregnancy
Oriented 5 Last meal
Confused 4
Event or Environment related to the injury
Inappropriate words 3
Incomprehensible words 2
None 1 ADJUNCTS TO SURVEYS
Motor Response Resuscitation should be initiated as the primary survey is being
Obeys command 6 done. The degree of resuscitation depends on available resources,
Localizes pain 5 experience of the rescuer(s), and environmental conditions. Under
Withdraw (pain) 4 the best circumstances, initial management of the wilderness
Flexion (pain) 3
trauma victim provides for airway control, adequate oxygenation
Extension (pain) 2
None 1 and ventilation, appropriate fluid resuscitation, and stabilization
Maximum Score 15 of cardiac function; monitoring and reassessment of vital signs
should continue. A urinary catheter and nasogastric (NG) tube can

380
be placed as adjunctive measures. This degree of resuscitation is
almost never possible in the wilderness setting; resuscitation may
be limited to oral administration of warm, high-calorie fluids and
maintenance of victim comfort and body temperature.
An NG tube and indwelling urinary (Foley) catheter should
be placed if available and appropriate. Aspiration of gastric con-
tents can be catastrophic in terms of patient survival after trauma.
Gastric decompression with an NG tube may help prevent this
adverse event in patients with a depressed level of conscious-
ness. It should be remembered that children can exhibit signifi-
cant hemodynamic consequences secondary to massive gastric
distention. In this setting, decompression becomes critical. If
possible, NG tubes should be placed in persons who are endo-
tracheally intubated in the field. The tube can be aspirated
sequentially with a syringe or left open to gravity drainage. Any
suspicion of facial fracture should deter attempts to place an NG
tube, and orogastric decompression should be chosen instead.
A Foley catheter can assist in volume assessment and hemo-
dynamic status determination in a critically injured victim. Hourly
urine output typically does not decrease until the onset of class
III hemorrhagic shock, with loss of 30% to 40% of blood volume.
Contraindications to urinary catheter placement in the field are
blood at the urethral meatus, high-riding prostate, and scrotal
hematoma; personnel not experienced in placement are also a
reason for caution.
ADVANCES IN WILDERNESS CARE
ADAPTED FROM COMBAT MEDICINE
Wilderness medicine has been enhanced in many ways
by the precepts of Tactical Combat Casualty Care.12 During the
recent conflicts in Iraq and Afghanistan, tourniquets and hemo-
static agents were packaged in easily carried, compact systems
so that exsanguinating hemorrhage from severe extremity injuries
could be controlled more rapidly.82 The equipment and the
lessons learned have been transferred to treatment of injuries in
the wilderness; when the easily mastered techniques are used
early, chances of survival increase.45,91
Throughout recorded history, trauma care in armed conflicts
has advanced the care of civilian trauma patients (see also
Chapter 28). Such care is uniquely suited for wilderness trauma.
Blackbourne and colleagues12 defined recent advances in trauma
care in Iraq and Afghanistan as revolutions in military medical
affairs, and Sward and associates recognized the rapid implemen-
tation of battlefield lessons in civilian care.133 The use of tourni-
quets, topical hemostatic agents, and freeze-dried plasma in
prehospital care, as well as procedures such as hypothermia
prevention, transport of patients by teams, and permissive
hypotension, has improved survivability from combat wounds.
Individuals wounded in Iraq and Afghanistan had higher survival
rates than those in any other conflict in U.S. history.49 The
A B
FIGURE 18-1  A, FAST1 intraosseous infusion system. B, Bone Injection Gun (BIG). C, EZ-IO.
advances in prehospital care can and should be applied to trauma
CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
emergencies in remote or austere environments.133
VASCULAR ACCESS
Obtaining vascular access is a basic tenet of ATLS. The best
procedure for initial access remains placing two large-bore
peripheral catheters in the veins of the antecubital fossa. If one
is unable to easily obtain peripheral IV access in the upper
extremities, the lower extremities may be considered.
Recent recommendations by the Eastern Association for the
Surgery of Trauma (EAST) suggest moving to intraosseous (IO)
access devices if peripheral access is not obtained after two
attempts.35 The U.S. and coalition military medical personnel have
used IO access extensively in Iraq and Afghanistan. There are
several commercially available devices for IO access in the
sternum, tibia, or humerus. The FAST1 IO device is designed to
obtain access to the manubrium. The EZ-IO device (a drill-based
device) and the Bone Injection Gun (a spring-loaded device)
can be used to obtain IO access in the tibia and humerus. The
skills for placing IO devices can be easily learned and simulated
in a multitude of models. The San Antonio Fire Department
recently demonstrated that with a short didactic and hands-on
training session, paramedics were able to successfully place
humeral IOs with the EZ-IO drill with a success rate of over
90%139 (Figure 18-1).
The EAST guidelines also suggested that, depending on the
expertise on hand, an attempt at central venous access using a
Seldinger technique is acceptable after two failed attempts at
peripheral venous access. The internal jugular, subclavian, and
femoral veins are usually chosen. Venous cutdown can be con-
sidered as a last resort.
PREHOSPITAL HEMORRHAGE CONTROL
Tourniquets
The first area of emphasis is on prehospital hemorrhage control.
Direct pressure is an excellent technique for control of hemor-
rhage, but this is not always feasible in the austere environment.
Direct pressure is practical if there is one casualty and sufficient
rescuers to control hemorrhage and facilitate transport or other
care. If there are multiple casualties or the rescuer needs to
perform tasks such as controlling the airway, evacuating the
patient, gathering supplies, or providing security, the rescuer is
going to need other tools. Tourniquets developed for combat
medics can and should be used by civilian rescuers. Use of tour-
niquets in the civilian world has traditionally been discouraged
because of concerns about harmful effects.88 Data on U.S. casual-
ties in Vietnam demonstrated that at least 2% of deaths resulted
from hemorrhage from isolated extremity wounds.93 Although
death is more common with combat injuries, it can also result
from isolated extremity injuries in civilian urban populations.44
C
381
 The Israel Defense Forces doctrine has mandated use of prehos-
pital tourniquets for control of extremity hemorrhage since the
late 1980s. Medical personnel demonstrated that tourniquets were
safe, easily applied (by medical and nonmedical personnel), and
potentially lifesaving.84 Use of tourniquets was not effectively or
widely taught in the U.S. military at the beginning of Operation
Enduring Freedom and Operation Iraqi Freedom. However, injury
patterns from these and previous conflicts demonstrate that most
injuries sustained by combatants are of the extremities.9 Kragh
and colleagues from the U.S. Army Institute of Surgical Research
(USAISR) prospectively evaluated the use of tourniquets at the
busiest Combat Support Hospital in Iraq in 2006. They concluded
that tourniquets can be lifesaving, especially when used early in
the prehospital setting prior to the onset of shock.82 A tourniquet
is defined as a limb-constricting device that is placed in an attempt
to arrest extremity hemorrhage; the device can be improvised or
one of the many commercially available devices. The author’s
experience is primarily with the Combat Application Tourniquet
(CAT; Composite Resources, Rock Hill, SC). The extensive USAISR
research on tourniquets in combat has led to development of
recommendations for their use81 (Figure 18-2 and Box 18-2).
Hemostatic Dressings
The high-tempo combat operations of Operation Iraqi Freedom
and Operation Enduring Freedom accelerated development of
hemostatic dressings. Both civilian and military data show that
the most common cause of potentially preventable death in
trauma patients is exsanguinating hemorrhage.49,118 Almost 20% of
these lethal hemorrhages will be from junctional anatomic loca-
tions, primarily the groin and axilla.49 To facilitate use in austere
locations or combat operations, the ideal hemostatic dressing
would be rapidly available, simple to use, lightweight, and rela-
TRAUMA
tively inexpensive and have a long shelf life.109 Several products
are on the market, with the largest reported experience being
with the mucoadhesive Chitosan-based HemCon (HemCon
Medical Technologies, Portland, OR) and the procoagulant sup-
plementor, kaolin-based product QuikClot Combat Gauze62
(Z-Medica, Wallingford, CT). Case reports from combat operations
PART 4
and civilian EMS support the preclinical data that have shown
that these products are effective in arresting hemorrhage in the
prehospital environment.24,111,140 Hemostatic dressings are easily
A and that one clamp will not provide adequate closure of a large
B rioration. DCR directly addresses the lethal triad that is often fatal
FIGURE 18-2  A, Combat Application Tourniquet. B, SAM Junctional
Tourniquet (A from North American Rescue, Greer, SC. B from SAM
Medical Products, Wilsonville, OR.)
382
BOX 18-2  Tourniquet Use Recommendations
Apply the tourniquet early, before the onset of shock.
Use scientifically designed, laboratory-tested, clinically validated
tourniquets.
Using an improvised tourniquet is acceptable if a commercially
available tourniquet is not available.
Continuing education on the use of tourniquets is essential for
personnel who will be expected to use them.
The goal of the tourniquet is to stop bleeding and stop the distal
pulse.
Avoid placement over Hunter’s canal (≈ 5 cm above the femoral
condyle).
Side-by-side use of tourniquets is acceptable if single tourniquet
application does not arrest hemorrhage.
Effectiveness of the tourniquet will be inversely proportional to the
girth of the extremity.
Tourniquets should be applied directly on the skin.
applied, and the mechanism of action is not complicated. When
the rescuer identifies bleeding that cannot be controlled with
direct pressure or a tourniquet, application of a hemostatic dress-
ing can potentially be lifesaving. Remove the product from its
packaging, place it on the bleeding area, and hold it with direct
pressure for at least 3 minutes. Once hemorrhage has been con-
trolled, the dressing stays in place. The dressing works by being
in direct contact with the bleeding source, so piling further hemo-
static dressings on top is not productive. The hemostatic dressing
must be removed eventually, but this can be done in a delayed
fashion once the victim reaches definitive care (Figure 18-3).
Junctional Tourniquet
Another product for the control of lethal hemorrhage is the junc-
tional tourniquet. Several types exist, with the basic premise being
that the belt encircles the pelvis or torso and has pressure devices
to occlude the axillary or external iliac vessels. The devices use
either direct mechanical or pneumatic pressure to achieve occlu-
sion. There are limited data to support use of these tourniquets,
but laboratory investigations of the SAM Junctional Tourniquet
(SAM Medical Products, Wilsonville, OR) suggest that they are
effective in hemorrhage control.74 Use of these tourniquets requires
familiarity with them and, often, hands-on instruction and experi-
ence prior to application. The manufacturers all provide written
and video educational tools to help users (see Figure 18-2).
Wound Closure Device
The iTClamp (Innovative Trauma Care, San Antonio, TX) wound
closure device is a recent innovation that brings the edges of a
wound together, causing a hematoma underneath the skin. This
hematoma causes pressure on the bleeding site, thus forming a
clot and stopping bleeding.52,97 This product is small, light, and
simple to use. The clamp has several pins that pinch the wound
together and lock in place. The disadvantages are the small size
or nonlinear wound (see Figure 18-3).
DAMAGE CONTROL RESUSCITATION: DIRECTLY
ADDRESSING THE LETHAL TRIAD
Of patients arriving at civilian trauma centers, only about 3%
require massive transfusion or damage control resuscitation
(DCR).33 Military wounds caused by high-energy blasts have a
much higher rate of DCR and massive transfusion.69 The term
damage control has become standard for describing a variety of
surgical tactics and techniques applicable across a wide range
of surgical disciplines. When DCR is extended to the prehospi-
tal and early resuscitation phases, it is called damage control
zero.8,31,73,86 Damage control zero takes place before the patient
arrives at the hospital, with the goal of preventing patient dete-
when patients become cold, coagulopathic, and acidotic.96 Hypo-
thermia in the austere environment is a significant challenge. The
U.S. military recognized in the combat environment that hypo-
thermia prevention was lacking in battlefield care. Therefore, the

A B
FIGURE 18-3  A, HemCon gauze-based chitosan dressing. B, QuikClot Combat Gauze. C, iTClamp.
(A courtesy Tricol Biomedical, Inc, Portland, OR; B courtesy Z-Medica, Wallingford, CT; C courtesy iTrau-
maCare, San Antonio, TX.)
Joint Theater Trauma System developed a clinical practice guide-
line to address hypothermia prevention at all levels of care. In
the austere environment, this should be the goal of the wilder-
ness medical team. A team or individual will use everything
available (e.g., jackets, blankets, improvised coverings) to protect
the patient from the environment. Several lightweight compact
adjuncts can be used to assist with prevention of hypothermia.
These essential items can easily be packed as part of the team’s
kit. Injury in a hot environment does not prevent hypothermia
in a seriously injured patient. One commercially available product
is the Hypothermia Prevention and Management Kit (North
American Rescue, Greer, SC), which is a self-contained, self-
heating shell liner to encompass the casualty. Eastridge and col-
leagues were able to show a significant drop in hypothermia
incidence after institution of a comprehensive clinical practice
guideline.48 Prehospital providers need to be proficient in iden-
tifying casualties who require the DCR approach. It may be dif-
ficult for a rescuer to rapidly identify this group of patients.
Although there are no uniformly accepted criteria for identifying
patients who will benefit from DCR, several groups have devel-
oped scoring systems (using a variety of anatomic, physiologic,
and laboratory variables) for identifying patients who will likely
require massive transfusion and thus be more likely to enter the
vicious cycle of hypothermia, coagulopathy, and acidosis.94,99,137,145
Each of these scoring systems is quite accurate, but two that are
most applicable to EMS are the shock index and the ABC system
(Boxes 18-3 and 18-4). In the austere environment, the shock
index by Vandromme and colleagues is most useful due to its
simplicity.99,137
The tenets of DCR are limited crystalloid resuscitation, permis-
sive hypotension, hemostatic resuscitation, and proper patient
selection.8,10,35,69,99,137 Limited crystalloid resuscitation has become
an accepted tenet for care of hemorrhaging patients. The EAST
guidelines35 on prehospital resuscitation state that there is a need
to (1) embrace permissive hypotension in penetrating torso
patients; (2) base resuscitation on mental status and presence of
radial pulse; (3) give patients a bolus with smaller aliquots of IV
fluids than the traditional 1 to 2 L; and (4) consider using hyper-
tonic saline as the resuscitative fluid.10,35,113 Although blood prod-
ucts may be difficult to obtain, depending on the austerity of a
particular expedition, early use of blood products needs to be
discussed, including a “walking blood bank” (using whole blood
donated by locally available personnel). In the past 15 years there
BOX 18-3  Shock Index
Shock index = Heart rate/Systolic blood pressure
Shock index > 0.9 identifies patients at risk for massive transfusion
CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
C
has been a paradigm shift toward use of blood products in
trauma resuscitation and limiting crystalloid infusion.69 During
Operation Iraqi Freedom, Borgman and associates showed the
utility of a high or nearly equivalent ratio of red blood cells to
plasma to platelet resuscitation.16 Most experts recommend deliv-
ery of these blood products in a ratio that resembles the normal
composition of whole blood, with 1 unit of red blood cells:1 unit
of plasma:1 unit of apheresis platelets.100 The complexity of
massive transfusion protocols may not apply to every austere
situation, primarily due to lack of resources. The medical team
should consider the ability to establish a walking blood bank as
part of the medical kit.
FRESH WHOLE BLOOD
Primarily a tool of the military, fresh whole blood has been used
in combat theaters dating back to World War I.103 The U.S. military
has continued the use of fresh whole blood extensively in ongoing
conflicts.130 Fresh whole blood is warm, the volume is close to
500 mL, the hematocrit is 38% to 50%, there are 150,000 to 400,000
platelets per microliter, there is 100% coagulation activity, and
1500 mg of fibrinogen is included. Fresh whole blood does not
possess the “storage lesion” of banked blood. Fresh whole blood
has the ultimate 1 : 1 : 1 ratio. There are several downsides to using
fresh whole blood: It must be type specific, and there are the
potential for transmission of blood-borne disease, a limited donor
pool, and potential deleterious effects on the donor (who in the
austere environment may have a job to do that prevents taking
the time to donate blood). Even with these known risks, we
strongly encourage use of fresh whole blood in certain austere
locations from which the patient cannot be easily transported or
at which blood products are not readily available.130
Organization of Walking Blood Bank
The process of obtaining fresh whole blood requires superb
planning and coordination. It is helpful to have a prescreened
donor pool; questionnaires are available to help determine a safe
BOX 18-4  Assessment of Blood Consumption (ABC)
Score for Massive Transfusion
The presence of two or more of the following factors identifies
patients at risk for massive transfusion:
Systolic blood pressure < 90 mm Hg
Heart rate > 120 beats per minute
Penetrating mechanism
Positive FAST signs (Face drooping, Arm weakness, Speech
difficulty, Time to call 9-1-1)
383
 donor pool. This must be done prior to the team’s expedition.
Trying to do this when a casualty has arrived would cause a
dangerous delay in the initiation of hemostatic resuscitation. The
beginning donor pool is all of the persons on the expedition.
The plan must include a predetermined method to activate and
operate the walking blood bank. A responsible individual must
have access to the blood donor pool and be able to manage the
walking blood bank. The authors recommend using the rapid
screening kits to evaluate for human immunodeficiency virus,
hepatitis, and human T-lymphotropic virus.130 These rapid immu-
noassays may not be as accurate as desired, but a positive result
can be helpful.
Collection of Fresh Whole Blood
When the decision to use fresh whole blood has been made
because blood components are unavailable or the normal blood
bank has been exhausted, the preassigned individuals mobilize
the donors and begin to collect the fresh whole blood. The basic
procedures require proper identification of individuals in the
donor pool, confirmation of an up-to-date screening question-
naire, and selection of individuals that have not recently donated.
If one is able to screen for blood-borne infectious diseases, this
should be done. Once a person has been deemed physically fit
to provide a donation (this should be done quickly), the walking
blood bank personnel should crossmatch the donor to the recipi-
ent, check the donor for significant anemia, and proceed with
collection of up to 500 mL of whole blood into a commercial
collection bag with anticoagulant citrate phosphate dextrose
adenine. The collection area should be as calm as possible,
because chaos breeds errors. A clerical error leading to transfu-
sion of the incorrect blood type could create a devastating
hemolytic reaction. The collection area may be within a few feet
TRAUMA
of the patient, but the collected blood must nonetheless be
properly labeled. After labeling, the unit of blood is “walked
over” to the patient and infused. This entire process can take less
than 25 minutes.
INJURIES TO THE HEAD, FACE,
PART 4
AND NECK
The secondary survey begins with examination of the entire head
and scalp for evidence of skull or facial fractures, ocular trauma,
lacerations, and contusions. The scalp is thoroughly palpated for
tenderness, depressions, and lacerations. The bones of the face,
including the zygomatic arch, maxilla, and mandible, are pal-
pated for fractures. Elements of the GCS are repeated.
Treatment of injuries to the eye is discussed in detail in
Chapter 48, but general examination principles are simple. Sig-
nificant periorbital edema may preclude examination of the
globe, so assessment should be carried out early. The eye should
be evaluated for visual acuity, retinal detachment, pupillary size,
conjunctival hemorrhage, lens dislocation, and entrapment. Indi-
viduals with significant facial trauma have a high incidence of
associated ocular or orbital injuries.122,124 Recent studies of ocular
injuries in trauma victims have emphasized underappreciation by
many disciplines of ocular and periocular signs indicative of
significant underlying injury.122 A black eye alone has a nearly
70% chance of having an associated underlying facial bone
fracture.26
HEAD INJURIES
Approximately 2 million cases of head injury occur in the United
States yearly, with a significant portion of them occurring in
remote locations as a result of outdoor activities such as hunting,
rock climbing, and hiking.58,106,135 Of these, approximately 16%
result in hospitalization; 3% of patients die before reaching the
hospital.135 Long-term disability associated with head injury is
significant, with 80,000 to 90,000 persons suffering various degrees
of permanent impairment. Because of the high-risk nature of
traumatic brain injury (TBI) and the impact of initial management
on disability and survival, clinical management objectives
must address both immediate survival and long-term outcome.
384
Management guidelines specific for head injuries in a wilderness
setting do not exist, and a wide range of clinical approaches are
used in hospital settings.58 However, the literature suggests that
morbidity and mortality can be reduced by means of a protocol
that includes early airway control with optimization of ventilation,
prompt cardiopulmonary resuscitation, induced hypothermia, and
rapid evacuation to a trauma care facility.63,131
Initial management of head injury in the wilderness should
follow established ATLS protocols. Prompt attention must then be
given to victim triage, evacuation strategies, and ongoing resus-
citative needs to prevent or minimize secondary brain injury from
hypoxia and hypotension. Expeditious evacuation to a trauma
center in which neurosurgery can be performed is essential.
Multiple clinical and experimental studies have demonstrated
the detrimental effects of hypoxia on the injured brain. A defini-
tive airway should be established if any degree of neurologic or
respiratory compromise exists, but not at the expense of risking
severe hypoxia to accomplish it in an otherwise well-ventilated
patient.55 Cervical spine injuries are common in patients with TBI.
Therefore, cervical spine immobilization is paramount to prevent
devastating neurologic injury.
After immobilization, attention is directed to prevention of
secondary brain injury. Given adequate resources, all efforts
should be made to avoid oxygen saturation levels of less than
90% and to maintenance of blood pressure of more than
90 mm Hg.55 The purpose of the wilderness head injury protocol
is to allow individuals with widely varying levels of experience
and expertise to identify signs of significant head injury, begin
proper resuscitation in the context of prevention of secondary
brain injury through airway maintenance and hemodynamic
support, and evacuate appropriately.
Anatomy of the Head
The scalp has five layers of tissue that cover the calvaria: skin,
connective tissue, galea aponeurotica, loose areolar tissue, and
periosteum of the skull. The galea is a fibrous tissue layer with
important ramifications in closure of scalp wounds, discussed
later in this chapter. Loose areolar tissue beneath the galea rep-
resents the site of accumulation of blood in scalp hematomas. A
rich vascular network located between the dermis and galea
supplies the scalp. When lacerated, these vessels can be a sig-
nificant source of hemorrhage, which may be important if evacu-
ation is impossible or delayed. As shown in Figure 18-4, these
injuries can be complex, deep, and associated with large-volume
blood loss. Hemostasis of these wounds should be achieved with
primary suture closure or some other mechanism.
The skull has two groups of bones that form the face and
cranium. The cranial bones are the bones of the calvaria and the
skull base. The calvaria is made up of frontal, ethmoid, sphenoid,
parietal, and occipital bones. Within the skull, the brain is covered
by three membranous layers that may be of pathophysiologic
importance after injury. However, in the wilderness, these layers
have little clinical relevance (except in terms of defining an open
versus a closed brain injury).
Pathophysiology of Traumatic Brain Injury
Traumatic brain injury (TBI) can be divided into primary and
secondary brain injuries. Primary injury consists of the physical
or mechanical insult at the moment of impact, and the immediate
and permanent damage to brain tissue. Little can be done in the
wilderness setting relative to primary brain injury. Secondary
brain injury is the biochemical and cellular response to the initial
mechanical trauma and includes physiologic derangements that
may exacerbate effects of the primary trauma, including hypoxia
and hypotension. Compounding these pathophysiologic altera-
tions in TBI is elevation of the intracranial pressure (ICP). In-
creased pressure increases cerebral ischemia and exacerbates
secondary brain injury. Without swift access to advanced medical
care, persons injured in the wilderness are at high risk for sec-
ondary brain injury.
Many forms of head injury result in elevated ICP, the duration
of which is significantly correlated with a poorer outcome. The
Monro-Kellie doctrine states that the volume of intracranial
contents must remain constant because the cranium is a rigid

A often result from falls, falling objects, or assaults. Penetrating
B pupillary responses suggest increased ICP. These clinical deterio-
FIGURE 18-4  A, Deep and complex scalp laceration. B, Raney clips
can be used to effectively achieve hemostasis in these types of wounds.
container. The normal compensatory response to increased intra-
cranial volume is to decrease venous blood and cerebrospinal
fluid (CSF) volume within the brain. If this normal response is
overwhelmed, small increases in intracranial volume result in
exponential increases in ICP. A rigid bony cranium cannot
expand to accommodate increases in brain volume and the
resultant increase in ICP. Brain parenchyma becomes compressed
and eventually displaced from its anatomic location. In the most
devastating circumstances, the brain parenchyma herniates
toward the brainstem through the largest cranial opening (foramen
magnum), and death rapidly follows. The volume-pressure curve
in Figure 18-5 shows the small, but critical, time period between
the development of neurologic symptoms, hemodynamic decom-
pensation, and brainstem herniation.
Elevation in ICP directly correlates with secondary brain
injury, and the field provider must attempt to minimize the ICP
of head-injured patients to the greatest extent possible.
The most important priority in minimizing secondary brain
injury in the field is optimizing cerebral perfusion pressure (CPP).
CPP is related to ICP and mean arterial pressure (MAP) as follows:
CPP = MAP − ICP
An ICP of less than 20 mm Hg after head injury should be
maintained, and the CPP should be between 50 and 70 mm Hg,
based on current recommendations.21,135 At a MAP of between 50
CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
and 160 mm Hg, cerebral autoregulation maintains the cerebral
blood flow at relatively constant levels. Not only is autoregulation
disturbed in injured regions of the brain, but a precipitous fall
in the MAP can further impair autoregulatory function, decreasing
the cerebral blood flow and exacerbating ischemia-induced sec-
ondary injury. The field provider is able to combat a rise in ICP
by simply optimizing the MAP through aggressive IV fluid resus-
citation. Body temperature regulation may also play a significant
role in secondary brain injury, especially on the cellular level.
Some investigators have demonstrated that controlled hypother-
mia may reduce the level of secondary injury in severe head
injuries.117 Standard methods of controlling ICP (hyperosmolar
therapy, sedation, intubation, chemical paralysis, barbiturate
coma) are rarely if ever available in the wilderness. Multiple trials
have shown that mild-to-moderate hypothermia may be of
benefit in reducing ICP in the head-injured patient, with potential
survival benefit.117
Diagnosis of Head Injury
The three useful descriptions of head injury that may be applied
to field recognition are history, severity, and morphology. History
includes the mechanism of injury, timing of the event, and related
circumstances. This knowledge assists in the decision-making
process with regard to initial assessment of severity of injury.135
Mechanism of injury is identified as blunt or penetrating trauma.
The anatomic demarcation between blunt and penetrating injury
is traditionally defined by violation of the outer covering of the
brain (dura mater). Blunt injuries in the wilderness setting most
injuries are most commonly gunshot or other projectile wounds.
Severity of injury can be estimated by quantifying the GCS and
pupillary response. The generally accepted definition of coma is
a GCS score of 8 or less; these patients often require endotracheal
intubation. Although the GCS score does not directly correlate
with the need for intubation, it is essential that all head-injured
patients be provided a stable, secure airway by the most appro-
priate means available in order to maintain adequate oxygenation
and avoid secondary injury due to hypoxia. It is important to
note the TBI victim’s best initial motor response because this is
most predictive of long-term neurologic outcome. Any victim
with a GCS score of less than 15 who has sustained a head injury
should be evacuated if possible. A low or declining GCS score
suggests increasing ICP. Abnormal pupil size or asymmetric
rations demand the rapid attention of rescue or evacuation per-
sonnel to optimize the MAP and CPP, minimize secondary brain
injury, and prevent brainstem herniation. Injury morphology may
be difficult to assess in the wilderness setting and relies on the
VOLUME-PRESSURE CURVE
60 Herniation
55
50
45
40
ICP (mm Hg)
35
30
25
20
15
10 Point of
hemodynamic
5
decompensation
Volume of mass
FIGURE 18-5  Pressure-volume curve for intracranial pressure (ICP).
385
 level of suspicion and clinical signs and symptoms. After atten-
tion to the primary survey, including airway provision and spinal
immobilization, the physical examination component of the sec-
ondary survey is imperative and can provide information about
the presence of a TBI.
Head Injury Classification
Intracranial injuries have a wide range of causes, with variable
severity. In order to simplify evaluation of the head-injured
patient, the GCS has been used.134 The initial GCS score of the
patient assists the treatment team in developing a treatment plan.
Mild injury is classified as a GCS score of 13 to 15; moderate, 9
to 12; and severe, 3 to 8. Patients with an initial GCS score of 8
or less in the field have a predictive value for a poor outcome
of at least 40%, and need urgent medical attention.7 This risk
increases proportionally with a lower GCS score. These individu-
als should be evacuated to a trauma center as soon as possible
if a favorable outcome is possible. Patients with mild TBI should
be assessed for limitations that would preclude them from con-
tinuing on the expedition, mission, or activity. Patients without
loss of consciousness associated with head injury only need
continuous monitoring for deterioration but are otherwise safe
to continue. Patients with loss of consciousness but a GCS of
more than 13 do not necessarily need to be transferred to a
trauma center but should be evaluated and undergo CT scanning
at the earliest and safest moment.7,71 Moderately injured patients
with a GCS of 9 to 12 or 13 are the ones in whom the outcome
can be affected by early, correct interventions. Avoidance of
hypotension in isolated head injury is paramount. As in combat-
related head trauma, use of mannitol, hypertonic saline, hy­
perventilation, and antibiotics is indicated for prophylaxis in
penetrating head trauma.20
TRAUMA
Physical Examination for Head Injury
After the primary survey and initial attempts to stabilize the
victim, a more complete physical examination should be done.
This examination should not delay patient evacuation. A hallmark
of TBI is an altered level of consciousness. Determination of the
PART 4
GCS score aids in recognition of TBI and should be regularly
reassessed to provide a mechanism for quantifying neurologic
deterioration. Physical signs that may denote underlying brain
injury include significant scalp lacerations or hematomas, contu-
sions, facial trauma, and signs of skull fracture. Findings specific
for basilar skull fracture include ecchymosis behind the ears
(Battle’s sign) and periorbital ecchymosis (raccoon eyes). Blood
behind the tympanic membrane on otoscopic examination
(hemotympanum), frank bleeding from the ears, and CSF rhinor-
rhea or otorrhea also suggest skull fracture and underlying TBI.
The pupillary examination may provide valuable data in
assessing an underlying TBI. Herniation of the temporal lobe of
the brain may be heralded by mild dilation of the ipsilateral pupil
with sluggish response to light. Further dilation of the pupil fol-
lowed by ptosis (drooping of the upper eyelid below its normal
level), or paresis of the medial rectus or other ocular muscle,
may indicate third cranial nerve compression by a mass lesion
or herniation. Table 18-1 relates pupillary examinations to pos-
sible underlying brain lesions.
Most dilated pupils (mydriasis) are on the ipsilateral side
to the mass lesion. With direct globe injury, traumatic mydriasis
may result, making evaluation of TBI more difficult. Also, 5% to
10% of the population has congenital anisocoria (a normal differ-
ence in pupillary size between the eyes); however, the pupil will
maintain a response to light. Casual inspection may overlook a
prosthetic eye, which is mistaken for a fixed pupil. Neither direct
trauma nor congenital anisocoria should be assumed in a head-
injured victim exhibiting mental status change in the wilderness.
After quantification of the GCS score, pupillary examination,
and examination of the head and face for signs of external
trauma, a concise neurologic examination should be performed.
The goal in the field is to identify motor or sensory focal deficits
suggestive of intracranial injury. Sensory deficits follow the
general dermatome patterns shown in Figure 18-6.
Unilateral hemiplegia may signify uncal herniation resulting
from mass effect in the contralateral cortex because of
386
TABLE 18-1  Interpretation of Pupillary Findings in
Victims with Head Injury
Pupil Size Light Response Interpretation
Unilaterally Sluggish or fixed Third nerve
dilated compression
secondary to
tentorial herniation
Bilaterally dilated Sluggish or fixed Inadequate brain
perfusion; bilateral
third nerve palsy
Unilaterally Cross-reactive Optic nerve injury
dilated or equal (Marcus Gunn pupil)
Bilaterally Difficult to determine; Opiates
constricted pontine lesion
Bilaterally Preserved Injured sympathetic
constricted pathway
compression of the corticospinal tract in the midbrain. Ipsilateral
pupillary dilation associated with contralateral hemiplegia is a
classic and ominous sign of tentorial herniation. Deep tendon
reflex changes in the absence of altered mental status or lateral-
izing signs are not indicative of TBI. Detailed evaluation of
brainstem function cannot be undertaken in the wilderness
setting. Evaluations of the gag and corneal reflexes may provide
some information helpful in triage and evacuation planning, but
the findings would not automatically obviate the need for
prompt evacuation.
Resuscitation with Head Injury
Resources and circumstances permitting, resuscitation should be
initiated as an adjunct to the primary survey. The main focus for
the head-injured victim, as for any traumatized victim, is the
airway.135 During the primary survey and performance of the
ABCDE sequence, IV access should be established. It is not advis-
able to administer fluids orally to the victim with head injury
because of the likelihood of vomiting, airway compromise, and
aspiration. In the patient with suspected head injury without
confirmatory imaging, the use of hypertonic IV fluids or mannitol
will effectively reduce the ICP.56,125
Individuals sustaining head trauma have a high incidence of
concomitant injuries, and many of these individuals, especially if
the injury is related to combat, have persistent postconcussive
symptoms for 6 months or longer.85,90 A victim who does not
have a palpable peripheral pulse or presents with other signs of
hypotension in the context of suspected head injury must not be
assumed to have a neurogenic cause of shock, so other causes
must be thoroughly and aggressively investigated. Recognition of
additional injuries is critical in the setting of head injury for mul-
tiple reasons. Management of a head injury should be secondary
to other life-threatening injuries, which, if not addressed, may
lead to hemorrhagic shock and preclude survival. As previously
discussed, maintenance of the MAP (and thus the CPP) and
adequate oxygenation are critical in preventing secondary brain
injury.
The type of resuscitative fluid administered to trauma victims
continues to be controversial. Previously, recommendations
warning of the dangers of overhydration in head injury led to
recommendations for restricting fluids. The need for resuscitation
and intravascular volume support has been well established.
Possible resuscitative fluids include isotonic crystalloid, hyper-
tonic crystalloid, or colloid solution. Osmotic agents, such as
hypertonic saline, have been shown to increase hypoperfused
regions of the brain after TBI.121 Hypotonic fluids, however, are
not appropriate in TBI secondary to an increase in whole-brain
water content and subsequent elevation in ICP. Data from animal
studies of TBI suggest that colloid solutions offer no advantage
over isotonic crystalloids, such as lactated Ringer’s solution, in
terms of augmenting cerebral blood flow or preventing cerebral
edema.146 As previously noted, no prospective trial has clearly
 CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
C2

C2 C3
Posterior cervical rami C4
C3 C5
C4 Posterior thoracic rami C6
C7
C5 Supraclavicular (C3,4) C8
T1 T1
T2
T2 Axillary (C5,6) T3
C6 T3 T4
Medial brachial cutaneous (C8–T1) T5
T4 T6
T7
T5 Radial (C5,8) T8
Anterior thoracic rami T9
T6 T10
T7 Lateral thoracic rami T11
T12
T8 Musculocutaneous (C5,6) L1
L2
T9 Medial antebrachial L3
T10 cutaneous (C8, T1) L4
L5
T11 Iliohypogastric (L1) S1
T12 Posterior sacral rami
S2
S3
L1
S2 Radial (C6–8) L3
Ulnar (C8,T1)
L2
Ilioinguinal Posterior
(L1) Median (C5–8) lumbar
L3 rami S2
Lateral femoral cutaneous (L2,3)
Obturator L1
(L2,3,4)
L4 L2
Anterior femoral cutaneous (L2,3)
Posterior femoral cutaneous (S1,2,3)

Common peroneal (L4,5,S1)

L5
Saphenous (L3,4)
S1

Superficial peroneal (L4,5,S1)

Sural (S1,2)
Superficial peroneal (L4,5,S1)
Deep peroneal (L4,5)

Dermatomes–anterior CUTANEOUS NERVES Dermatomes–posterior

FIGURE 18-6  Dermatome distribution map.

documented an advantage of colloid over crystalloid administra-
tion in the victim with multiple systemic injuries. Evidence is
accumulating that hypertonic solutions, particularly mannitol
or hypertonic saline, may be beneficial in TBI.56 However, an
advantage has not been demonstrated in trauma victims overall,
especially with concomitant injuries. The recommended resusci-
tative fluid for the head-injured victim in the wilderness setting
is isotonic crystalloid in the form of lactated Ringer’s solution,
with a target MAP of 80 to 90 mm Hg based on cuff blood pres-
sure determinations or extrapolation from evaluation of distal
pulses.
Further Management of Head Injury
Numerous adjuncts exist for management of the head-injured
victim, few of which are applicable in the wilderness setting.
Once the primary and secondary surveys are complete, the
airway is secured, resuscitation has been initiated, and spine
immobilization has been achieved, the victim should be placed
in a 30-degree head-up position. This position assists in control
of ICP, and thus CPP, through augmentation of venous outflow.
This maneuver should not be attempted if the spine cannot be
adequately immobilized.
If endotracheal intubation is possible, ventilation should be
optimized without hyperventilating the victim. Hyperventilation
has been used aggressively in the past to promote hypocarbia-
induced cerebral vasoconstriction and, theoretically, to decrease
brain swelling. However, if the PaCO2 falls below 25 mm Hg,
severe vasoconstriction ensues, effectively reducing cerebral
blood flow, promoting ischemia, and possibly augmenting sec-
ondary brain injury. Studies have demonstrated worse outcomes
in victims with severe head injury who were hyperventilated.98
Inability to measure or titrate the PaCO2 in the wilderness man-
dates that respiration be controlled to approximate near-normal
minute ventilation while maintaining oxygen saturation of more
than 95%.
All bleeding from the scalp or face should be controlled with
direct pressure. Scalp hematomas, regardless of size, should not
be decompressed. Open wounds, particularly skull fractures,
should be irrigated and covered with the most sterile dressing
available. Fragments of displaced cranium overlying exposed
brain tissue should not be replaced. If signs of skull fracture are
present, broad-spectrum antibiotic prophylaxis and immunization
against tetanus are administered. Although diuretics have been
widely used in the intensive care management of intracranial
hypertension, no rationale exists for their use in the field. The
wilderness trauma victim may have many injuries that are impos-
sible to evaluate fully in the field. In this setting, particularly in
the presence of hemorrhagic shock, attempts to induce osmotic
diuresis to decrease ICP may be life-threatening. Diuretics such
as furosemide or mannitol may exacerbate hypotension, cause
metabolic alkalosis, and induce renal complications in the
absence of physiologic monitoring.4 Corticosteroids have no role
in head injury in the field or intensive care unit. Studies have
documented no beneficial impact on ICP or survival. Attempts
at brain preservation by slowing the metabolic rate and oxygen
consumption have no role in the wilderness setting. Barbiturates
have been used for elevated ICP refractory to other measures,
but they may induce hypotension, depress myocardial function,
and confound the neurologic examination.4 Feasibility of these
advanced interventions may not be advisable in the wilderness,
especially if skilled providers are not available. The use of
hypertonic saline empirically in the treatment of TBI has little

387
 likelihood of complication and is often deployed in combat by
today’s military embedded medical technician.47
Approximately 50% of persons with severe head injury experi-
ence posttraumatic seizures.21 Phenytoin, valproate, or levetirace-
tam, if available, can be safely administered in the field.
Prophylactic administration has not been shown to change long-
term survival rates, but seizure prophylaxis may benefit patients
with TBI by reducing additional accidental injury, psychological
effects, and loss of driving privileges. Controlling seizures may
reduce secondary injury due to hypertension, increased ICP,
changes in oxygen delivery, and excess neurotransmitter release.21
Skull Fracture
Skull fracture in the wilderness mandates evacuation. Therapeutic
options in the field are few, with intervention limited to identify-
ing the injury and arranging rapid transport. Skull fractures may
be open or closed, linear or stellate, and may occur in the vault
or skull base. These fractures are associated with a high incidence
of underlying intracranial injury. Skull fractures with depression
greater than the thickness of the skull may require elevation. No
attempt at elevation should be made in the field. Any exposed
brain surface should quickly be covered with the most sterile
covering available, preferably moistened with crystalloid solu-
tion. Loose bone or brain fragments should not be manipulated.
If a broad-spectrum antibiotic is available, it should be adminis-
tered. After attention to the wound and stabilization of associated
injuries, the victim should be rapidly evacuated.
Penetrating Head Injuries
Most penetrating head injuries in the wilderness are gunshot
wounds; knives and arrows may also penetrate the cranium. Such
penetrating injuries are usually catastrophic; more than 60% of
TRAUMA
patients with gunshot wounds to the head succumb prior to
reaching a medical treatment facility.115 Some persons have sur-
vived small-caliber, low-velocity injuries and tangential wounds
that need only local debridement or antimicrobial therapy without
an operation.115 As with closed-head injury, management priori-
ties consist of maintenance of the airway, prevention of second-
PART 4
ary brain injury, and rapid evacuation. If the cranium has been
violated, the victim should receive antibiotics and tetanus immu-
nization in the same manner as for open skull fracture. In the
rare instance that the projectile is embedded in the skull, no
attempt at removal should be undertaken. If the length of the
projectile makes immobilization or transport cumbersome, the
excess length may be removed but only if this can be done
without displacement of the intracranial segment.
Evacuation of Patients with Head Injury
Survival and outcome of head injury in the wilderness correlate
directly with rapidity of evacuation. Certain situations dictate
immediate evacuation. Any person with evidence of an open or
closed skull fracture should be evacuated. There is reasonable
evidence to suggest that 30% to 90% of persons with raccoon
eyes or the Battle’s sign will show abnormalities on computed
tomography (CT) scanning.15,30 Similarly, any person who sustains
a penetrating injury should be evacuated. Decisions concerning
evacuation of victims who have sustained closed-head injuries
can be simplified by dividing the victims into three groups based
on probability of injury. The experience provided by the military
from recent conflicts in Iraq and Afghanistan suggests that all
patients with a GCS score of 9 to 13 be transported to a trauma
center immediately for evaluation.20 The low-risk group with a
GCS score of 14 or greater includes persons who have suffered
a blow to the head but are asymptomatic, did not lose conscious-
ness, and complain only of mild headache or dizziness. These
individuals do not necessarily require evacuation but may not
return to duty or activity until disorientation resolves.20 Finally,
persons with a GCS score of 3 to 8 must be evacuated to a trauma
center with neurosurgical capability.20
Persons who meet low-risk criteria with a GCS score of 15
and have no loss of consciousness, minimal symptoms, and an
unlikely mechanism may have suffered a concussion. The Quality
Standards Subcommittee of the American Academy of Neurol-
ogy60 defines concussion as a trauma-induced alteration in mental
388
status that may or may not involve loss of consciousness. The
neurologic impairment is short lived and resolves spontaneously
without any structural injury to the brain. These individuals
should not be allowed to return to activity until they are asymp-
tomatic and are no longer taking any medications. The following
signs indicate that more advanced medical care is necessary:
(1) inability to be awakened; (2) severe or worsening headaches;
(3) somnolence or confusion; (4) restlessness, unsteadiness, or
seizures; (5) difficulties with vision; (6) vomiting, fever, or stiff
neck; (7) urinary or bowel incontinence; and (8) weakness or
numbness involving any part of the body. No prospective vali-
dated guidelines for return to activity have been established,
although level III evidence recommends a graded plan for return
to activity.60 Generally, one should not return to an environment
in which concussion is a risk (e.g., contact sports) until symptoms
have been absent for 14 days and the individual is no longer
taking medications.
The group for which the evacuation decision is most difficult
is the moderate-risk group. These persons have a history of a
brief loss of consciousness or change in consciousness at the
time of injury, or a history of progressive headache, vomiting, or
posttraumatic amnesia. If any of these signs is present in the
face of concurrent systemic injury, the victim should be evacu-
ated immediately. Studies associating clinical variables and
abnormal results on CT scan have demonstrated the significance
of a decreased GCS score, presence of symptoms, and loss of
consciousness. If these signs are present in isolation and the
evacuation can be completed in less than 12 hours, the evacua-
tion should proceed. If the evacuation is impossible or will
require longer than 12 hours, the victim should be closely
observed for 4 to 6 hours. If the examination improves to nor-
mality during the observation period, it is reasonable to con-
tinue observation.
NECK INJURIES
Blunt Neck Injuries
Injuries to the neck may be classified as blunt or penetrating.
Significant blunt injuries include cervical spine injuries and laryn-
gotracheal injuries. The neck is divided into three distinct zones
that help predict injury and guide management (Figure 18-7).
Fracture of the larynx and disruption of the trachea usually
require surgical intervention that is unavailable in the wilderness.
The sooner laryngeal repair is accomplished, the better the
outcome with respect to phonation.39 Victims present with a
history of a significant blow to the anterior neck. Physical exami-
nation findings include difficulty with phonation, subcutaneous
emphysema that may extend as far inferiorly as the abdominal
wall, stridor, odynophagia, and often acute respiratory distress.
Blunt cerebrovascular injuries pose unique challenges in the
wilderness because they are difficult to diagnose. Practice
III
II
I
FIGURE 18-7  Zones in neck trauma.
management as well as diagnostic and surveillance guidelines
have been suggested for these injuries, but they fall outside the
scope of wilderness medicine.23,25,34
The airway is frequently in jeopardy, and treatment is focused
on establishing and maintaining an airway until evacuation can
occur. Because of the propensity for injuries of this type to result
in significant, progressive edema, endotracheal or nasotracheal
intubation is often necessary. If these options are unavailable,
airway maintenance techniques, as described in the Primary
Survey section, should be used. If intubation fails or is not avail-
able and hypoxic death is impending, a surgical cricothyrotomy
may be needed. A recent study of prehospital cricothyrotomies
demonstrated that trained personnel had success rates of more
than 90% regardless of the environment in which the cricothy-
rotomy was performed.67 For further descriptions of airway man-
agement, refer to Chapter 19.
Vertebral column injury, with or without neurologic deficits,
must be identified in any wilderness multiple-trauma victim.
Fifteen percent of victims sustaining an injury above the clavicles
and 5% to 10% with a significant head injury have a cervical
spine injury. In addition, 55% of spinal injuries occur in the cervi-
cal region.135 In the wilderness setting, fractures or dislocations
of the cervical spine are a result of falls from a significant height
or of high-velocity skiing or vehicular accidents. Approximately
10% of persons with cervical spine fractures have discontinuous
fractures elsewhere in the spine, necessitating early and complete
spine immobilization.135
Anatomy of the Neck.  The cervical spine has seven verte-
brae. The anteriorly placed vertebral bodies form the weight-
bearing structure of the column. The bodies are separated by
intervertebral disks and held in place anteriorly and posteriorly
by longitudinal ligaments. The paraspinal muscles, facet joints,
and interspinous ligaments contribute as a whole to stability of
the spine. The cervical spine, based on its anatomy, is more
susceptible to injury than are the thoracic spine or lumbar spine.
The cervical canal is wide from the foramen magnum to C2, with
only 33% of the canal constituting the spinal cord itself. The
clinically relevant tracts in the spinal cord include the corticospi-
nal tract, spinothalamic tract, and posterior columns.
Classification and Recognition.  Fractures of the cervical
spine may result in neurologic deficit, with total loss of function
below the level of injury. Spinal cord injuries should be classified
according to level, severity of neurologic deficit, and spinal cord
syndrome. Fractures of the C1-C2 complex generally result from
axial loading (a C1 ring fracture, or Jefferson’s fracture) or an
acute flexion injury (a C2 posterior element fracture, or hang-
man’s fracture). Approximately 40% of atlas (first cervical verte-
bra) fractures have an associated fracture of the axis (second
cervical vertebra). The atlas fracture, if survived, is rarely associ-
ated with cord injury but is unstable and requires strict immobi-
lization. A complete neurologic injury at this level is usually
unsurvivable due to paralysis of respiratory muscle function.
One-third of victims sustaining a severe upper cervical spine
injury die at the scene. The severity of cervical spine fractures
is a result of the neurologic compromise incurred. The most
common mechanism of injury is flexion. The most common
cervical fracture is of C5, and the most common level of injury
is C5-C6 due to the relative fulcrum associated with this
position.135
Fractures and dislocations may result in partial or complete
neurologic injury distal to the fracture or in no neurologic injury
at all. Partial injuries to the spinal cord result from typical patterns
of injury. Because flexion injuries are the most common type of
injury to the cervical spine, the anterior cord syndrome (see later)
is the most commonly seen serious neurologic picture. A careful
neurologic examination in the field to grade motor strength and
document sensory response to light touch and pinprick yields
important information that should be documented and reported
to the treating physician at the definitive care facility.
When appropriate resources are available, a rectal examina-
tion should be performed. Complete lack of tone and failure of
the sphincter muscles to contract when pulling on the penis or
clitoris (the bulbocavernosus reflex) indicate the presence of
spinal cord injury.
CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
BOX 18-5  Sensory and Motor Deficit Assessment
Sensory
C5: Area over deltoid
C6: Thumb
C7: Middle finger
C8: Little finger
T4: Nipple
T8: Xiphisternum
T10: Umbilicus
T12: Symphysis pubis
L3: Medial aspect of thigh
L4: Medial aspect of leg
L5: First toe web space
S1: Lateral foot
S4 and S5: Perianal skin
Motor
C5: Deltoid
C6: Wrist extensors
C7: Elbow extensors
C8: Finger flexors, middle finger
T1: Small finger abductors
L2: Hip flexors
L3: Knee extensors
L4: Ankle dorsiflexors
L5: Great toe extensors
S1: Plantar flexors
When individuals with cervical spine fractures or dislocations
are transported, the neck must be stabilized to prevent further
injury to the spinal cord or nerve roots at the level of the fracture
or dislocation. Approximately 10% of persons with cervical spine
fractures have discontinuous fractures elsewhere in the spine135;
therefore, the entire spine must be protected during transport.
A pure flexion event can result in dislocation of one or both
of the posterior facets without fracture or neurologic injury. The
victim may complain only of neck pain and limitation of motion.
If so, the victim should be transported with the neck rigidly
immobilized. With this injury, posterior instability is present
(because the interspinous ligament is ruptured), and any further
flexion stress could produce a spinal cord injury.
Physical Examination.  A thorough neurologic examina-
tion should be performed. Initial documentation of deficits and
frequent repeat examinations are critical to follow-up care. The
classification of injury in the field begins with determination of
the level of injury. Knowledge of sensory dermatomes (see Figure
18-6) and motor myotomes is invaluable. The sensory level is
the lowest dermatome with normal sensation and may differ on
each side of the body. Vertebrae C1-C4 are variable in their
cutaneous distribution, so assessment should begin at C5. The
examiner should not be confused by the occasional innervation
of the pectoral skin by C1-C4, known as the cervical cap. Light
touch and pinprick should be assessed.
Motor function should be assessed by the myotomal distribu-
tion listed in Box 18-5. Each muscle should be graded on a six-
point scale:
0: Total paralysis
1: Palpable or visible contraction
2: Full range of motion without gravity
3: Full range of motion against gravity
4: Full range of motion with decreased strength
5: Normal strength
Each muscle must be tested bilaterally and its function docu-
mented. The reflexes alluded to in the classification section, as
well as anal sphincter tone, must be tested.
Spinal Cord Syndromes.  There are three clinically useful
spinal cord syndromes:
Central cord syndrome is characterized by a disproportionate
loss of motor power between the upper and lower extremities,
with greater strength retained in the lower extremities. Sensory
loss is variable. The mechanism of injury usually involves a
forward fall with facial impact and hyperextension of the
spine.
389
 Mechanism of injury suggestive of cervical spine injury?
Yes/unknown
Alert and oriented, no distracting injury, not intoxicated?
Yes
Tenderness, pain spontaneously or with movement?
No
Normal neurologic exam?
Yes
A Immobilization unnecessary?
TRAUMA
B between the cricoid cartilage and the angle of the mandible. Zone
FIGURE 18-8  A, Clinical assessment of cervical spine stability. Failure
of any criterion suggests need for immobilization. B, Proper spine
PART 4
immobilization.
Anterior cord syndrome is characterized by paraplegia and
loss of pain and temperature sensation. It is the most common
manifesting syndrome caused by cervical spine injury and carries
a poor prognosis.
Brown-Séquard syndrome results from hemisection of the
cord. It consists of ipsilateral motor loss and position sense with
contralateral sensory loss two levels below the level of injury. It
is usually secondary to penetrating injury.
Immobilization.  After identification of injury, the caregiver
faces the critical decision, with important ramifications, of whether
to immobilize the patient.110 Victims who would as a matter of
course be immobilized in an urban setting might not be appropri-
ate candidates for immobilization in the wilderness. The decision
to immobilize converts an otherwise ambulatory victim who can
actively participate in his or her own evacuation to one requiring
more involved evacuation procedures. The subsequent evacua-
tion can be dangerous to the victim and rescuers and demands
significant expense and use of resources.
Risk criteria for cervical spine injury and the need for immo-
bilization have been defined.135 All criteria for the exclusion of
immobilization must be satisfied. These include normal mental
status without chemical influence; lack of distracting injury;
normal neurologic examination; and a reliable neck examination
without midline neck pain, deformity, or tenderness. Figure
18-8A presents an evidence-based algorithm for determining the
need for immobilization; although such a need poses hazards for
the evacuation process, if criteria are met, immobilization takes
precedence over ease of evacuation. Additionally, using the trap
squeeze technique for positioning and moving the patient with
a suspected cervical spine injury has been shown to be safe and
effective.110 A difficult balance must be struck in the wilderness
between the likelihood of true injury and the danger to the
390
expedition members and rescuers that may ensue when the
victim is immobilized. If a rigid litter is not available, the victim
should be maintained on the flattest surface possible. A rigid
cervical collar should be placed. All collars allow some degree
of movement, particularly rotation; soft collars provide the least
amount of immobilization.51 The Philadelphia collar allows 44%
of normal rotation and 66% of normal lateral bending.92 To
achieve 95% immobilization, a halo and vest are necessary. Any
number of materials may be used to improvise an immobilizing
device (see Chapter 46). Restriction of flexion, extension, and
rotation must be achieved to the greatest degree possible. Optimal
immobilization consists of a long spine board or litter, rigid collar,
bolsters to the sides of the head, and tape or straps restricting
movement (see Figure 18-8B).
Treatment.  Because little definitive treatment for cervical
spine injury can be accomplished in the field, survival and
outcome depend on speed of transport and maintenance of the
airway. This is particularly true when cervical spine injury is
associated with head injury and major systemic trauma. Transport
all victims with proven or suspected cervical spine injury to a
definitive care facility.
Penetrating Neck Injuries
Like penetrating head injuries, penetrating neck injuries are
usually due to gun or knife wounds. Most do not confer bony
instability; however, stability should not be assumed. Neurologic
deficits, if present, can progress with further movement of an
unstable spine. Projectiles should not be removed if embedded
in the neck. Penetrating injuries to the neck may not directly
injure the spine, but neurologic sequelae may result from a blast
effect. The same immobilization criteria should be implemented
as when dealing with blunt injuries.
Penetrating injuries to the neck are classified according to
anatomic zones of injury (see Figure 18-7). Zone I injuries extend
from the clavicles to the cricoid cartilage. Zone II injuries occur
III injuries occur superior to the angle of the mandible.
Historically, treatment has been based on penetration of the
platysma muscle. In the wilderness setting, if the examiner is
confident that platysmal penetration has not occurred, the victim
may be observed and the wound considered a laceration. Much
debate has taken place over management of platysmal penetra-
tion within respective topographic zones, with treatment arms
consisting of surgical exploration versus radiographic evaluation.
In the wilderness setting, such considerations remain relevant,
including the definition of what constitutes a life-threatening
penetrating neck injury. Injuries that produce hard signs of bleed-
ing (arterial bleeding, expanding hematoma, airway compression,
neurologic symptoms, palpable thrill, audible bruit) should be
treated with direct compression, and movement to immediate
evacuation should begin.50 These penetrating injuries violating
the platysma muscle not only indicate the possibility of significant
neurovascular injury but also esophageal or tracheal injuries.
These victims should be evacuated promptly with close attention
to the airway.
INJURIES TO THE THORAX
Thoracic trauma accounts for about 25% of all fatalities in trauma
patients, yet only 10% require major surgical intervention. In most
injuries, especially in the austere environment, supportive man-
agement with supplemental oxygen and pain relief are all that
is required. However, on occasion chest drainage may be neces-
sary. The key is to rapidly identify patients that require urgent
intervention.135 The most common mechanism in the wilderness
is blunt trauma from falls or direct blows to the chest. Penetrating
injuries can be caused by gunshot wounds, knife and arrow
injuries, or impalements. The approach to thoracic injuries
depends on the mechanism, severity, and location and whether
the injury is through the chest wall only or through the wall plus
the pleura and into the lung parenchyma.
Rapid examination of the thorax by inspection, palpation, and
auscultation can assess life-threatening injuries, which are delin-
eated in Box 18-6.
 Most rib fractures can be managed with oral analgesics. Deep

CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES

BOX 18-6  Life-Threatening Chest Injuries
breathing, incentive spirometry, pain control, and possibly sup-
Airway obstruction plemental oxygen usually allow the patient to be evacuated
Tension pneumothorax safely. Taping, splinting, or use of a rib belt is contraindicated
Open pneumothorax (sucking chest wound) in chest wall injury because these measures hinder movement
Massive hemothorax and decrease chest wall expansion, leading to atelectasis and
Cardiac tamponade worsening hypoxia. Extremely painful shallow respirations can
be associated with multiple rib fractures. Intercostal nerve block
or subcutaneous block over the area of injury may help the
patient hike out of the wilderness.68,76 Multiple segmental rib
fractures associated with a significant underlying lung injury,
The typical patient will complain of chest pain and shortness pneumothorax, hemothorax, or pulmonary contusion will neces-
of breath with point tenderness at the site of the impact. As with sitate emergent evacuation. Sternal fractures are caused by
any injury, the physical examination first requires assessment of impact to the sternum by blunt force, most commonly in the
the airway. Intercostal or supraclavicular retraction suggests upper or middle portion of the bone. The patient complains of
airway obstruction. The chest wall in general should rise sym- anterior chest pain with or without ecchymosis. A palpable
metrically. The best way to visualize and inspect the chest is from deformity may be evident with motion of the fracture fragments
the foot of the patient, looking for retraction and a possible flail upon respiration. The primary treatment is analgesia and pulmo-
segment, wherein the chest wall moves paradoxically. Dyspnea, nary toilet. Sternal fractures are seen in combination with other
cyanosis, and use of accessory muscles are indications of impend- major chest injuries when multiple injuries are present, including
ing respiratory compromise. Hypotension, tachycardia, and ashen rib fractures, pulmonary contusion, and blunt myocardial injury.
or cyanotic skin suggest shock. Diaphoresis is common in low- In these cases, it may be important to rule out a myocardial
flow states such as cardiac tamponade and commonly precedes injury.46,102,143
hypotension, especially in the young trauma patient with tam-
ponade. If the patient has distended neck veins, suspect tension
pneumothorax or pericardial tamponade. However, the absence
of distended neck veins does not exclude these two entities,
especially in a hypovolemic patient.
It is important to examine the patient’s back by logrolling the
patient while maintaining in-line position and immobilization.
Palpation can identify significant chest wall and sternal segment
movement when both hands are placed on the two hemithoraces
to palpate for symmetric chest wall motion. This technique can
also identify a flail segment. Crepitus is common with chest
trauma and may indicate subcutaneous emphysema from an
underlying pneumothorax. Subcutaneous emphysema can extend
up into the neck and down into the inguinal ligaments, and is
almost always associated with a significant pneumothorax. Palpa-
tion of the thoracic cavity should occur symmetrically, beginning
at the distal clavicles and working medially toward the sternum,
palpating and inspecting each rib individually for tenderness,
contusion, or fracture. Auscultation of both chest walls can aid
in diagnosis. Dullness to percussion may suggest a hemothorax;
hyperresonance or tympani may indicate a large pneumothorax
or tension pneumothorax.51
Portable ultrasound can be used in the austere environment
to diagnose traumatic conditions of the chest, including pericar-
dial fluid collections, pneumothorax, and hemithorax. Pneumo-
thorax is identified by loss of “comet tails” or pleural sliding
(Figure 18-9).6 Numerous articles in the literature have found this
to be a sensitive and specific means of diagnosing significant
chest wall injuries (see Chapter 109).13,37,77,127
A
SPECIFIC THORACIC INJURIES
Blunt chest trauma in the wilderness is associated with decelera-
tion injury, a fall from a significant height, or a direct blow.
Compression of the chest wall by moving or falling debris can
contribute to major intrathoracic injuries.
Rib Fractures
Rib fractures range from isolated nondisplaced, single-rib frac-
tures that cause minor discomfort to a major flail segment with
associated underlying hemothorax and/or pneumothorax with or
without pulmonary contusion. Rib fractures usually cause pain,
especially during inspiration. The patient will often have a rapid,
shallow breathing pattern and point tenderness. The health care
provider can occasionally feel displacement or crepitus overlying
the rib fracture. Lower rib fractures should provoke consideration
of associated liver or splenic injury. In these situations, the patient B
should be examined for intraabdominal tenderness and ultra-
sound may be useful to detect peritoneal fluid indicative of FIGURE 18-9  A, Portable ultrasound devices are easily transported for
hemorrhage. Figure 18-10 demonstrates fluid in the right upper rapid assessment of physiologic and anatomic parameters. B, Example
quadrant.116 of pneumothorax on ultrasound.

391

A first-aid kit.
B as midazolam, will help with pain and anxiety relief during the
FIGURE 18-10  A, Ultrasound image demonstrating fluid in Morison’s
TRAUMA
pouch. B, Fluid around the spleen.
Pneumothorax
As air enters the pleural cavity, causing the intrapleural pressure
PART 4
to equal the atmospheric pressure, the lung collapses (pneumo-
thorax). The three types of pneumothorax are simple, tension,
and open pneumothorax.
In simple pneumothorax, symptoms include tachypnea, dys-
pnea, and hyperresonant breath sounds in the affected hemi­
thorax. Treatment of a simple pneumothorax, depending on its
symptoms and size, is decompression of the pleural cavity.41 In
the wilderness, tube thoracostomy can be difficult to perform. A
small pneumothorax can often be managed without placing a
chest tube, especially if the patient can ambulate with adequate
analgesia. Frequent rest breaks may be necessary. Suspicion of
a pneumothorax alone on physical examination does not neces-
sitate placement of a catheter or chest tube.22,128 However, if the
patient develops incapacitating symptoms, decompression may
be necessary to avoid a life-threatening situation. Portable ultra-
sound can be used to make the diagnosis (see Chapter 109). The
patient should be monitored with physical examination and pulse
oximetry.
Tension pneumothorax develops when the intrapleural pres-
sure increases, so that the heart and great vessels are shifted away
from the pneumothorax. This commonly impedes venous return
from the superior and inferior venae cavae, decreases cardiac
output, and causes hypotension leading to shock. The patient
may have distended neck veins and tracheal deviation away from
the side of the lesion. Other physical findings are absent breath
sounds, hyperresonance on percussion, respiratory distress, cya-
nosis, and cardiovascular collapse. This life-threatening injury
demands immediate chest decompression, followed by evacua-
tion. A temporizing treatment is to insert a needle or catheter into
the pleural space, which converts the tension pneumothorax into
a simple pneumothorax. This is done by inserting a 14-gauge
catheter percutaneously over the second rib in the midclavicular
space or laterally in the anterior axillary line in the fifth intercostal
space.72 The needle is placed over the anterosuperior surface of
the rib through the intercostal muscles to avoid the inferiorly
located neurovascular bundle. If successful, a rush of air is usually
392
heard upon release of the tension pneumothorax. In muscular or
obese individuals, the catheter needle must be long enough to
reach the pleural cavity. The lateral approach may be easier. A
plastic catheter can be advanced over the needle, the needle
withdrawn, and the catheter left in place to ensure ongoing
decompression. A rubber glove or a finger cot can be attached to
the catheter to create a unidirectional flutter valve that allows
egress but not ingress of air from the pleural cavity. A commer-
cially available system for this purpose is the Asherman Chest Seal
(Chinook Medical Gear, Durango, CO).5 With limited resources,
one might use a sharp instrument and a finger thoracostomy or
placement of a hollow tube. The skin is optimally first cleansed
with an antiseptic. A premade kit such as a Heimlich Chest Drain
Valve kit (Chinook Medical Gear, Durango, CO) can be used for
decompression. This is a valued addition to any expedition’s
Open pneumothorax is described in the section on Penetrating
Chest Wounds, below.
Chest Tube Placement.  Appropriate positioning of the
patient will aid in the placement of a tube thoracostomy. The
patient should be supine and the ipsilateral arm raised and placed
behind the patient’s head to open the space between the latis-
simus and pectoralis muscles and allow a better window for
insertion. It is important in females to place the chest tube lateral
to the breast tissue. The area should be cleaned with an antiseptic
and anesthetized with 1% lidocaine if possible. All layers of the
chest wall, including the intercostal muscles, rib surface, and
especially pleura, should be infiltrated with anesthetic to provide
adequate analgesia. Oral or IV narcotics and a mild sedative, such
insertion period. A 2- to 3-cm incision is made through the skin
and subcutaneous tissue down to the ribs and intercostal space.
A blunt instrument, such as a clamp, is carefully inserted into the
pleural space and directed close to the superior surface of the
rib. Confirmation of entry into the pleural space can be made
digitally to ensure that the underlying lung parenchyma is dis-
sected away from the pleura, so that chest tube insertion will be
done properly. For a simple pneumothorax, a 20 or 22 French
tube is used, or a pigtail catheter if available. The catheter or
chest tube should be directed posteriorly and apically, and
secured with a suture or tape. If possible, the tube should
be connected to suction or an underwater seal. The tube can be
left open to the atmosphere to accomplish decompression and
the end of the tube covered with a rubber glove, finger cot, or
plastic bag modified to permit unidirectional egress flow of air.
Preinsertion antibiotics, oral or parenteral, to cover gram-positive
skin flora will reduce the chance of a subsequent pleural
infection.38
Hemothorax
A hemothorax is the presence of blood in the pleural space,
usually associated with an overlying major chest wall injury with
multiple rib fractures. The most common cause is a direct blow
to the chest that causes laceration of the lung, intercostal vessels,
or pulmonary vasculature. Tenderness, inspiratory pain, and
dyspnea can be associated with a hemothorax. In the wilderness,
a tube thoracostomy is rarely required or feasible, but can be
placed if the equipment is available and the patient is symptom-
atic, especially with prolonged evacuation. A 32F to 36F chest
tube should be inserted if a hemothorax is suspected. If more
than 1500 mL is evacuated after placement of the chest tube, this
is indicative of a massive hemothorax. This mandates rapid
evacuation and ongoing resuscitation in anticipation of operative
intervention. The major goal in treatment is to evacuate the
pleural space and allow expansion of the lung, which helps
appose the lung pleura and visceral pleura and potentially
decreases bleeding from the lung and other low-pressure
sources.51
Flail Chest
When two or more ribs are fractured in two or more places, that
segment of the chest wall has lost bony continuity with the rest
of the bony thorax. An unstable segment will have paradoxic
motion inward upon inspiration. This is often associated with an
underlying pulmonary contusion, which may blossom only after
PENETRATING CHEST WOUNDS

CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES

12 to 24 hours. These injuries, especially in the elderly, can be
associated with significant oxygenation and ventilation compro- Penetrating chest trauma above the nipples is most often associ-
mise and may require mechanical ventilation2; therefore, rapid ated with pneumothorax, hemothorax, or cardiac injury, and
evacuation may be necessary. Intercostal nerve blocks may below the nipples with intraabdominal penetration.
provide short-term management of pain and pulmonary toilet. An open pneumothorax, or “sucking” chest wound, is a trau-
Bilateral fractures of the costochondral cartilage can cause a matic defect of the chest wall at least two-thirds the diameter of
central flail segment, where the entire sternum paradoxically the trachea. This injury causes decreased ventilation owing to
moves with respirations. preferential movement of air through the chest wall defect instead
of the major airway. This injury requires rapid reconstruction of
chest wall integrity to avoid hypercarbia and hypoxia. A hand
BLUNT CARDIAC INJURIES can first be placed over the sucking chest wound, and field treat-
Pericardial tamponade or major symptomatic blunt myocardial ment can include placing petroleum gauze on top of the wound,
injuries are relatively rare in the wilderness. Most blunt myocar- covered by a patch of gauze 4 inches square taped to the skin
dial injuries are self-limited and improve within the first 24 hours. on three sides. The untaped side serves as a flutter valve mecha-
However, the risk of significant dysrhythmias is high within the nism to prevent a tension pneumothorax by allowing air to move
first 24 hours. The classic presentation of a blunt myocardial out with expiration but not back into the pleural space during
injury is sinus tachycardia refractory to analgesia. Other dysrhyth- relaxation or inspiration. An Asherman Chest Seal kit serves the
mias include premature ventricular contractions and bundle same purpose. Additionally, a chest tube can be placed remote
branch block. Any patient with symptomatic dysrhythmias or from the wound to decompress air and blood in the pleural cavity
development of hemodynamic instability should be evacuated (Figure 18-11). Most often, these large wounds require surgical
immediately. Rare major blunt cardiac injuries include chamber intervention for closure, and, thus, the patient should be trans-
rupture or valvular disruption. In the wilderness, major cardiac ported urgently to definitive care.
injury is likely nonsurvivable.14,32
Acute pericardial tamponade can be life-threatening. Even a
small amount of blood acutely contained within the pericardial
cavity can cause severe restriction of cardiac function. As little
as 15 to 20 mL is sufficient to produce shock. The classic clini-
cal finding is Beck’s triad (distended neck veins, hypotension,
and muffled heart sounds), which is difficult to diagnose in the
wilderness. Less than one-third of patients with tamponade
have all three findings. The patient is often agitated, diapho-
retic, and tachycardic. Another sign of cardiac tamponade is
pulsus paradoxus, in which there is a decrease in systolic blood
pressure of more than 10 mm Hg with inspiration. Diagnosis of
cardiac tamponade in the wilderness has been made much
easier with the use of portable ultrasound. Once the diagnosis
of tamponade has been made, immediate evacuation of the
patient is necessary, because nearly all require median sternot-
omy for definitive treatment. A temporizing measure that can be
performed prior to definitive management is pericardiocentesis.
If there is high suspicion of pericardial tamponade and shock
that is unresponsive to resuscitation has developed (and death A
is impending), a long (16-cm) 16- to 18-gauge needle with over-
lying catheter can be introduced 1 to 2 cm below and to the
left of the xiphoid, and advanced superiorly at a 45-degree
angle with the tip aimed at the tip of the left scapula. The cath-
eter should be aspirated as the needle is advanced until blood
is obtained. Traditional teaching states that pericardial blood is
nonclotting; however, with a large amount of fresh blood in the
pericardium, clots may form. Once the blood is aspirated, the
needle is removed and the catheter left in place and secured.
Repeat aspiration may be required according to the hemody-
namic status as the patient is being evacuated for definitive
care. Cardiac tamponade can also result from penetrating trauma
to the “box,” which is an area outlined by the nipples, sternal
notch, and xiphoid.

TRAUMATIC ASPHYXIA B
Traumatic asphyxia can occur with burial during landslides, ava- Lateral edge of
lanches, or earthquakes, particularly when there is a severe crush pectoralis major
injury of the chest wall. Craniocervical cyanosis presents with
symptoms of facial edema, diffuse upper body petechiae, sub-
conjunctival hemorrhage, and hypoxia-related neurologic symp-
toms. The pathophysiology is an acute increase in intrathoracic
pressure, which is dissipated to the inferior and superior venae Base of
cavae. In this circumstance, venous flow reverses in the veins of axilla Fifth intercostal
the head and venous hypertension causes capillary rupture, with space
subsequent facial edema and petechiae. C Lateral edge of
The patient can have significant facial and laryngeal edema. latissimus dorsi
Care is supportive. Death is associated with pulmonary dys­ FIGURE 18-11  A, Asherman Chest Seal device. B, Heimlich valve
function and associated injuries. Expeditious evacuation is attached to a pigtail pleural catheter. C, Proper position for chest tube
essential.75,101 insertion.

393

INJURIES TO THE ABDOMEN
Intraabdominal injuries in the wilderness setting are difficult to
recognize. Once recognized, all require appropriate resuscitation
and immediate evacuation. The abdomen is the most frequent
site of life-threatening hemorrhagic shock; however, in the wil-
derness setting, few diagnostic and treatment options exist.
BLUNT ABDOMINAL TRAUMA
Blunt intraabdominal injury is commonly associated with falls.
Abdominal injuries are often associated with fractures or closed-
head injuries. Often the decision for evacuation is made on the
basis of other injuries; however, the wilderness physician must
be attuned to the potential for intraabdominal hemorrhage as an
occult injury.
Anatomy of the Abdomen
For descriptive purposes, the abdomen may be divided into
thoracic, true, and retroperitoneal compartments. The thoracic
abdomen contains the liver, spleen, stomach, and diaphragm.
The liver, spleen, and, more rarely, stomach may be injured by
direct blows to the ribs or sternum. Twenty percent of persons
with multiple left lower rib fractures have a ruptured spleen. A
direct blow to the epigastrium may result in increased intraab-
dominal pressure, with subsequent rupture of the liver or dia-
phragm. The true abdomen contains the small bowel, large
bowel, and bladder. Isolated bowel injuries are rare in the wil-
derness setting. Blunt bladder or rectal injury usually occurs in
conjunction with severe pelvic fracture and carries a high risk of
death. The retroperitoneal abdomen contains the kidneys, ureters,
pancreas, and great vessels. It is notoriously difficult to evaluate
TRAUMA
by physical examination. Life-threatening hemorrhage can occur
into the true abdomen or retroperitoneal space.
Diagnosis
The wilderness physician must have a high index of suspicion
and perform a superlative history and physical examination. With
PART 4
the advance of ultrasound technology, access to a small portable
unit may be helpful in determining the absence or presence of
free abdominal fluid (see Figure 18-9 and Chapter 109).
Handheld ultrasound devices are as sensitive and specific as
more powerful units designed for inpatient use; they are no less
accurate and their positive and negative predictive values are the
same.78 In the wilderness, invasive diagnostic procedures such as
peritoneal lavage are not recommended.
Physical Examination
Look for signs of early shock, with tachycardia, tachypnea,
delayed capillary refill, a weak or thready pulse, and cool or
clammy skin. Physical examination of the abdomen begins with
visualization and inspection. Contusions and abrasions may be
the only harbingers of occult visceral injury. Periumbilical ecchy-
mosis associated with abdominal hemorrhage (Cullen’s sign) is
virtually never present in acute abdominal trauma. Abdominal
distention due to hemorrhage is a late sign and is never present
before shock and cardiovascular collapse have developed.
Abdominal inspection should survey the flanks, lower chest, and
back. Inspection of the back should follow palpation of the spine
while the victim is supine. The victim should be carefully log-
rolled if there is any suspicion of spinal injury.
Looking for muscle guarding, the examiner gently palpates
the abdomen in all four quadrants. Persistent guarding or tender-
ness after trauma mandates rapid evacuation. Percussion tender-
ness is an indicator of peritoneal irritation, also mandating
evacuation. The presence or absence of bowel sounds has little
prognostic significance. Bowel sounds may be present in the face
of significant intraabdominal hemorrhage or, conversely, absent
when extraabdominal injuries induce ileus.
Referred pain to the left shoulder (Kehr’s sign) strongly sug-
gests a ruptured spleen. This pain is often exaggerated by placing
the victim in the Trendelenburg position, increasing the amount
of left upper quadrant blood irritating the diaphragm. Pain from
the retroperitoneal abdomen associated with injuries to the
394
kidneys or pancreas may be referred to the back. However,
referred pain is usually a late finding and is not helpful in evalu-
ation of acute trauma.
Gross hematuria that does not clear immediately or that is
coupled with an associated injury, such as pelvic fracture or
abdominal or back pain, requires immediate evacuation. To
minimize blood loss, the victim should be kept stationary and
the evacuation team brought as close to the victim as possible.
In a wilderness setting, rectal and vaginal examinations add
little to the evacuation decision when evaluating for abdominal
trauma. The unstable pelvic fracture associated with rectal and
vaginal injuries is usually the determinant for evacuation.
PENETRATING ABDOMINAL TRAUMA
Penetrating intraabdominal injuries may result from blast, gun-
shot, stab, or arrow wounds. The social context in which these
injuries occur (accidental, intentional, or self-inflicted) makes
little difference in the wilderness setting. Recrimination, guilt,
and blame only interfere with the paramount goal of immediate
evacuation.
Gunshot Wounds
A low-caliber gunshot injury often manifests with a small entrance
wound and no exit wound. A high-caliber, high-velocity gunshot
injury may have a relatively innocuous entrance wound but a
large, disfiguring exit wound and extensive internal injuries. No
matter what the caliber or trajectory and no matter where the
entrance and exit wounds, all gunshot wounds from the nipple
line to the inguinal ligament should be presumed to have pen-
etrated the abdominal cavity and created an intraabdominal
injury. These injuries mandate immediate surgical intervention.
A victim of gunshot wounds to the head, neck, chest, abdomen,
or groin should undergo immediate evacuation and should
receive a single-agent broad-spectrum antibiotic, such as an oral
fluoroquinolone, second-generation cephalosporin, or extended
beta-lactam drug. Hunting injuries are discussed in Chapter 26.
Shotgun Injuries
Shotgun injuries to the torso are managed in the same manner
as gunshot wounds. Shotgun injuries have a potentially lower
incidence of underlying visceral injury than do gunshot wounds,
but there is often extensive soft tissue damage requiring surgical
debridement. The potential exists for delayed development of
peritonitis from a single penetrating pellet to the viscera. Conse-
quently, shotgun injuries should also be treated with emergency
evacuation and a broad-spectrum antibiotic, as recommended
previously for gunshot wounds.
Occasionally, a close-range shotgun blast results in a soft
tissue defect large enough for bowel to extrude through the
wound. The bowel should not be placed back into the abdomen.
Injured bowel displaced from the abdominal cavity conceptually
should be treated as though it were an enterocutaneous fistula.
Because evacuation is often delayed in the wilderness, it is better
to have fecal contents outside, rather than inside, the peritoneal
cavity. The exteriorized bowel should be kept moist and covered
at all times. Uncovered bowel outside the peritoneal cavity
rapidly desiccates and becomes nonviable, mandating later surgi-
cal resection. Exposed bowel should be covered with an abdomi-
nal pack or cloth moistened with sterile saline at best, or at worst
with potable water. The dressing should be checked and remoist-
ened at least every 2 hours.
Stab Wounds
The penetrating object is usually a knife but may be as varied
as a piton, ski pole, or tree limb. Any deep skin laceration from
the nipple line to the groin should be considered to have dam-
aged an intraabdominal organ. Whereas the odds of an abdomi-
nal gunshot wound injuring a visceral organ exceed 85%, the
odds of a stab wound injuring a visceral organ are less than 50%.
In certain urban hospitals, the high incidence of negative
surgical explorations for stab wounds had led to a more selective
approach toward patients with abdominal stab wounds.11 Sig­
nificant injuries from penetrating trauma have been statistically
decreasing in most trauma centers. The practice of nonoperative

CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES

management for penetrating abdominal trauma has its place in
the right setting, including one where hemodynamics can be
continuously monitored, frequent physical examinations can take
place, and the patient can be taken immediately to the operating
room if the condition changes or peritonitis develops. This
approach uses local wound exploration and frequent physical
examinations. This is not appropriate for the wilderness environ-
ment; all patients with suspected violation of the fascia from
penetrating abdominal trauma should be promptly evacuated.
Although there are no data addressing the management of
stab wounds in the wilderness, the following approach is practi-
cal and reasonable. If the wound extends into the subcutaneous
tissue, the evacuation decision depends on local wound explo-
ration. This procedure is simple to perform, even in the wilder-
ness. The skin and subcutaneous tissue are infiltrated with local A
anesthetic, and the laceration is extended several centimeters to
clearly visualize the underlying anterior fascia. It is helpful to
use lidocaine 1% with epinephrine to minimize slight but annoy-
ing bleeding that can impair visualization. The wound should
never be probed with any instruments, particularly if overlying
the ribs.
Wound exploration is confined to the area from the costal
margin to the inguinal ligament. Local exploration is contraindi-
cated in wounds that extend above the costal margin, because
it is possible for such exploration to communicate with a small
pneumothorax, potentially exacerbating respiratory distress.
If thorough exploration of the wound shows no evidence of
anterior fascial penetration and there is no evidence of peritoneal
irritation, the wound can be closed with tape (e.g., Steri-Strips)
or adhesive bandages and dressed, and the evacuation process
may be delayed. Physical examination should be performed
every few hours for the next 24 hours. If no peritoneal signs B
develop and the victim feels constitutionally strong, a remote
expedition may resume with caution and an eye to evacuation FIGURE 18-12  A, Pelvic sling improvised with a jacket provides com-
should the victim become ill. pression to the pelvis to control bleeding. B, Pelvic binder.
In the wilderness, it is prudent to have a low threshold for
evacuation because of technical difficulties in performing wound
exploration, such as insufficient light and inadequate instruments. The flank, scrotum, and perianal areas should be inspected
Persons who have been impaled by long objects, such as tree for blood at the urethral meatus, swelling or bruising, or a lac-
limbs or ski poles, should have the object left in place and care- eration in the perineum, vagina, rectum, or buttocks suggestive
fully shortened, if possible, to facilitate transport. of an open pelvic fracture. Rectal and vaginal examinations
should be performed by an experienced provider to recognize a
possible “open pelvis.” The pelvis should be examined carefully
PELVIC TRAUMA once, without any aggressive rocking motion. The first indica-
In the wilderness setting, fractures of the pelvis are generally tion of mechanical disruption is leg length discrepancy or rota-
associated with a fall from a significant height, a high-velocity tional deformity in the absence of an obvious leg fracture or
ski accident, or a vehicular accident. hip dislocation. For more information on pelvic fracture, see
Pelvic fractures have a significant risk of death; if the fracture Chapter 22.
is open, the risk at least doubles.53,144 With opening of the pelvic
ring, there may be hemorrhage from the posterior pelvic venous
complex and occasionally from branches of the internal iliac
EXTREMITY TRAUMA
artery. For hemodynamically unstable victims with severe pelvic Most wilderness-related extremity injuries are fractures and
fractures, resuscitative efforts should be instituted. In addition, sprains, which are discussed in Chapter 22. This section focuses
simple techniques to reduce increased pelvic volume using cir- on general field management of significant extremity vascular
cumferential binding sheets or slings may slow bleeding.129 injuries, traumatic amputation, and recognition and treatment of
Several pelvic binders provide circumferential pressure to mini- rhabdomyolysis.
mize the pelvic volume with essentially equal efficacy.79 Even the
improvised use of a sheet has been shown to provide adequate
compression of the pelvis in cadaver models.108 In the field, a
VASCULAR INJURIES
blanket, sheet, binder, or jacket may be used to hold compres- Injury to the major vessels supplying the limbs can occur with
sion (Figure 18-12). penetrating or blunt trauma. Fractures can produce injury to the
The key factor in the initial management of pelvic fractures vessels by direct laceration (rarely) or by stretching, which pro-
is early suspicion, identification, and proper management and duces intimal flaps. Penetrating injuries can be devastating if
transport of the victim. Posterior ring fractures or dislocations are transection of a vessel occurs. Significant vascular injuries, from
associated with a greater incidence of significant hemorrhage, penetrating or blunt causes, can result in subtypes of multiple
neurologic injury, and death than are other pelvic fractures. The vessel injuries, each of which may threaten the limb. Injury sub-
diagnosis of pelvic fracture should be identified early in the types include laceration, transection, contusion with spasm,
primary/secondary survey. The examiner may see pain, swelling, thrombosis, true or false aneurysm, external compression, and
and ecchymosis. The authors do not recommend repeated or arteriovenous fistula. Accurate history taking, expeditious physi-
aggressive stressing or compression on the pelvis during exami- cal examination, and prompt evacuation are the keys to life and
nation. A person with a pelvic ring fracture must be immediately limb salvage.
evacuated on a backboard, with care taken to minimize leg and Significant vascular injuries result in one of two clinical pre-
torso motion.87 sentations, hemorrhage or ischemia. The main priority is stopping

395
 hemorrhage. The victim of trauma may die in short order from
a major vascular injury. Ideally, control of hemorrhage can be
accomplished without resultant ischemia of the distal extremity.
Hemorrhage from an extremity wound can almost always be
controlled with direct pressure and pressure dressings. These
measures permit circulation to and from the extremity outside
the area of pressure application. In some circumstances, a tour-
niquet may be required.
History of the Injury
A complete history of the time and mechanism of injury is invalu-
able in planning further management. Although no absolute
ischemia time has been established, a goal of less than 6 hours
to reperfusion is prudent.135 Recent military experience demon-
strates that tourniquets are an effective method of stopping
hemorrhage. The optimal ischemia time is less than 2 hours;
however, minimal morbidity has been achieved with longer
applications.80,81 The amount of blood present at the scene should
be quantified. A history of pulsatile bleeding of bright-red blood
that abates suggests arterial injury. Thirty-three percent of victims
with arterial injuries have intact distal pulses.
Physical Examination
Vascular examination in the field can be difficult. Hypovolemia,
hypothermia, and hostile conditions make accurate examination
challenging. Skin color and extremity warmth should first be
assessed. Distal pallor and asymmetric hypothermia suggest vas-
cular injury. Pulses should be palpated. In the upper extremity,
the axillary, brachial, radial, and ulnar pulses should be assessed.
In the lower extremity, the femoral, popliteal, posterior tibial,
and dorsalis pedis pulses should be assessed. Location and direc-
tion of the wound, amount of hemorrhage, and presence of
TRAUMA
hematomas or palpable thrill should be noted.
A neurologic examination that quantifies motor and sensory
deficits is critical. Because of the high metabolic demands
of peripheral nerves, disruption of oxygen delivery makes neu-
ronal cells highly susceptible to ischemic death. Conversely,
skeletal muscle is relatively resistant to ischemia. Loss of sensa-
PART 4
tion or limb paralysis is an alarming sign of impending anoxic
necrosis.
Treatment of Vascular Injuries
All external hemorrhages should be identified during the primary
survey and controlled with direct pressure at the site of injury.
Tourniquets should be applied only when direct pressure fails
to control bleeding or cannot be applied (as while a casualty is
being evacuated by hoist to an aircraft). Tourniquets should be
released every 5 to 10 minutes to attempt to limit ischemia, unless
severe hemorrhage continues when the tourniquet is loosened.
In this case, it should be left tightened. Efforts to control bleed-
ing with pressure should be undertaken. Direct pressure permits
collateral flow to provide some perfusion to the distal extremity.
Hematomas should never be explored or manually expressed
without surgical capability readily available. Attempts to clamp
or ligate vessels are not recommended. Frequent repeat neuro-
vascular examinations are mandatory.
Once bleeding is controlled and the wound is covered with
a sterile but nonconstrictive dressing, completion of the primary
survey, identification and stabilization of associated injuries, and
appropriate resuscitation with normal saline should follow. After
hemostasis is achieved, a nonconstrictive dressing will obviate
the chance for unintended venous outflow obstruction. The
extremity should be splinted to prevent movement. The need
for evacuation depends directly on the results of the physical
examination. Examination results can be grouped into “hard
signs,” indicative of ischemia or continued hemorrhage, and “soft
signs,” suggestive of, but not indicative of, ischemia (Boxes 18-7
and 18-8).
All victims with hard signs should be evacuated emergently.
Based on current data, an isolated soft sign may warrant observa-
tion alone, depending on the remoteness of the expedition and
the risks of evacuation. The data for observation of soft signs
have emerged from hospital settings and must be applied with
great caution in the wilderness. If soft signs are present, clinical
396
BOX 18-7  Vascular “Hard Signs”
Pulsatile bleeding
Palpable thrill
Audible bruit
Expanding hematoma
Six Ps of regional ischemia
  Pain
  Pulselessness
  Pallor
  Paralysis
  Paresthesia
  Poikilothermia
suspicion is high, and evacuation can be accomplished safely,
the victim should be transported and observed in a medical
facility.
Although not feasible in the wilderness, the use of vascular
shunts has been shown to be a viable option for increased limb
salvage without an increasing risk of death.28 Based on recent
military conflict data, the use of battlefield temporary vascular
shunts does not lead to increased limb loss rates.17 Porcine
models have demonstrated safety of temporary vascular shunt
use without increased thrombosis rates within 48 to 72 hours of
placement.29 Additionally, the more proximal the shunt on the
extremity, the better the patency. This is also true of shunted
venous injuries.112
TRAUMATIC AMPUTATION
In the wilderness, amputation victims require immediate evacu-
ation. Hemorrhage is controlled during the primary survey with
direct pressure, and resuscitation is instituted. Tourniquets are
rarely required. The victim should be kept warm and calm. Reas-
surance and analgesics should be administered. Amputations
should be completed only if minimal tissue bridges exist and it
is clear that the neurovascular supply has been interrupted.
Amputation of a mangled extremity, defined as an extremity
with a high-grade open fracture and significant soft tissue injury,
should not be carried out in the wilderness except to free a
trapped victim to avoid further severe injury or even death, or
in the case of uncontrollable hemorrhage threatening the life of
the victim, and then only by experienced surgical personnel. All
other severely injured extremities should be wrapped in available
sterile materials, splinted, and kept moist.
Amputated extremities should be cooled if possible, optimally
in a plastic bag in ice or ice water. Avoid placing the extremity
in direct contact with ice. Without cooling, the amputated extrem-
ity remains viable for only 4 to 6 hours; with cooling, viability
may extend to 18 hours. The amputated extremity should accom-
pany the victim throughout the course of the evacuation.
CRUSH INJURIES AND RHABDOMYOLYSIS
Rhabdomyolysis is a potentially fatal syndrome that results from
lysis of skeletal muscle cells. In its fulminant form, rhabdomyoly-
sis can affect multiple organ systems. Compartment syndrome,
renal failure, and cardiac arrest are the major complications.
Any condition resulting in significant acute or subacute stri-
ated muscle damage can precipitate rhabdomyolysis. Crush inju-
ries of the extremities and pelvis, revascularization of ischemic
tissue, ischemic extremities, animal bite and snakebite, frostbite,
and traumatic asphyxia can all result in rhabdomyolysis in a
wilderness setting. Crush injuries are frequently results of ava-
lanches, falls from heights, or rock slides.
BOX 18-8  Vascular “Soft Signs”
Injury in proximity to major vessel
Diminished but palpable pulses
Isolated peripheral nerve deficit
History of minimal hemorrhage
 The pathophysiology of rhabdomyolysis remains controver- spider bite or mushroom ingestion, both of which can simulate

CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES

sial. The exact mechanism of muscle injury appears not to
be simple direct force or isolated ischemia and is probably mul-
tifactorial. The common cellular derangement is interference of
the normal function of muscle cell membrane sodium-potassium
adenosine triphosphatase with intracellular calcium influx and
cell death through activation of proteases and phospholipases.147
After cell death, multiple intracellular constituents, including
myoglobin, creatine kinase, potassium, calcium, and phosphate,
are released into the systemic circulation.
The metabolic derangements of rhabdomyolysis depend
directly on release of intracellular muscle constituents. Myo­
globinemia, hypercalcemia, hyperphosphatemia, hyperkalemia,
hyperuricemia, metabolic acidosis, coagulation defects, and con-
tracted intravascular volume result.
The clinical presentation of rhabdomyolysis may include
muscle weakness, malaise, fever, tachycardia, abdominal pain,
nausea and vomiting, or encephalopathy. The danger of the
syndrome lies in the cardiovascular effects of electrolyte distur-
bances and renal failure secondary to changes in renal perfusion
and direct toxicity of myoglobin to tubular cells.
Successful treatment relies on prompt diagnosis based on
clinical signs and urinalysis, aggressive hydration, and forced
diuresis. Myoglobin turns urine the color of tea; this is an impor-
tant indicator of significant muscle death and the need for aggres-
sive treatment.
Crystalloid solution should be administered intravenously at
1 to 2 L/hr to achieve a urine output of 100 to 300 mL/hr. Signs
of fluid overload should be monitored. Victims who are trapped
in rubble should have resuscitation initiated before extrication if
possible. The addition of agents to alkalinize the urine and
promote diuresis has been shown to improve clearance of myo-
globin but not to alter survival rates. In addition, diuretics
may be detrimental in multisystem trauma victims who are hypo-
volemic. All victims demonstrating myoglobinuria should be
evacuated.
WILDERNESS SURGICAL EMERGENCIES
In the wilderness it is important to distinguish between a surgical
and a nonsurgical emergency for evacuation purposes. Table
18-2 reviews the differential diagnosis of abdominal pain. Certain
differential diagnoses can be difficult, such as a black widow
an acute surgical abdomen. The key is to identify surgical prob-
lems related to peritoneal inflation and conditions that will need
evacuation and urgent operative intervention. Common genito-
urinary problems that can cause abdominal pain in males include
appendicitis, renal colic, urinary retention, and testicular torsion.
Common genitourinary problems causing abdominal pain in
females include pelvic inflammatory disease, urinary tract infec-
tions, dysmenorrhea, ruptured ovarian cysts, and ectopic preg-
nancy. Pain is the hallmark of the surgical abdomen, and therefore
it is important to obtain an accurate history and physical exami-
nation to determine the nature and onset of pain, and its severity,
location, and precipitating factors. The onset of pain can be
explosive, rapid, or gradual. Explosive agonizing pain is most
common with rupture of a hollow viscus into the peritoneal
cavity. Renal or biliary colic may also cause acute severe pain,
but it is not as excruciating as that with a perforated viscus. Pain
that is of rapid onset and progressively worsens is most often
indicative of acute pancreatitis, mesenteric thrombosis, or small
bowel strangulation. Gradual onset of pain is usually from pro-
gressive peritoneal inflammation, as commonly occurs with
appendicitis or diverticulitis. Unrelenting and excruciating pain
that is unresponsive to narcotics should alert the clinician to an
acute vascular insult, such as a ruptured abdominal aortic aneu-
rysm or intestinal infarction. Vague or poorly localized pain
usually means an inflammatory process of the parietal perito-
neum, as is initially present with appendicitis. Colicky pain with
cramps and rushes is indicative of gastroenteritis. Small bowel
obstruction can also cause colicky pain, but it is more rhythmic
in nature, with pain-free intervals.
Patients who are unable to lie still often have renal or biliary
colic, but those lying perfectly still may have peritoneal inflam-
mation. Auscultation can reveal rushes and tinkles of a small
bowel obstruction or the completely silent abdomen related to
ongoing peritoneal inflammation. Any patient with severe pain
upon shaking or percussing the abdomen, along with nausea,
fever, or vomiting, most likely needs to be evacuated, because
many require surgical intervention.
Volume depletion from both surgical and nonsurgical disease
processes is common in the wilderness. Severe dehydration and
electrolyte depletion can result from vomiting and/or diarrhea,
especially in the later stages of disease and if evacuation has
been delayed. Crystalloid resuscitation in the field should be

TABLE 18-2  Features Considered in the Differential Diagnostic of Abdominal Pain

Associated
Location of Pain and Mode of Onset and Gastrointestinal
Disease Prior Attacks Type of Pain Problems Physical Examination

Acute appendicitis Periumbilical region or
localized generally to right
lower abdominal quadrant
Intestinal Diffuse
obstruction
Perforated Epigastric; history of ulcer in
duodenal ulcer many
Diverticulitis Left lower quadrant; history
of previous attacks
Acute cholecystitis Epigastric or right upper
quadrant; may be referred
to right shoulder
Renal colic Costovertebral or along
course of ureter
Acute pancreatitis Epigastric penetrating to
back
Acute salpingitis Bilateral adnexal; later, may
be generalized
Ectopic pregnancy Unilateral early; may have
shoulder pain after rupture
Insidious to acute and Anorexia common; Low-grade fever; epigastric
persistent nausea and tenderness initially; later, right
vomiting in some lower quadrant pain
Sudden; crampy Vomiting common Abdominal distention;
high-pitched rushes
Abrupt; steady Anorexia; nausea and Epigastric tenderness; involuntary
vomiting guarding
Gradual; steady or Diarrhea common Fever common; mass and
crampy tenderness in left lower quadrant
Insidious to acute Anorexia; nausea and Right upper quadrant pain
vomiting
Sudden; severe and Frequently nausea Flank tenderness
sharp and vomiting
Acute; persistent, dull, Anorexia; nausea and Epigastric tenderness
severe vomiting common
Gradually becomes Nausea and vomiting Cervical motion elicits tenderness;
worse may be present mass if tuboovarian abscess is
present
Sudden or intermittently Frequently none Adnexal mass; tenderness
vague to sharp

397

A to an hour, and then abates. It is occasionally associated with
B floxacin 750 mg twice a day) to cover gram-negative enteric
FIGURE 18-13  A, OPTION-vf (female) catheter. B, OPTION-vm (male)
catheter. (Courtesy Practica Medical Manufacturing, Inc, Dublin, Ohio.)
initiated to counteract potential sepsis and hypovolemic shock.
Decompressing the stomach with a NG tube may alleviate severe
nausea and vomiting if antiemetics are ineffective, which is often
the case with a small bowel obstruction. Confirmation of proper
placement of a NG tube is made by aspirating gastric contents
TRAUMA
or oscillating gastric air when one insufflates the stomach through
the tube. Monitoring the urine output is a good estimate of intra-
vascular volume status. Therefore, placing an indwelling urinary
catheter in circumstances of major volume depletion may be
helpful to determine the adequacy of the resuscitation (Figure
18-13). Portable ultrasound can also be used to diagnose certain
PART 4
intraabdominal conditions and is valuable in determining the size
of the vena cava as an estimate of intravascular volume.
ACUTE APPENDICITIS
About 7% of people have a chance of developing acute appen-
dicitis during their lifetime.1 In normal circumstances, early diag-
nosis and definitive surgical treatment result in a low complication
rate. In the wilderness, however, delayed diagnosis or late pre-
sentation can cause severe illness and sepsis. It is important to
carefully assess and evacuate the patient early if acute appendi-
citis is suspected. The most common differential diagnosis with
acute appendicitis is mesenteric adenitis, which is often preceded
by an upper respiratory tract infection and associated with vague
abdominal pain beginning in the right lower quadrant. Pelvic
inflammatory disease in young women usually occurs within a
week of menses. With gastroenteritis, vomiting often precedes
abdominal pain and is often associated with diarrhea.
Clinical presentation of acute appendicitis revolves around the
associated abdominal pain. Classically, the pain is initially achy
in nature and located in the periumbilical area. As the disease
progresses, the pain becomes sharper and localized in the right
lower quadrant. It is associated with fever, anorexia, and malaise.
In later stages, the patient often remains still, occasionally with
the right hip flexed, complaining of pain on passive hip exten-
sion (psoas sign). The patient may have indirect tenderness in
the right lower quadrant upon palpation of the left lower quad-
rant. As mentioned, if acute appendicitis is suspected, evacuation
is required to avoid perforation. Once the appendix is ruptured,
the patient develops generalized peritonitis and abdominal rigid-
ity. Initial field treatment of appendicitis includes IV hydration
and initiation of broad-spectrum antibiotics covering anaerobic
and gram-negative bacteria (e.g., cefoxitin 2 g, or piperacillin-
tazobactam 3.375 g). If only oral antibiotics are available, a fluo-
roquinolone, such as oral ciprofloxacin 750 mg twice a day, is
recommended.
398
ACUTE CHOLECYSTITIS AND BILIARY COLIC
About 15% of the population develops gallstones, but only about
25% develops biliary colic. An even smaller percentage of these
patients develop acute cholecystitis or gallstone pancreatitis.
Biliary colic occurs when a gallstone obstructs the neck of the
gallbladder. The pain is usually constant and aching, and
the patient often states that similar episodes have occurred in the
past. The pain is mostly localized in the right upper quadrant or
epigastric region, and radiates to the right scapula and back. This
type of pain often follows a spicy or fatty meal, usually lasts up
nausea and vomiting but usually not with fever. In this circum-
stance, evacuation may not be necessary unless the condition
advances to acute cholecystitis, which occurs when the stone
obstructs the duct and the gallbladder becomes inflamed. In this
circumstance, the pain often persists for more than an hour and
is accompanied by fever, tachycardia, and worsening right upper
quadrant pain. Acute cholecystitis requires evacuation and often
hospitalization, because it can progress to gangrenous changes
and perforation, or cholangitis and gallstone pancreatitis. Initial
management is IV hydration and broad-spectrum antibiotics (e.g.,
IV piperacillin-tazobactam 3.375 g every 6 hours, or oral cipro-
bacteria and Streptococcus species.27
PEPTIC ULCER DISEASE
Peptic ulcer disease is on the decline in the United States, espe-
cially with the advent of acid-reducing agents and the treatment
of Helicobacter pylori infection. Duodenal ulcer perforation is a
serious complication and should be in the differential diagnosis
of upper abdominal pain in the wilderness. Patients often have
a history of peptic ulcer disease, which is much more common
in males than females. The use of nonsteroidal antiinflammatory
drugs and smoking are the most common risk factors. These
patients have an acute onset of constant epigastric pain that radi-
ates to the midback. There is tenderness and tympany of the
upper abdomen. Signs of peritonitis mandate evacuation. Tem-
porizing measures may include insertion of a NG tube and
administration of broad-spectrum antibiotics and a proton pump
inhibitor. If the perforation is anterior, the patient more often
develops peritonitis; posterior perforation causes upper gastroin-
testinal bleeding. The differential diagnosis may include pancre-
atitis, acute cholecystitis, myocardial infarction, or a perforated
viscus.
DIVERTICULITIS
Most patients with diverticulitis remain asymptomatic. Patients
that present with uncomplicated diverticulitis usually have non-
specific symptoms, including vague, colicky, left lower quadrant
abdominal pain. Diverticulitis can involve the entire lower
abdomen and is occasionally associated with diarrhea and fever.
Classically, the patient is in moderate discomfort with left lower
quadrant pain with or without localized guarding. Perforation
and abscess formation can present with minimal symptoms if the
perforation is contained in the retroperitoneum. However, if the
perforation extends into the peritoneal cavity, it can present with
generalized peritonitis. Treatment in the wilderness for diverticu-
litis includes hydration, bowel rest, and broad-spectrum antibiot-
ics; if evacuation is delayed, IV antibiotics covering gram-negative
enterics and anaerobes are given. Oral antibiotic coverage with
ciprofloxacin and metronidazole may be adequate for mild cases
of diverticulitis. Because of the unpredictable response to anti-
biotics and potential for progression, evacuation is most often
indicated when patients develop diverticulitis.
MECHANICAL SMALL BOWEL OBSTRUCTION
Small bowel obstruction is a common surgical condition; in the
wilderness, it is a true emergency. The most common cause is
postoperative adhesions, followed closely by an incarcerated
abdominal wall incisional hernia. The clinical presentation varies
between patients according to the level of obstruction, the time
course, and the presence of or potential for strangulation. Initially
there may be hyperperistalsis as the bowel attempts to overcome
the obstruction with proximal dilation. This leads to acute diffuse
crampy abdominal pain, which can be associated with vomiting
and obstipation. Late physical findings include a very distended
tympanitic abdomen; many liters of fluid may be sequestered in
the abdominal cavity and within the bowel wall, causing signifi-
cant dehydration. If the process progresses to strangulation of
the bowel, the result may be fever, tachycardia, and subsequent
peritonitis from a perforation. Therefore, it is important to identify
impending or actual strangulation, because the patient requires
immediate evacuation and emergent operative intervention. In
the interim, NG decompression and IV hydration should be initi-
ated. Serial examinations of the abdomen are important to note
any changes in symptoms. The colicky pain can become local-
ized and constant, or signs of peritonitis may develop.
INCARCERATED ABDOMINAL WALL DEFECT
Most incarcerated hernias developing in the wilderness will be
in the inguinal region, followed by incisional and umbilical
hernias. Many patients had previously been aware of the asymp-
tomatic bulging hernia. New or known hernias that cannot be
reduced are concerning. Constant point tenderness, especially
when associated with vomiting, fever, and tachycardia, is indica-
tive of incarceration and potential strangulation. Physical exami-
nation shows a palpable tender groin or scrotal mass for inguinal
hernias. The differential diagnosis for a tender groin mass includes
lymphadenopathy, testicular torsion, and epididymitis. A painful
mass below the inguinal ring is highly suspicious of a femoral
hernia. Other areas of potential incarceration or strangulation
include a painful mass at the site of an abdominal wall incision
or at the umbilicus. The bowel that becomes incarcerated within
the hernia sac can progress to necrosis within 3 to 5 hours; the
decision to evacuate the patient depends greatly on whether the
hernia can be reduced. Any patient with an incarcerated hernia
and signs of toxicity must be evacuated immediately. A newly
incarcerated hernia without contraindication can be reduced by
personnel who are experienced in this technique. This includes
gentle pressure that is exerted on the hernia mass. If the incar-
ceration is in the inguinal region, the patient should be lying flat
with hips elevated. This technique can also be attempted with
incarcerated umbilical or incisional hernias in the early stages of
obstruction. Analgesia and sedation are helpful adjuncts in assist-
ing with attempts at reduction.64 An absolute contraindication to
attempts at reduction includes the presence of a femoral hernia
or any signs of intestinal ischemia or necrosis where the mass is
exquisitely tender and the overlying skin may be erythematous
and warm to the touch. These patients require emergent evacu-
ation and early operative intervention.3
ANAL FISSURE AND HEMORRHOIDS
An anal fissure is a superficial, linear tear in the anoderm distal
to the dentate line. It is often associated with constipation and
passage of hard stools or anal trauma (Figure 18-14). Patients
complain of severe pain during a bowel movement that continues
for several minutes to hours and recurs after each bowel move-
ment. About 70% present with bright-red blood on the toilet
paper. Most occur in the posterior midline. First-line treatment
includes relief of constipation with stool softeners and fiber
supplements, along with hydration. Mineral oil (15 mL twice a
day), along with warm sitz baths after bowel movements, helps
lubricate the stool and reduce pain. Second-line treatment
includes topical analgesics such as 1% to 3% lidocaine jelly and,
if available, topical nitrates (0.4% nitroglycerin ointment) or
calcium channel blockers (e.g., 2% diltiazem ointment) directly
applied to the internal sphincter to relieve the pain associated
with sphincter spasm.
A hemorrhoid is an abnormal dilated venous plexus that can
protrude from the anus. Most patients are aware of the problem
before the excursion. The condition can be first recognized or
exacerbated by constipation. Symptoms include severe itching
and discomfort. Hemorrhoids can be very painful if prolapsed or
CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
FIGURE 18-14  Anal fissure.
thrombosed. Blood may be noted on the toilet paper after a hard
bowel movement. If a hemorrhoid becomes bothersome in the
field, begin measures to soften and lubricate the stool with hydra-
tion, stool softeners, and mineral oil. Avoid bearing down during
a bowel movement, take a sitz bath several times a day, and use
hemorrhoidal suppositories or creams.
These lesions often present as dark, firm, tender purple
nodules protruding from the anal opening, or they can be pal-
pated within the anal canal. Small thrombosed hemorrhoids often
resolve spontaneously. Those greater than 2.5 cm in diameter
may require incision and evacuation of the clot to relieve pain.
Wash the anal area with soap and water and provide local or
topical analgesia if available. Pressing ice against the nodule can
provide effective analgesia. Incision on the top of and into the
thrombosed hemorrhoid and evacuation of the clot often causes
dramatic relief of pain. The incision should be left open and
abdominal pads placed to absorb drainage. Warm sitz baths for
the next several days will improve symptoms.66
UROLOGIC EMERGENCIES
RENAL COLIC
Renal colic is a symptom complex resulting from acute obstruc-
tion of the urinary tract secondary to calculus formation. The goal
of the wilderness physician is to recognize the symptom complex
and institute treatment. After obstruction of the urinary tract, the
pain crescendo of renal colic begins in the flank. The pain pro-
gresses anteriorly over the abdomen and radiates to the groin
and testes in men and labia in women. Because the autonomic
nervous system transmits visceral pain, many abdominal com-
plaints may manifest. Nausea and vomiting are common. With
severe colic, the victim writhes in pain and is unable to find a
comfortable position. Diagnosis in the wilderness is assisted by
the presence of gross hematuria.
Management of ureteral colic is pain control. Although almost
universally deployed, forced diuresis may reduce ureteral peri-
stalsis. Thus, forced oral fluids or aggressive IV hydration is of
questionable benefit.142 Most calculi pass spontaneously in 4 to
6 hours. The goal of management is to control pain until passage
of the stone has occurred. A number of pharmacologic approaches
may be used. Nonsteroidal antiinflammatory drugs such as
ibuprofen and ketorolac have been effective for management
of renal colic. For symptoms uncontrolled by antiinflammatory
agents, narcotics may be added. Narcotic analgesics are most
effective if given parenterally; however, agents such as meperi-
dine, codeine, and hydromorphone may be given orally. Antiin-
flammatory agents and analgesics can be combined. An antiemetic
may be added to relieve nausea. When administering pain medi-
cation in the field, particular attention should be given to airway
399
 maintenance, induced nausea, and vomiting.138 Any person
whose symptom complex cannot be controlled must be evacu-
ated. Additional indications for evacuation include calculus
anuria, evidence of obstruction-induced infection, and signs of
systemic infection.
URINARY RETENTION
Urinary retention is a painful experience in which the patient is
unable to voluntarily urinate. This condition requires immediate
medical, and sometimes surgical, intervention.123,141 Causes of
urinary retention can be categorized as obstructive, infectious,
inflammatory, pharmacologic, or neurologic.123 Twenty-three
percent of men reaching 80 years of age will experience acute
retention at some time.19 Acute urinary retention can lead to
incapacitating symptoms in the wilderness; prompt recognition
and intervention are necessary and can be addressed with limited
resources.136
Principal symptoms are bladder distention and pain that may
mimic acute abdomen, overflow incontinence, dribbling, and
hesitancy. Physical examination findings include prostatic enlarge-
ment in men and lower midline abdominal tenderness and
distention. If painful distention of the bladder is present, decom-
pression should be undertaken.
Medical therapy may be considered before complete obstruc-
tion to urinary flow. Third-generation α-adrenergic blockers may
provide some relief. The α-adrenergic blockers such as terazosin
promote bladder neck and prostatic urethral relaxation.59
Bladder decompression should be initially attempted with a
standard Foley catheter. In men with prostatic hypertrophy,
passage of the catheter may be challenging, and a large catheter
or coudé catheter should be used if a standard Foley catheter
TRAUMA
cannot be passed.123 Instrumentation of the urethra with hemo-
stats or dilators is dangerous and should not be attempted in the
field.
There are several valved urinary catheters that eliminate the
need for the urine drainage bags and connecting tubes normally
required with Foley catheters. These catheters incorporate a
PART 4
manually activated valve at the end of the catheter that allows
the patient to store urine in the bladder and to mimic normal
voiding behavior.141 The catheters may be used with a continuous
drainage adapter when appropriate, so that a bag may be placed
and the urination rate and volume assessed.
If multiple attempts are unsuccessful and symptoms are
severe, needle decompression is indicated. The skin of the supra-
pubic region should be anesthetized, if possible. The distended
bladder is palpated to guide aspiration. If ultrasound is available,
it can be used to guide the decompression. A 22-gauge needle
attached to a syringe is introduced through the skin of the lower
abdomen two fingerbreadths above the pubic symphysis and
directed at the anus. The needle is advanced with simultaneous
aspiration of the syringe until free-flowing urine is visualized.
Palpation of the bladder in combination with adherence to this
technique should lead to successful decompression.
Complications related to decompression can occur. Drainage
of more than 300 mL/hr can induce mucosal hemorrhage. A small
number of victims develop obstructive diuresis that may lead to
dehydration, in which case aggressive oral hydration or crystal-
loid repletion should be undertaken.105 Finally, surgical decom-
pression is temporizing, and retention will recur. Treatment may
need to be continued or repeated. Drainage of the bladder
acutely relieves symptoms and may allow ambulatory evacuation,
but the underlying cause must be addressed once the patient is
undergoing definitive care.
ACUTE SCROTUM
Acute onset of scrotal pain and swelling requires immediate
attention. Causes are multiple, but the three that should be con-
sidered as soon as possible are incarcerated hernia, testicular
torsion, and necrotizing infection. Although any one aspect of
the history and physical examination may not be diagnostic,
when all aspects are taken as a whole, they frequently suggest
the cause of the scrotal pathology.36
400
Testicular torsion can occur at any age, but it is more likely
near puberty. The likelihood of testicular salvage is inversely
proportional to the elapsed time from torsion; this is a true surgi-
cal emergency. Acute onset of severe testicular pain is the hall-
mark. Mild to moderate pain is more suggestive of torsion of a
testicular appendage or epididymitis. It has been stated that
victims who can ambulate with minimal pain are less likely to
have testicular torsion. In addition, nausea and vomiting may
accompany torsion, whereas fever, dysuria, and frequency are
associated with epididymitis.
Physical examination reveals a patient in extreme discomfort
with a swollen scrotum and a tender testicle; the affected testicle
may be higher than normal and have a horizontal lie.36 Scrotal
skin may be edematous and discolored. Unilateral scrotal swell-
ing without skin changes is more indicative of a hernia or hydro-
cele. In testicular torsion, the affected testis is often larger than
the unaffected testis. Prehn’s sign (relief of pain accomplished
by elevation of the testicle) may be helpful to some degree in
differentiating testicular torsion from acute epididymitis.119 With
torsion, which twists the spermatic cord and elevates the testicle,
pain is not relieved by elevation (negative Prehn’s sign); with
epididymitis, pain is relieved by elevation (positive Prehn’s sign).
This maneuver has low sensitivity in distinguishing the two con-
ditions, but may be helpful in conjunction with other findings.119
Treatment consists of surgical detorsion, which should be
accomplished within 12 hours of torsion.36 Manual detorsion is
not the treatment of choice; however, remoteness of the wilder-
ness environment may mandate manual attempts. Studies of
manual detorsion are scant and the cohorts small.36
If manual detorsion is necessary, the victim should be placed
supine. The procedure can be assisted with IV sedation with or
without local anesthetic. Classic teaching has suggested that tes-
ticular torsion typically occurs in the medial direction. Therefore,
detorsion is initially attempted with outward rotation of the testis
(toward the ipsilateral thigh). Simultaneous rotation in the caudal
to cranial direction may be necessary to release the cremasteric
muscle.114
The surgical treatment of testicular torsion includes pexing the
testes to prevent recurrent torsion. Thus, although detorsion may
be a temporary treatment for an acute situation in the field, all
victims must be evacuated for definitive treatment.
PROSTATITIS
A number of forms of prostatitis have been defined, including
viral, bacterial, nonbacterial, and chronic forms. The acute bacte-
rial form may potentially lead to severe infection.
Bacterial prostatitis is an infection of the prostate caused pri-
marily by gram-negative bacteria, with 80% attributable to Esch-
erichia coli. It is an acute, febrile illness characterized by perineal
pain radiating to the low back, chills, malaise, and voiding symp-
toms, such as urgency, frequency, and dysuria. Urinary retention
is common, and cystitis frequently accompanies the infection. On
rectal examination, the prostate gland is usually boggy, warm,
and tender, and enlargement is variable.
In an ideal situation, treatment is individualized to the cause,
which may be difficult to discern in the wilderness. The infection
may respond to an oral antibiotic such as ciprofloxacin (750 mg
orally twice a day), ampicillin (500 mg orally 4 times a day), or
trimethoprim (160 mg) with sulfamethoxazole (800 mg) orally
twice a day. Penetration of prostatic secretions has been shown
to be best achieved by trimethoprim/sulfamethoxazole. The
chosen antibiotic should be administered for 30 days. If retention
is present, catheterization or suprapubic aspiration should be
undertaken.
Acute bacterial prostatitis can escalate in severity to systemic
toxicity. Persons with evidence of systemic toxicity unresponsive
to a trial of oral or parenteral antibiotic therapy should be
evacuated.
URINARY TRACT INFECTION
Urinary tract infections (UTIs) are extremely common and in-
clude episodes of acute cystitis and pyelonephritis occurring in
otherwise healthy individuals. These infections predominate in
women; approximately 25% to 35% of women 20 to 40 years of
age report having had a UTI. Conversely, men between the ages
of 15 and 50 years rarely develop UTI.
Despite the striking difference in prevalence, symptoms are
similar in men and women. The symptoms may represent ure-
thritis, cystitis, or an upper UTI; the distinction is often difficult.
Common symptoms include frequency, urgency, dysuria, supra-
pubic pain, flank pain, and hematuria. Flank pain with tender-
ness to percussion suggests pyelonephritis. On urinalysis, pyuria
is nearly invariably present, and hematuria may assist in the
diagnosis. The definitive diagnosis is based on significant bacte-
riuria. The leukocyte esterase test has a screening sensitivity of
75% to 96% and a specificity of 94% to 98% in detecting more
than 10 leukocytes per high-power field.70
Treatment in the wilderness setting for both men and women
should be directed at the most common causative agents,
although 50% to 70% of cases resolve spontaneously if untreated.
Causative bacteria include E. coli (70% to 95%); Staphylococcus
species (5% to 20%); and, less frequently, Klebsiella, Proteus, or
Enterococcus. Fortunately, oral antibiotics are highly effective.
Although resistant E. coli strains are being reported, trimethoprim/
sulfamethoxazole is an excellent first-line drug. Alternative
regimens include nitrofurantoin, a fluoroquinolone, or a third-
generation cephalosporin. A 3-day course of therapy has been
shown to be more effective than single-dose therapy.70 For pyelo-
nephritis, a similar antibiotic in a 10-day course is an acceptable
initial treatment. Evacuation should be reserved for systemic
toxicity unresponsive to oral antibiotics.
SKIN AND SOFT TISSUE INFECTIONS
A variety of conditions ranging from minor skin infections to
localized abscesses to necrotizing soft tissue infections can occur
in any austere environment. The nomenclature has recently been
changed to acute bacterial skin and skin structure infections
(ABSSSIs).107 The vast majority of these superficial skin infections
are self-limited. However, some can progress to a systemic condi-
tion and in a few cases be life-threatening, requiring emergency
surgical treatments. Coagulase-positive Staphylococcus aureus is
the predominant organism present in skin and soft tissue infec-
tions. Coagulase-negative organisms, such as Staphylococcus
epidermidis, have lower virulence and are a less common cause
of infection in healthy people. Of the Streptococcus species, it
is the beta-hemolytic group that is primarily responsible for
severe infections and sepsis. Other clinically important organisms
are anaerobic gram-negative rods, such as Clostridium per­
fringens, and gram-negative bacilli, such as Pseudomonas
aeruginosa.
CELLULITIS
Cellulitis is acute infection of the dermis and subcutaneous tissue
that causes erythema, pain, and swelling of the affected area.
There are often well-demarcated borders that advance as the
infection worsens. The most common cause of cellulitis in the
wilderness is trauma. It is important to mark the boundaries of
the erythema and monitor its progress. Rapid advancement
A B
FIGURE 18-15  A, Two incisions are placed approximately 1 inch apart to allow the loop technique for
abscess drainage. B, The rubber is tied off to create a loose loop. (From Auerbach PS. Medicine for the
outdoors: the essential guide to first aid and medical emergencies, ed 6, Philadelphia, 2016, Elsevier.)
despite treating with antibiotic therapy could be related to an
CHAPTER 18  WILDERNESS TRAUMA AND SURGICAL EMERGENCIES
underlying soft tissue infection that may need surgical interven-
tion. In most circumstances, treatment for cellulitis is wound
hygiene and skin flora coverage with antibiotic therapy directed
at the most common pathogen, which is group A S. aureus.
Methicillin-resistant S. aureus (MRSA) is an increasingly common
infection in the field; it is discussed in further detail later in this
chapter. It is important to regularly examine the affected area
and determine if there is fluctuance or swelling that would indi-
cate an underlying subcutaneous abscess requiring surgical
drainage.
LYMPHANGITIS
Lymphangitis is infection of the subcutaneous lymphatic system
and often follows a puncture wound, commonly in the hand
from an animal bite. This entity causes linear erythematous
streaks along the lymphatic drainage basin of the wound. The
treatment is antibiotics, moist soaks, immobilization, and eleva-
tion of the affected limb. Broad-spectrum antibiotics covering
gram-positive bacteria are important; often a combination of a
fluoroquinolone to cover Staphylococcus and penicillin to cover
Streptococcus is necessary to treat this entity.
CUTANEOUS ABSCESS
If left untreated, many of the superficial infections described
previously can convert to an abscess, which is a localized col-
lection of exudate contained within a membrane. These abscesses
tend to “point” to the nearest epithelial surface, which is pre-
dominately the skin. Physical examination shows a raised fluctu-
ant mass with overlying warmth and erythema. The mainstay of
treatment for subcutaneous abscess is incision and drainage.
Local anesthesia administered as a field block before the incision
may aid with pain relief. The mass should be incised in the line
of the tissue planes over the area of maximum fluctuance. The
incision should be large enough to adequately drain the cavity.
All of the purulent material should be evacuated and the cavity
copiously irrigated with saline or water. Also, finger fracturing of
internal cavities is important to ensure adequate drainage. If
packing is performed, it is important to not pack too tightly to
avoid surrounding ischemia and pain. Not all abscesses require
packing, but they should be frequently irrigated and the dress-
ings changed. The wound should be covered with a sterile dress-
ing. Another option that might work is to use an incision/
counterincision technique where two incisions are made to enter
the abscess cavity so that an irrigation path is created. Irrigation
of sterile solution can be flushed through both incisions until the
purulent material is evacuated. A Penrose or other rubber drain
can be inserted that traverses both incisions, and the ends tied
together to create a moveable loop (Figure 18-15).
COMMUNITY-ACQUIRED METHICILLIN-RESISTANT
STAPHYLOCOCCUS AUREUS INFECTIONS
Staphylococcus aureus is the most common cause of skin and
soft tissue infections. About a third of healthy people are colo-
nized with Staphylococcus bacteria, which live in the nose and
401

A Myiasis is infestation of the skin by developing larvae (maggots)
B as mafenide acetate, Dakin’s solution (diluted sodium hypochlo-
FIGURE 18-16  Cutaneous MRSA infection.
on the skin of humans. About 2% of the population is colonized
TRAUMA
with community-acquired S. aureus (CA-MRSA), which is resis-
tant to beta-lactam antibiotics. CA-MRSA can spread by contact
with an infected person or by exposure to a contaminated object
or surface. Sharing personal items, such as towels or razors, is a
common mode of spread.
About 80% of MRSA infections involve the skin and soft tissue
PART 4
(Figure 18-16). MRSA infection can also involve bones and joints,
leading to severe sepsis. Outbreaks have been reported during
wilderness excursions. Areas of skin violation that are most vul-
nerable include lacerations, burns, blisters, abrasions, and insect
bites. Areas of increased body hair, such as the buttocks, axillae,
back of the neck, and beard, are more likely to be infected. The
most frequent presenting sign is a red, swollen, painful lesion
resembling an infected spider bite. Subsequent yellow or white
central pustules or boils may drain spontaneously. The spectrum
of CA-MRSA infections includes cellulitis, furuncles, carbuncles,
and cutaneous abscesses.
CA-MRSA has been found in 75% of cutaneous abscesses in
the community. The mainstay of treatment is adequate drainage.
Oral antibiotics that have been effective include clindamycin and
trimethoprim/sulfamethoxazole. These infections can occasion-
ally disseminate and become life-threatening, with associated
bacteremia, septic arthritis, or endocarditis. Avoidance of dis-
semination is best accomplished with preventive measures,
which include washing the hands on a regular basis, using a
hand sanitizer with 60% alcohol, wearing long pants and protect-
ing the skin from injury, and not sharing personal items such as
towels and clothing. If skin injuries occur, keep them covered
and clean and report all suspected skin infections promptly.42,132
These life-threatening conditions are caused by virulent toxins
produced by bacteria, the most common being group A beta-
hemolytic Streptococcus, with or without Staphylococcus present.
Frequently these infections are caused by multiple mixed flora
of both anaerobic and facultative aerobes, especially C. perfrin-
gens and Bacteroides. The depth of tissue involvement may
include subcutaneous tissue, fascia, or even muscle. These infec-
tions most commonly occur in the extremities, abdominal wall,
or perineum and occur within a week of the inciting event.
Necrotizing infections occur with increased frequency in immu-
nosuppressed patients, including those with diabetes, peripheral
vascular disease, and chronic renal failure; drug abusers; and
persons of advanced age. The area of cellulitis spreads progres-
402
sively, which causes pain and fever with spreading erythema,
induration, blue-black discoloration, and blister formation. The
extent of infection often exceeds what is evident from the skin.
Treatment in the wilderness is limited. An experienced provider
may want to consider debriding as much visible necrotic tissue
as possible while plans for immediate evacuation are initiated.
Administration of IV broad-spectrum antibiotics is necessary, and
evacuation must be done expeditiously because time is of the
essence and the mortality rate is extremely high.120
WOUND MYIASIS (MAGGOT INFESTATION)
of a variety of species of the arthropod order Diptera. The two
main clinical types are furuncular (follicular) myiasis and wound
myiasis. Fly larvae may infest open wounds in a living host.
Myiasis is usually self-limited with minimal morbidity in most
cases but can be complicated by wound cellulitis. The diagnosis
is typically made by identifying the larvae in an open wound.
Severe cases may be associated with fever, chills, bleeding from
the infested site, and secondary infection. Treatment requires
removal of the maggots, which is accomplished by irrigation and
debridement of dead host tissue. Local anesthesia may be
required and the wound should be packed with a broad-spectrum
topical antimicrobial in a wet-to-dry dressing, using agents such
rite), or 0.25% acetic acid.54,126
STERILITY IN THE AUSTERE
ENVIRONMENT
One of the major disadvantages of operative procedures in the
austere environment is inability to sterilize instruments and estab-
lish a sterile field. The goal is to decrease the risk for bacterial
contamination as much as possible.
Antiseptics are agents used to decontaminate skin. Chlorhexi-
dine is an antiseptic with excellent antimicrobial activity and
prolonged length of activity. In many health care facilities,
chlorhexidine has replaced iodophors as the antiseptic of choice.
Isopropyl alcohol may be used if no other antiseptic is available.
It is particularly ineffective on dirty skin and has little persistent
activity. If nothing is available, soap and water may be of benefit.
Soap removes unattached bacteria from the surface of skin, but
does not remove adherent bacteria.
If sterile fluid is not available for wound irrigation, potable
water may be used. Boiling water before irrigation does not rid
the water of spores. If water is to be boiled, the boiling should be
“rolling” for 20 minutes to be effective. Any fluids used should
be removed from the wound as best as possible. Wounds should
be managed to ensure that no devitalized tissue or foreign bodies
remain in them.
If preparations are made for the possibility of surgical proce-
dures during an expedition, instruments taken into the field
should be packed sterile in durable containers. Paper wrappers
can become perforated, permitting contamination. A disinfectant
is an agent that will decontaminate inanimate objects. If surgical
instruments are not sterile, disinfectants can be used to decrease
the bacterial count on the surface. Of course, all instruments
should be clean of debris. Unfortunately, many of the disinfec-
tants used in health care facilities are not practical for the austere
environment. Ortho-phthaladehyde, peracetic, and glutaralde-
hyde are effective disinfectants, but hazardous for personnel and
the environment and impractical in the field environment.43 The
antiseptic chosen, such as chlorhexidine, for skin preparation
may be applied to the instruments.
Placing instruments into boiling water decreases the bacterial
count but will not completely eliminate bacterial spores. Apply-
ing flame to instruments may kill bacteria but leave products of
combustion on the instruments that are then left in the wound
as foreign material.
The U.S. Army has developed a field sterilization system that
is lightweight and does not require an external energy source.
The system is the size of a suitcase and has the capacity to
accommodate a surgical tray. A mixture of water and dry reagents
controllably generates chlorine dioxide. The chlorine dioxide
kills all vegetative cells and bacterial spores within 30 minutes.43
Although the specific system used by the army may not be avail-
able to the public, there are a number of commercially available
products that can be easily found on the Internet for the purpose
of field sterilization.
ANESTHESIA IN THE WILDERNESS
Local and regional anesthesia will be the techniques of choice
to provide comfort during minor operative procedures. General
anesthesia should not be considered without a full complement
of trained personnel and equipment. Procedural sedation
and analgesia may be used with the availability of adequate
monitoring, and the capability of establishing a definitive airway
should be immediately available. Common agents used to sup-
plement local or regional anesthesia are opioids and benzodiaz-
epines. Should these agents be used, reversal agents of naloxone
and flumazenil should be available. Ketamine is an excellent
agent for providing dissociative sedation and pain reduction.
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403.e3

CHAPTER 19 
Emergency Airway Management
ANDREW J. EYRE AND CALVIN A. BROWN III
Emergency airway management skills are crucial in the care of
critically ill or injured patients. Airway management consists of
a structured patient assessment, methodical approach, and effec-
tive oxygenation and ventilation, typically by inserting a cuffed
endotracheal tube. Effective airway management takes prece-
dence over all other clinical considerations.
In resource-limited, austere environments, airway manage-
ment is by definition challenging. Many resources that are readily
accessible in a hospital or emergency department setting are
not available in remote settings. Improvisation may prove
invaluable.
AIRWAY ANATOMY
The airway consists of the mouth, nasal and oral cavities, pharynx,
nasopharynx, hypopharynx, glottis, and tracheobronchial tree
(Figure 19-1). It begins at the oral and nasal apertures. The nasal
cavity extends from the nostrils to the posterior nares (i.e.,
choanae). Due to anatomic features (e.g., turbinates), resistance
to nasal airflow is approximately twice that of oral airflow. The
nasopharynx extends from the posterior nasal cavity to the level
of the soft palate. Primary impediments to airflow through the
nasopharynx are the tonsils. The oral cavity is bounded by the
teeth anteriorly, the hard and soft palates above, and the tongue
and floor of the mouth below. The oropharynx communicates
with the oral cavity and nasopharynx and extends from the soft
palate to the tip of the epiglottis.
The oropharynx continues into the hypopharynx, which
extends from the epiglottis to the upper border of the cricoid
cartilage (level of the C6 vertebral body). The larynx connects
the laryngopharynx and trachea, and serves as the organ of
phonation. The larynx and epiglottis serve to protect the lower
airway from aspiration. The larynx is made up of muscles, liga-
ments, and cartilages (i.e., thyroid, cricoid, arytenoids, cornicu-
lates, and epiglottis).
The epiglottis is flexible. It originates from the hyoid bone
and base of the tongue and covers the glottis during swallowing.
During laryngoscopy, the epiglottis is an important landmark
because it serves as a guidepost for the glottic inlet and laryn-
goscopic blade placement. The vallecula is the space at the base
of the tongue that is bounded posteriorly by the epiglottis and
CHAPTER 19  Emergency Airway Management
anteriorly by the anterior pharyngeal wall. The base of the val-
lecula contains the hyoepiglottic ligament. This structure is key
to successful visualization during direct laryngoscopy with a
curved blade. Engaging the hyoepiglottic ligament with the
bulbous end of a MacIntosh laryngoscope blade elevates the
epiglottis and reveals the glottic aperture. Failure to fully engage
the hyoepiglottic ligament can result in a poor glottic view and
intubation failure. The laryngeal inlet is the opening to the larynx
that is bounded by the epiglottis, aryepiglottic folds, and aryte-
noid cartilages. The glottis is the vocal apparatus. The glottis
consists of the true and false vocal cords and glottic opening
(i.e., the triangular fissure between the vocal cords and the nar-
rowest segment of the adult larynx).
Externally identifiable landmarks are important for airway
assessment and management (Figure 19-2). The mentum is the
anterior aspect of the mandible that forms the tip of the chin.
The hyoid bone forms the base of the floor of the mouth. The
thyroid cartilage forms the laryngeal prominence (Adam’s apple)
and thyroid notch. The cricoid cartilage, which lies inferior to
the thyroid cartilage, forms a complete ring that provides struc-
tural support to the lower airway. The cricothyroid membrane
lies between the thyroid and cricoid cartilages and serves as an
access point during surgical airway management.
Knowledge of anatomic differences between adults and
infants is integral to effective pediatric airway management.
These important differences are summarized in Table 19-1 and
Figure 19-3.
THE DECISION TO INTUBATE
A decision to intubate is based on three criteria: (1) failure to
maintain or protect the airway, (2) failure of ventilation or oxy-
genation, and (3) the patient’s anticipated clinical course and
likelihood of deterioration.23
FAILURE OF AIRWAY PROTECTION
A patent airway is essential for ventilation and oxygenation. If a
patient is unable to maintain an unobstructed airway, the pro-
vider should establish patency by repositioning, performing a
chin lift and/or jaw thrust, or inserting an oral or nasopharyngeal
403
 Nasal
cavity
Nasopharynx
Oral
cavity
Oropharynx
Vallecula
Laryngeal inlet
Laryngopharynx
Epiglottis
Glottis
Larynx
FIGURE 19-1  Lateral airway anatomy.
airway. The patient must be able to protect against aspiration of
gastric contents. The presence of a gag reflex is neither sensitive
nor specific for predicting the need for intubation. A patient’s
ability to swallow or handle secretions is a more reliable indica-
tor. The recommended approach is to evaluate the patient’s
mental status, phonation, response to verbal commands, and
ability to manage secretions. If a patient has pooling secretions,
has difficulty phonating, is comatose, or cannot respond to
TRAUMA
simple verbal cues, the patient likely cannot adequately protect
against aspiration. Intubation is required. In most patients, if a
maneuver for establishing an airway is needed, definitive airway
management is also required.
FAILURE OF VENTILATION OR OXYGENATION
PART 4
Oxygen is required for vital organ function. Removal of carbon
dioxide (i.e., ventilation) is equally as important. Cardinal indica-
tions for intubation include hypoxemia despite maximal oxygen
supplementation and ventilatory failure that is not immediately
reversible (e.g., opioid overdose). Assessment of the patient’s
clinical status and peripheral oxygen saturations, augmented by
TABLE 19-1  Anatomy of the Airway in Infants Compared with Adults
Infant Anatomy
Large intraoral tongue that occupies a relatively large portion of
oral cavity
High tracheal opening: C1 in infancy; C3 or C4 at age 7 years;
C4 or C5 in adulthood
Large occiput may cause flexion of airway; large tongue easily
collapses against posterior pharynx
Cricoid ring is the narrowest portion of the trachea as compared
with vocal cords in adults
Airway anatomy varies consistently by patient age; there are
fewer abnormal variations related to body habitus, arthritis, or
chronic disease
Large tonsils and adenoids may bleed; more acute angle
between epiglottis and laryngeal opening results in
nasotracheal intubation attempt failures
Small cricothyroid membrane
Modified from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, 2nd ed, Philadelphia, 2004, Lippincott Williams & Wilkins.
404
Hyoid bone
Thyroid
Thyroid membrane cartilage
Thyroid notch
Laryngeal
Cricothyroid prominence
membrane
Cricoid cartilage Thyroid
gland
Tracheal rings
FIGURE 19-2  External airway anatomy.
capnography (if available), provides critical data. In the absence
of objective data (i.e., pulse oximetry), central cyanosis and poor
respiratory effort are key physical examination findings that can
indicate the need for airway management.
ANTICIPATED CLINICAL COURSE
Patients with a moderate to high likelihood of airway deteriora-
tion often require endotracheal intubation despite airway patency,
adequate oxygenation, and normal vital signs. For instance, a
patient with significant blunt trauma from a climbing accident
may require intubation due to pain severity and likelihood of
deterioration. Assess the structural integrity of the central face
and mandible. Injuries to these structures may lead to airway
distortion and compromise. Inspect the anterior neck and chest
for penetrating wounds, asymmetry, or swelling that may herald
impending airway compromise. Anticipating deterioration or pro-
gression of disease that may confound subsequent intubation
attempts is crucial.
In children, visual signs of airway compromise and respiratory
distress include tachypnea, cyanosis, drooling, nasal flaring, and
intercostal retractions. A child with severe upper airway obstruc-
tion may sit upright with the head tilted back (sniffing position)
to straighten the airway and reduce occlusion. A child with severe
lower airway obstruction may sit up and lean forward on out-
stretched arms in the tripod position to augment accessory
muscle function.
Clinical Significance
High anterior airway position of glottic opening compared with that of
adult
Straight blade preferred over curved blade to push distensible anatomy
out of the way to visualize larynx
Sniffing position is preferred; large occiput elevates head into sniffing
position in most infants and children a towel may be required under
shoulders to elevate torso relative to head in small infants
Uncuffed tubes provide an adequate seal because they fit snugly at the
level of the cricoid ring; correct tube size is essential because variable
expansion cuffed tubes are not used
Age less than 2 years, high anterior airway
Age 2 to 8 years, transitional airway
Age older than 8 years to small adult; “normal” adult positioning of airway
Blind nasotracheal intubation not indicated for children; nasotracheal
intubation failure
Needle cricothyroidotomy difficult and surgical cricothyroidotomy
impossible in infants and small children
 HEAD POSITIONING

CHAPTER 19  Emergency Airway Management

Head positioning can play a critical role in airway management.
If there is concern for cervical spine injury, the head and neck
should be stabilized in a neutral position and care should be
taken to avoid all unnecessary head and neck movements. In the
field, certain actions (e.g., evacuation from a dangerous setting)
may take priority over strict cervical spine immobilization.

Tongue Recovery Position

Vocal cords
Unconscious, spontaneously breathing patients that are judged
Epiglottis Cricoid not at risk of cervical spine injury should be placed in the recov-
membrane ery position (Figure 19-4). This encourages airway patency while
Cricoid ring reducing the risk of aspiration. In the recovery position, the
Junction of tongue is less likely to occlude the airway and vomitus is less
chin and neck likely to be inhaled.
Infant
MANUAL AIRWAY TECHNIQUES
Manual airway techniques employ specialized positioning of the
head and facial structures to elevate the tongue and soft tissues
of the pharynx to open the airway. These techniques are often
effective but require continuous involvement of a single provider
in order to maintain airway patency. Typically, manual airway
techniques are used as temporizing treatments until an airway
adjunct or definitive airway is placed.
Head Tilt and Chin Lift
The head tilt/chin lift is a simple and effective technique for
opening the airway in patients assessed as unlikely to have cervi-
cal spine injury (Figure 19-5). Place one palm on the patient’s
Tongue Vocal cords forehead. Apply firm downward and backward pressure to
extend the neck and tilt the head posteriorly. Fingers of the
Cricoid other hand are placed under the chin’s bony anterior and lifted
Epiglottis membrane forward. These fingers support the jaw and maintain the head-tilt
Cricoid ring position.
Junction of Jaw Thrust
chin and neck If a cervical spine injury is suspected or if the head tilt/chin lift
is not effective, a jaw thrust should be performed to maintain
airway patency. A jaw-thrust airway positioning maneuver lifts
Adult the mandible forward, thereby lifting the tongue away from the
FIGURE 19-3  Anatomic airway differences between infants and adults. posterior pharyngeal wall. To perform this maneuver, take a
Anatomic differences particular to infants include (1) a higher and more position behind the supine patient’s head. Place both hands
anterior position for the glottic opening (note relationship of the vocal alongside the patient’s jaw. Rest thumbs and thenar eminences
cords to the chin-neck junction); (2) a relatively larger tongue that lies along the maxilla and zygoma. Place the rescuer’s remaining
between the mouth and glottic opening; (3) a relatively larger and fingers along the mandibular margin and angle of the mandible.
floppier epiglottis; (4) a cricoid ring that is the narrowest portion of Pull up (i.e., anteriorly) to displace the jaw while using the
the pediatric airway (in adults, the narrowest portion is the vocal cords); thumbs for support (Figure 19-6). This maneuver is tiring, yet
(5) the position and size of the cricothyroid membrane; (6) a sharper
and more difficult angle for blind nasotracheal intubation; and (7) a
larger relative size of the occiput. (Redrawn from Walls RM, Murphy
MF, Luten RC, et al, editors: Manual of emergency airway manage-
ment, 2nd ed, Philadelphia, 2004, Lippincott Williams & Wilkins.)

BASIC AIRWAY MANAGEMENT

Opening the airway and ensuring airway patency are essential
for adequate oxygenation and ventilation. In an outdoor environ-
ment, these priorities are critical because definitive airway man-
agement may be delayed due to the distance to a medical facility,
weather conditions, or a lack of equipment. Conscious patients
maintain airway patency and protect against aspiration (e.g., of
foreign substances, gastric contents, or secretions) using protec-
tive reflexes of the innervating musculature of the upper airway.
In severely ill or injured patients, these protective airway mecha-
nisms may be impaired or absent. In obtunded patients, upper
airway obstruction most commonly results from posterior dis-
placement of the tongue against the posterior pharynx. The
presence of foreign bodies, blood, or secretions, as well as airway
edema, commonly leads to partial or complete airway obstruc-
tion. Head positioning, manual airway techniques, and mechani-
cal airway adjuncts may be employed to alleviate upper airway
obstruction. FIGURE 19-4  Recovery position.

405

FIGURE 19-5  Head tilt with chin lift.
TRAUMA
FIGURE 19-6  Jaw thrust without head tilt.
PART 4
quite effective. If cervical spine injuries are not suspected, it can
be used in combination with a head tilt/chin lift.
MECHANICAL AIRWAY ADJUNCTS
After a patent airway has been established, it is critical that the
airway remain open. This requires continual reassessment of
airway patency. An oropharyngeal airway (OPA) or nasopharyn-
geal airway (NPA) device can be placed to create a patent
conduit for spontaneous or assisted ventilation. Each device has
specific indications and contraindications and must be properly
selected to avoid causing harm. Although OPAs and NPAs help
to maintain airway patency, they do not protect against aspira-
tion. They serve as temporizing measures until a definitive airway
can be established or the patient’s condition improves.
Oropharyngeal Airway
The OPA is a curved, rigid device designed to hold the tongue
away from the posterior pharyngeal wall (Figure 19-7). When
FIGURE 19-7  Oropharyngeal airway.
406
properly placed, an OPA prevents the tongue from obstructing
the hypopharynx and creates a conduit for ventilation. Certain
types of OPAs allow for airway suctioning. These devices should
only be used in minimally arousable or unconscious patients.
Using an OPA in an alert patient with a gag reflex or cough is
generally contraindicated because the OPA will likely stimulate
retching, vomiting, or laryngospasm. OPAs are typically made of
disposable plastic and come in varying styles and sizes to accom-
modate patients of all ages. The size is based on the distance in
millimeters from the OPA flange to its distal tip. The proper OPA
size is estimated by placing the OPA’s flange at the corner of the
mouth so that the bite-block segment is parallel with the victim’s
hard palate. The distal tip of the airway should reach the angle
of the jaw.
To place an OPA, select an appropriate size and manually
open the mouth. The pharynx should be cleared of any debris
(e.g., foreign bodies, secretions, or emesis). Insert the OPA into
the mouth horizontally or in an upside-down orientation, with
the distal tip facing superiorly. Gently advance the OPA tip until
it reaches the junction between the hard and soft palates (approx-
imately at the level of the uvula), and slowly rotate it 90 or 180
degrees. After rotation, continue inserting the OPA’s curved
aspect along the base of the tongue until the OPA flange reaches
the lips or teeth. Alternatively, use a tongue blade to push down
on the tongue while inserting the OPA with its inner curve along
the tongue. After placement, ensure that the OPA has created a
patent airway by lifting the tongue (and not displacing it into the
pharynx) and that it has not stimulated the patient’s gag reflex.
Nasopharyngeal Airway
The NPA is a soft, uncuffed, rubber cylinder that provides a
conduit for airflow between the nares and the hypopharynx
(Figure 19-8). The NPA is inserted through the nose. The NPA
has a distal flange to prevent insertion beyond the nostril. The
device is less likely to stimulate a patient’s gag reflex and so is
better tolerated than an OPA. An NPA is most commonly used
in a semiconscious patient (e.g., under the influence of sedative
drugs or alcohol). It is effective when trauma, trismus, or other
obstacles preclude OPA placement. NPAs are contraindicated in
victims with suspected basilar skull or significant midface frac-
tures because inadvertent intracranial placement may occur.
NPAs are made of pliable rubber or plastic and come in
varying designs and sizes to accommodate patients of all sizes.
The sizes (as indicated by the internal diameter) range from 12
to 36 French. The proper NPA length is determined by measuring
the distance from the tip of the patient’s nose to the tragus of
the ipsilateral ear.
After selecting the appropriate size, the NPA is lubricated with
a water-soluble lubricant. Insert it gently into the nostril with its
beveled end pointed toward the nasal septum. Continuing to act
gently, advance the NPA along the floor of the nasal passage and
into the nasopharynx. If resistance is met, gently rotate the NPA,
select a smaller size, or attempt to insert it through the other
nostril. In position, the flange should rest against the patient’s
nostril. The distal end should rest behind the tongue in the pos-
terior pharynx. Ensure that the NPA has created a patent airway.
If necessary, an NPA can be placed in each nostril.
FIGURE 19-8  Nasopharyngeal airway.

FIGURE 19-9  Improvised nasal trumpet.
Improvised Nasopharyngeal Airway
Any flexible tube of appropriate diameter and length can be used
as a temporary NPA substitute. Various types of tubing that may
be present in camping or wilderness situations include a solar
shower hose, siphon tubing, an inflation hose from a kayak flota-
tion bag, and a Foley catheter. Round and bevel one end of the
substitute nasal airway to minimize its potential for injuring the
nasal mucosa. An endotracheal tube (ETT) can be shortened and
softened in warm water to substitute for a commercial nasal
trumpet. Improvise a flange by placing a safety pin through the
nostril end of the tube (Figure 19-9).
AIRWAY OBSTRUCTION FROM A
FOREIGN BODY
Foreign bodies (e.g., food, dislodged teeth) may cause airway
obstruction. A patient with partial airway obstruction can usually
phonate or produce a forceful cough in an attempt to expel the
foreign body. In a patient with a partially obstructed airway, if
air exchange is adequate, encourage forceful coughing and
closely monitor the patient’s condition. If obstruction persists
or if air exchange becomes inadequate, manage the situation
as a complete airway obstruction. Ominous signs that indicate
the need for immediate aggressive airway management include
a weak or ineffective cough, increased respiratory difficulty,
decreased air movement, and cyanosis.
A patient with a complete airway obstruction cannot speak
(aphonia), exchange air, or cough. The person will often grasp
the neck in the universal distress signal for choking and open
the mouth widely. An unconscious patient with a complete
airway obstruction will not demonstrate chest movement or other
signs of adequate air exchange. Failure to relieve a complete
airway obstruction leads to hypoxia-induced cardiac arrest. If a
patient collapses with suspected complete airway obstruction,
attempt immediate laryngoscopy to remove obvious foreign
debris. If the patient remains unresponsive and apneic despite
the removal of foreign material (or if no foreign body is identi-
fied), the patient should be endotracheally intubated. If a midtra-
cheal foreign body is suspected, advance the ETT (with stylet in
place) to move the foreign body into the right mainstem bron-
chus. The ETT can then be retracted above the carina and the
left lung ventilated, taking care not to cause barotrauma.
SUCTION
Sick or injured patients are at risk for airway obstruction and
pulmonary aspiration of secretions, vomitus, or blood. Many
lifesaving interventions, such as manual ventilation, increase this
risk. If foreign material cannot be cleared manually, suction
becomes essential to create and maintain a patent airway and to
CHAPTER 19  Emergency Airway Management
prevent aspiration.
Portable suction devices for austere environments may be
manually or externally powered, by oxygen, air, or electricity.
Hand-operated units are lightweight, compact, reliable, and inex-
pensive. All units should have large-bore, nonkinking suction
tubing; an unbreakable collection container; and a sterile dispos-
able suction catheter, and should provide sufficient negative
pressure for adequate pharyngeal suctioning.
Flexible (French) suction catheters are used to suction the
nose, mouth, and oropharynx. Rigid suction catheters are used
to suction the mouth and oropharynx. Suction catheters should
not be inserted beyond the base of the tongue, and suction
should occur as the catheter is withdrawn from the pharynx. To
prevent oxygen deprivation, do not suction adults for more than
10 to 15 seconds. Infants and children should be not be suctioned
for more than 5 seconds at a time. In children, take care when
using rigid suction catheters, because oropharyngeal stimulation
may result in cardiac muscarinic stimulation that leads to brady-
cardia. Infants up to 4 months old are obligate nose breathers.
Use a bulb syringe to suction their noses and mouths.
A “mucus trap” suction device can be improvised from a jar
with two holes poked in its lid and two tubes taped into the
holes (Figure 19-10). One tube goes to the source of the suction
(i.e., a suction device or rescuer’s mouth) and the other goes
toward the patient’s airway. The jar serves as a trap to capture
secretions and decrease the likelihood of a rescuer being directly
exposed to suctioned bodily fluids or foreign substances, such
as mud.
SUPPLEMENTAL OXYGEN
Supplemental oxygen therapy should be provided to all sick or
injured persons with cardiac disease, respiratory distress, shock,
or trauma, even if measured arterial oxygen tension is normal.
Oxygenation in preparation for intubation should be provided
using the oxygen delivery system that can provide the highest
inspired amount of oxygen. This typically is a face mask with an
oxygen reservoir that delivers a fraction of inspired oxygen of
approximately 70%. Leave this in place as the patient breaths
tidally for 3 minutes. Supplemental oxygen applied as part of an
overall resuscitation strategy should start with a high oxygen
concentration and then be titrated downward to maintain the
desired oxygenation.
Various oxygen delivery techniques may be employed,
depending on the desired oxygen concentration and clinical
circumstances (see Chapter 103).
VENTILATION
Even if the airway is patent and supplemental oxygen is being
received, a patient is not necessarily being ventilated. Adequate
ventilation requires sufficient air exchange between ambient
conditions and the lungs to deliver oxygen to the alveoli and
Duct tape
Tubing
Jar
FIGURE 19-10  Improvised mucus trap suction device.
407
 facilitate carbon dioxide removal. To establish adequate ventila-
tion, open the airway and assist with ventilation or provide
manual ventilation using positive pressure. When providing
manual ventilation, employ barrier protection (e.g., a mask with
a one-way valve) to avoid contact with patient secretions, blood,
or infectious agents. Persistent hypoventilation without an
obvious reversible component is one of the cardinal indications
for intubation.

MOUTH-TO-MOUTH VENTILATION
Mouth-to-mouth ventilation is an efficient way of providing
manual ventilation. Failure to use a barrier device during mouth-
to-mouth ventilation places a rescuer at risk for exposure to
infectious bodily fluids. To provide mouth-to-mouth ventilation,
open the airway and clear any foreign bodies, secretions, or
debris. If there is no concern for cervical spine injury, open the
airway using the head tilt/chin lift maneuver. Once the airway is
open, pinch the patient’s nostrils tightly shut and use the other
hand to keep the patient’s mouth slightly open. After establishing
a tight mouth-to-mouth seal, deliver full, slow breaths. Deliver
enough breath volume to create a visible chest rise. Between
breaths, break the mouth seal to allow for passive exhalation.
When the rescuer is the sole provider for a patient with cardiac
arrest, rescue breaths should occur at 2 breaths per 30 chest FIGURE 19-11  Rescuer using mouth-to-mask ventilation. The rescuer
compressions. is providing rescue breathing with a face mask and supplemental
oxygen during cardiopulmonary resuscitation. The rescuer is using the
cephalic technique (i.e., the rescuer is positioned at the top of the
MOUTH-TO-NOSE VENTILATION patient’s head). Both of the rescuer’s hands are used to hold the mask
securely in position while keeping the patient’s airway open. The res-
In a patient with mouth injuries or abnormal anatomy that pre- cuer’s thumbs and forefingers hold the mask in place while the third,
cludes effective mouth-to-mouth ventilation, mouth-to-nose ven- fourth, and fifth fingers lift the jaw (i.e., jaw thrust) and maintain an
tilation should be considered. The mouth-to-nose technique is
TRAUMA

similar to that for mouth-to-mouth ventilation. Open the airway
in a similar fashion, and then close the mouth using the thumb
and forefinger to seal the lips. The patient’s nostrils are left open,
and the rescuer’s mouth is sealed around the patient’s nose.
Breaths are delivered until chest rise is observed.
PART 4
open airway with the head tilted. Alternatively, the thumbs and a
portion of the rescuer’s palms can anchor the mask, and the index and
remaining fingers can lift the jaw and hold it against the mask. (Redrawn
from American Heart Association: Guidelines 2000 for cardiopulmo-
nary resuscitation and emergency cardiovascular care. Circulation
102:I95, 2000.)

MOUTH-TO-MASK VENTILATION
Mouth-to-mask ventilation is the safest and most effective tech-
nique for rescue breathing (Figure 19-11). A pocket face mask
or a similar barrier device allows the rescuer to provide ventila-
tion without making direct contact with the patient’s mouth and
nose. The mask has a one-way valve in the stem to prevent
exhaled gases and bodily fluids from reaching the health care
provider. A disposable filter may be added to trap infectious air
droplets and secretions.
The pocket face mask is made of pliable plastic material and
can be easily carried. Some masks have an oxygen inlet so that
supplemental oxygen can be administered. Devices are available
in a number of sizes. If an infant mask is not available, an adult
mask can be turned upside-down for a better fit. To use a pocket
mask, first open the airway and clear any obvious obstruction
using the head tilt/chin lift or jaw thrust. Take a position behind
the patient’s head. In an unresponsive patient, insert an OPA or
NPA to help maintain a patent airway. Stretch the mask and apply
it to the patient’s face. Apply pressure to both sides of the mask
with the thumbs and base of the palm to create an air-tight seal.
As with a jaw thrust, place the remaining fingers underneath the
patient’s jaw and apply upward pressure. Provide breaths directly
to the mask, ensure adequate chest rise, and allow for passive
exhalation between breaths.
BAG-VALVE-MASK VENTILATION
A self-inflating ventilation bag with face mask (i.e., bag-valve-
mask [BVM] device) allows for emergency ventilation with a high
concentration of oxygen. Devices are equipped with several
one-way valves to allow coordinated airflow into and out of the
patient without creating dead space ventilation (Figure 19-12, A
and B). Used correctly and attached to a high-flow oxygen source
(15 L/min), BVM devices can supply approximately 100% oxygen.
Patient characteristics associated with difficult rescue mask ven-
tilation include traits that prevent an adequate mask seal (e.g.,
beard, facial trauma) or limit flow to gas-exchanging portions of
the lungs (e.g., chronic obstructive pulmonary disease, airway
obstruction, morbid obesity).12,13 The MOANS mnemonic outlines
predictors of difficult bag-and-mask ventilation (see Box 19-2).
Face mask fittings are interchangeable with distal ETT adapters.
The same bag can be used after intubation.
Competence with a BVM device is a vital emergency skill and
a prerequisite for the use of paralytic agents for endotracheal
intubation. Whenever possible, use a two-handed and two-
person technique. Holding the mask with a thenar grip results
in more effective ventilation, even by novice airway managers.
With thumbs pointed toward the patient’s chest, place the thenar
eminences against the lateral walls of the mask. Wrap the other
fingers around the mandibles and pull the jaw up into the mask.
Ensure an even mask seal.9 If a single-handed mask hold is
required, the operator must remain vigilant to prevent mask
leakage and ineffective ventilation. When rescue ventilating a
supine, apneic, and unresponsive patient, an oral airway is
imperative because the tongue falls against the posterior pharynx
and occludes the airway. During prolonged mask ventilation,
apply cricoid pressure to limit gastric insufflation. For infants and
children, use smaller BVM devices to prevent overinflation and
barotrauma. In the absence of a BVM device that precisely
regulates the volume of air transferred, the amount of air trans-
ferred by a BVM is a clinical estimate based on the patient’s
weight, approximately 5 to 7 mL/kg, or enough to create visible
chest rise.
ADVANCED AIRWAY MANAGEMENT
A definitive airway requires patency and protection provided by
a stabilized, inflated cuffed structure in the trachea attached to

408

A Predicting Difficult Direct Laryngoscopy with the
B L—Look externally. Use the operator’s clinical impression and
FIGURE 19-12  View of a bag-mask ventilation device. A, Rescuer
provides ventilation with a bag and mask attached to an oxygen
supply. Rescuer uses E-C technique to hold the mask to the face by
creating a “C” with thumb and forefinger while lifting the jaw along
the bony portion of the mandible with the last three fingers of the
same hand; these fingers make the “E.” The second hand squeezes
the bag while the rescuer watches the patient’s chest to ensure that it
rises with each ventilation. B, Common elements of a standard bag-
mask ventilation system with supplemental oxygen. A system consists
of a self-refilling bag with an oxygen inlet, valve, and standard fittings
(in this case, the bag is joined with a standard fitting to a mask).
(Redrawn from American Heart Association: Guidelines 2000 for car-
diopulmonary resuscitation and emergency cardiovascular care. Circu-
lation 102:I95, 2000.)
an oxygen source. Failure to secure a definitive airway in a timely
manner can lead to disastrous consequences. Once it has been
determined that a patient requires intubation, use an algorithmic
approach to airway management. Successful algorithms depend
on the caregiver’s knowledge of airway anatomy, pharmacology,
difficult airway recognition, and rescue techniques. The most
common approach to emergency airway management is orotra-
cheal intubation facilitated by rapid sequence intubation (RSI).3
Other methods may be used if a difficult airway is predicted or
when the need for airway management is immediate (e.g., a
patient with rapidly progressing lingual edema due to anaphy-
laxis or one who is deteriorating to an agonal ventilatory effort
and critical hypoxia). Approaches to definitive airway manage-
ment include immediate oral endotracheal intubation, awake oral
intubation, rapid sequence oral intubation, nasotracheal intuba-
tion, and surgical airway (e.g.,cricothyrotomy).
PREDICTORS OF AIRWAY DIFFICULTY
For most patients, intubation is accomplished without complica-
tions.3,14 Modern observational registries of emergency depart-
ments report cricothyrotomy rates of less than 0.5%.3 Difficult
BVM ventilation occurs in approximately 2% of operative patients.
In emergency patients, the percentage of difficult BVM ventila-
tions is higher because preoperative assessment and patient
selection cannot occur.
To assess for RSI, evaluate for (1) difficult intubation, (2) dif-
ficult rescue mask ventilation, (3) difficult placement or use of
an extraglottic device (EGD), and (4) difficult cricothyrotomy.
Although specialist backup, difficult airway devices, and rescue
techniques may be limited in wilderness settings, knowledge of
the four aspects of assessment is crucial to successful planning.
Preintubation discovery of difficult airway characteristics is highly
predictive of a challenging intubation. Providers should always
CHAPTER 19  Emergency Airway Management
be ready for a difficult-to-manage airway because unseen com-
plications may not be discovered by bedside assessment.14
Aspects of a difficult airway are recalled by the mnemonics
LEMON, MOANS, RODS, and SMART.24 Some patients have an
isolated anatomic or pathophysiologic feature responsible for
airway challenges, and others may have multiple features. Patients
with evidence predicting a difficult airway may still be candidates
for neuromuscular blockade. Patients with multiple markers of a
difficult airway may be best managed using an “awake” tech-
nique without paralysis because neuromuscular blockade may
place the patient at high risk for a failed intubation situation. In
a patient with a concerning bedside assessment, neuromuscular
blockade may be used in conjunction with a double setup (i.e.,
prepared for cricothyrotomy) as part of a planned approach.
LEMON Mnemonic
Successful intubation is strongly associated with the ability to see
the glottis (whether using conventional direct laryngoscopy or
video-assisted laryngoscopy). Video laryngoscopy typically pro-
vides better glottic views than does direct laryngoscopy.2,18,21
To predict difficult direct laryngoscopy, use the LEMON mne-
monic (Box 19-1):
initial gestalt. If judged difficult simply by bedside inspec-
tion (e.g., patient with a distorted face following a fall from
a tree), the patient is likely to be challenging to intubate.
E—Evaluate 3-3-2. Direct laryngoscopy requires adequate
mouth opening to admit the laryngoscope, sufficient space
in the floor of the mouth to displace the tongue into the
mandibular fossa, and laryngeal placement that is suffi-
ciently “low” (i.e., caudal) that it is not hidden by the base
of the tongue. Mouth opening, thyromental distance, and
thyrohyoid distance are measured by the 3-3-2 rule. Patients
who fail a 3-3-2 assessment may have a challenging direct
laryngoscopy (see Figure 19-1)
M—Mallampati scale. The four-class Mallampati scale assesses
the important relationship between mouth opening and
tongue size. The degree to which an operator can visualize
posterior pharyngeal structures predicts the difficulty with
laryngoscopy. The Mallampati scale in isolation is not a
sensitive assessment tool. It can have limited utility in
emergency situations because it requires an awake, compli-
ant patient. Forty percent of emergency department patients
cannot yield this assessment.1
O—Obstruction or obesity. Upper airway (supraglottic) ob-
struction can make visualization of the glottis or intubation
impossible. Mechanical upper airway obstruction can be
caused by head and neck cancer, pharyngeal infection, or
anaphylaxis. Any form of airway obstruction should be
considered a difficult airway. Obesity can increase the dif-
ficulty of laryngoscopy and complicate other aspects of
airway management, such as mask ventilation.
N—Neck mobility. Patients with potential cervical spine injury
should be placed in cervical precautions. A neutral head
position limits direct laryngoscopy because the sniffing
position is contraindicated. Neck extension is most impor-
tant, but the full sniffing position is best for an optimal
laryngeal view.8
BOX 19-1  LEMON Mnemonic for Evaluation of Difficult
Direct Laryngoscopy
Look externally for signs of obvious difficulty
Evaluate the 3-3-2 rule
Mallampati classification
Obstruction or Obesity
Neck mobility (reduced)
Adapted with permission from The Difficult Airway Course: Emergency and
Walls RM, Murphy MF, editors: Manual of emergency airway management,
4th ed, Philadelphia, 2012, Lippincott, Williams & Wilkins.
409
 BOX 19-2  MOANS Mnemonic for Challenging Rescue
Bag-and-Mask Ventilation
Mask seal (beard or altered anatomy)
Obstruction or Obesity
Aged (> 55 years old)
No teeth
Stiffness (resistance to ventilation or intrinsic lung pathology)
Adapted with permission from The Difficult Airway Course: Emergency and
Walls RM, Murphy MF, editors: Manual of emergency airway management,
4th ed, Philadelphia, 2012, Lippincott, Williams & Wilkins.
Predicting Difficult Bag-Mask Ventilation with the
MOANS Mnemonic
Attributes of difficult BMV are well validated. They are reflected
in the mnemonic MOANS (Box 19-2).12,13 Patients in whom rescue
ventilation by face mask is difficult or impossible typically have
features that interfere with an adequate mask seal (e.g., patients
with beards or altered lower craniofacial anatomy) or qualities
that impair adequate delivery of oxygen to gas-exchanging por-
tions of the lungs. This can be due to advanced age, morbid
obesity, airway obstruction, or intrinsic lung pathologic condi-
tions (e.g., asthma, chronic obstructive pulmonary disease).
The difficulty with BVM management of the edentulous
patient is the basis of the advice, “Teeth out to intubate; teeth in
to ventilate.”6 In patients without teeth, place the mask or a rolled
gauze inside the lower lip to limit air leakage and eliminate the
risk of aspiration associated with dental prosthetics.
Predicting Difficult Extraglottic Device Placement with
TRAUMA
the RODS Mnemonic
When faced with difficult rescue mask ventilation due to an
inadequate mask seal, consider placing an extraglottic device
(EGD) (e.g., intubating laryngeal mask airway [I-LMA], King
laryngeal tube). An EGD (internal bagging) is placed directly
above the glottic opening. Difficulty with placement and ventila-
PART 4
tion with an EGD is predicted by the mnemonic RODS (Box
19-3). If the LEMON and MOANS assessments have been com-
pleted, only the D (distorted anatomy) remains to be evaluated.
Distorted upper airway anatomy may result in an incomplete seal
and air leakage that cause ineffective ventilation. Restricted
mouth opening, airway obstruction, and intrinsic lung pathologic
conditions can make ventilation difficult with a mask or EGD.
Predicting Difficult Cricothyrotomy with the
SMART Mnemonic
Predicting difficult cricothyrotomy is outlined by the SMART
mnemonic (Box 19-4). Difficult cricothyrotomy occurs when
there is limited access to the anterior neck or when laryngeal
landmarks are obscured. Inspect and palpate the neck for signs
of prior surgery, hematoma, tumor, abscess, or radiation changes.
IMMEDIATE ORAL INTUBATION
(“CRASH” INTUBATION)
Patients in cardiorespiratory arrest or with agonal vital signs
require immediate oral intubation. These patients often have little
or no muscular tone and can be intubated without the need for
RSI drugs. Attempt immediate intubation without medications. If
BOX 19-3  RODS Mnemonic for Potentially Difficult
Extraglottic Device Placement and Use
Restricted mouth opening
Obstruction or Obesity
Distorted anatomy
Stiffness (resistance to ventilation)
Adapted with permission from The Difficult Airway Course: Emergency and
Walls RM, Murphy MF, editors: Manual of emergency airway management,
4th ed, Philadelphia, 2012, Lippincott, Williams & Wilkins.
410
BOX 19-4  SMART Mnemonic for Evaluation
of Difficult Cricothyrotomy
Surgery
Mass (head and neck cancer, hematoma)
Access/anatomy problems (obesity, edema)
Radiation
Tumor
Adapted with permission from The Difficult Airway Course: Emergency and
Walls RM, Murphy MF, editors: Manual of emergency airway management,
4th ed, Philadelphia, 2012, Lippincott, Williams & Wilkins.
intubation is unsuccessful (e.g., due to residual muscular contrac-
tion and limited mouth opening), a neuromuscular blocking
agent (NMBA) (e.g., succinylcholine [1.5 mg/kg intravenously])
can be administered, followed by another intubation attempt. If
an ETT has not been placed after three attempts, place an EGD.
If at any point the oxygen saturation drops and cannot be main-
tained with an EGD or rescue ventilation technique, a failed
airway has developed and the operator should move quickly to
create a surgical airway.
RAPID SEQUENCE INTUBATION
If a patient does not require an immediate (crash) airway inter-
vention and assessment does not predict a sufficiently difficult
airway such that neuromuscular blockade might be contraindi-
cated, pursue RSI. RSI follows a coordinated series of steps to
allow safe and effective airway management without interposed
BVM. It is the method of choice for most acutely ill or injured
patients.3 RSI involves administration of weight-based doses of
potent sedative and NMBAs given consecutively by IV push
without intervening time delay. Prior to drug administration, a
period of preoxygenation creates an oxygen-rich reservoir in the
patient’s functional residual capacity and helps prevent desatura-
tion during apnea.
RSI is described in discreet steps termed the seven Ps of RSI
(Table 19-2).25
Preparation
Prior to the intubation attempt, gather the proper equipment and
medications for use during airway management. This may include
pretreatment, induction, and paralytic agents (see below). Attach
cardiac and oximetry monitors. In an austere environment, this
process may be quite limited.
Preoxygenation
The goal of preoxygenation is to prolong the period of safe
apnea (from the onset of paralysis to desaturation below 90%)
by creating an oxygen reservoir in the patient’s lungs. This is
typically accomplished by supplying nonrebreather face mask
oxygen at approximately 100% for 3 minutes of normal, tidal
volume breathing. In a healthy patient, this may allow 6 to 8
minutes of safe apnea. This time will be much less in children,
obese patients, and patients with critical illness or injury for
whom oxygen use is increased. Preoxygenation is essential to
the “no bagging” approach of RSI. If time is insufficient for a full
TABLE 19-2  The Seven Ps of Rapid Sequence
Intubation
Time Action
Zero minus 10 minutes Preparation
Zero minus 5 minutes Preoxygenation
Zero minus 3 minutes Pretreatment
—Time zero— Paralysis with induction
Zero plus 20-30 seconds Positioning
Zero plus 45 seconds Placement with proof
Zero plus 1 minute Postintubation management

TABLE 19-3  Clinical Characteristics of Induction Agents*
Induction Induction Dose Onset of Duration
Agent (Intravenous) Action of Action
Midazolam 0.2-0.3 mg/kg 30 to 60 15 to 30
seconds minutes
Etomidate 0.3 mg/kg 15 to 45 3 to 12
seconds minutes
Ketamine 1 to 2 mg/kg 45 to 60 10 to 20
seconds minutes
Propofol 1.5 mg/kg 30 to 60 2 to 5
seconds minutes
*All doses should be halved in the setting of profound refractory shock in order to prevent circulatory collapse.
3-minute preoxygenation phase, eight vital capacity breaths with
high-flow oxygen can achieve oxygen saturations and apnea
times that match or exceed those obtained with traditional pre-
oxygenation. For an obese patient, if contraindications do not
exist, preoxygenation should be performed with the patient
upright. After neuromuscular blockade, passive oxygenation is
accomplished by continuing supplemental oxygen by nasal
cannula (at a flow rate of 2 to 6 L/min) during laryngoscopy,
and the time to 95% desaturation is extended from 3.5 to 5.3
minutes.16,26
Pretreatment
Laryngoscopy may have detrimental physiologic effects (e.g.,
increased intracranial pressure, heart rate, blood pressure, vascu-
lar sheer forces, and bronchospasm). Pretreatment agents are
used to mitigate these effects. Pretreatment regimens have
evolved, and many formerly traditional methods (e.g., defascicu-
lating doses of competitive neuromuscular blockers before
administering succinylcholine; routine use of atropine in chil-
dren) have largely been abandoned. Patients who may still be
considered for pretreatment are those with reactive airway
disease, elevated intracranial pressure, or a cardiovascular or
neurovascular condition for which increased vascular sheer
forces might be dangerous. In patients with asthma, lidocaine
has been recommended as a pretreatment drug to limit the bron-
chospastic response to laryngoscopy. Given that data are limited
and beta agonists are universally recommended for acute asthma
exacerbations, lidocaine is unlikely to confer benefit. It is reason-
able to administer lidocaine (1.5 mg/kg) as a pretreatment drug
for asthmatic patients who have not received albuterol. Lidocaine
is no longer indicated for pretreatment in head-injured patients
with presumed elevated intracranial pressure. A patient intubated
in the setting of a vascular emergency (e.g., ischemic coronary
disease, aortic dissection) may benefit from a sympatholytic dose
(3 µg/kg) of fentanyl to blunt the release of catecholamines
caused by laryngeal manipulation. Fentanyl can also be used in
patients with primary cerebral processes associated with pre-
sumed elevated intracranial pressure if the blood pressure and
heart rate are normal.
Paralysis with Induction
Rapidly administer an intravenous (IV) bolus of an induction
agent to produce complete loss of consciousness, followed
immediately by rapid administration of a NMBA to induce com-
plete motor paralysis.
Induction Agents.  With few exceptions, patients should
receive an induction agent before neuromuscular blockade. Para-
lyzing a conscious patient without providing adequate sedation
can lead to detrimental physiologic and psychological sequelae.
Unless the patient has a Glasgow Coma Scale score of 3 or suffers
from profound refractory shock (i.e., those for whom even a
small dose of an induction agent might precipitate cardiovascular
collapse), induction is mandatory.
CHAPTER 19  Emergency Airway Management
Benefits Precautions
Readily available Slow onset, apnea and hypotension
Amnestic No analgesia
Anticonvulsant Often underdosed for RSI
Decreased intracranial pressure Myoclonic jerks
Rarely, decreased blood pressure Vomiting
No analgesia
Increased blood pressure and Increased secretions
bronchodilation
Dissociative amnesia and pain control Emergence phenomenon
Reversible, rapid offset; Apnea and hypotension;
anticonvulsant variable dosing
Principal induction agents used in the emergency setting are
etomidate, propofol, and ketamine. In North America, more than
90% of inductions in adult patients in the emergency department
involve etomidate, indicating widespread familiarity and confi-
dence with this drug.3 Previous controversy regarding the poten-
tial harmful effects of etomidate in septic patients has not been
substantiated.10 Clinical characteristics of the most commonly
used induction agents and their typical doses are summarized in
Table 19-3.
Neuromuscular Blockade.  NMBAs induce rapid, transient
paralysis to facilitate laryngoscopy and ETT placement. These
agents do not provide analgesia, sedation, or amnesia. The ideal
NMBA has a rapid onset and short duration of action and few
adverse side effects. Succinylcholine, a depolarizing NMBA,
comes closest to fulfilling these traits. It is the most commonly
used NMBA, although rocuronium is becoming increasingly
popular.3 At the neuromuscular junction, succinylcholine binds
tightly to acetylcholine receptors that control potassium channels.
Efflux of potassium ions results in motor end-plate depolarization
and muscle contraction. Succinylcholine prevents repolarization,
causing flaccid paralysis. Clinically, this manifests as muscle fas-
ciculations (10 to 15 seconds following IV bolus administration)
followed by complete muscle relaxation and paralysis (at 45 to
60 seconds). It has a short duration of action. Patients may
resume spontaneous breathing within 3 to 5 minutes.
Succinylcholine is administered at a dose of 1.5 mg/kg via
rapid IV bolus. It is contraindicated in patients with postsynaptic
receptor upregulation following neurologic injury (i.e., stroke or
spinal cord injury). In this population, succinylcholine depolar-
ization can cause severe hyperkalemia. This risk presents 3 days
after a discreet neurologic insult and lasts approximately 6
months. Nondepolarizing NMBAs (e.g., rocuronium) cause paral-
ysis by competing with acetylcholine for receptors at the neuro-
muscular junction. Rocuronium is the most commonly used
competitive NMBA for emergency airway management. It is
administered at a dose of 1 to 1.2 mg/kg given via rapid IV push,
and provides intubating conditions similar to those created by
use of succinylcholine.15 Vecuronium and pancuronium should
not be used for emergency airway management unless neither
succinylcholine nor rocuronium is available (Table 19-4).
Positioning
The airway can be considered to have three separate axes: oral,
pharyngeal, and laryngeal. In neutral head position, these axes
approximate a right angle (Figure 19-13). By combining proper
head positioning with head elevation and cervical spine exten-
sion, these axes become more aligned and the trajectory to
establish an airway is made straighter (Figure 19-14). The sniffing
position can be accomplished by placing rolls, a daypack, or
even shoes under the posterior occiput (Figure 19-15).
The sniffing position is helpful in all patients. It is crucial in
morbidly obese patients, where alignment of upper airway axes
can be even more challenging.
411
 TABLE 19-4  Neuromuscular Blocking Agents

Intubating
Dose
Agent (Intravenous) Onset Duration

Depolarizing Agent OA
Succinylcholine 1.5 mg/kg 45-60 seconds 6-12 minutes PA
(adult) LA
2 mg/kg
(child)
3 mg/kg
(infant)
Nondepolarizing Agents
Rocuronium 1 mg/kg 50-70 seconds 30-60 minutes
Vecuronium 0.15 mg/kg 90-120 seconds 60-75 minutes

Adapted from Mahadevan SV, Garmel GM, editors: An introduction to clinical

emergency medicine: guide for practitioners in the emergency department,
Cambridge, UK, 2005, Cambridge University Press.
Patients with potential cervical spine injury should be main-
tained in neutral position and intubated with cervical spine
precautions and manual in-line cervical stabilization. Sellick’s
maneuver (undirected posterior displacement of the cricoid
ring) has been taught as a mandatory step during RSI to prevent
TRAUMA
FIGURE 19-15  Head elevated on a pad, head extended on neck. LA,
Laryngeal axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls
RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway
management, 2nd ed, Philadelphia, 2004, Lippincott Williams &
Wilkins.)
aspiration, nominally by blocking the cervical esophagus. It is
not clear that Sellick’s maneuver prevents aspiration. It is associ-
ated with worsened glottic views, distortion of the cricoid ring,
and added difficulty with ETT passage.7,19 It is no longer routinely
recommended.

Placement
Once the patient is fully paralyzed, perform laryngoscopy, place
the ETT, and confirm proper placement by colorimetric or quan-
OA titative carbon dioxide detection.
Manage difficult direct laryngoscopy using several augmenta-
tion maneuvers. First, ensure that the patient and laryngoscope
PA
PART 4

blade are both optimally positioned. If the glottic aperture is not

LA
FIGURE 19-13  Head on a bed, neutral position. LA, Laryngeal axis;
OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM, Murphy
MF, Luten RC, et al, editors: Manual of emergency airway manage-
ment, 2nd ed, Philadelphia, 2004, Lippincott Williams & Wilkins.)
readily visible, consider manual repositioning of the larynx to
improve glottic visualization using optimal external laryngeal
manipulation (OELM). In OELM, the operator uses the right hand
to move the larynx into optimal viewing position. OELM was
previously known as the BURP maneuver. If the glottis is visual-
ized, have an assistant hold the larynx in place while intubation
takes place.
Other helpful airway adjunct devices include intubating stylets
(e.g., Eschmann intubating stylet, Frova intubating stylet). Stylets
(bougies) can be used to help intubate when the only airway
structure visible is the epiglottis (Cormack-Lehane grade III
view). Place the angled tip of the bougie under the tip of the
epiglottis and gently advance it. Correct bougie placement can
be confirmed by feeling vibratory transmission of movement over
the anterior tracheal rings through the bougie, or feeling the
bougie stop after it has been advanced a few inches beyond the
glottis, indicating that it has lodged in the right mainstem
bronchus.

OA Proof (Confirmation of Endotracheal Tube Placement)

Immediately after every intubation, confirm proper ETT position-
ing within the trachea. Monitor through several breaths. Failure
to recognize an esophageal intubation can be disastrous. Confirm
correct ETT placement by using clinical assessment, pulse oxim-
PA etry, end-tidal carbon dioxide detection, and aspiration tech-
LA niques. Clinical assessment alone is insufficient to confirm ETT
location, which ideally should always be accomplished by colo-
rimetric or quantitative end-tidal carbon dioxide detection. Chest
radiography assesses the ETT position but is highly unlikely to
be available in austere settings.

FIGURE 19-14  Head elevated on pad, neutral position. LA, Laryngeal CLINICAL ASSESSMENT
axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM,
Murphy MF, Luten RC, et al, editors: Manual of emergency airway man- Classic clinical observations used to confirm correct ETT place-
agement, 2nd ed, Philadelphia, 2004, Lippincott Williams & Wilkins.) ment include (1) watching the ETT pass through the vocal cords

412
during intubation; (2) auscultation of clear and equal breath
sounds over both lung fields; (3) absence of breath sounds when
auscultating over the stomach; (4) observation of symmetric chest
rise during ventilation; and (5) observation of ETT “fogging”
during ventilation. Because any one clinical finding is subject to
failure, it is safest to confirm ETT placement with multiple
findings.
PULSE OXIMETRY
A drop in oxygen saturation after intubation raises concern for
an esophageal intubation. If the patient has been adequately
preoxygenated, this drop may be delayed for several minutes. In
certain patients (e.g., those with severe hypotension or marked
peripheral vasoconstriction from cold exposure), the oxygen
saturation measurement may be unreliable or difficult to detect.
It is important to monitor pulse oximetry after endotracheal
intubation, but one must remember the previous cautionary state-
ment that no one method should be the sole indicator of suc-
cessful ETT placement.
End-Tidal Carbon Dioxide Detection
When adequate circulation is present, detection of end-tidal
carbon dioxide is a highly reliable method for identifying proper
ETT placement within the trachea. When unequivocal color
change persists after six full breaths, this ensures that the tracheal
tube tip is either within or directly above the trachea. Prolonged
bagging prior to intubation may result in initially weak but fati-
gable color change with an esophageal intubation. A false-
negative “color change” (no change in color despite correct ETT
placement) may occur in some cases of cardiac arrest and circula-
tory collapse as carbon dioxide delivery to the lungs abruptly
declines.
ASPIRATION DEVICES
Bulb and syringe aspiration devices may be used for confirmation
of ETT placement. Bulb aspiration devices are round and com-
pressible plastic globes (i.e., turkey baster) that are compressed
and deflated, attached to the ETT, and released to allow them to
inflate. If the bulb reexpands rapidly, the ETT is likely in the
trachea. Failure of or delay in reexpansion suggests that the ETT
is in the esophagus. Syringe aspiration devices are large syringes
(usually 30 mL [1 oz]) that are attached to the ETT. The syringe
plunger is pulled back rapidly. Rapid and easy flow of air sug-
gests tracheal intubation, whereas resistance suggests esophageal
intubation. Such devices are reliable at detecting esophageal
intubation (sensitivity > 95%); however, false-positive intubations
(i.e., a correctly placed tracheal tube is incorrectly labeled as an
esophageal intubation) can occur in up to 25% of cardiac arrest
patients.
POSTINTUBATION MANAGEMENT
After verification of correct ETT placement within the trachea,
secure the ETT (i.e., tape or tie it) to prevent movement or migra-
tion. Closely monitor the patient’s vital signs. Bradycardia after
intubation is worrisome for hypoxia or gastric distention and
should prompt detection of a possible esophageal intubation.
Hypertension after intubation suggests inadequate sedation.
Hypotension after intubation may result from a tension pneumo-
thorax, decreased venous return, large induction agent dose, or
cardiac cause.
After intubation, especially if a longer-acting neuromuscular
blocker (e.g., rocuronium or vecuronium) is used, sedation is
mandatory. An IV benzodiazepine (e.g., midazolam [0.1 to
0.2 mg/kg], diazepam [0.2 mg/kg], or lorazepam [0.05 to 0.1 mg/
kg]) may be administered initially for sedation and repeated for
any sign of awakening with awareness. Propofol (0.3 mg/kg) and
ketamine (1 to 2 mg/kg) are less commonly used, but are becom-
ing more popular both as induction agents and as postintubation
sedatives.3 An opioid agent such as fentanyl (3 to 5 µg/kg)
or morphine sulfate (0.1 mg/kg) may also be administered for
additional patient comfort. Nondepolarizing NMBAs (e.g., pan-
curonium [0.1 mg/kg] or vecuronium [0.1 mg/kg]) may be used
CHAPTER 19  Emergency Airway Management
for long-term paralysis. If any motor activity is detected after 45
to 60 minutes, give a repeat dose that is one-third the initial dose.
Ensure adequate sedation when long-acting paralysis is employed.
This is especially true when pancuronium is used, because it can
render a patient paralyzed for nearly 2 hours. Recent data suggest
that emergency department patients are not uncommonly para-
lyzed without adequate sedation.5
ALTERNATIVE STRATEGIES FOR THE
DIFFICULT AIRWAY
AWAKE ORAL INTUBATION
Awake oral intubation is an approach that makes use of titrated
IV sedation and liberal topical airway anesthesia to allow inspec-
tion and intubation of an awake patient’s airway. This approach
allows the patient’s protective airway reflexes and spontaneous
respirations to be preserved while the laryngoscopist takes a
gentle awake look at the glottis, vocal cords, and internal airway
anatomy. This approach is typically used when significant airway
difficulty is anticipated and direct laryngoscopy and/or rescue
mask ventilation are judged likely to fail. In these patients, use
of neuromuscular blockers may result in a failed airway. During
awake airway inspection, the clinician can elect to intubate
unstable patients (e.g., those with airway burns or anaphylaxis
with progressive airway swelling), because that moment may be
the most opportune time for definitive airway management. Key
components of an awake look are airway preparation, topical
anesthesia, and limited sedation. First, prepare the airway by
using a topical nasal vasoconstrictor (e.g., oxymetazoline 0.05%)
and drying agent (e.g., glycopyrrolate [Robinul] 0.01 mg/kg intra-
venously). Topical anesthesia is accomplished by using atomized
or nebulized aqueous lidocaine. The presence of blood or secre-
tions or distorted anatomy can make topical analgesia and visu-
alization challenging.
NASOTRACHEAL INTUBATION
When oral access is limited (e.g., fractured mandible, severe
lingual edema from Hymenoptera envenomation), awake naso-
tracheal intubation may be a better alternative, because it can be
performed while preserving the patient’s spontaneous respira-
tions. This technique does not require many of the tools needed
for other airway management techniques and so is well suited
for austere conditions.
Prepare the mucosa to facilitate tube passage and minimize
the risk for epistaxis. Instill 2 to 3 drops of a topical vasoconstric-
tor agent (e.g., phenylephrine hydrochloride [0.25%] or oxy­
metazoline [0.05%]) in each nostril. Anesthetize the nasal mucosa
using a 4% cocaine pack or 2% lidocaine jelly. After vasoconstric-
tion, use atomized or nebulized 4% aqueous lidocaine to provide
topical anesthesia. Select a cuffed ETT that is sized 1 mm smaller
than would be selected for orotracheal intubation. Lubricate the
tube with a water-soluble lubricant to facilitate its passage. Lido-
caine jelly is ideal for simultaneously providing lubrication and
topical anesthesia. Insert the ETT into the more patent nostril.
The right side is preferred because the ETT bevel will face the
septum and so avoid Kiesselbach’s plexus, decreasing epistaxis
risk. Direct the ETT straight back along the nasal floor toward
the occiput, and rotate it 15 to 30 degrees during advancement.
When the distal ETT nears the glottis, listen for airflow within
the tube with each breath. When maximal airflow is heard,
quickly and gently advance the ETT. A cough will likely be heard
with successful passage of the tube into the trachea, and the
patient will not be able to phonate. Advance the ETT to 32 cm
at the nares in adult males and to 27 to 28 cm in adult females.
Inflate the cuff. ETT confirmation should be established in stan-
dard fashion as described above. When ETT placement is assured,
immediately sedate the patient. NTI is contraindicated in patients
with apnea, significant midface trauma (i.e., with suspicion for
basilar skull fracture or cribriform plate injury), severe coagu-
lopathy, or presumed altered upper airway anatomy.
413
 Epistaxis and nasal turbinate injury from blind nasotracheal
intubation can be reduced by pretreatment with vasoconstrictor
agents and proper technique. If sufficient topical anesthesia is
provided, patients typically tolerate this procedure well. Long-
term complications (e.g., sinusitis, turbinate destruction) are
uncommon and result from multiple intubation attempts or pro-
longed intubation.
ALTERNATIVE AIRWAY ADJUNCTS
AND TECHNIQUES
In certain wilderness settings, tracheal intubation may be difficult
or impossible. Under such circumstances, alternative airway
adjuncts or techniques may be employed to provide an airway.
Alternative airways that require blind passage of an ETT into the
airway may be simpler to master than passing an ETT under
direct vision. To achieve good outcomes with these devices
and techniques, providers must maintain a high level of knowl-
edge and skills through frequent practice (e.g., simulation) and
field use.
LARYNGEAL MASK AIRWAY
The laryngeal mask airway (LMA) is a modified ETT with an
inflatable oval cuff (i.e., the laryngeal mask) at its base (Figure
19-16A-D). Blindly insert the LMA into the pharynx and advance
it until resistance is felt as the distal portion of the LMA lodges
in the laryngopharynx. Inflating the collar seals the LMA around
the laryngeal inlet and facilitates tracheal ventilation.
Although LMAs do not ensure protection against aspiration,
studies have shown that aspiration is uncommon and regurgita-
TRAUMA
PART 4
tion less likely with an LMA than with a BMV device. LMAs
provide ventilation equivalent to that of ETTs. LMA use may be
preferred to ETT intubation when access to the patient is limited,
when unstable neck injury may exist, or when appropriate victim
positioning for tracheal intubation is impossible. With elective
anesthesia, the LMA has an extremely high rate of successful
insertion and a low rate of complications, including a low inci-
dence of tracheal aspiration. Evaluations of LMA insertion by
experienced and inexperienced personnel alike consistently have
shown ease of insertion, high rates of successful insertion, and
successful ventilation.20
The LMA Fastrach is designed to facilitate blind intubation
through a specially designed mask employing an epiglottic eleva-
tor bar. Placement of the iLMA results in successful ventilation
in nearly all cases and successful subsequent intubation in 85%
to 95% of cases. When augmented by flexible fiberoptic endos-
copy, the rate of successful subsequent intubations rises to
approximately 100%. The LMA Fastrach has significant advan-
tages when compared with a standard LMA. It provides a means
for rescue ventilation and intubation. The LMA Fastrach comes
in adult sizes 3, 4, and 5. It is not suitable for use in patients
weighing less than approximately 30 kg (66 lb).
Newer-style LMA devices (e.g., air-Q and Aura-i) perform as
well as standard LMAs for ventilation and oxygenation, and can
also facilitate blind intubation with standard adult ETTs. Both
work well for intubating a difficult airway, especially when aug-
mented by flexible endoscopy.11
Combitube
The Combitube is a double-lumen, adult-only, dual-cuffed airway.
One lumen contains ventilating side holes at the hypopharyngeal
level. The distal end is closed. The other lumen has an open

A B

C D
FIGURE 19-16  Laryngeal mask airway (LMA). A, The LMA is an adjunctive airway that consists of a tube
with a cuffed masklike projection at its distal end. B, Introduce the LMA through the mouth into the pharynx.
C, When the LMA is in position, a clear and secure airway is present. D, During insertion, advance the LMA
until resistance is felt as the distal portion of the tube lodges in the hypopharynx. Inflate the cuff. This seals
the larynx and leaves the distal opening of the tube just above the glottis to provide a clear and secure
airway (dotted line). (Redrawn from American Heart Association: Guidelines 2000 for cardiopulmonary
resuscitation and emergency cardiovascular care. Circulation 102:I95, 2000.)

414

.2
No No.1
No.1
2
No.
A Insertion B Esophageal placement
FIGURE 19-17  Esophageal-tracheal Combitube. (Redrawn from Skinner D, Swain A, Peyton R, et al, editors:
Cambridge textbook of accident and emergency medicine, Cambridge, UK, 1997, Cambridge University
Press.)
distal end with a cuff similar to an ETT. One lumen functions as
an esophageal airway, and the other functions as a tracheal
airway (Figure 19-17). A Combitube is typically blindly inserted
and advanced until two guide marks printed on the tube reach
the patient’s teeth. The pharyngeal and distal balloons are
inflated. This isolates the oropharynx above the upper balloon
and the esophagus or trachea below the lower balloon. The
tube’s distal end most commonly finds its way into the esopha-
gus. It will intubate the trachea in 3% to 5% of cases. Determine
the location (i.e., esophagus or trachea) of the distal orifice and
ventilate through the appropriate opening.
Advantages of a Combitube over a BVM include isolation of
the airway, reduced aspiration risk, and more reliable ventilation.
Disadvantages include large size, more difficulty with placement,
and competition with newer and more easily applied devices.
Fatal complications with the Combitube may result from incorrect
identification of the position (trachea or esophagus) of the distal
lumen. An end-tidal carbon dioxide or esophageal detector
device should be used in conjunction with the Combitube.
KING LT
The King LT airway is a single-lumen, dual-cuffed airway with
ventilation outlets between a large pharyngeal and a smaller
esophageal balloon (Figure 19-18). The King LT airway is inserted
blindly. A single pilot balloon inflates both cuffs simultaneously.
Although it is similar to the Combitube, the King LT is shorter,
easier to insert, and easier to inflate, and does not inadvertently
intubate the trachea.4 Newer versions of the King LT have a
Figure 19-18  King Laryngeal Tube (LT) inflated with the prepackaged
syringe.
CHAPTER 19  Emergency Airway Management
No.1
2
No.
C Tracheal placement
posterior channel that accepts a nasogastric tube, allowing tube
passage through the device to allow aspiration of gastric con-
tents. The device’s airway seal may be lost after insertion and
requires deflation of the balloons and repositioning. The King LT
airway is available in newborn through adult sizes.
VIDEO LARYNGOSCOPY
Video laryngoscopes consist of a video camera functionally asso-
ciated in one of many ways with a laryngoscope blade and
handle, or other intubation device. For instance, the blade and
handle may be attached by video cable to a high-resolution color
display, or a miniaturized display may be attached directly to the
handle. This technology effectively places the operator’s eye on
a screen that transmits an image of the leading edge of the
laryngoscopy blade. The blade may have a hypercurved (Glide-
Scope) or traditional (Storz C-MAC) laryngoscope shape (Figures
19-19 and 19-20). The video laryngoscopes with integrated moni-
tors (e.g., McGrath MAC Series 5) on the end of the handle make
them attractive options for prehospital providers or other opera-
tors in austere settings (Figure 19-21). Compared with conven-
tional laryngoscopes, the video scope improves glottic exposure
in both operative and emergency department populations, and
it has higher first-pass success rates when compared with con-
ventional laryngoscopes.3,17,18,21 Video laryngoscopy is replacing
direct laryngoscopy as a first-line maneuver. Video laryngoscopes
tend to be expensive, but lower-cost devices (e.g., King Vision
video laryngoscope) are available (Figure 19-22). The King Vision
is powered by three standard AAA batteries that provide 90
minutes of continuous use.
Video screens used in bright outdoor environments are subject
to glare and reduced visibility. Modified shade (e.g., using natural
Figure 19-19  GlideScope titanium blades.
415

Figure 19-20  C-MAC video laryngoscope. (Photo courtesy Karl Storz
GmbH & Co. KG, Germany.)
TRAUMA
PART 4
Figure 19-21  McGrath MAC Series 5 video laryngoscope.
canopies or blankets) improves visualization. Small, lightweight
devices with fixed screens (e.g., McGrath Series 5, King Vision)
are attractive options. Visualization may be adversely affected
more in conditions of bright light because there is no separate,
mobile screen that can be positioned for optimal viewing.
FIBEROPTIC INTUBATION
Fiberoptic techniques for endotracheal intubation (e.g., fiberoptic
intubating bronchoscopes and rigid fiberoptic laryngoscopes) are
invaluable tools for difficult airway management. Their role in
out-of-hospital airway management is negatively affected by low
availability, high cost, requirements for power supplies for illu-
mination, and complex cleaning procedures after use. Devices
can be used for awake intubation in patients for whom RSI or
insertion of a laryngoscope blade may be disadvantageous. In
Figure 19-22  King Vision video laryngoscope.
416
patients with uncontrolled secretions or active bleeding, visual-
ization with fiberoptic devices may be impaired.
New, single-use, lightweight, fully disposable flexible video-
scopes (Ambu aScope 3) are available. The cost is low, and the
device is portable, so that fiberoptic technology can be used in
remote locations. A power supply is required.
DIGITAL INTUBATION
Digital (tactile) intubation is a technique in which the index and
long fingers of the nondominant hand are used to identify the
epiglottis and manually direct an ETT into the larynx. It may be
useful when poor lighting, poor positioning, copious airway
secretions, or equipment failure make laryngoscopy difficult or
impossible. Digital intubation requires a profoundly unresponsive
victim. It is relatively contraindicated in the semiconscious victim
with intact oropharyngeal reflexes. Other relative contraindica-
tions include caustic ingestion, thermal burns, and upper airway
foreign bodies.
SURGICAL AIRWAY MANAGEMENT
Surgical airway management (e.g., cricothyrotomy, needle crico-
thyrotomy with percutaneous transtracheal ventilation) involves
creation of an opening directly into the trachea by surgical
means.
CRICOTHYROTOMY
Video laryngoscopy may be reducing the “salvage” surgical
airway rate, currently at 0.3% in emergency department popula-
tions.3 Needle cricothyrotomy (i.e., insertion of a large needle
through the cricothyroid membrane into the airway for transtra-
cheal jet ventilation [TTJV]) is rarely, if ever, the correct choice
for an adult airway emergency. Cricothyrotomy creates an
opening in the cricothyroid membrane through which a cannula,
usually a cuffed tracheostomy tube, is inserted to permit oxygen-
ation and ventilation. When surgical airway management is
required, cricothyrotomy is the procedure of choice in the emer-
gency setting. It is faster, more straightforward, and more likely
to be successful than is tracheotomy. Alternate techniques are
described elsewhere.22
Cricothyrotomy is indicated when oral or nasal intubation fails
or is technically impossible to accomplish in the setting of declin-
ing oxygen saturation. Cricothyrotomy is relatively contraindi-
cated by altered neck anatomy, hematoma, overlying cancer, or
coagulopathy. There is no absolute contraindication to a surgical
airway, with the exception of age. The procedure should be
avoided in children younger than 10 years, in whom anatomic
limitations make it difficult.
A number of commercial kits can be used to perform a cri-
cothyrotomy. When landmarks are clear, cutaneous cricothyrot-
omy employing the Seldinger’s technique (i.e., cricothyrotomes)
appears comparable to formal open cricothyrotomy. In patients
with poor landmarks, standard open cricothyrotomy is more suc-
cessful. Bougie-assisted cricothyrotomy may improve surgical
airway success rates for inexperienced practitioners. The safety
and efficacy of cricothyrotomy kits are not clearly established.
Two percutaneous cricothyrotomy sets allow a cuffed tracheos-
tomy tube to be placed. One is a dedicated Seldinger cricothy-
rotomy set. The other is a combination set with equipment for
either a Seldinger percutaneous cricothyrotomy or a standard
surgical cricothyrotomy. Complications of cricothyrotomy include
incorrect location of airway placement, hemorrhage, tracheal or
laryngeal injury, infection, pneumomediastinum, subglottic ste-
nosis, and voice change.
Standard Surgical Cricothyrotomy
Standard surgical cricothyrotomy is performed as follows and as
shown in Figure 19-23:
Identify the thyroid cartilage. This is the only V-shaped
structure encountered when palpating the anterior neck. The
cricothyroid space is the gap immediately below the thyroid
cartilage.
 CHAPTER 19  Emergency Airway Management
Cricoid Cricothyroid
cartilage membrane
Cricoid
cartilage

Thyroid
cartilage

Cricothyroid
space
A B C

Left hand takes

trachea hook
from right hand
L
R

L R

Right hand picks

R
up scalpel

D E F

Right hand takes L R

trachea hook
from left hand

Left hand
picks up
L trachea
G H I spreader

J K L
FIGURE 19-23  Standard surgical cricothyrotomy. (Redrawn from Walls RM: Cricothyrotomy. In Rosen P,
Chan TC, Vilke GM, et al, editors: Atlas of emergency procedures, St. Louis, 2001, Mosby.)

417
 Prepare the neck in sterile fashion. With the nondominant
hand holding the thyroid cartilage, make a vertical midline
incision with a No. 11 scalpel blade from the thyroid cartilage
caudad approximately 3 to 4 cm (1.2 to 1.6 inches) (see Figure
19-23A).
Place a tracheal hook through the cricothyroid space. Hold
cephalad traction with the nondominant hand (see Figure
19-23B-D).
Make a transverse incision across the exposed cricothyroid
membrane (see Figure 19-23E,F). If time permits, insert silk stay
sutures in the trachea (see Figure 19-23G,H). Dilate the opening
in the cricothyroid membrane using a Trousseau dilator while
maintaining traction with the hook (see Figure 19-23I-K).
Place a Shiley cuffed tracheostomy tube through the opening
created in the cricothyroid membrane. Initially aim posteriorly
and then redirect caudally once through the opening (see Figure
19-23L). The tracheal hook may be removed before insertion of
the tube to avoid damaging the tube. If a tracheostomy tube is
not available, an ETT may be substituted.
Rapid Four-Step Cricothyrotomy
The rapid four-step cricothyrotomy is accomplished as follows
and as shown in Figure 19-24:
From a position at the head of the victim, palpate and identify
landmarks, especially the cricoid and thyroid cartilages and cri-
cothyroid membrane.
Using a No. 20 scalpel, incise the cricothyroid membrane and
overlying skin simultaneously with a single horizontal 1.5-cm
(0.6-inch) incision. While maintaining the blade within the
airway, slide a tracheal hook alongside the caudal side of the
blade into the wound.
Orient the hook caudally. Place gentle traction on the cricoid
TRAUMA
Improvised Cricothyrotomy
If formal cricothyrotomy equipment is not available, a knife and
a hollow object (i.e., substitute for the tracheostomy tube) may
be used. An improvised cricothyrotomy could be performed
using a modified IV macro drip chamber or the cut barrel of a
1-mL or 3-mL syringe (see Chapters 28 and 46). Any small hollow
object (e.g., ballpoint pen casing, sports-bottle straw, inflation
tube for white-water floatation bag) may be employed as a cri-
cothyrotomy tube. Objects with an internal diameter of at least
3 mm (0.12 inch) provide the best gas exchange.
NEEDLE CRICOTHYROTOMY WITH
PERCUTANEOUS TRANSTRACHEAL
(TRANSLARYNGEAL) JET VENTILATION
An alternative surgical airway procedure is needle cricothyrotomy
with percutaneous transtracheal jet ventilation (TTJV). With this
technique, a transtracheal catheter is inserted through the crico-
thyroid membrane into the trachea and connected to a jet ventila-
tion system consisting of high-pressure tubing, an oxygen source
at 50 psi, and an in-line one-way valve to intermittently admin-
ister oxygen. One hundred percent oxygen is delivered at 12 to
20 bursts/min. The inspiratory phase should last 1 second. The
expiratory phase should last 2 to 4 seconds. Advantages of this
technique include simplicity, safety, and speed. In adults, this is
an appropriate procedure only in the most dire circumstances;
even then, it should be considered a temporizing measure
because the tube’s small diameter makes oxygenation and
removal of carbon dioxide incredibly challenging. In TTJV, there
is typically less bleeding than with cricothyrotomy. Age is not a
contraindication. In children less than 10 years old, this is the
preferred surgical airway technique. During TTJV, the upper

ring; this typically widens the incision. Then remove the blade airway must be free of obstruction to allow complete exhalation.
from the airway. If not, the patient is at risk for barotrauma from air “stacking.”
Place the ETT through the opening into the airway. Secure All patients receiving TTJV should have an oral and nasal airway
the ETT. placed.
PART 4

A B

C D
FIGURE 19-24  Rapid four-step cricothyrotomy. A, Step 1: Palpation (location of the cricoid membrane
externally). B, Step 2: Incision (horizontal incision of skin and soft tissues through the cricoid membrane).
C, Step 3: Traction (application of caudal traction to the cricoid ring). D, Step 4: Intubation (passage of the
tracheal tube). (Redrawn from Brofeldt BT, Panacek EA, Richards JR: An easy cricothyrotomy approach:
The rapid four-step technique, Acad Emerg Med 3:1060, 1996.)

418
 Ventilation bag

CHAPTER 19  Emergency Airway Management

Universal
adaptor

Standard
endotracheal
tube connector

3-mL syringe barrel

Cannula Cricothyroid
membrane
Trochar

FIGURE 19-25  LifeStat emergency airway device. (Redrawn from Life-

Stat product information.) 14-gauge IV
catheter-over-needle

The technique for needle cricothyrotomy with TTJV is as

follows:
Stand at the patient’s side at the level of the neck. Expose the Cricoid
neck, and identify landmarks, especially the cricoid and thyroid Thyroid ring
cartilages and cricothyroid membrane. cartilage
Prepare the neck with an antiseptic solution, and provide local FIGURE 19-26  A simple setup for translaryngeal ventilation using
anesthesia if time permits. standard equipment found in any emergency department. This setup
Immobilize the larynx between the thumb and middle finger, is inadequate for adults. A high-pressure (50-psi) ventilation system is
while the index finger identifies the cricothyroid membrane. optimal. Even with the pressure relief valve on the bag-valve device
Attach a large-bore (12- to 16-gauge) over-the-needle catheter turned off, only suboptimal pressure can be developed. However this
to a 20-mL syringe. Hold the needle and syringe in the dominant technique may be satisfactory for infants and small children. (Redrawn
hand. Direct the needle caudally through the cricothyroid mem- from Roberts JR, Hedges JR, editors: Clinical procedures in emergency
brane at a 30-degree angle to the skin while maintaining negative medicine, 4th ed, Philadelphia, 2004, Saunders.)
pressure on the syringe. As soon as the needle tip enters the
trachea, the syringe should fill easily with air.
Advance the catheter to its hub while simultaneously remov- BOX 19-5  Sample Contents of a Wilderness Airway
ing the needle. Reconfirm the catheter position within the trachea. Management Kit
Connect the catheter to a jet ventilation system.
In terms of expedition kit portability, one transtracheal punc- Basic Airway Equipment
ture emergency airway device deserves special mention. LifeStat Laerdal pocket mask
(French Pocket Airway, Inc.) manufactures a keychain emergency CPR microshield barrier
airway set. It consists of a sharp-pointed metal trocar introducer Nasal airway kit
Oral airway kit
inside a straight metal cannula that screws into a metal extension
Stethoscope
with a universal 15-mm (0.6-inch) male adaptor. Lightweight and Bulb suction device
less than 7.6 cm (3 inches) long, the three-component apparatus
is attached to a detachable keychain (Figure 19-25). It is approved Advanced Airway Equipment
by the Food and Drug Administration for surgical access and is Bag-mask ventilation device with pediatric and adult masks
for a single use only. The device can be left in place during Manual suction device
subsequent attempts at intubation. For circumstances in which a Endotracheal tubes with stylet
jet ventilator is not readily available, care providers may impro- Compact and battery-operated video laryngoscope system
Laryngoscope handles and blades
vise by using a self-inflating bag-valve device to ventilate the
Magill forceps
patient through the transtracheal catheter. The bag-valve device Esophageal detector device
may be connected to a 3.0-mm-ID ETT adapter inserted directly Colorimetric end-tidal carbon dioxide detector
into transtracheal catheter or to a 7.5-mm-ID ETT adapter inserted Laryngeal mask airway, King LT, or Combitube
into a 3-mL (0.1-oz) syringe barrel and then into the transtracheal Needle cricothyrotomy catheter or device
catheter (Figure 19-26). Ventilation with this device is temporary Commercial cricothyrotomy kit
at best, but may have usefulness in children younger than 5 years Oxygen cylinder with toggle handle
of age. Nasal cannula, oxygen mask with strap, and nonrebreather bag
Oxygen tubing
Pulse oximeter
AIRWAY EQUIPMENT FOR
THE WILDERNESS
Box 19-5 lists standard airway equipment, video devices, and
REFERENCES
rescue tools for expedition airway management. Emergency Complete references used in this text are available
medical kits with basic or advanced airway equipment (e.g., Stat online at expertconsult.inkling.com.
Kit) are commercially available.

419
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25. Walls RM. Rapid sequence intubation. In: Walls RM, Murphy MF,
Luten RC, editors. Manual of emergency airway management. 3rd ed.
Philadelphia: Lippincott, Williams & Wilkins/Wolters Kluwer Health;
2008. p. 23–35.
26. Weingart SD, Levitan RM. Preoxygenation and prevention of desatura-
tion during emergency airway management. Ann Emerg Med 2012;
59(3):165–75 e1.
419.e1
 CHAPTER 20 
Management of Facial Injuries
DAVID SHAYE, VICKI MAZZORANA, AND ROBIN W. LINDSAY
Wilderness medicine is often defined in part by the amount of
time that an individual is in a remote place, far from definitive
hospital-based care. This occurs in disaster medicine, military and
tactical medicine, rural medicine, and traditional wilderness med-
icine. These fields have in common environments with con-
strained resources, the necessity for robust prehospital patient
care, and delayed access to definitive care. These conditions
require integrating evacuation and rescue training, evaluating
environmental threats, and understanding and managing re-
sources during disasters. A more expansive definition of wilder-
ness medicine takes into consideration the type of injury, the
setting in which the injury occurred, and how a particular injury
relates to human interaction with the environment.41 In all of
these environments and situations, facial injuries occur and
require urgent initial management to diminish the morbidity,
chance of mortality, and disruption of recreational activities.
The Joint Theater Trauma Registry is responsible for collecting
and organizing medical treatment data about patients from
combat operations who are treated at U.S. medical facilities.
Although the head, face, and neck account for only 12% of the
body surface area, approximately 40% of all injuries currently
sustained during military conflicts are to these areas. This propor-
tion is higher than reported for previous military conflicts, and
most likely results from improved body armor and relative lack
of protective devices for the head and face.32,38,50 Soldiers are at
high risk for sustaining oral and facial trauma during training and
assaults.52 Traumatic facial injuries account for significant rates of
morbidity and mortality among the U.S. armed forces, so improved
functional protection for the vulnerable facial region must be
developed. Experience and data gathered during military con-
flicts have been of tremendous value with regard to further
education of medical providers about the emergency care of
facial trauma. Military research has been instrumental in advanc-
ing trauma care principles and guidelines used to manage trauma
in both civilian and military populations.
In addition to military-related injuries, sports-related accidents
and outdoor recreational activities are responsible for a signifi-
cant number of facial injuries. Skiing, bicycling, soccer, and
mountain biking account for more than 60% of sports-related
accidents. Traumatic injuries from falls, collisions, and self-
inflicted injuries result in facial bone fractures, dentoalveolar
trauma, and soft tissue damage. The injury pattern depends on
the sporting activity, with high-speed and high-impact sports
causing more fractures and low-speed and low-impact sports
producing more dental injuries.48
A growing number of people participate in a wide variety of
outdoor recreational activities that take them far away from
definitive medical services.14,46 Wilderness recreation and adven-
ture activities create many situations that place individuals at risk
for facial traumatic injuries. The National Outdoor Leadership
School collects and publishes data about injuries, illnesses, near-
miss incidents, nonmedical incidents, and evacuation profiles
among its participants. According to recent unpublished data
from the leadership school, facial trauma accounted for 4% of
reported injury incidents over a period of 25 years from 1984 to
2009; the majority of these were soft tissue injuries.26
HISTORY AND EXAMINATION OF
FACIAL INJURIES
Before evaluating and treating a patient in the wilderness, the
safety of the setting and situation must be evaluated. Evaluating
420
a patient with facial trauma proceeds as it does with any other
medical condition. In emergency situations, the chief complaint
and history of the present illness are obtained as one is perform-
ing the primary survey, which evaluates and treats inadequacies
of airway, breathing, and circulation. The patient’s baseline
mental status is assessed, and any neurologic disabilities are
identified.
Airway assessment begins with examination of the mouth and
pharynx for foreign bodies, such as blood clots, tooth or bone
fragments, and dentures. If the airway is obstructed, perform a
chin lift or jaw thrust, or insert an oropharyngeal airway to hold
the tongue forward. If there is a potential cervical spine fracture,
keep the head and neck in a neutral position without hyperex-
tension. Position the patient to maintain the airway and facilitate
respiration; in many instances, this will be the prone position.
Raise the head above the heart to decrease bleeding and swell-
ing, or position the victim seated with the head forward so that
blood drains from the mouth or nose. If these measures fail,
perform endotracheal intubation or cricothyrotomy. Do not leave
the patient unattended, especially when in a supine position.
After the airway is secured and the patient stabilized, perform
a secondary survey to obtain an abbreviated history of the
present injury or illness and to extract pertinent information, such
as a history of allergies, any medications taken, the medical
history, the last oral intake, and the events leading up to the
injury. If the patient has sustained significant head or facial
trauma, determine if the patient experienced loss of conscious-
ness or has symptoms of nausea, vomiting, visual disturbances,
or headache. Assess the patient’s pain, and ask about its charac-
ter, onset, location, radiation, duration, and exacerbating or alle-
viating factors.
A systematic approach to examination in oral and maxillofa-
cial emergencies allows for efficient collection of relevant infor-
mation. Clean the face, mouth, head, and neck of blood and
debris; this unmasks soft tissue injuries and facilitates diagnosis.
Next, observe the head, neck, and face, and note any asymmetry.
Palpate all facial bones, temporomandibular joints, muscles, and
areas of suspected injury for tenderness, crepitus, swelling,
instability, dislocation, fracture, and foreign bodies. Bimanually
palpate the lips, cheeks, and floor of the mouth. Observe the
patient slowly opening the mouth, and examine for the range of
motion and any deviation with opening. Evaluate facial soft tissue
swelling for hematoma formation, especially in areas associated
with underlying cartilage, such as the ear and nose.
Perform an intraoral examination of the lips, cheeks, mouth,
tongue, hard palate, soft palate, and pharynx. Examine facial
lacerations carefully to determine if they penetrate into the oral
cavity or contain foreign material. Gently retract the lips with the
teeth closed to examine the soft tissues and occlusion. Examine
the dentition for fractures and mobility. Observe the gingiva for
bleeding, swelling, trauma, color, firmness, and recession.
DIAGNOSIS AND TREATMENT OF
FACIAL INJURIES
TEMPOROMANDIBULAR JOINT DISORDERS
Temporomandibular Joint Dislocation
Temporomandibular joint (TMJ) dislocation is more commonly
referred to as mandibular dislocation. Dislocation of the man-
dibular condyles causes inability to close the mouth and may
result from external trauma or, more frequently, from mandibular
 Articular

CHAPTER 20  Management of Facial Injuries

Temporal bone eminence

Mandibular
fossa

1 Mandibular condyle 2 3 4 5

FIGURE 20-1  Reduction of temporomandibular joint dislocation. The temporomandibular joint is shown in
both normal and dislocated positions. 1, Closed position, with the mandibular condyle resting in the man-
dibular fossa behind the articular eminence. 2, In maximally open position, the condyle is just under and
slightly behind the eminence. 3, In dislocated position, the condyle moves forward and upward slightly
above the eminence; muscle spasm then occurs. 4, To reduce dislocation, place thumbs intraorally and
lateral to the lower molars, and apply downward pressure to the lower molar ridge area near the jaw angle
in a downward and backward direction. 5, When the condyle has cleared the articular eminence, muscle
contraction will return the jaw to a normal closed position. The patient sits on a low chair with the back
straight. Face the patient, wrap the thumbs with gauze for protection, place them in the mouth on the back
molars, and then push down and back. A rocking motion may help. (From Amsterdam JT: Oral medicine.
In Marx JA, Hockberger RS, Walls RM, editors: Rosen’s emergency medicine: concepts and clinical practices,
6th ed, Philadelphia, 2006, Mosby, p 1041.)

hyperextension. This may occur while yawning, taking a large or mandibular ridge while exerting steady and constant down-
bite when eating, vomiting, laughing, or performing oral sex. ward pressure by moving the mandible down, then posteriorly,
This condition may be bilateral or, less often, unilateral, and it and then up with the remainder of the fingers and hand around
frequently recurs.8 the jaw and chin, levering upward. Downward pressure clears
Although posterior, lateral, and superior dislocations occur, the condyle of the articular eminence, and posterior pressure
anterior dislocation is most common, and it occurs when the repositions the condyle within the glenoid fossa. This technique
mandibular condylar heads and their respective cartilaginous may be difficult if muscle spasm is severe8,28 (Figure 20-2).
discs move anteriorly along the articular eminence out of the For the recumbent approach, lay the patient on his or her
glenoid fossa and become locked in the anterosuperior aspect back, and standing either behind or in front of the patient, apply
of the articular eminence of the temporal bone. Dislocation is caudal pressure on the mandibular ridge8 (Figure 20-3).
complicated by involuntary spasms of the muscles of mastication, For the posterior approach, seat the patient either on the floor
including the masseter, temporalis, and medial pterygoid, thereby or in a chair, and stand behind and above the patient. Place the
making it extremely difficult for the condyles to return to their thumbs on the retromolar gums posterior to the patient’s last
normal position during reduction.1,8,37 molar along the mandibular ramus, and exert downward pressure
Diagnosis.  Diagnosis of mandibular dislocation is not dif- on the mandible8 (Figure 20-4).
ficult, but without the benefit of a medical history the disorder
can be confused with an acute dystonic reaction. Patients present
with difficulty speaking, acute jaw pain anterior to the ear, mal-
occlusion, and inability to open or close the mouth. They may
be extremely uncomfortable and anxious. Patients present with
an open mouth and a prominent-appearing lower jaw. In a uni-
lateral dislocation, the chin appears to deviate to the side oppo-
site the dislocation. More frequently, dislocation is bilateral
without chin deviation. Clinically, the patient may have a palpa-
bly absent condyle within the glenoid fossa and visible periau-
ricular depression.8,27,28
Ideally, with traumatic dislocation, radiographs are performed
to eliminate a condylar fracture. In the wilderness, radiography
is impossible, and fractures are excluded on the basis of clinical
examination.
Treatment.  A variety of methods may be attempted to
reduce anterior mandibular dislocations without procedural seda-
tion or local anesthesia. The goal is to reduce the mandibular
condyle to the glenoid fossa from its current location anterior to
the articular eminence of the temporal bone. This requires relax-
ing the muscles of mastication, and is accompanied by properly
positioning the provider and patient so that direct pressure can
be placed on the mandible during reduction8 (Figure 20-1).
The classic reduction technique is performed having the
patient seated lower than the provider. Stand facing the seated
patient, and ask the patient to open the mouth widely against
resistance; this reduces muscle tone of the elevator muscles
through reciprocal inhibition and allows for concurrent manual
reduction. Simultaneously exert a maximal downward reduction FIGURE 20-2  Classic technique for reduction of anterior mandibular
force with the use of gloved thumbs on the patient’s lower molars dislocation.

421
 musculature posteriorly and inferiorly to induce relaxation of the
muscles and reduction of the condyle into the glenoid fossa.8,21
For the wrist pivot method, face the seated patient while
standing, and place your thumbs on the apex of the patient’s
chin while wrapping the remainder of the fingers laterally over
the mandible onto the inferior molars of the patient. With this
method, push upward with the thumbs on the patient’s chin
while simultaneously pushing downward on the body of the
mandible with the remaining fingers in a pivoting action. Flex
your wrists, and move in the direction of ulnar deviation. The
pivoting action uses the angle of the jaw as a fulcrum, resulting
in rotation of the mandibular condyles back into the glenoid
fossa. To prevent mandibular injury, this technique must be
applied to both sides of the jaw concurrently8,27 (Figure 20-6).
For the gag reflex method, elicit the patient’s gag reflex by
stimulating the soft palate. This results in relaxation of the
muscles of mastication and descent of the mandible caudally as
part of the reflex. During the gag reflex, jaw muscles relax,
causing transient descent of the mandible inferiorly and forcing
condyle reduction back into the glenoid fossa.2,8 Alternatively,
have the patient open the mouth widely or against resistance to
cause reciprocal relaxation of the elevator muscles to allow for
simultaneous manual reduction.

FIGURE 20-3  Recumbent approach for reduction of anterior mandibu-

lar dislocation.
TRAUMA
PART 4

FIGURE 20-5  Ipsilateral extraoral approach for reduction of anterior

mandibular dislocation.

FIGURE 20-4  Posterior approach for reduction of anterior mandibular

dislocation.

For the ipsilateral approach, use a sequential combination of

intraoral and extraoral manipulation. Focus on one side of the
jaw at a time. Stand at the patient’s side, and, while stabilizing
the patient’s head with one hand, use the thumb of the other
hand to exert external downward pressure on the displaced
mandibular condyle, located anterior and inferior to the zygo-
matic arch. If this is unsuccessful, exert downward pressure
intraorally on the ipsilateral lower molar teeth or the mandibular
ridge. If this is still unsuccessful, a combination of intraoral
downward pressure on the posterior molars, along with external
downward pressure on the mandibular condyle, may be success-
ful8,43 (Figure 20-5).
For an alternative manual method, place your fingers over the FIGURE 20-6  Wrist pivot method for reduction of anterior mandibular
periauricularly dislocated condyle and then gently massage the dislocation.

422

FIGURE 20-7  Masseteric nerve block for reduction of anterior man-
dibular dislocation. The index finger locates the zygomatic arch and
moves inferiorly until it reaches the mandibular notch at a point halfway
between thumb and middle finger. The needle is introduced posterior
to the index finger to hit the neck of the condyle.
With the nerve block method, the peripheral masseteric nerve
is anesthetized where it has passed through the mandibular notch
and before it penetrates the masseter. The deep temporal nerve
may be anesthetized by locating the anterior temporalis muscle
within a depression just above the zygomatic bone. The greater
wing of the sphenoid bone is located deep below this portion
of the muscle. The anesthetic needle is directed into this area
until the needle hits the sphenoid bone and the anesthetic agent
is deposited. These blocks result in reduction of pain and muscle
spasm, thereby allowing manual reduction. Administration of a
local anesthetic agent around the TMJ capsule may diminish joint
pain but will not diminish muscular pain or spasm51 (Figure 20-7).
Complications of reduction techniques include intraoral
trauma from significant downward pressure on the teeth and
gums, fractures, joint cartilaginous injuries, and torn ligaments
and muscles. The provider’s fingers may be injured during intra-
oral reduction techniques when the jaw snaps shut after success-
ful reduction. Using gloves, gauze, bite blocks, and plastic finger
splints, as well as placing the thumbs on the mandibular ridge
rather than the teeth or gums, during reduction can prevent this
complication.8
After reduction, advise patients to apply ice or cool com-
presses to the TMJ, avoid hyperextending the mandible, take
a nonsteroidal antiinflammatory agent such as ibuprofen, and
A B
FIGURE 20-8  A, The normal temporomandibular joint with cartilaginous disc. B, In a closed lock, the liga-
ments have stretched, and the disc is trapped anterior to the condyle.
maintain a soft diet for 1 week. Wrap a bandage around the head
CHAPTER 20  Management of Facial Injuries
and jaw to prevent mandible hyperextension and to limit jaw
movement.8,16
Internal Derangements of the Temporomandibular Joint
There is a cartilaginous disc interposed between the articulating
components of the movable mandibular condyloid process and
articular eminence of the temporal bone. The disc stabilizes the
joint and allows for rotational movements.
Diagnosis.  The intraarticular cartilaginous disc may displace
anteriorly, which results in joint dysfunction and abnormal joint
sounds such as clicking or popping. When closing the mouth, if
the cartilaginous disc of the TMJ displaces anteriorly relative to
the mandibular condyle with reduction to its normal position
when the mouth opens, clicking of the joint may occur. This may
manifest as a “pop,” the sound heard when the condyle moves
under the anteriorly displaced disc; this may or may not be
associated with joint pain and dysfunction25 (Figure 20-8).
However, if the cartilaginous disc is displaced but does not
return to its normal position with mouth opening, the patient
may experience occlusive instability associated with jaw locking.
There are two types of lockjaw. With closed lock, the mandibular
condyle is unable to slide under the anteriorly displaced disc.
With open lock, the mandibular condyle is unable to slide back
over the disc into its normal position.36 Clinically, there is joint
tenderness on palpation, and the chin may be deviated toward
the affected side on attempted mouth opening. Functionally, the
disc is trapped anterior to the mandibular condyle and the liga-
ments are stretched and become inflamed. This can occur spon-
taneously while eating or talking, but also may be present on
awakening from sleep, or be associated with mandibular trauma.
Treatment.  The provider can assist the patient to self-
reduce a closed lock. To do this, the patient should close the
mouth until the teeth almost touch, move the mandible laterally
as far as possible to the affected side, and finally swing the mouth
fully open.36 If these maneuvers fail, consider manual reduction
using TMJ reduction techniques. Spasm of muscles of mastication
may cause a similar restriction in mandibular function, but typi-
cally the affected muscles are firm and extremely tender; alter-
natively, with closed lock, the muscles are usually normal.
EPISTAXIS
Although most cases of epistaxis are trivial, some become life-
threatening, because aspiration can lead to respiratory compro-
mise and extensive blood loss can result in hemodynamic
instability. Therefore, the condition should never be neglected. It
is more common among the young and the elderly. Most causes
are traumatic and occur in the winter.37 Spontaneous epistaxis is
423
 Septal branch of anterior
ethmoidal artery
Frontal sinus
Ethmoid bone
Watershed area
(Kiesselbach’s plexus) Sphenopalatine
artery
(septal branch)
Septal
cartilage Sphenoid
sinus
Vomer
Septal branch
of superior
labial artery
Palate Great palatine
A artery
FIGURE 20-9  A, Vascular supply to the septum. The most common site of anterior epistaxis is the area
labeled Kiesselbach’s plexus. B, Vascular supply to the lateral wall. The most common site of posterior
epistaxis is the sphenopalatine artery as it emerges posterior to the middle turbinate. (From Maceri DR:
Epistaxis and nasal trauma. In Cummings CW, editor: Otolaryngology: head and neck surgery, 2nd ed,
St Louis, 1993, Mosby, p 728.)
more common in cold, dry, dusty, or smoke-filled environments.
Epistaxis is normally classified as anterior or posterior, depending
on the anatomic location. A particularly rich collection of vessels
and common site of anterior nosebleed is Kiesselbach’s plexus
on the lower anterior part of the nasal septum (i.e., Little’s area).
TRAUMA
Ninety percent of episodes of epistaxis occur in this area. Poste-
rior bleeding originates primarily from a branch of the spheno-
palatine artery called the posterior nasal artery, which forms part
of Woodruff’s plexus19,49 (Figure 20-9). Anterior epistaxis may be
managed definitively in the wilderness, but posterior epistaxis
requires immediate evacuation because of continued hemorrhage
PART 4
and the potential for airway compromise.29
Evaluation
The initial evaluation includes determining if bleeding is unilat-
eral or bilateral and whether it is coming from an anterior or
posterior site. A nosebleed usually occurs on one side of the
nasal cavity. However, with profuse bleeding, blood can pass
behind the nasal septum and also appear on the unaffected side.
Most individuals bleed from an anterior site, which is visualized
on intranasal speculum examination; with posterior epistaxis, the
bleeding site cannot be seen on intranasal examination.
Treatment
Have the patient sit upright with the head tipped slightly forward.
This maneuver decreases blood flow through the nasopharynx
and allows blood to drip passively out of the nose rather than
flowing posteriorly and causing choking, aspiration, and vomiting
of swallowed blood. Have the patient blow the nose to remove
clots immediately before examination. Warm saline lavage of
each nostril may accelerate activation of the clotting cascade and
allow for better visualization of the bleeding areas.49 Bleeding
may resume, but there will be improved access and visibility for
application of a vasoconstrictor drug or chemical cautery. Ask
the patient if he or she has placed anything inside the nose to
stop the bleeding, so that it can be removed before additional
packing is placed. Examine the nasal cavity with a nasal specu-
lum to determine the site of bleeding. If anterior bleeding is
suspected, instruct the patient to pinch the fleshy alae tightly
against the cartilaginous septum of the nose between the thumb
and index finger for at least 20 minutes. Applying cold com-
presses to the nose and instructing the patient to suck on ice can
improve this.39 Pinching the bony bridge of the nose does not
provide direct pressure on the bleeding vessels. Alternatively,
hands-free techniques that involve using commercial or impro-
vised (e.g., from taping together two tongue depressors) external
pressure devices or clips work well.19
424
Anterior ethmoidal artery
Frontal Posterior ethmoidal artery
sinus
Sphenoid sinus
Sella turcica
Sphenopalatine artery
(lateral nasal branch)
Eustachian tube
Site of posterier
epistaxis
B
If nose pinching does not stop the bleeding, apply a local
anesthetic and vasoconstrictor to the nasal mucosa over Little’s
area. Anesthetic preparations include topical tetracaine 1%,
cocaine 1% to 4%, lidocaine 5%, ephedrine 5%, and aqueous
epinephrine 1 : 1000. Vasoconstrictive nasal sprays include phen-
ylephrine 0.5% (Neo-Synephrine) and oxymetazoline 0.05%
(Afrin). Apply anesthetics and vasoconstrictors by drip or spray,
on a cotton pledget, or with a cotton-tipped applicator. Objects
placed in the nose should be inserted along the floor of the nose
and have a string attached or include another method for easy
removal. Avoid pushing material laterally into the turbinates or
superiorly toward the cribriform plate. Leave the vasoconstrictor
in place until it effectively staunches bleeding. This may take
from 10 minutes to 24 hours.29
Epistaxis refractory to pressure and topical vasoconstrictors
may require chemical cauterization using a silver nitrate (75%
concentration) stick that reacts to the mucosal lining to produce
local chemical damage. After applying a topical anesthetic, apply
the cautery stick to the bleeding point with firm pressure for 5
to 10 seconds. Apply cautery only to one side of the septum,
and be careful not to perforate the septum by applying too much
pressure.13
When there is more vigorous anterior nasal bleeding, nose
pinching, topical chemical vasoconstrictors, and cautery may not
be effective. In such an instance, inject the anterior bleeding site
with 0.5 to 1 mL of lidocaine 0.5%, 1%, or 2% that contains
1 : 100,000 epinephrine. This tamponades bleeding and provides
a vasoconstrictive effect. Alternatively, insert into the nares
directly over the bleeding site a small piece of absorbable or
degradable material that does not require removal. Such materi-
als include oxidized regenerated cellulose (Oxycel or Surgicel),
purified bovine collagen foam or paste (Gelfoam), microfibrillar
collagen (Avitene), porcine gelatin (Surgiflo), bovine gelatin-
human thrombin (FloSeal), QuikClot, recombinant factor VIIa,
topical thrombin, hemostatic matrix, nosebleed gauze, and fibrin
glue.19,33,34,39 When bleeding has stopped, instruct the patient not
to blow the nose or probe the area for 48 hours. After the bleed-
ing episode is over, increasing the humidity, warming inspired
air, and moisturizing the nasal mucosa with topical gels, lotions,
and ointments help to prevent recurrent bleeding.
Treat persistent epistaxis by packing the anterior cavity or
posterior cavity, or both. If bleeding is not controlled by the
previous methods, insert a lubricated anterior nasal sponge or
tampon. Improvise with gynecologic tampons, sponges, and
gauze. Current commercial options include Merocel, Medtronic,
Rapid Rhino, ArthroCare, Weimert Epistaxis Packing, and Rhino
Rocket34 (Figure 20-10).

A
B E
FIGURE 20-10  Commercial nasal packing is commonly used in place of traditional gauze packing. A, Rhino
Rocket. B, Epi-Stop Balloon Catheter. C, Rapid Rhino. D, Rapid-Pac. E, Rapid Rhino Dual Nasal Pack.
(A and B courtesy Shippert Medical, Centennial, Colorado; C to E courtesy ArthroCare Corporation, Austin,
Texas.)
If a nasal tampon fails to stop the bleeding, then formal ante-
rior packing is necessary. The basic technique involves placing
a 12-mm (0.5-inch) petrolatum- or antibiotic-impregnated strip of
gauze into the nasal cavity. An adult patient requires 90 to 120 cm
(3 to 4 ft) of such gauze to pack the nose adequately and
tamponade bleeding. Layer the gauze in tiers beginning on the
nasal floor and proceeding to the roof of the nose. Leave both
ends of the gauze outside of the nose and taped to the face to
prevent inadvertent aspiration. Improvised anterior nasal tam-
ponade can be accomplished with a Foley catheter (Figures 20-11
and 20-12).
Nasal packing blocks sinus drainage and can predispose to
sinusitis. Some studies in the literature contradict the following
recommendation when in an emergency department setting, but
we recommend that any patient who has the nose packed in the
field be placed on a prophylactic antistaphylococcal antibiotic,
such as 875 mg of amoxicillin with 125 mg of clavulanic acid
(Augmentin) by mouth three times daily, 500 mg of dicloxacillin
by mouth four times daily, 150 to 450 mg of clindamycin by
mouth four times daily, or 160 mg of trimethoprim and 800 mg
of sulfamethoxazole (Bactrim) by mouth twice daily until the
packing is removed after 48 hours.29
If the bleeding site is posterior and cannot be visualized, insert
a formal posterior nasal pack, commercially available nasal
balloon device, or Foley catheter. These methods rely on direct
pressure or blood accumulation within the nasal cavity, which
leads to tamponade. Placing a formal posterior nasal pack is dif-
ficult and involves gently inserting a lubricated soft tube into
each nostril until the ends can be visualized in the back of the
throat and then grasping the pack with a hemostat and bringing
it out through the mouth. Use Foley catheters, nasogastric tubes,
chest tubes, or improvised substitutes. Prepare a cylindrical pack
of 10- by 10-cm (4- by 4-inch) gauze, and hold it in shape by
tying three silk sutures around it and leaving the ends approxi-
mately 10 cm (4 inches) long. The pack should be the same
diameter as a circle made by the patient’s thumb and forefinger
(i.e., the “OK” sign). Attach the two end sutures to the oral ends
of the catheters. Pull the nasal ends of the catheters carefully
back out of the nose until the pack is firmly positioned against
the posterior aspect of the nasal cavity above the soft palate.
CHAPTER 20  Management of Facial Injuries
Detach the sutures from the catheters, and tie them over a bolster
placed underneath the nose. Secure the middle suture outside
the mouth to allow for removal 48 hours later (Figure 20-13).
Commercially available preshaped nasal balloons (e.g., Brigh-
ton, Nasostat, Naso-Blymp, Simpson plug, and EpiStat nasal
catheter) are manufactured specifically for treatment of posterior
epistaxis. They have a postnasal balloon and mobile anterior
balloon that are inflated independently. These are contraindi-
cated in cases of severe head trauma, basilar skull fracture, or
suspected craniofacial fractures that involve cerebrospinal fluid
(CSF) rhinorrhea19,34 (Figure 20-14).
A standard 14F to 16F Foley urinary catheter with a 30-mL
balloon can function as a posterior pack. Trim the distal catheter
tip to prevent irritation. Insert the lubricated catheter through the
nose into the posterior pharynx until it is visualized in the oro-
pharynx; inflate with a minimum of 3 to 5 mL of air or saline,
gently pull it forward into the nasopharynx until the balloon
engages, and hold it in position by clamping the external end
with a hemostat or an umbilical clamp. Balloons filled with air
tend to deflate over time, and those filled with water may rupture
and cause aspiration.13,49 Pack the anterior nasal cavity with a
nasal sponge or gauze.
Hot water irrigation has been documented as an alternative
strategy for posterior epistaxis. Occlude the posterior pharynx
with a balloon catheter, and irrigate the nares with heated water
(i.e., 45° C to 50° C [113° F to 122° F]). This reduces blood flow
by causing mucosal edema and clears blood clots from the
nose.19,34
FACIAL BONE FRACTURES
Anyone suffering from head or facial injury should be closely
examined for facial fractures. Proper management includes a
detailed examination for signs and symptoms of bony fractures,
stabilizing measures, and a plan for repair. The vast majority of
facial fractures are not surgical emergencies, and if they are
attended to within 2 weeks, can be properly treated without
long-term sequelae. In the acute setting, the level of concern
should be higher for facial fractures that occur with visual loss,
entrapment of extraocular muscles, CSF leak, and airway edema.
425
 A B

C D
FIGURE 20-11  The key to placing an anterior nasal pack that will control epistaxis adequately and stay in
place is to lay the packing into the nasal cavity in an “accordion” manner so that part of each layer of
packing lies anteriorly, thereby preventing the gauze from falling posteriorly into the nasopharynx. A, Grasp
the first layer of 0.25-inch petrolatum gauze strip approximately 2 to 3 cm (0.8 to 1.2 inches) from its end.
TRAUMA

B, Place the first layer on the floor of the nose through the nasal speculum (not pictured), and then withdraw
the bayonet forceps and the nasal speculum. C, Reintroduce the nasal speculum on top of the first layer
of packing, and place a second layer in an identical manner. After several layers have been placed, it is
often useful to reintroduce the bayonet forceps to push the previously placed packing down onto the 
floor of the nose to make it tighter and more secure. D, A complete anterior nasal pack can tamponade a
bleeding point anywhere in the anterior nasal cavity and will stay in place until the clinician or patient
removes it.
PART 4

Upper Face Fractures may preclude appreciation of obvious deformity. Functional

Nasal Fractures.  Nasal bones are the most commonly frac-
tured facial bones. The projected and prominent nasal vault is a
delicate, pyramid-shaped structure made up of paired nasal
bones centrally and the frontal processes of the maxilla laterally.
The remainder of the nose is composed of interconnecting car-
tilaginous structures that provide stability and support.
Nasal fracture typically manifests with midface swelling, epi-
staxis, periorbital ecchymosis, subconjunctival hemorrhage, and
bony nasal deformity. A few hours after injury, facial swelling
FIGURE 20-12  A Foley catheter is placed into the nasopharynx,
inflated with water, and retracted into position. The distal tip of the
catheter has been cut off. Place an anterior pack (not shown) around
the catheter. Protect the ala and columella with gauze padding, and
apply a plastic umbilical clamp or nasogastric clamp to the catheter to
maintain slight tension on the balloon.
changes in breathing and anosmia may also occur. Sweet or salty
watery drainage suggests CSF leak.10
After soft tissue injuries and epistaxis have been appropriately
managed, examine the nose to determine the extent of nasal
trauma. This requires an external examination followed by an
internal view using a light source. Deviation or fracture of the
nasal septum should be noted, along with the presence of a
septal hematoma. CSF fluid rhinorrhea, which is appreciated on
internal nasal examination as clear fluid, is indicative of skull
base fracture and/or intracranial trauma. CSF fluid separates from
blood when the liquid is placed on filter paper and produces a
clinically detectable double-ringed, or halo, sign (Figure 20-15).
When palpating the nasal bridge, the provider may appreciate
bony crepitus, nasal segment mobility, point tenderness, and
displacement that may not be visible on external examination.
Remove intranasal clots with cotton swabs. Close deep intranasal
lacerations with absorbable sutures or cover with Oxycel,
Gelfoam, Surgicel, or Avitene to control bleeding.31
Advise patients to apply ice to the area and to keep the head
elevated to reduce soft tissue swelling. Most surgeons prefer to
treat nasal fractures either immediately before significant edema
has evolved, or after the edema has subsided, within 5 to 10
days after injury. Immediate treatment and evacuation are not
necessary unless there are complications, such as persistent epi-
staxis, difficulty breathing, or deeper lacerations that require
definitive repair. If the nose appears to be straight after swelling
has subsided and the patient can breathe easily through both
nostrils, further treatment may not be necessary. If the nose
remains deformed after swelling has resolved or if the patient
experiences breathing problems, refer the patient to an otolar-
yngologist or a plastic surgeon within 3 to 5 days so that the

426
 CHAPTER 20  Management of Facial Injuries
Rubber Palate
catheter Turbinates
Catheter Nasopharynx
in nostril
in nostril
Palate

Tongue Tongue

Ring
forceps
Gauze wrapped
around cotton ball

A B
*

4” x 4” pad

Folded
gauze pad Fold

Long tapes
Roll

* Umbilical tape Two ties

C

Palate
Traction Gauze roll
Silk ties
Tongue

*
*
D E F
FIGURE 20-13  Traditional posterior nasal pack. A, After applying topical anesthesia, pass a red rubber
catheter through the nose, carefully grasp it in the oropharynx with ringed forceps, and bring it out through
the mouth. B, Make a posterior nasal pack by wrapping a cotton ball in a 4 × 4 inch gauze pad and tying
two long silk sutures or umbilical tapes around the neck of the pack. Leave one tie long so that it can be
taped to the cheek until it is needed for removal of the pack. C, Alternatively, fold a gauze pad, roll it into
a cylinder, and tie it with two strings. Use two of the long strings to tie the pack to the tip of the catheter,
and use the other two to remove the pack. D, As an option, use a second catheter that has been passed
through the nonbleeding side and brought out through the mouth to retract the palate forward to help
with the placement of the pack (not shown). E, Remove the optional “retraction” catheter after the pack
is in proper position. Digitally guide the pack into the nasopharynx. F, Use a gauze roll to secure the pack
to the nose, and tape the rescue ties to the cheek.

bones do not heal while misaligned. Children with nasal fractures
may have premature closure of sutures and uneven growth;
therefore, a consultant should evaluate the injury, preferably
within 4 days of its occurrence10,30 (Figure 20-16).
Digital manipulation of a displaced nasal bone fracture can in
some instances quickly reduce the fracture with minimal effort.
It is important to note that due to swelling at the time of injury,
deformity may result even with proper reduction.31,37 With any
nasal fracture, make a protective splint by cutting a triangular
piece of a SAM splint large enough to fit the nasal contours. Rest
the splint on the adjacent part of the face without placing pres-
sure on the nasal bridge. Secure the splint with strips of adhesive
tape. Do not pack the nose unless it is necessary to control
epistaxis or drain a septal hematoma. No antibiotics are needed
for a nasal fracture unless packing is placed. If packing is
required in a wilderness setting to control epistaxis or after drain-
age of a septal hematoma, administer 500 mg of penicillin V
potassium or amoxicillin by mouth four times a day for 5 days.10

427
 A
FIGURE 20-14  A, The Epi-Max balloon catheter. The balloon tamponade device serves as both an anterior
and posterior pack. It is easily inserted and is often successful for temporarily controlling posterior epistaxis
in the emergency department. B, The inflated Epi-Max. If the balloon pack is used for more than a few
days, protect the nasal opening with a piece of gauze, because skin breakdown is possible. (Courtesy Ship-
pert Medical, Centennial, Colorado.)
Anterior nasal septal trauma may cause tearing of the submu-
cosal blood vessels. If the mucosa remains intact, blood will
accumulate between the septal cartilage and mucoperichondrium
and cause formation of a hematoma, either immediately or within
the first 24 to 72 hours after injury. Septal hematoma appears
TRAUMA
Blood
PART 4
CSF
FIGURE 20-15  CSF fluid separates from blood when the liquid is
placed on filter paper and produces a clinically detectable double-
ringed, or halo, sign.
Unilateral
fracture of
nasal pyramid
Dislocation
of septum
FIGURE 20-16  Nondisplaced and minimally displaced nasal fractures
often do not require manipulation, but the true extent of deformity is
often difficult to appreciate initially. Note that the septum may require
subsequent intervention. Reduction of a depressed and dislocated
nasal bone fracture is usually performed after 3 to 7 days, when swell-
ing has subsided and the true deformity is obvious.
428
B
as a deviation, bulging, or widening of the nasal septum. Symp-
toms include nasal obstruction, pain, rhinorrhea, and fever
(Figure 20-17).
Inspect the nasal septum for asymmetry, swelling, pain, and
a fluctuant area. The mucosa of the fluctuant area will usually
have a bluish or reddish hue. The bulging area of the septum,
when compressed with a cotton-tipped applicator, feels boggy
and may be temporarily indented by the pressure. Increased
mobility that occurs with palpation with the applicator suggests
septal fracture. Insert a gloved small finger into each side of the
nares, and palpate the entire septum for swelling, fluctuance, and
crepitus.
Nasal cartilage receives nourishment from the surrounding
perichondrium and the supporting tissues. Septal hematoma
separates the cartilage from the nutrient-rich perichondrium and
requires urgent drainage to prevent complications such as septal
perforation, necrosis, and loss of nasal support, which can result
in a saddle-nose deformity. Bacterial growth of Staphylococcus
aureus, Streptococcus pneumoniae, and group A β-hemolytic
streptococcus within stagnant blood may form an abscess, which
can destroy the septum.10
Before drainage, anesthetize the bulging area by infiltrating
with a local anesthetic such as lidocaine 1% or by applying a
topical anesthetic such as benzocaine 20%. Aspirate the hema-
toma with an 18-gauge needle attached to a syringe, or make a
small incision at the most inferior (dependent) aspect of the
hematoma. Evacuate the blood clot and reapproximate the peri-
chondrium to cartilage, but leave the incision open. It may be
necessary to excise a small amount of mucosa to prevent pre-
mature closure and blood reaccumulation. Pack the nasal cavity
with 0.5-inch antiseptic-impregnated gauze or petrolatum to
prevent recurrent bleeding and to maintain apposition of the
perichondrium to the cartilage (Figure 20-18).
Frontal Sinus Fractures.  The frontal bone is one of the
strongest parts of the craniofacial skeleton. It overlies the frontal
Hematoma
FIGURE 20-17  Nasal septal hematoma requiring drainage.

A B
C D
FIGURE 20-18  A, A small, left-sided septal hematoma. B, After apply-
ing appropriate topical anesthesia (which can be supplemented with
local infiltration, if necessary), make a horizontal incision through the
mucosa and perichondrium that cover the hematoma. C, Use a small
cup forceps or scissors to remove enough mucosa to prevent prema-
ture closure of the wound and reaccumulation of hematoma. D, Place
a sterile rubber band as a drain, and pack the naris.
sinus, which adds additional protection for the brain. Any frontal
bone or sinus fracture should be evaluated for underlying brain,
dura, or CSF involvement. If a forehead laceration is present, it
is explored for visible bone, and if present, characteristics of the
bony fractures are noted. If clear, watery drainage is seen, this
could be indicative of CSF leak. These wounds are irrigated and
closed in layers until the patient can be seen at a tertiary center
for definitive care. The patient will require imaging to investigate
the fracture further and to determine whether surgical repair is
necessary.
Naso-Orbito-Ethmoid Fractures. Naso-orbito-ethmoid frac­
tures rarely occur. They are extremely complex fractures involving
the nasal skeleton, medial orbital walls, and interorbital area.
Clinical signs and symptoms include periorbital ecchymosis,
proptosis, dystopia, anosmia, nasal obstruction, enophthalmos,
subcutaneous emphysema, subconjunctival hemorrhage, edema,
lacerations, a flattened nasal bridge, rhinorrhea, and blindness.
Medial canthal ligament attachments may become disrupted,
resulting in telecanthus or abnormally widely spaced eyes.22,47
Naso-orbito-ethmoid fractures should be referred to tertiary
centers for proper imaging, evaluation, and possible surgical man-
agement, which can be extensive.
Midface Fractures
Midface fractures include isolated orbital fractures, zygomatico-
maxillary complex (ZMC) fractures, and malar (cheekbone) frac-
tures. Fractures of the lower maxilla can occur in the Le Fort
pattern.
Orbital Fractures.  An orbital fracture is often part of the
ZMC fracture pattern. Orbital fractures can also occur in isolation.
An orbital fracture that occurs with a ZMC fracture sometimes
has a palpable bony step-off along the infraorbital rim, which
represents the anteriormost projection of the orbital fracture. With
any orbital fracture, a detailed ophthalmologic examination,
including visual acuity, range of extraocular motion, pupillary
response, and light perception, should be performed. Orbital
fractures can cause diplopia as a result of displacement or hernia-
tion of the globe into the maxillary sinus, or extraocular muscle
entrapment. Ocular injuries, such as ruptured globe, retinal
detachment, vitreous hemorrhage, lens dislocation, and hyphema,
CHAPTER 20  Management of Facial Injuries
may be associated with these fractures (see Chapter 48).
Visual loss (or loss of light perception) should elicit concern
for orbital hematoma, a true surgical emergency. A proptotic eye
with loss of light perception should be decompressed immedi-
ately with a lateral canthotomy and cantholysis. The lateral can-
thotomy is made by incising sharply through the skin laterally
for a distance of approximately 1 to 1.5 cm. Next, the lower lid
is grasped and retracted inferiorly to expose the tension of the
lateral canthus. The scissors are used to cut sharply through the
lateral canthus, performing a lateral cantholysis to relieve or
reduce intraorbital and, therefore, intraocular pressure. If one is
unsure of the anatomic arrangement of the lateral canthus, an
alternative but less aesthetically preferred area of release is the
central lower lid. With either release, the patient is monitored for
return of light perception.
In the acute setting, orbital injuries can result in intractable
vomiting or bradycardia through the oculocardiac reflex. This and
entrapment are indications for urgent surgical repair of orbital
fractures.
Zygomaticomaxillary Complex Fractures (Malar Frac-
tures).  The most common midface fracture patterns are zygo-
maticomaxillary complex (ZMC) fractures, also known as malar
(cheekbone) fractures. These fractures occur across the anterior
maxilla, through the infraorbital foramen, through the orbital
floor, across the lateral orbital wall, through the zygomaticofron-
tal sutures, and across the zygomaticomaxillary suture (zygomatic
arch). This leaves an unstable, mobile malar segment that may
be displaced.
Clinical findings in maxillary fractures should be carefully
noted on examination. Inspect the face for asymmetry, hemato-
mas, ecchymosis, swelling, bleeding from the nose or conjuncti-
vae, intraoral tears, and ecchymosis of the palatal mucosa. Palpate
for crepitus, deformities, and step-offs of the orbital rims, nasal
bones, zygomatic arches, zygomas, and intraoral prominences of
the maxilla. It is common for ZMC fractures to pass through
the infraorbital foramen, an area of structural weakness. The
infraorbital nerve is often injured, leaving the patient with
decreased sensation from the lower eyelid down to the upper
lip, and over the nose and cheek on the injured side. Reassure
the patient that sensation usually returns with time. Malar flat-
tening is commonly found on examination. If the injury has
caused retropositioning of the fractured segment, the malar emi-
nence is posteriorly displaced and overlying soft tissue shows
loss of malar projection. With isolated ZMC fractures, patients
report pain with mastication; however, there should not be dental
malocclusion.
Treatment of ZMC fracture is not an emergency, so the patient
is stabilized until more definitive imaging and care can be pro-
vided. The degree of loss of malar projection, severity of the
orbital floor fracture, and trismus are the main indications for
surgical repair, which should be performed within 2 weeks of
injury prior to bone healing.
Zygomatic Arch Fractures.  Zygomatic arch fractures
usually result from force to the lateral cheek. Findings include a
depression along the lateral zygomatic arch, which can be visual-
ized on examination or palpated. Bony depression results in a
flat-appearing face with dimpling over the arch. Trismus and pain
with mandibular movement may occur. The coronoid process of
the mandible is located beneath the zygomatic arch. Therefore,
this fracture may result in inability to fully open the mouth by
impingement of the underlying temporalis tendon.7,18,47 Zygo-
matic arch fracture is not a surgical emergency and should be
repaired within 2 weeks of fracture.
Le Fort Fracture of the Maxilla.  The Le Fort classification
of maxillary fractures was established based on areas of structural
weakness in the maxilla.22 Le Fort pattern fractures all have sepa-
ration of the lower maxilla from the craniofacial skeleton in
variable locations along the midface. The Le Fort I transverse
fracture is the most common maxillary fracture. It occurs above
the apices of the teeth and runs transversely across the maxilla;
this involves the alveolar process, maxillary sinus walls, palate,
and pterygoid processes. The Le Fort II pyramidal fracture starts
in the nasal bones and frontal processes of the maxilla and then
429

Le Fort I Le Fort II
Le Fort III
TRAUMA
FIGURE 20-19  Classification of midface fractures. (Redrawn from the
American Association of Oral and Maxillofacial Surgeons: Oral and
maxillofacial surgery services in the emergency department, Rose-
mont, Illinois, 1992, American Association of Oral and Maxillofacial
Surgeons. With permission.)
PART 4
passes laterally and inferiorly through the lacrimal bones, inferior
orbital rims, and orbital floors near the zygomaticomaxillary
suture. It continues posteriorly along the lateral walls of the
maxilla, and through the pterygoid plates into the pterygomaxil-
lary fossa. The Le Fort III fracture pattern is frank craniofacial
disjunction, occurring through the frontomaxillary, zygomatico-
frontal, and orbital floors; nasofrontal sutures; cribriform plate of
the nose; and ethmoid and sphenoid sinuses. The fracture forces
are so great that there is a complete separation of the facial bones
from the cranial base47 (Figure 20-19).
Examine a patient for a Le Fort I maxillary fracture by grasping
the anterior maxillary segment by the central incisors between
the thumb and forefinger and gently rocking the maxilla antero-
posteriorly. If a Le Fort I fracture is present, the entire maxilla
and palate will move in relation to the upper midface. With a
unilateral fracture, the two halves of the maxilla may move
independently.
With a Le Fort II fracture, palpation will identify movement at
the nasofrontal junction and medial portion of the inferior orbital
rims where a step-off fracture may be palpated. Rock the maxilla
gently while grasping the nasal bridge between the thumb and
forefinger of the opposite hand. Any movement of the midface
complex is indicative of a Le Fort II pattern fracture. Palpate the
infraorbital rim for the presence of a step-off deformity.
Manipulation of a Le Fort III craniofacial disjunction fracture
results in separation and movement of the entire midface in rela-
tion to the cranium. This injury is often accompanied by intra-
cranial trauma. There is usually subconjunctival hemorrhage,
ecchymosis, and bilateral periorbital edema that causes eyelid
closure. Fractures that involve dural tears and meningeal lacera-
tion cause CSF rhinorrhea. When this is suspected, the nose
should not be packed, and prophylactic antibiotics (e.g., 500 mg
azithromycin by mouth once a day) should be initiated.
Rarely, a posteriorly displaced Le Fort fracture can cause
airway compromise. Only in this case should the maxilla be
disimpacted in the field by using forward traction.
430
Lower Face Fractures
Fractures of the Mandible.  Signs and symptoms of man-
dibular fractures include malocclusion, trismus, mental nerve
paresthesias, edema, intraoral and extraoral lacerations, buccal
or lingual ecchymosis, crepitus, facial asymmetry, jaw deviation
with mouth opening, and palpable step-off deformity along the
inferior mandibular border.6,18 Mandibular fractures are described
based on anatomic location within the mandible47 (Figure 20-20).
Inspect the skin, mucosa, dentition, and associated alveolar
and basilar structures. If there is no obvious tooth or bony dis-
placement, perform a bimanual examination. Note any loose
teeth. If any teeth are completely dislodged, remove them
because they pose an airway risk. Place the thumbs on the
occlusal edges of the teeth and the forefingers bilaterally on the
inferior border of the mandible to evaluate for crepitus, instabil-
ity, tenderness, and mobility. In addition to abnormal movement,
a grating sound can occasionally be heard when a fracture is
present. It is particularly important to evaluate any area of soft
tissue contusion. Palpate the inferior border of the mandible for
step-off defects and the mandibular condyles for limitation of
mobility. Evaluate the TMJ by placing a finger in the external
auditory canal.44 Normally, the condyles can be palpated by
placing a forefinger in front of the external auditory meatus. If
the condyle cannot be palpated or does not move significantly
when the mouth is opened, a fracture may be present. Place a
tongue blade in the patient’s mouth across the posterior molars,
and ask him or her to bite down and then to resist when you
attempt to pull out the blade. If this is accomplished without too
much pain, a fracture is unlikely to be present. A unilateral con-
dylar fracture is suspected when there is a shift of the mandibular
midline to the fractured and painful side on mouth opening.
Bilateral condylar fractures often result in an anterior open bite
and premature contact of the posterior teeth (Figure 20-21).
Asking the patient if the teeth do not properly align is a highly
sensitive way of assessing malocclusion. If there is malocclusion,
a cross bite, or an anterior open bite, there is a high likelihood
of a mandibular fracture.
Hemotympanum and external auditory meatus lacerations
indicate fractures of the temporal bone with condyle retrodis-
placement. To evaluate occlusion, have the patient bite down.
Any deviation of the bite or change in level of the occlusal plane,
especially in the mandible, should raise suspicion for a fracture.
There will sometimes be a gingival tear with bleeding and ecchy-
mosis at the site of discontinuity. Sublingual hematoma is a
common sign of mandibular fracture. In edentulous areas, there
will also be a discrepancy in the level of the bone, sometimes
accompanied by a disruption in the mucosa18 (Figure 20-22).
Definitive repair of a simple mandibular fracture is not usually
a surgical emergency. However, it is wise to note that airway
distress may occur with bilateral mandibular fractures or complex/
comminuted mandibular fractures in which significant edema has
arisen in the floor of the mouth. Delay in repair does not increase
the risk of infectious complications, but persons who are treated
after 3 days have a higher incidence of operative technical com-
plications, such as infected hardware, nonunion, or malunion.
Region of the
coronoid process
Region of
the condylar
process
Region of
Region of the ramus
the alveolar
process
Region of
Region of the Region of the angle
symphysis the body
FIGURE 20-20  Anatomic regions of the mandible. (Modified from
Dingman RO, Natvig P: Surgery of facial fractures, Philadelphia, 1964,
Saunders.)

FIGURE 20-21  Condylar fracture. With a condylar fracture, the joint is
positioned normally, but the muscles of mastication have pulled the
posterior portion of the mandible upward to create premature contact
of the posterior teeth.
A involves the facial nerve or salivary glands and ducts.24
B
FIGURE 20-22  Mandibular fracture. A, Note the malocclusion before
reduction. B, Normal.
Treatment within 24 to 36 hours after injury minimizes patient
discomfort and avoids significant soft tissue edema and fibrinous
deposition within the fracture.4,22 Even if perfect alignment is not
achieved, fixation makes the patient more comfortable, reduces
bleeding, and avoids further fracture fragment displacement.
Fractures that pass through the tooth-supporting portion of the
mandible are quickly stabilized with a bridle wire or more
securely held with an arch bar. More rigid fixation can be
obtained with intermaxillary wiring, which involves placing arch
bars on the upper and lower arches, placing teeth in the proper
occlusion, and connecting the upper arch bar to the lower bar
with elastic bands or 22- or 24-gauge wire.30
Temporarily immobilize more posteriorly located fractures
CHAPTER 20  Management of Facial Injuries
with a Barton bandage; this pulls the mandible in a superior
direction, obtains dental occlusion, and diminishes pain. Form
the bandage by wrapping a 0.25- to 0.5-inch gauze bandage or
ace wrap underneath the jaw and alternating around the top of
the head and back of the neck, with care taken to supply enough
force to maintain occlusion.16 Do not pull the chin posteriorly,
because this may displace the fracture and compromise the
airway (Figure 20-23).
All mandibular fractures are considered open fractures because
the gingiva is fixed to the underlying bone and mucosal disrup-
tions, visible or not, allow for oral flora to communicate with the
fracture zone. Prophylactic antibiotics are suggested, especially
in a setting where the time until surgical fixation may be unknown.
The most frequently recommended treatments are 500 mg of
penicillin V or 150 to 450 mg of clindamycin by mouth four times
daily for 5 to 7 days. The patient should remain on a soft, pureed
diet until surgical fixation has been accomplished.
Facial fractures are usually not immediate surgical emergen-
cies but should be seen by a specialist to allow for potential
surgical repair before 2 weeks has elapsed, at which point bone
healing begins. Pediatric patients experience faster bone healing
and should be seen within 1 week of injury. Pending evacuation,
apply ice to reduce edema and medicate for pain.17 Strong nar-
cotics are avoided if there is an associated head injury to avoid
respiratory depression in an obtunded patient.
SOFT TISSUE INJURIES
During evaluation and treatment of facial soft tissue injuries, it is
important to remember that these wounds may have significant
psychosocial and emotional impacts on the patient, with cosmetic
outcome and function being priorities. Treatment of these wounds
in the wilderness environment must take into consideration long-
term sequelae associated with an unfavorable cosmetic result. A
patient may recover from a traumatic experience only to be
reminded of it daily by a large scar or deformity.
Contusions, abrasions, and superficial lacerations are repaired
primarily or treated with wound debridement and wound care.
More complex lacerations that involve underlying muscles,
nerves, and ducts that must be identified at the time of injury
are referred for appropriate definitive care, especially if the injury
Treatment
Abrasions and contusions can be treated topically. Manage contu-
sions with cool compresses or ice, and have the patient sleep
with the head elevated to diminish periorbital edema and ecchy-
mosis.23 Abrasions can be cleaned with mild soap and warm
water to prevent infection and remove crusting. Once thoroughly
FIGURE 20-23  Barton bandage. A simple bandage can be used to
temporarily stabilize a jaw fracture.
431
 cleaned, abrasions should be covered with antiseptic ointment,
such as mupirocin or bacitracin, and a sterile dressing. Infection
rates do not differ between wounds cleaned with decontaminated
water or sterile saline.12 Hydrogen peroxide can be used to
remove crusts that form on the wound surface.
Complicated wounds with associated devitalized tissue may
necessitate delayed primary closure or closure by secondary
intention. Thoroughly clean, irrigate, and debride all soft tissue
injuries with a soft brush and decontaminated water to remove
foreign material and prevent traumatic tattooing and infection.42
Consider using a local or topical anesthetic agent so the patient
can tolerate adequate scrubbing. Keep tissue debridement to a
minimum. Significant tissue loss or avulsion usually necessitates
specialty referral to achieve the best cosmetic result.
Clean, simple, superficial, and uncontaminated facial wounds
less than 6 hours old may be closed with surgical glue or adhe-
sive tape strips if they are not under tension.20 Irrigate and
explore complex deeper wounds for underlying foreign bodies
or fractures. A layered closure using 4-0 or 5-0 absorbable inter-
rupted subcuticular sutures and 5-0 or 6-0 nonabsorbable mono-
filament interrupted skin sutures will remove tension from skin
edges and improve the appearance of the scar if sutures are
removed after 5 to 7 days. Adhesive tape strips can be used to
stabilize wound margins after suture removal.
The face has an excellent vascular supply, which allows for
wound closure with minimal risk of infection if treatment can be
accomplished within 6 hours of the injury. Topical antibiotics are
useful, but prophylactic oral antibiotics should not be initiated,
because these wounds rarely become infected. More complicated
wounds, including those that involve ear or nose cartilage,
through-and-through lip or buccal mucosa lacerations, bites, and
wounds with any evidence of maceration, contamination, or
TRAUMA
devascularization, require prophylactic oral antibiotic treatment
against normal bacterial flora associated with the affected site
and consideration for the mechanism of trauma. Inspect all facial
wounds frequently for evidence of vascular compromise or infec-
tion, or both. Significant infections require bandage removal,
possible surgical drainage, and intravenous antibiotics.
PART 4
Any injury that involves the eyelids, auricular helical rims,
nasal alar rims, or vermilion border has potential significant cos-
metic and functional implications and must be evaluated and
managed with extreme caution.
INJURIES TO THE LIPS
Lips are mobile muscular folds that have three distinct regions:
oral mucosa, skin, and a noncornified layer of stratified epithe-
lium called the vermilion. The vermilion border is the junction
between the skin and the dry vermilion. Realigning the border
and restoring the natural architecture of the philtrum are crucial
to successful cosmetic repair.
During repair of a through-and-through lip laceration, first
close the muscular layer with 5-0 absorbable sutures, and then
realign and stabilize the vermilion border with a vertical mattress
nonabsorbable suture. Next, close the inner mucosal layer with
4-0 absorbable sutures, the wet and dry vermilion with 5-0
absorbable sutures, and the external skin with 6-0 nonabsorbable
sutures. Through-and-through lacerations of the lower lip that do
not involve the vermilion border occur when lower incisors
impale tissue during facial blunt trauma. First, cleanse and close
the mucosal layer from an intraoral approach. Irrigate to remove
foreign material and oral bacteria, and then rescrub the extraoral
wound. Close the remaining layers, finishing with the skin. Large
soft tissue lip avulsions may require plastic surgery to achieve
the best cosmetic result (Figure 20-24).5
A mental nerve block anesthetizes the chin and lower lip; an
infraorbital nerve block anesthetizes the cheek, upper lip, lower
eyelid, and lateral aspect of the nose. These blocks provide
adequate anesthesia without tissue distortion and are easily per-
formed. The mental nerve exits the mandible through the mental
foramen in the midpupillary line 1 cm (0.4 inch) inferior to the
apex of the second bicuspid. While retracting the lower lip with
the nondominant hand, insert the needle 5 mm (2 inches) inferior
to the tooth, and inject 2 mL of anesthetic. The infraorbital nerve
432
FIGURE 20-24  Lip laceration involving the vermilion border.
exits the infraorbital foramen 1 cm (0.4 inch) below the infraor-
bital ridge. Place the third finger of the nondominant hand on
the infraorbital foramen, and use the second finger and thumb
to lift the upper lip. Insert the needle over the canine tooth at
the level of the gingival buccal sulcus. Aspirate while advancing
toward the foramen, and inject 2 mL of anesthetic (Figures 20-25
and 20-26).
TONGUE LACERATIONS
Tongue lacerations may be difficult to suture because of poor
visualization. Simple, small, linear lacerations less than 1 cm (0.4
inch) long and located centrally usually heal well without sutur-
ing. All lacerations that are deep or gaping or that bisect the
tongue should be closed with absorbable 4-0 or 5-0 suture.5 Suf-
ficient local anesthesia can be provided by a combination of
topical lidocaine and a nerve block. Apply local anesthesia by
applying gauze soaked with lidocaine 4% to the tongue for 5
minutes, and then locally infiltrate the wound with lidocaine 1%
with epinephrine, and/or perform an inferior alveolar or lingual
nerve block. The inferior alveolar and lingual nerves are termi-
nal branches of the trigeminal nerve. Palpate the vertical ridge
of the anterior border of the mandibular ramus with your thumb.
Using a tongue blade, push away the buccal surface of the
cheek to expose the target area. Position the syringe barrel over
the opposite premolar and parallel to the occlusive surface of
the lower teeth. Insert the needle into the oral mucosa medial
to the ridge, 1 cm (0.4 inch) above the occlusive surface of the
mandibular third molar. Aspirate while slowly advancing the
needle 2 cm (0.8 inch), and inject 2 mL of anesthetic to block
the inferior alveolar nerve. The lingual nerve runs with the infe-
rior alveolar nerve at the mandibular foramen. It supplies the
anterior two-thirds of the tongue, floor of the mouth, and gums.
Block the lingual nerve by withdrawing the needle 1 cm (0.4
inch) while aspirating, and then injecting another 1 mL of anes-
thetic. Prescribe a liquid or soft diet after any intraoral repair.
Advise the patient to gently swish and spit four times a day
and after eating with warm saline, antiseptic mouthwash,
chlorhexidine gluconate 0.12%, or half-strength hydrogen perox-
ide (Figure 20-27).
INJURIES TO THE EYELID
It is essential that providers recognize eyelid lacerations that
require referral to an ophthalmologist. Simple upper and lower
lid lacerations may be managed without consultation, but
complex lacerations that involve tissue avulsion or the tarsal
plate, lid margins, orbital septum, levator palpebrae superioris,
or lacrimal drainage system may require semiurgent ophthalmo-
logic referral for definitive care. The presence of a penetrating
globe injury must be identified.24 Upper eyelid lacerations with
exposure of orbital fat and ptosis in the presence of a horizontal

A meticulously close the skin with nonabsorbable 6-0 sutures.
B External ear injury may be associated with hearing loss, facial
FIGURE 20-25  Mental nerve block. A and B, Infiltrate anesthetic at
the mental foramen opening. To prevent neurovascular damage, do
not introduce the needle into the foramen.
lid laceration suggest levator palpebrae superioris muscle
damage.9 Lacerations involving the lateral aspect of the upper lid
may involve the lacrimal gland, which may be mistaken for
orbital fat and inadvertently excised. Evaluate for laceration of
the canalicular drainage system by instilling fluorescein into
the eye and assessing for its presence within the wound.5 Any
laceration that involves the medial portions of the upper and
lower eyelid or that is medial to the puncta should be assumed
to involve the canalicular system and requires evacuation
and ophthalmology referral. If unrecognized or untreated, lacera-
tion or obstruction of the lacrimal ducts will cause tears to over-
flow.42 Stenting the canalicular system is required to prevent
obstruction.
Superficial lacerations of less than 25% of the lid are candi-
dates for healing by secondary intention and may be treated
conservatively without suture repair. Clean and irrigate wounds
with clean, disinfected water, and instill topical antibiotic drops
(e.g., ciprofloxacin, ofloxacin, tobramycin) into the wound.5
Apply tape strips to approximate wound edges if the laceration
cannot be properly sutured. Lid margin lacerations require a
three-layer closure. Close the conjunctival side and tarsal plate
with 6-0 or 7-0 absorbable sutures, and close the external
surface with a nonabsorbable monofilament suture. Repair other
CHAPTER 20  Management of Facial Injuries
simple superficial lacerations that do not involve the lid margin
with either 6-0 or 7-0 absorbable or nonabsorbable sutures
(Figure 20-28).
INJURIES TO THE NOSE
Superficial nasal lacerations can be repaired with interrupted 5-0
or 6-0 nonabsorbable sutures, but complex nasal lacerations
involving the nasal mucous membrane and cartilaginous frame-
work require layered closure. Lacerations involving the nostril
margin or alar rim require precise alignment and eversion of skin
edges for a satisfactory cosmetic result and to prevent alar notch-
ing (Figure 20-29). Close full-thickness lacerations involving car-
tilage with a three-layered closure. First, suture the cartilage
together to restore the normal anatomic configuration. Next,
Finally, close the mucosa with absorbable 5-0 sutures. Contrac-
tion and retraction of the nasal margin may occur if there has
been poor approximation of the mucosa, or with scar con­
traction. All patients with nasal lacerations should be instructed
that scar revision may be required and appropriate referral
recommended.
Most nasal laceration repairs are facilitated by performing an
infraorbital nerve block with lidocaine 1% with epinephrine5 or
injection of local anesthetic into the area of injury. If the nasal
laceration involves the superior aspect of the nose or forehead,
a supraorbital nerve block may be useful. The supraorbital nerve
exits the skull at the supraorbital foramen, and then branches
cephalad into the medial and lateral branches to supply the
forehead and anterior scalp. The supratrochlear nerve supplies
the midforehead and lies under the medial 1 cm (0.4 inch) of
the eyebrow. It exits the skull 0.5 to 1 cm (0.2 to 0.4 inch) medial
to the supraorbital foramen. The infratrochlear nerve exits the
orbit superior to the medial canthus and travels inferiorly to
supply the medial eyelid, lateral nose superior to the medial
canthus, medial conjunctiva, and lacrimal apparatus. Use the
nondominant hand to locate the supraorbital notch, insert
the needle into the lateral edge of the middle one-third of the
eyebrow, and advance the needle while aspirating toward the
medial canthus. Then, inject 2 mL of anesthesia (Figure 20-30).
INJURIES TO THE EAR
nerve palsy, tympanic membrane rupture, and temporal bone
fracture. Evaluate ear trauma with an otoscope to observe the
integrity of the external canal and assess for hemotympanum and
otorrhea, which suggests underlying temporal bone injury that
requires evacuation. External cartilaginous ear trauma may result
in lacerations, tissue avulsion, and formation of a hematoma
within the ear itself.
Local ear anesthesia can be used to close lacerations or drain
auricular hematomas. Innervation of the ear is by the greater
auricular nerve, lesser auricular nerve, auricular branch of the
vagus nerve, and auriculotemporal nerve. Partial or complete
anesthesia of the ear can be accomplished using a variety of field
blocks. Inject approximately 2 to 4 mL of lidocaine 1% without
epinephrine, or bupivacaine 0.25% with a 25- to 27-gauge needle
subcutaneously into the skin around the ear (Figure 20-31).
To repair through-and-through lacerations, cleanse and irri-
gate the ear without dissecting the cartilage from the perichon-
drium. Debridement should be minimized to prevent a poor
cosmetic result. Reapproximate the cartilage with 5-0 or 6-0 clear
nonabsorbable sutures. Place sutures through the anterior and
posterior perichondrium as well as through the cartilage to
re-create the normal auricular contour. Suture the anterior and
posterior skin with 6-0 or 7-0 nonabsorbable interrupted sutures.
Simple superficial ear skin wounds are closed in a single layer
with 6-0 or 7-0 nonabsorbable sutures. Repairing complex ear
lacerations requires adequate coverage of the exposed cartilage
to prevent infection, chondritis, and cartilage necrosis. Lacera-
tions of the auricular helical rim are repaired with a three-layer
process that involves precisely realigning the auricular cartilage
433
 Area of
anesthesia

B
A C
FIGURE 20-26  Infraorbital nerve block. A, The unilateral infraorbital nerve block anesthetizes the lower
eyelid and upper lip. B, The nerve is located directly under the pupil when the patient is looking forward.
C, Avoid the orbit by keeping the needle tip under the orbital rim. (From Roberts JR, Hedges JR: Clinical
procedures in emergency medicine, 5th ed, St Louis, 2009, Saunders.)

Inferior
alveolar
Inferior Finger on
nerve
alveolar
TRAUMA

pterygomandibular
artery triangle

Coranoid
notch
Mandible Inferior
Lingual
alveolar
PART 4

nerve
nerve
Needle enters
1 cm above
tooth surface

A B

Second
premolar

First
premolar

C D
FIGURE 20-27  Inferior alveolar and lingual nerve blocks. A, Pterygomandibular triangle. B, Identify the
anterior border of the ramus of the mandible with the left index finger or thumb. C, Grasp the ramus with
the intraorally placed thumb and an extraorally placed index finger to allow visualization of the pterygo-
mandibular triangle. D, The syringe is angled, with the barrel of the syringe overlying the first and second
premolar teeth on the opposite side of the mandible. (From Roberts JR, Hedges JR: Clinical procedures in
emergency medicine, 5th ed, St Louis, 2009, Saunders.)

434

FIGURE 20-28  Eyelid laceration involving the tarsal plate and lacrimal
apparatus. (Courtesy Dr. Chang Hee Kim.)
FIGURE 20-29  Nasal laceration involving the alar cartilage. (Courtesy
Dr. Ross Stutman.)
FIGURE 20-30  Supraorbital, supratrochlear, and infratrochlear nerve
blocks. This is the site for local injection of the supratrochlear and
infratrochlear nerves, as well as for the lateral and medial branches of
the supraorbital nerve. (From Roberts JR, Hedges JR: Clinical proce-
dures in emergency medicine, 5th ed, St Louis, 2009, Saunders.)
to prevent notching (Figure 20-32). Precise realignment of the
CHAPTER 20  Management of Facial Injuries
helix and antihelix is vital for a good cosmetic result.
A potential space exists between the avascular cartilage and
perichondrium, where blood can accumulate. Shearing forces of
moderate intensity, which occur frequently during fights, wres-
tling matches, and mixed martial arts activities, may cause blood
extravasation and hematoma formation in the subperichondrial
potential space, thereby separating perichondrium from cartilage.
If the hematoma is not drained acutely, neocartilage formation
develops at the site of the clot, subsequently deforming the ear
and leading to a “cauliflower ear.”30
Treating an auricular hematoma involves complete evacuation
of the subperichondrial hematoma, elimination of dead space,
and reapproximation of the perichondrium to the underlying
cartilage. Prevent reaccumulation of hematoma by applying a
compressive dressing, and reexamine this frequently, with reaspi-
ration as necessary. If the provider does not have the tools
necessary to drain or aspirate the hematoma within 7 to 10 days,
patient evacuation is necessary because new perichondrial
growth must be debrided to prevent ear disfigurement and defor-
mity caused by cartilaginous necrosis, chondritis, or fibrosis35
(Figure 20-33).
An auricular hematoma may be drained either by aspiration
or by incision. Aspirate by perforating the hematoma with a
20-gauge needle, and compress the hematoma between the
thumb and forefinger until all blood is evacuated (Figure 20-34).
If the hematoma is less than 7 to 10 days old and if aspiration
is unsuccessful, incision and drainage may be required. With a
No. 15 scalpel blade, incise the hematoma by following along a
natural anatomic crease or curvature of the pinna. The incision
should be sufficiently long that simple compression adequately
drains the hematoma. After completely evacuating the hematoma,
irrigate the remaining pocket with normal saline (Figure 20-35).
Next, apply a topical antibiotic or antiseptic ointment. Reex-
amine the ear frequently for reaccumulation of hematoma. Create
a bolster dressing by placing petrolatum-coated cotton within all
fissures and folds of the ear until the dressing is level with the
helix, and then place a dry cotton gauze behind the ear to
provide padding and prevent the ear from being compressed
against the skull. Then, place dry cotton gauze anterior to the
ear and secure it with a circumferential compressive head
bandage that does not include the other ear. Another technique
is to suture dental rolls over the area to create a compressive
bolster dressing. The dressing should firmly reapproximate the
perichondrium to the cartilage without vascular compromise.40
Evacuate the patient for consultation and definitive repair if there
is significant tissue and cartilage loss that precludes cosmetic
closure (Figure 20-36).30,42
A number of methods are available to eliminate dead space
and prevent hematoma recurrence. However, incision and drain-
age of hematoma followed by placement of absorbable mattress
sutures has been shown to result in fewer reaccumulations and
complications. In addition, this technique eliminates the need for
a bulky bolster. Perform this technique after incision, drainage,
and irrigation of the hematoma, followed by manipulation of the
ear into its normal anatomic appearance. Weave absorbable 4-0
chromic or plain gut suture from posterior to anterior through
the skin and cartilage as many times as is necessary to achieve
appropriate ear contour while apposing skin to cartilage. Place
topical antibiotic or antiseptic ointment on both sides of the ear,
and apply a loose head dressing (rather than a compressive
dressing) for the next 24 to 48 hours.15
If medical-grade soft silicone putty is available, the lateral part
of the external auditory meatus and contours of the lateral pinna
surface are filled with putty, which hardens after a few minutes.
From the anterior aspect of the pinna, fold the malleable silicone
backward to cover the medial surface and mold to the pinna
before placing a head bandage.11
INJURIES TO THE CHEEK
Contusions and lacerations of the cheek or parotid region may
involve other structures, including the external auditory meatus,
TMJ, underlying zygomatic or maxillary bones, parotid gland,
435
 A

C
TRAUMA
PART 4

B D
FIGURE 20-31  Field blocks of the auricle. A, One method makes use of approximately 3 to 4 mL of anes-
thetic, both in the posterior sulcus and at a point just anterior to the tragus. B, An alternative field block
technique that involves depositing 2 to 3 mL of anesthetic with each needle pass. C and D, The locations
of anesthetic injections. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, 5th ed,
St Louis, 2009, Saunders.)

FIGURE 20-32  Ear laceration involving auricular cartilage. (Courtesy FIGURE 20-33  Auricular hematoma that requires drainage. (Courtesy
Dr. Ross Stutman.) Dr. Alicia Pilarsky.)

436
 CHAPTER 20  Management of Facial Injuries
Perichondrium

Cartilage

A B
FIGURE 20-34  Auricular hematoma aspiration. A, Subperichondrial hematoma within the concha of the
ear. B, Needle aspiration of auricular hematoma. A topical antiseptic is used to clean the ear, but local
anesthesia is seldom required. While stabilizing the pinna between thumb and fingers, puncture the most
fluctuant part of the hematoma with a 20-gauge needle. Use the thumb to “milk” the hematoma into the
syringe until the entire hematoma has been evacuated. Be careful not to puncture your thumb with the
needle. The thumb maintains continuous pressure on the ear for 3 minutes after the needle has been
withdrawn. A pressure dressing is then applied, and the ear is checked for reaccumulation of blood in
24 hours. Repeated aspirations may be required, and persistent accumulations require incision and drain-
age. (B redrawn from Ruddy RM: Aspiration of an auricular hematoma. In Fleisher GR, Ludwig S, Henretig
FM, et al, editors: Textbook of pediatric emergency medicine, 5th ed, Philadelphia, 2006, Lippincott
Williams & Wilkins, p 1889.)

Perichondrium Stensen’s duct, branches of the facial nerve, and transverse facial
artery. Failure to recognize these injuries may lead to significant
morbidity. Injuries to these structures require repair that occurs
Cartilage concurrently with laceration repair.
The parotid duct arises from the anterior aspect of the parotid
gland and runs superficially over the masseter muscle. The duct
Incise pierces the buccinator muscle and oral mucosa at the level of
Hematoma the second maxillary molar. A line that connects the midportion
of the upper lip with the tragus delineates the path of the parotid
duct over the cheek. The duct runs in proximity to the transverse
facial artery and buccal branch of the facial nerve. Suspect parotid
duct damage if there is saliva leakage from the wound when the
Stensen’s duct is irrigated with saline. A sialocele, cutaneous
fistula, or salivary duct cyst may occur from salivary fluid reten-
A B tion if a parotid duct injury is not initially recognized45 (Figure
Skin 20-37). Evacuation is required for definitive repair if a cheek
laceration involves Stensen’s duct.
Injuries to branches of the facial nerve (e.g., cranial nerve VII)
frequently occur in association with parotid duct injury. Delay
Incision injection of local anesthetic until facial nerve function has been
site evaluated. Evaluate facial nerve damage by observing the patient
move the eyebrows, eyelids, and mouth. Evacuate any patient
Posterior Anterior for immediate repair of facial nerve injury lateral to a vertical line
auricular auricular through the lateral canthus of the eye, because nerve transection
requires early repair to maximize recovery of facial nerve
function.

C FOREIGN BODIES IN THE NOSE AND EAR

D
FIGURE 20-35  Auricular hematoma incision. A, Hematoma separates
the perichondrium from the cartilage. B, Incision (arrows) made along
the skin curvature at the posterior edge of the hematoma. The hema-
toma is evacuated, and the area is irrigated. C, Two anterior dental
rolls are secured with sutures to a posterior dental roll to maintain
normal anatomy of the pinna. D, A side view illustrates the position of
sutures and dental rolls in relation to the incision site. Note that the
perichondrium is in apposition to the cartilage. (From Clemons JE,
Seveneid LR: Otohematoma. In Cummings CW, editor: Otolaryngol-
ogy: head and neck surgery, 2nd ed, St Louis, 1993, Mosby, p 2866.)
In contrast with children, who insert foreign bodies for no appar-
ent reason, adults insert foreign bodies into the nose and ear
deliberately to control epistaxis or to clean and relieve irritation.3
Insects may find their way into the nose or ear and prove to be
quite distressing, although not associated with trauma. The
patient can usually blow out insects from within the nostril by
occluding the unaffected nostril and blowing, and this rarely
requires provider instrumentation. Insects within the ear may be
problematic, because the inner ear canal is extremely sensitive.
The patient is usually aware that something is in the ear. If the
insect is alive, the patient may be extremely agitated and feel
movement of the insect or hear buzzing. This may be associated
with pain, fullness, impaired hearing, itching, canal edema, and
drainage. The insect may damage the canal and cause bleeding,

437
 Cotton soaked in mineral oil or 3 layers
saline-soaked packing gauze covering of gauze
a small dry cotton pledget that has
been placed in the ear canal.

A B
TRAUMA

Fluffed Elastic or
gauze gauze roll

C D
PART 4

FIGURE 20-36  Compression dressing of the ear. After successful aspiration of an auricular hematoma, use
a compression dressing to prevent reaccumulation of the hematoma or fluid. A, First, place dry cotton into
the ear canal, then carefully mold a conforming material into all of the convolutions of the auricle. One may
use petroleum jelly–impregnated gauze, saline-soaked 0.25-inch packing gauze, or cotton soaked in mineral
oil or saline. Inset, Note the gauze pack behind the pinna and use of saline-soaked packing gauze to conform
to the auricle. B, When the convolutions are fully packed, place a posterior gauze pack behind the ear. A
V-shaped section has been cut from the gauze to allow it to fit easily behind the ear. C, Place multiple
layers of fluffed gauze over the packed ear, and hold the entire dressing in place with Kling Gauze or an
elastic gauze roll. Do not wrap this too tight. D, The ear is thus compressed between two layers of gauze,
and the packing ensures even distribution of pressure to all parts of the auricle. (From Roberts JR, Hedges
JR: Clinical procedures in emergency medicine, 5th ed, St Louis, 2009, Saunders.)

tympanic membrane perforation, and infection. Tympanic perfo-
ration may cause tinnitus, vertigo, and hearing loss.
Before examining the ear, it is important to ascertain if
attempts have been made to remove the foreign body by the
patient, because this may have caused ear canal injury, tympanic
membrane perforation, or worsening foreign body impaction.
Ear canal irrigation may cause enlargement of some foreign
bodies.
Within the external auditory ear canal, there are two areas of
anatomic narrowing where foreign objects usually become stuck.
These include a point of bony narrowing called the isthmus at
the junction between bone and cartilage, and a point near the
inner end of the cartilaginous portion of the canal lateral to the
tympanic membrane.37 Examine the ear with adequate lighting,
an otoscope, and a large-size speculum to visualize the ear canal
and allow injection of a local anesthetic. Grasp the superior pinna
and retract it in a posterosuperior direction to straighten the
tortuous canal and to achieve a more complete view of the
external auditory canal.
Anesthetize or immobilize an insect within the ear canal to
decrease patient distress and facilitate removal. Immobilizing
agents include lidocaine 2% gel, lidocaine 10% spray or liquid,
mineral oil combined with lidocaine 2% or 4%, and alcohol. If
attempts are made to remove a moving insect, the insect or
device may cause ear damage.
With appropriate tools, foreign body removal may be
attempted in the wilderness. Instill a topical anesthetic, such as
lidocaine 1% to 2%, into the canal. Unfortunately, topical anes-
thetics are poorly absorbed through the impermeable keratinized
epithelial surface of the external auditory canal. Auralgan, a
topical combination of benzocaine and other ingredients, does
not provide adequate anesthesia for painful procedures. Local
anesthetic injection within the canal is painful and difficult to
perform, and frequently does not provide adequate anesthesia
of the inner ear and tympanic membrane.
A common technique to provide local anesthesia of the canal
requires insertion of a large speculum immediately inside the
auditory meatus to facilitate use of a 25- to 27-gauge needle that
is 3 to 5 cm (1.2 to 2 inches) in length in order to inject 0.25 to
0.5 mL of lidocaine 1% or a 1 : 10 mixture of sodium bicarbonate
8.4% with lidocaine into the subcutaneous tissue, stopping after
a small bulge in the skin is raised. Inject all four quadrants, as
well as deeper tissues along the anterior wall and at the posterior
wall of the bone–cartilage junction (Figure 20-38).

438

1
C A
Lacrimal
apparatus
2
3 B
5 4
FIGURE 20-37  Structures that may be injured by facial lacerations.
A, The lacrimal drainage system. B, The parotid duct. C, A line drawn
through the lateral canthus of the eye. Facial nerve injuries posterior
to this line should be repaired as soon as possible. 1 through 5,
Branches of cranial nerve VII. (Redrawn from the American Association
of Oral and Maxillofacial Surgeons: Oral and maxillofacial surgery ser-
vices in the emergency department, Rosemont, Ill, 1992, American
Association of Oral and Maxillofacial Surgeons.)
Speculum
Syringe
FIGURE 20-38  Four-quadrant field block anesthesia of the external
auditory canal. Local anesthetic is injected subcutaneously into the four
quadrants of the lateral portion of the ear canal. The largest speculum
that will fit is used to guide injections. The speculum is withdrawn
slightly and tilted toward each of the four quadrants; the needle is then
inserted subcutaneously. Inject a very small amount of anesthetic (i.e.,
0.25 to 0.50 mL) to produce a slight bulge in the soft tissue. A total
of 1.5 to 2 mL of anesthetic is usually sufficient to anesthetize the ear
canal and allow for painless removal of a foreign body. (From Roberts
JR, Hedges JR: Clinical procedures in emergency medicine, 5th ed, St
Louis, 2009, Saunders.)
CHAPTER 20  Management of Facial Injuries
FIGURE 20-39  External auditory canal anesthesia; diagram of injection
sites for an alternative technique to anesthetize the ear canal and
central concha. Each site should be injected with approximately 0.5 mL
of lidocaine 1%. Do not perform these injections if external signs of
infection are present. (From Roberts JR, Hedges JR: Clinical proce-
dures in emergency medicine, 5th ed, St Louis, 2009, Saunders.)
Another technique involves injecting approximately 0.5 to
1 mL of lidocaine 1% externally into each of five points around
the auditory meatus and the tragus (Figure 20-39).
Various instruments can be used to successfully remove a
foreign body from the ear canal. Alligator forceps, bayonet
forceps, and right-angle probes are frequently used.
Foreign body removal is often successful using indirect irriga-
tion of the canal. If tympanic membrane perforation is suspected,
this technique is contraindicated. Using a 20-mL syringe and a
14- or 16-gauge catheter, direct a stream of room-temperature
water or saline around the (nonvegetable) foreign body. Irriga-
tion directed past the object will collide with the tympanic mem-
brane and bounce against the posterior aspect of the foreign
body, thereby driving it out of the canal. This technique has a
low complication rate and is well tolerated.3
Cyanoacrylate adhesive–tipped swabs have been used to
remove foreign objects from the ear. Complications associated
with this method include contaminating the ear canal with glue
that is difficult to remove and accidental perforation of the tym-
panic membrane.
After successfully removing an insect, inspect the external
auditory canal for trauma and retained material. Evaluate the
tympanic membrane for perforation caused by the insect itself
or by removal attempts. Confirm that there is not tympanic mem-
brane perforation. If irrigation was implemented, instill several
drops of isopropanol within the canal to facilitate moisture evap-
oration. Initiate a prophylactic oral antibiotic (e.g., 500 mg of
cephalexin by mouth twice daily) if the tympanic membrane was
ruptured or perforated, because the middle ear is at risk for
infection. Administer topical steroid–containing antibiotic suspen-
sion drops (e.g., hydrocortisone with ciprofloxacin) to alleviate
pain and potentially decrease the risk of developing otitis externa
as a result of the foreign body and removal efforts.
WILDERNESS MEDICAL KIT FOR FACIAL TRAUMA
The wilderness medical kit, described in Box 20-1, should be
prepared to anticipate treating facial trauma.
PREVENTION OF FACIAL TRAUMA
Prevent significant head and facial trauma by wearing a helmet
for recreational activities such as technical rock climbing, rock
scrambling, mountaineering, caving, skiing, snowboarding, bik-
ing, whitewater kayaking and rafting, and horseback riding. Wear
439
 BOX 20-1  Wilderness Medical Kit for Facial Trauma

Temporomandibular Joint Relocation Supplies Surgical tissue glue

Bite blocks Adhesive strips
Plastic finger splints No. 15 scalpel blade
18-gauge needles
Mandibular Dislocation and Fracture Supplies
Ophthalmoscope
Barton bandage Fluorescein paper and blue light
0.25- to 0.5-inch bandaging gauze
Traumatic Ear Injury Evaluation
Nasal Fracture and Epistaxis Supplies
Otoscope
Nasal speculum and light source Alligator forceps, bayonet forceps, and right-angle probes
Nasal clips and tongue depressors Viscous lidocaine
Cotton pledgets and cotton-tipped applicators Medical-grade soft silicone putty
Silver nitrate–tipped sticks Cotton pledgets
Topical anesthetics:
  Tetracaine 1% Prophylactic Antibiotics
  Cocaine 1% to 4% Oral antibiotics:
  Lidocaine 5%   Cephalexin
  Ephedrine 5%   Amoxicillin-clavulanate
  Aqueous epinephrine 1 : 1000   Dicloxacillin
  Benzocaine 20%   Clindamycin
Vasoconstrictive nasal sprays:   Trimethoprim-sulfamethoxazole
  Phenylephrine 0.5% (Neo-Synephrine)   Penicillin V
  Oxymetazoline 0.05% (Afrin)   Amoxicillin
Commercial nasal tampons or sponges Topical steroids containing antibiotic suspension drops:
Nasal balloon devices   Hydrocortisone with ciprofloxacin
Petroleum jelly–impregnated gauze Topical antibiotic drops:
Absorbable degradable nasal packing materials   Ciprofloxacin
Foley urinary catheters   Ofloxacin
  Tobramycin
Wound Evaluation and Repair
Nonabsorbable nylon 6-0 and 7-0 sutures
Absorbable chromic 6-0 and 7-0 sutures

safety goggles and custom-fitted mouth protective devices when REFERENCES

training for and participating in contact sports or any activity
that may injure the eyes, mouth, and face. Wear properly fitted
protective equipment, such as helmets, face masks, padded chin Complete references used in this text are available
straps, and mouth guards, for all sporting activities to prevent online at expertconsult.inkling.com.
orofacial trauma.
REFERENCES
1. Amsterdam JT. Oral medicine. In: Marx JA, Hockberger R, Walls R,
editors. Rosen’s emergency medicine: concepts and clinical practices.
7th ed. St Louis: Mosby; 2009.
2. Awang MN. A new approach to the reduction of acute dislocation of
the temporomandibular joint: a report of three cases. Br J Oral Maxil-
lofac Surg 1987;25:244.
3. Belleza WG. Otolaryngologic emergencies in the outpatient setting.
Med Clin North Am 2006;90:329.
4. Biller JA, Pletcher SD, Goldberg AN, et al. Complications and the time
to repair of mandible fractures. Laryngoscope 2005;115:769.
5. Brown DJ, Jaffe JE, Henson JK. Advanced laceration management.
Emerg Med Clin North Am 2007;25:83.
6. Ceallaigh PO, Ekanaykaee K, Beirne CJ, et al. Diagnosis and manage-
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7. Ceallaigh PO, Ekanaykaee K, Beirne CJ, et al. Diagnosis and manage-
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8. Chan TC, Harrigan RA, Ufberg J, et al. Mandibular reduction. J Emerg
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9. Chang EL, Rubin PA. Management of complex eyelid lacerations. Int
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10. Chegar BE, Tatum SA. Nasal fractures. In: Cummings CW, Flint PW,
Haughey BH, et al., editors. Otolaryngology: head and neck surgery.
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11. Choung YH, Park K, Choung PH, et al. Simple compressive method
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13. Frazee TA, Hauser MS. Nonsurgical management of epistaxis. J Oral
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14. Gentile DA, Morris JA, Schimelpfenig T, et al. Wilderness injuries and
illnesses. Ann Emerg Med 1992;21:853.
15. Giles WC, Iverson KC, King JD, et al. Incision and drainage followed
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16. Green BE. Use of modified head halter for a Barton bandage. Plast
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17. Haug RH. Selecting the appropriate setting for management of maxil-
lofacial trauma. J Oral Maxillofac Surg 1999;57:983.
18. Haug RH, Likavec MJ. Evaluation of the craniomaxillofacial trauma
patient. In: Greenburg AM, editor. Craniomaxillofacial fractures. New
York: Springer-Verlag; 1993.
19. Hill CS, Hughes O. Update on management of epistaxis. West Lond
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20. Hollander JE, Richman PB, Werblud M, et al. Irrigation in facial and
scalp laceration: does it alter outcome? Ann Emerg Med 1998;31:73.
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temporomandibular luxations. Gen Dent 1990;38:147.
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23. Lammers RL. Principles of wound management. In: Roberts JR,
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24. Lammers RL. Methods of wound closure. In: Roberts JR, Hedges JR,
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25. Laskin DM. Temporomandibular joint disorders. In: Cummings CW,
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26. Leemon D, Schimelpfenig T. Wilderness injury, illness, and evacua-
CHAPTER 20  Management of Facial Injuries
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2002. Wilderness Environ Med 2003;14:174.
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29. Massick D, Tobin EJ. Epistaxis. In: Cummings CW, Flint PW, Haughey
BH, et al., editors. Otolaryngology: head and neck surgery. 4th ed.
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30. McKay MP, Mayersak RJ. Facial trauma. In: Marx JA, Hockberger R,
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34. Pope LER, Hobbs CGL. Epistaxis: an update on current management.
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36. Quinn FB: Temporomandibular joint disorders. <http://www.utmb
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Hedges JR, editors. Clinical procedures in emergency medicine. 5th
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38. Rustemeyer J, Kranz V, Bremerich A. Injuries in combat from 1982-
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39. Schlosser RJ. Epistaxis. N Engl J Med 2009;360:784.
40. Sharma K, Goswami SC, Baruah DK. Auricular trauma and its manage-
ment. Indian J Otolaryngol 2006;58:232.
41. Sholl MJ, Curcio EP. An introduction to wilderness medicine. Emerg
Med Clin North Am 2004;22:265.
42. Shumrick KA, Chadwell JB. Facial trauma: soft-tissue lacerations and
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43. Shun TA, Wai WT, Chiu LC. A case series of closed reduction for
acute temporomandibular joint dislocation by a new approach. Eur J
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44. Stacey DH, Doyle JF, Mount DL. Management of mandibular fractures.
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45. Steinberg MJ, Herrera AF. Management of parotid duct injuries. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 2005;99:136.
46. Stephens BD, Diekman DS, Klein EJ. Recreational injuries in Wash-
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47. Tiner BD. Facial fractures. In: Montgomery MT, Redding SW, editors.
Oral-facial emergencies. Portland, Ore: JBK Publishing; 1994.
48. Tuli T, Hachl O, Hohlrieder M, et al. Dentofacial trauma in sports
accidents. Gen Dent 2002;50:274.
49. Viehweg TA, Roberson JB, Hudson JW. Epistaxis: diagnosis and treat-
ment. J Oral Maxillofac Surg 2005;64:511.
50. Wade AL, Dye JL, Mohrle CR, et al. Head, face, and neck injuries
during Operation Iraqi Freedom II: Results from the U.S. Navy-Marine
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52. Zadik Y, Levin L. Orofacial injuries and mouth guard use in elite
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440.e1
 CHAPTER 21 
Wound Management
RAMIN JAMSHIDI
Management of wounds sustained in remote and wilderness
environments requires special preparation and knowledge. The
basic elements of wound care can be outlined so that a provider
in a remote, austere, or wilderness environment can safely
manage the acute wound and thereby limit secondary injury.
In the care of acute trauma, attention is frequently focused
on wound closure. In truth, most traumatic wounds fare well if
left open to heal by secondary intention because this allows
drainage of infected or necrotic tissue.21 However, open wounds
incur a prolonged healing time, wound care discomfort, and
vulnerability to further injury, and they leave larger scars.
The critical goals of immediate wound care are to stop hemor-
rhage and limit complications related to infection. Secondary
goals are to promote rapid healing and optimize the cosmetic
outcome.55
440
TYPES OF WOUNDS AND DEFINITIONS
Abrasions result from tangential (shearing) forces. Although abra-
sions are most commonly superficial, they can be extensive and
involve deep tissues. Superficial abrasions pose no threat to the
patient but may require use of analgesics. Deep abrasions that
have completely obliterated skin and denuded underlying fascia
are at increased risk for infection and must be kept clean. By
virtue of the mechanism of injury, abrasions involve more surface
area than they do depth. As a consequence, they are not ame-
nable to suture closure. Abrasions are treated with extensive
irrigation to remove all debris (often dirt or gravel) and with
application of nonadherent dressings. Topical antiseptic solutions
are not necessary but are useful adjuncts in preventing gauze
dressings from adhering to raw tissue. Such dressings should be
changed once daily or more frequently as needed for soilage or
adherence (drying out). Abrasions do not form abscesses, because
they have no deep spaces to contain infection. They may become
superinfected and develop cellulitis; although this is uncommon,
the possibility is more real in the exposed wilderness environ-
ment. Diagnosis and management of cellulitis are discussed later
in this chapter.
Burns (see Chapter 15) may be caused by thermal, chemical,
or radiation sources. These injuries span a spectrum from trivial
sunburn to deep tissue necrosis. The first principle of manage-
ment is to limit further injury by extinguishing the source, seeking
shade, washing out chemicals, and moving the person away from
the source. For chemical exposures, voluminous irrigation is the
key to limiting further injury. This should be done with clean
(not necessarily sterile) water, and the run-off irrigant should be
prevented from injuring more skin.8,19,43 Chemical quenchers (i.e.,
alkaline solution for an acid burn) should never be used because
the resulting exothermic reaction will cause secondary injury. The
practice of avoiding chemical quenchers has a long history. There
is some animal evidence to suggest that this may not be such a
problem, but accepted practice is to avoid use of chemical
quenchers and concentrate on dilution and removal. Once the
burning process is arrested, burn care must focus on antisepsis
because infection poses the single most important immediate
threat.
Burn wounds should be fastidiously cleaned to remove all
foreign material and devitalized skin. Depth was formerly
described as first, second, or third degree, but modern descrip-
tion relies on the descriptors partial thickness and full thickness
(Figure 21-1). Blisters should be left intact unless they interfere
with function. There is some debate about the management of
blisters, but in a wilderness environment, the “biologic bandage”
provided by an intact blister supersedes any academic debate
about the presence of inflammatory mediators in the blister fluid.
Blisters over the palms or joints are exceptions to this rule,
because their presence will significantly limit motion and poten-
tially engender contraction or decrement in function. One school
of thought is that these blisters should be unroofed and gently
scrubbed away with moistened gauze or trimmed with scissors.
Once cleaned, burns should be dressed and kept clean. Topical
antiseptic agents should be applied to burns with invasion deep
enough to result in blistering or erosion through the skin to white
tissue or burned muscle underneath. Silver sulfadiazine is an
excellent agent, and can be reapplied once or twice daily to
prevent the wound from desiccating. In the absence of silver
sulfadiazine (and for burns < 1% of the body surface area), anti-
biotic or antiseptic ointment (e.g., bacitracin) can be employed.
Lacerations can be deep or superficial, or simple or irregular
(Figure 21-2). Generally, lacerations are amenable to primary
repair (i.e., closure at the time of injury). Closure simplifies
wound care and optimizes cosmetic outcome. Much of the fol-
lowing discussion is dedicated to management of lacerations.
FIGURE 21-1  Campfire burns, mostly partial-thickness burns, with
both intact and ruptured blisters. The distal forearm is pale white
without capillary refill, representing full-thickness injury. (Courtesy
Ramin Jamshidi, MD.)
CHAPTER 21  Wound Management
FIGURE 21-2  A deep and irregular laceration that is suitable for irriga-
tion and multilayer closure with interrupted mattress sutures (see text).
(Courtesy Ramin Jamshidi, MD.)
Punctures are lacerations with a very small entry site injury
but an extended depth. Generally these injuries should not be
closed, because they cannot be adequately cleansed. There is
little cosmetic benefit to closure, whereas there is significant risk
for trapping infectious agents deep within the wound because
of the inherent difficulty of properly irrigating the tract.
CLINICAL PRESENTATION
Immediate evaluation of traumatic wounds should include deter-
mination of the type of injury. Focused assessment includes
determination of the surface area and apparent depth. Distal
sensation and passive and active range of motion must be
assessed to elucidate any associated nerve injury, tendon disrup-
tion, or fracture. Nerve and tendon injuries will not affect acute
management but are important as a baseline examination. Frac-
tures require immobilization, a topic discussed in Chapter 22.
Distal perfusion must be assessed to determine the likelihood of
vascular injury. If there is suspicion of vascular injury based on
examination, depth of the wound, or blood at the scene, the
wound should not be probed (nor blood clots dislodged) until
one is prepared to place direct pressure to control hemorrhage
and potentially ligate or suture the injured vessel.
Time since injury is very important when considering wound
closure. Within several hours of injury, traumatic wounds become
colonized with bacteria. Even without frank infection, heavy
colonization impedes proper wound healing.21,28,56 A bacteria-
laden wound that has its edges approximated will generally not
heal and has increased risk for developing an abscess. Histori-
cally, the accepted dogma has been that traumatic wounds older
than 6 hours should not undergo primary closure, but this is
based only on animal experiments by P.L. Friedrich that date
back to 1898. Efforts to establish a firm time limit beyond which
traumatic wounds should not be closed have previously yielded
inconsistent results.4,12,34,60 More recently, a randomized prospec-
tive trial in the Netherlands demonstrated no increase in infection
rates between wounds closed before or after 6 hours from
injury.62
With copious irrigation and removal of foreign bodies, most
wounds that are otherwise suitable for closure (see earlier discus-
sion) can be closed if this is accomplished within 6 hours of
injury.25 This deadline may be extended in the hospital setting,
where thorough sharp debridement can be undertaken in a con-
trolled environment. In some circumstances, wounds may be
closed days or even weeks after they have been initially gener-
ated, but this involves sophisticated surgical care.35 This situation
should not be confused with an acute wound in the wilderness,
which in all circumstances should be thoroughly irrigated, have
foreign bodies removed, and have dressings applied. These ele-
ments are critical, whereas closure is usually optional.
Acute wounds in the wilderness should be closed only if they
are clean, if suitable materials and instruments are at hand, and
441
 A B
FIGURE 21-3  A, Irrigation of a deep inguinal wound to remove debris. B, Placement of an interrupted
vertical mattress suture to approximate the deep tissue defect with eversion of the edge and relief of
tension. C, Completed interrupted closure. (Courtesy Ramin Jamshidi, MD.)
if the care provider has had proper training. If less than 6 hours
have passed since injury, closure is generally safe. If conditions
are fitting and the provider has sufficient experience, this author
supports closure up to 24 hours after injury. An intermediate
option is partial wound closure, in which the “corners” and/or
deeper layers of tissue are reapproximated while a portion of the
wound is left open to heal by secondary intention. This helps
TRAUMA
minimize wound morbidity and discomfort while allowing drain-
age if infection were to develop.
TREATMENT
Personal protective equipment should be donned before inter-
PART 4
rogating, preparing, possibly closing, and dressing a wound. Eye
shields and gloves are considered mandatory equipment. Eye
shields are particularly important in preventing exposure of
mucous membranes to bodily fluids. Gloves are essential; they
should be made of a material other than latex and should contain
no talcum or other lubricant. Talcum, calcium carbonate, and
cornstarch are common glove lubricants, and all have been
shown to cause wound granulomas, foreign body reactions,
adhesions, and chronic sinuses. Sterile gloves are less cumber-
some to work with but are not required, because they do not
reduce the incidence of infection in an austere setting.47 Use of
a mask has also not been demonstrated to reduce rates of acute
wound infection but certainly provides a protective barrier for
the care provider. Hair coverings are not necessary, because
studies have failed to demonstrate reduction in wound infection
rates.
CLEANSING TECHNIQUES
Cleansing involves removing devitalized tissue, clearing debris,
and copiously irrigating the area.25 This may involve vigorous
manipulation of painful and sensitive tissues, so if oral analgesics
are available, they should be used. Constricting jewelry and
equipment should be removed from the affected area (e.g., rings,
piercings). Ideally, hair around the wound is trimmed because
the roots harbor bacteria. Hair should be trimmed to a few mil-
limeters in height because shaving at the surface increases wound
infection rates by causing superficial skin trauma.3 Eyebrow hair
is an important exception, because trimming or shaving can result
in permanent abnormal hair growth. If hair trimming is not pos-
sible, an antiseptic ointment can be used to paste the hair down
away from the wound.
Water should be used to clean the wound. There is no dem-
onstrated benefit to use of saline solutions, and there is no
absolute need for the irrigant to be sterile.8,19,43 Although some
persons mention use of dilute (1%) povidone-iodine as an
442
C
irrigant, this has not proved to be more efficacious. Whatever the
method available to generate potable water (e.g., iodine tablets,
mechanical filter, irradiation, boiling), it is sufficient to generate
irrigation fluid for wound care. Hydrogen peroxide is injurious
to deep tissues and should not be used as an irrigant.
The greatest impact on wound cleanliness is gained from the
volume of irrigant and simple mechanical debridement. Debride-
ment is achieved by removal of obvious foreign material (as with
forceps) and also by pulsing irrigant at the wound (the fluid
agitation is an effective debrider) (Figure 21-3).37 The available
volume should be used in successive bursts rather than a single
“gush,” because dilution of wound contaminants is far superior
with small serial volumes. Although the matter has not been
systematically researched, a guideline that is often used is a
minimum of 100 mL per centimeter of wound length. Optimal
stream pressure has been determined to be 5 to 10 psi, but in a
remote setting, use of pressure gauges or regulators is unneces-
sarily cumbersome; it is sufficient to realize that excessive pres-
sures are not required.54,60 A large (20- to 60-mL) syringe attached
to a 19- or 20-gauge needle or catheter is an effective instrument
for this purpose, and will approximate that pressure. Alterna-
tively, holes can be punched into the cap of a squeezable water
bottle to generate a similar effect. A splash shield at the tip of
the instrument decreases the risk of personal exposure. If not
available as a specific commercial product for this purpose, one
can easily be fashioned from a paper or plastic plate, or the base
of a disposable water bottle or drinking cup.
Preparing for the actual wound closure, the skin edges may
be prepared with an iodine, povidone-iodine, chlorhexidine,
hydrogen peroxide, or isopropyl alcohol solution, but these
antiseptic agents should not be used within the wound itself
because of potential toxicity. If concentrated ethyl alcohol (i.e.,
liquor) is available, it may be effective in reducing wound con-
tamination, but this has not been systematically evaluated. These
agents should be used to cleanse the skin surrounding the
wound, using gauze soaked with the liquid to paint an overlap-
ping spiral from the wound outward to a distance of approxi-
mately 5 cm. The cleansed skin must be allowed to dry to
achieve the full effect; this takes 3 to 5 minutes at 20° C (68° F).
Honey has been used for thousands of years as an antimicro-
bial dressing, but only in recent years has it been scientifically
evaluated for effects on wound healing. The antibacterial effects
are believed to be due to acidity, osmolarity, and chemical factors
such as hydrogen peroxide and methylglyoxal. The latter is
present only in manuka honey (a generally edible honey), which
has been formulated into commercial wound care products.
Despite regulation by the Food and Drug Administration (FDA),
purity and potency vary greatly among honey products, and
clinical research into their efficacy is ongoing.41 Some of the
commercial dressings available are lightweight, weather-resistant,
and useful adjuncts for wilderness wound care. For example,
Medihoney (Derma Sciences) and TheraHoney (Medline Indus-
tries) are manuka honey products that come in a variety of
formulations, including hydrocolloid gel, adhesive bandage, and
combination alginate dressings. Some of these can be left in place
for 5 days at a time and reduce the need for frequent dressing
changes.
Honey in wound care is a promising and evolving area but
cannot be recommended as a routine adjunct at this time.,31 If
honey products are employed in wound care, this author recom-
mends verified products regulated by the FDA. It is estimated
that more than 80% of products labeled as manuka honey are
counterfeit. Furthermore, while there is allure to this centuries-old
practice, simply pouring table honey onto a wound, especially
in the austere environment, is not advised. Modern honey prod-
ucts contain a variety of natural and synthetic products that do
not necessarily provide medicinal benefit. There is also potential
harm to pouring a “sealing” gel of honey into a wound because
this may encourage bacterial proliferation and limit drainage of
exudate or pus.
VASCULAR INJURIES
Evaluation of hemorrhage is a major component of acute wound
management; even if bleeding has stopped, there may be a risk
for delayed rebleeding. The wound should be irrigated vigor-
ously so that if bleeding is to occur, it happens while the wound
is being interrogated and one is poised to address it. Inadequate
hemostasis during initial treatment comes at the cost of avoidable
delayed blood loss, which can be particularly hazardous in the
wilderness setting.
Bleeding from wounds can almost always be controlled with
direct pressure. The most common reason for failure of direct
pressure to control bleeding is too short a compression time.
Initial pressure should be applied for 5 minutes (checked with
a timepiece to ensure accurate timing). If bleeding persists, pres-
sure should be reapplied for 10 minutes or pressure should be
applied at both the wound and a proximal inflow point (e.g.,
popliteal, femoral, or brachial artery).29 The second most common
reason for failure of direct pressure is that pressure is not applied
in a focused manner over the site of bleeding. A broadly applied
towel over a large wound will not be as effective at controlling
bleeding as will finger-point pressure applied over the actual site
of greatest bleeding.
In the face of profuse diffuse bleeding (as from a large raw
wound), topical adjuncts are available to promote thrombosis.5,9,36
The original such product is QuikClot, a granular coagulant
powder designed to be poured onto wounds to stop diffuse
bleeding. The mechanism of action of the original product is
adsorption of water onto zeolites, which activates factor XII and
catalyzes platelet aggregation. However, the granular form of this
material was difficult to use for two reasons: the poured material
is unwieldy and difficult to control in windy situations, and the
reaction is exothermic, causing pain and risking burn injury.
QuikClot has now been modified and integrated into a gauze
dressing (also marketed as Combat Gauze). The active element
is now kaolin, an alumina silicate that activates and accelerates
the enzymatic clotting cascade. The solid consistency of Combat
Gauze is more manageable and generates no heat on application.
Celox Gauze is based on chitosan, a natural product derived from
shellfish. Initial versions of this product, too, were granules to
be poured into a wound, but it is now embedded into an actual
gauze dressing and also has no exothermic properties. HemCon
bandages are also chitosan based and not exothermic. These
agents are all designed to be applied directly to bleeding wounds
and compressed with direct pressure. Before wound closure,
these dressings must be removed and bulky gelatinous deposits
in the wound irrigated out (although mild residual coatings are
reportedly safe to leave in place). All of these agents are sup-
ported by anecdotal reports of success and are clearly superior
to simple gauze dressings, reducing bleeding by nearly an order
of magnitude. To date, head-to-head studies of these agents have
been underpowered and are difficult to interpret, but these
agents have found widespread use in the military and are becom-
CHAPTER 21  Wound Management
ing increasingly popular in civilian prehospital trauma care.
In contrast to the above products, which are designed to
control gross hemorrhage, there are adjuncts intended to assist
with lower-volume bleeding within the wound. Surgicel products
are procoagulant materials composed of a scaffold of cellulose
polymer. They have been in clinical use for more than 60 years
and are manufactured in fibrillar consistency as well as woven
sheets. The major benefit of these agents is that they are totally
absorbable, so they can be left on or within the wound; the
wound can even be sutured closed over them. Gelita-Cel is a
procoagulant dressing that is similar to Surgicel. It is a knitted
sheet of resorbable cellulose that boasts complete dissolution in
as little as 96 hours (more rapidly than Surgicel and therefore
theoretically less likely to result in an encapsulated collection
within the wound).
Tourniquets have often been considered a last resort to stop
life-threatening hemorrhage. Considerable debate continues over
the use of tourniquets and who should be allowed to apply them
(laypersons, emergency first responders, midlevel health care
providers, physicians, or even specialty-specific physicians). The
more proximal a tourniquet is applied, the greater the risk of
devastating tissue or limb loss. With experience from recent mili-
tary and civilian terrorist attacks, tourniquet use is making a
comeback and garnering support from authoritative groups. The
best potential use of a tourniquet is for a traumatic amputation
in which there is copious, diffuse bleeding at the open end that
cannot be controlled by other means (such as direct pressure).
In this case, a tourniquet can be firmly applied just proximal to
the open wound so that distal ischemic tissue is minimized
(Figure 21-4). This practice has been supported by the American
College of Surgeons Committee on Trauma.12
Commercial tourniquets such as the Combat Action Tourni-
quet are available, but a blood pressure cuff can serve as an
effective instrument. Whatever device is employed, it should be
applied and intensified until pressure exceeds arterial pressure
and then increased at least another 20 mm Hg or until bleeding
stops. Controversy also exists as to whether tourniquets should
be intermittently released during prolonged application. This
debate is fueled by contradictory experimental evidence.40,46
Nonetheless, most groups now suggest avoiding intermittent
release because of the possibility of additional blood loss without
a clear benefit.15 If a tourniquet is released (as when testing
whether hemorrhage has been controlled and it is no longer
necessary), it should be done slowly over a minute or two,
because recirculation of stagnant, acidic, and hyperkalemic blood
from the nonperfused distal limb can lead to hemodynamic
instability. If dysrhythmia is noted, the tourniquet should not
be released further until the patient stabilizes. Hypotension and
even cardiac arrest may result when a tourniquet is released;
these dangers are sometimes overlooked and can cause tragic
outcomes.
FIGURE 21-4  Severe complex crush injuries of both legs. These
wounds mandate immediate evacuation, but profound hemorrhage
may require tourniquet placement to prevent exsanguination until
advanced surgical care is available. (Courtesy Ramin Jamshidi, MD.)
443
 TABLE 21-1  Relative Indicators of Vascular Injury
turgor from infiltration of the solution. Conventional teaching is
that epinephrine-containing local anesthetic solutions should not
Hard Signs Soft Signs be used in end-vascular beds such as the nose, fingers, toes, and
penis because of concern for ischemia. However, there is litera-
Active or pulsatile hemorrhage Hypotension or shock ture to support safe use of these solutions for digital blocks.57,63
Pulsatile or expanding Neurologic deficit immediately Using anesthetics without epinephrine allows maximum flexibil-
hematoma following injury ity in terms of allowable location of use. Pain of injection for any
New thrill or bruit Stable, small, nonpulsatile local anesthetic can be attenuated by mixing 1 mEq of sodium
Limb ischemia or compartment hematoma bicarbonate with each 9 mL of anesthetic to buffer the solution.
syndrome Proximity of wound to major It should be noted that this delays the onset of action by approxi-
Diminished or absent distal pulse vessels mately 5 minutes.
The most common reasons for apparently ineffective local
anesthetic effect are use of an insufficient dose and inadequate
time allowed for onset of effect. Time to onset depends on the
Although profuse external hemorrhage is easy to localize, agent’s ability to cross cell membranes, which is determined by
ischemic complications of vascular injuries are more subtle and the compound’s intrinsic pKa. In general, a minimum of 3 minutes
sometimes overlooked. Examination findings are classically is required for onset of effect (as with lidocaine), but sometimes
divided into “soft” and “hard” signs of vascular trauma, indicating as much as 15 minutes is required (as with bupivacaine). This
the relative likelihood of a significant vascular injury (Table chemistry explains the delayed onset of action when the anes-
21-1).29 The presence of a hard sign is more than 90% predictive thetic is mixed with bicarbonate.
of the need for vascular intervention. Only about one-third of For all agents, intravascular administration or overdose will
patients with a single soft sign have an abnormality on arteriog- first cause agitation, tremor, and tinnitus, then seizures, and,
raphy, and few of these require emergent intervention. Any finally, cardiac arrest through aberrant conduction.23 These risks
patient with a hard sign of vascular injury requires immediate are particularly important to consider in children, in whom toxic-
evaluation by a surgeon. A simple, reliable, classic evaluation is ity occurs at lower doses. Table 21-2 lists maximum doses of
the arterial pulse index (ratio of systolic blood pressure in the commonly employed local anesthetics, along with weight-based
affected extremity to the contralateral side). An index of less than guidelines for children. Although ample anesthetic should be
0.9 is 95% sensitive for major arterial injury, and an index of administered, caution must be exercised to ensure that no intra-
more than 0.9 rules out injury, with a negative predictive value vascular administration occurs and to avoid nearing the maximum
of 99%.30 dose. This principle is complicated by the fact that maximum
doses are ill defined and are set at different levels in different
nations.48 Of note, patients with liver disease and those taking
ANESTHESIA
TRAUMA

medications (such as systemic antifungals) interfering with cyto-

Manipulation of traumatic wounds can be painful and provoke
anxiety. Studies have demonstrated that music can reduce pro-
cedural anxiety.39,52 For most patients, explaining the steps
involved can improve tolerance by guiding expectations.65 If
vigorous debridement or suture closure is to be attempted, infil-
PART 4
chrome P-450 metabolism will have decreased capacity to metab-
olize aminoesters. In patients with renal failure, the metabolism
of bupivacaine is altered, which requires a dose reduction of
15% to 20%. Concern frequently arises over administration of
epinephrine-containing local anesthetics to patients with heart

tration of local anesthetic can provide tremendous comfort for disease. However, these dilute local or regional doses do not
the patient and thus facilitate technically superior closure. Anes- cause significant systemic hemodynamic effects.
thetic solutions can be applied locally within tissue, as topical Local anesthetics can be applied topically as well and have
agents or as regional nerve blocks. demonstrated efficacy in numbing the skin, although 20 to 30
Direct intradermal or subcutaneous injection is the most minutes is required for onset. Topical anesthetics are particularly
common technique of local anesthetic use. These agents are useful for superficial wounds over a large surface, such as burns
synthesized in two related chemical classes: aminoamides and abrasions.33 A variety of formulations are available: TAC
(lidocaine, bupivacaine, dibucaine, etidocaine, mepivacaine, (0.5% tetracaine, 0.027% epinephrine, 11.8% cocaine), LET (4%
prilocaine, and ropivacaine) and aminoesters (chloroprocaine, lidocaine, 0.1% epinephrine, 0.5% tetracaine), and EMLA (2.5%
procaine, tetracaine, and cocaine). Characteristics of the most lidocaine, 2.5% prilocaine in a eutectic mixture containing a
commonly used local agents are listed in Table 21-2. Inclusion thickener, emulsifier, and distilled water buffered to pH 9.4), and
of epinephrine in the solution causes local vasoconstriction by 5% lidocaine jelly. Characteristics of these agents are summarized
α1-adrenoceptor agonism and nearly doubles the duration of the in Table 21-3. Care must be taken to avoid application near
local effect of the medication. By slowing systemic absorption of mucous membranes because of the potential for systemic absorp-
the anesthetic, epinephrine also increases the maximum allow- tion and toxicity. Compared with TAC, LET has less potential for
able total dose. Inclusion of epinephrine in the anesthetic solu- toxicity, is not a controlled substance, and is less expensive.1 LET
tion is believed by some to improve local hemostasis, but this is should be stored in a light-resistant container and is stable for 6
a minor contribution relative to the effect of increased tissue months if refrigerated and 4 weeks at room temperature. It
should be discarded if the solution becomes discolored. Near
mucous membranes, 3 mL of LET solution can be combined with
150 mg of methylcellulose (4000 cps) by stirring for a few
TABLE 21-2  Properties of Select Local Anesthetics minutes, to create a gel preparation that should be used imme-
diately. This lessens the likelihood of having the topical prepara-
Maximum Weight-Based tion run onto the mucous membranes.
Agent* Duration Dose Dose True IgE-mediated allergic reactions to local anesthetics are
very rare, particularly with aminoamide anesthetics.14,23,48 Typi-
Amide Class cally these reactions are actually caused by preservatives such as
Lidocaine 30-60 minutes 300 mg 5 mg/kg methylparaben in multidose vials. One alternative is to use an
  with epi 60-120 minutes 500 mg 7.5 mg/kg aminoester anesthetic such as chloroprocaine. However, the prin-
Bupivacaine 90-240 minutes 175 mg 2 mg/kg cipal metabolite of the aminoesters is paraaminobenzoic acid,
  with epi 180-360 minutes 225 mg 3 mg/kg which is chemically similar to methylparaben and can induce the
Ester Class same reactions. A reasonable approach to a reported allergy to
Chloroprocaine 15-30 minutes 800 mg 7 mg/kg a particular anesthetic is to use a preservative-free anesthetic of
  with epi 30-60 minutes 1000 mg 10 mg/kg the other class.
Use of diphenhydramine has been described as an alternative
*With epi, epinephrine 1:200,000 (5 µ/mL). to traditional local anesthetics.45 At 1% concentration, it can be

444
 CHAPTER 21  Wound Management
TABLE 21-3  Properties of Topical Anesthetics

Agent Composition Time to Onset Notes

TAC 0.5% tetracaine 30 minutes Seizures and cardiac arrest reported; controlled substance; avoid
0.057% epinephrine mucosal surfaces
11.8% cocaine
LET 0.5% tetracaine 15-30 minutes Inactivated by extensive light exposure
0.14% epinephrine
4% lidocaine
EMLA 2.5% lidocaine 30-120 minutes Longer duration; requires occlusive dressing; methemoglobinemia
25% prilocaine reported; do not place over open wound
LMX 4 or 5 4% or 5% liposomal lidocaine 15-40 minutes

injected subcutaneously or subdermally but causes more pain particularly useful in a wilderness setting involving exposure to
from injection than do the classic anesthetics, and this pain is the elements. Available agents include Dermabond, SurgiSeal,
not diminished by dilution or mixing with bicarbonate.49 More Indermil, and Histoacryl. Each of these differs slightly in time to
importantly, diphenhydramine injection can result in vesicle for- drying, maximum tensile strength, and viscosity. In general, the
mation and tissue necrosis.22 Because of these characteristics, it butyl agents (Indermil and Histoacryl) dry more quickly, but
is not recommended as a local anesthetic. In the absence of any the octyl agents (Dermabond and SurgiSeal) are more flexible.
pharmacologic anesthetics, ice may be applied around the wound The variability in clinical worth is relatively slight, so the selection
edges for 5 minutes to diminish sensation. should be based on availability and cost. Although many are
Regional anesthetic techniques can be useful for dealing with stable at lower than 30° C (86° F), it should be noted that storage
extremity wounds or fractures. This involves infiltrating the anes- of Indermil for longer than 4 weeks requires refrigeration (Table
thetic around the nerve(s) innervating the affected region.27 These 21-4). In the absence of a medical glue, Krazy Glue can be
techniques rely on specific anatomic landmarks and are beyond applied a ways distant from tender areas or mucosal surfaces. It
the scope of this chapter. will not remain in place as long as the glues that are approved
by the FDA for clinical use, and some of the breakdown products
can be injurious if they enter a wound. In clinical practice,
WOUND CLOSURE TECHNIQUES however, it can be useful, particularly in areas such as the hands
The first determinant of whether or not to close a wound is the and fingers.
type of trauma sustained. The next is the degree of contamination Improvised wound closure has been described using only
and time since injury. If the wound clearly has foreign material tape, needle, and thread. Two strips of adhesive tape are cut to
that cannot be removed or devitalized tissue that cannot be 2.5 cm (1 inch) longer than the wound. One-quarter of each strip
completely debrided, the wound should be left open to heal by of tape is folded over lengthwise (sticky to sticky) to create a
secondary intention. Critical factors are the experience of the long nonsticky edge on each piece (Figure 21-5). One strip of
health care provider and availability of instruments. Wound the tape is attached to each side of the wound, 0.6 to 1.3 cm
closure is almost never so necessary that an untrained provider (0.25 to 0.5 inch) from the wound, with the folded (nonsticky)
should attempt it. Even in experienced hands, wound closure in edge toward the wound. Using a needle and thread, the folded
remote settings may beget serious complications, including cel- edges are sewn together, cinching them tightly enough to bring
lulitis, abscess, wound dehiscence, necrotizing soft tissue infec- the wound edges together properly (Figure 21-6). The tape will
tion, and systemic sepsis.53
A variety of materials and approaches may be taken to close
wounds. Sutures are generally required to approximate deep
tissues, but the superficial aspects of wounds can be addressed
with adhesive strips, sutures, glues, or staples, or some combina-
tion thereof.26
Small superficial lacerations in areas with modest skin tension
may be amenable to reapproximation with dressing strips such
as Steri-Strips, Leukostrips, or Episeal. This can also be achieved
with clean, semiporous medical paper tape. These strips of tape FIGURE 21-5  Folding a longitudinal piece of tape to prepare for a
are laid perpendicular to the direction of the wound while suture anchor strip.
holding the edges together. Small gaps should be left between
strips to ensure ventilation. Different manufacturers boast supe-
rior adhesiveness, but the greatest impact on tape adherence is
the use of liquid adhesive on the skin before applying the tape.
Tincture of benzoin and Mastisol are equally effective for this
purpose as long as they are allowed to dry for a minute before
the strips are applied. The modern genesis of these products was
the use of plastic medical tape to approximate wounds in remote
locations when providers found the skin too thin or delicate to
retain sutures. Modern adhesive strips can still be used for this
purpose, or even in a hybrid fashion; strips can be placed along
wound edges to reinforce the skin and help it “hold” suture. This
practice actually dates back to the 16th century, when Ambroise
Paré pasted linen strips to wound edges to reinforce suture
closure.
Modern cyanoacrylate skin glues are effective, affordable, and
more versatile than adhesive strips.10,26,50 Although they do not
provide as much wound strength as does suture closure, they FIGURE 21-6  Sewing the tape suture strips together to close the
boast the added benefit of sealing the incision, which may be wound.

445
 TABLE 21-4  Characteristics of Selected Topical Adhesives

Product Layers of
(Manufacturer) Chemical Class Application Storage Recommendations Comments*

Butyl-CA Polymers (Faster to Dry)

Histoacryl n-butyl-CA 1 layer Store at 22° C (72° F) Low viscosity
(Aesculap) Not more than 8 hours at 40° C (104° F)
SwiftSet n-butyl-CA 1 layer 5° C (41° F) to 25° C (77° F)
(Covidien)
Octyl-CA Polymers (More Flexible)
Dermabond 2-octyl-CA 1-3 layers Below 30° C (86° F) Applies a thick coat
(Ethicon) Away from direct heat or moisture
LiquiBand Exceed 2-octyl-CA 1 layer 5° C (41° F) to 25° C (77° F) Leaves a flexible seal
(Advanced Medical Solutions)
Skin Affix 2-octyl-CA 1 layer 5° C (41° F) to 25° C (77° F)
(Medline Industries)
SurgiSeal 2-octyl-CA 1-2 layers N/A
(Adhezion Biomedical)
Butyl-CA/Octyl-CA Blends
Dermaflex 60% 2-octyl-CA 1 layer Room temperature
(Derma Sciences) 40% n-butyl-CA
GLUture 60% 2-octyl-CA 1 layer Below 30° C (86° F) Marketed for veterinary applications
(Abbott Labs) 40% n-butyl-CA Multiple-use tube
Low cost
Other
Krazy Glue ethyl-CA N/A N/A Not marketed for medical application
(Krazy Glue) Multiple-use tube
TRAUMA

Low cost

*Comments are the opinion of the author, based on personal experience.

CA, cyanoacrylate; N/A, not available.

stick much better if a thin layer of benzoin is applied to the skin Sutures are the workhorse of wound closure because of dura-
PART 4

before beginning.6 This use of tape can also be employed when
suturing delicate skin, as in elderly patients or those receiving
chronic steroid therapy. Preparing the skin with adhesive and
tape adds strength to the closure and decreases the likelihood
of the suture tearing through the skin. This is performed as
described above except that the entire tape length is applied to
the skin without creation of a nonsticky edge. Full-thickness
sutures are then passed through skin and tape as though they
were one tissue layer.
bility and versatility; characteristics of the most versatile sutures
for acute traumatic wounds are listed in Table 21-5.16,20,51 When
suturing deep tissue, absorbable materials of immediate durabil-
ity, such as polyglactin (e.g., Vicryl) or copolymeric glycolic, and
lactic acids (e.g., Polysorb) should be used. At 2 weeks, these
materials retain approximately three-quarters of their original
strength.13,18 Nondyed varieties are preferred within 5 mm (0.2
inch) of the skin surface to avoid wound tattooing. For mucosal
lesions (such as within the mouth), rapid-absorbing gut suture is

TABLE 21-5  Properties of Select Sutures

Suture Material Structure Tensile Strength Absorption Uses

Chromic gut Bovine intestinal serosa Monofilament 0% at 2 weeks 21 days Mucosal repair
treated with a
chromium salt
Biosyn Glycolide and Monofilament 75% at 2 weeks; 40% 90-110 days Skin
dioxanone at 3 weeks
Vicryl Polyglactic acid Braided 75% at 2 weeks; 50% 55-70 days Deep tissue, including ligation
at 3 weeks of small bleeding vessels
Polysorb Glycolic and lactic acid Braided 80% at 2 weeks; 30% 55-70 days Deep tissue, including ligation
copolymer at 3 weeks complete of small bleeding vessels
absorption
Prolene, Surgipro, Polypropylene Monofilament Long-term hydrolysis Not absorbed Skin or full-thickness wound;
Surgilene major vessel ligation/repair
Ethilon, Dermalon, Nylon Monofilament Long-term hydrolysis Not absorbed Skin or full-thickness wound
Monosof
Nurolon, Surgilon Nylon Braided Long-term hydrolysis Not absorbed Skin or full-thickness wound
(holds knots better than
monofilament nylon)
Sofsilk Silk Braided Poorly defined Permanent Can be used to ligate vessels,
but falling out of use because
of high tissue reactivity

446
the most suitable.11 In all these cases, a tapered-tip needle should
be used so that deep tissue is not lacerated. Ideally, skin suturing
should be done with monofilament nonabsorbable material
attached to a cutting needle. Nylon (e.g., Ethilon, Dermalon) and
polypropylene (e.g., Prolene) are typical nonabsorbable sutures.
Polypropylene is blue but does not tattoo skin as noted above
for absorbable sutures. If proper materials are not available,
nondyed absorbable suture with a tapered needle can be used
on the skin, but nonabsorbable suture should not be buried
within the wound; in this case, deep mattress sutures should be
placed so that deep tissue is approximated but the suture can
still be removed once healing is complete. Size selection is based
on visibility and the degree of tension expected on the wound.
For skin approximation, the recommended sizes are 5-0 or 6-0
for the face, neck, or ears; 5-0 or 4-0 for the fingers or hand; 4-0
or 3-0 for the scalp, arms, legs, feet, chest, or abdomen; and 3-0
or 2-0 on the back or over a major joint. Deeper layers (below
the skin) generally require suture one size larger than or the
same size as is being used for the skin (e.g., a deep upper arm
laceration receives 4-0 absorbable suture to approximate the
deep layer, followed by 4-0 for the skin).
The goals of deep tissue closure are to take tension off the
skin closure and to obliterate the gap in the deep tissue so that
a seroma or abscess is less likely to form.16,20,51 Muscle sheaths
(i.e., fascia) should be reattached, and subcutaneous tissues
should be sutured together in interrupted fashion. A deep wound
may require multiple layers of suture before skin closure, but
usually one or two suffice. Each “layer” of suture is indicated not
by the absolute depth of the tissue but by the presence of distinct
anatomic “planes” (e.g., separate fascial sheaths) that must be
approximated. If significant muscle, tendon, or nerve injuries are
recognized, suture repair should not be attempted in the acute
setting, but written notes should be recorded for long-term
follow-up (Figure 21-7). If required later, these repairs are per-
formed in an elective setting after healing has occurred and
functional deficits are delineated.
Traumatic wounds are typically irregular in shape and thus
lend themselves to closure by interrupted technique. Running
closure may be employed if there is a truly linear laceration. A
straight or smoothly curved incision may be closed with a running
suture to save time. An irregularly shaped wound should be
closed with interrupted sutures to achieve optimal alignment
(Figure 21-8, A; see Figure 21-3, B and C). Mattress techniques
can be applied for deep wounds, thin skin, or wounds under
tension.51,66 Vertical mattress sutures approximate the wound at
two depths and evert wound edges for optimal healing (see
Figure 21-8, B). Horizontal mattress sutures close a single depth,
evert wound edges, and distribute tension along the length of
the incision (see Figure 21-8, C). More complex wounds can
benefit from application of advanced techniques, such as local
rotational or advancement flaps.59,61
Mechanical clips can be applied more rapidly than can sutures.
Ancient Hindus used ant mandibles to pinch skin edges together
and then twisted off the ant bodies.64 Modern skin staplers are
A B
FIGURE 21-8  A, Interrupted simple sutures. B, Interrupted vertical mattress sutures. C, Interrupted hori-
zontal mattress sutures.
CHAPTER 21  Wound Management
FIGURE 21-7  Deep laceration over the wrist that is likely to involve
nerve, tendon, and vascular injury. There is no role for attempting
tendon or nerve repair in the field; care should focus on irrigation,
control of hemorrhage, and aseptic aftercare. (Courtesy Ramin
Jamshidi, MD.)
made by various manufacturers and are useful for rapid closure
of wounds on thick skin such as the scalp or back. They can be
particularly effective for rapidly achieving hemostasis in the scalp,
which is richly perfused and frequently rebleeds after direct pres-
sure is released.
Wounds of the abdomen and chest have the potential to
involve the viscera. If air is felt, heard, or seen emanating from
a chest wound, or if the patient is complaining of shortness of
breath, some form of pneumothorax must be present. The wound
should not be closed tightly but rather should be covered with
a nonocclusive dressing. This will minimize contamination while
allowing outflow of air so that tension pneumothorax does not
develop. If intestine or omentum protrudes from an abdominal
wound, there is considerable likelihood of visceral injury (Figure
21-9). Such a wound should be covered with a moist, secure
dressing and not be sutured. Both of these conditions require
prompt evaluation by a surgeon.
Scalp wounds occur frequently, can be very bloody, and have
unique management options. The scalp is richly perfused, so
even superficial lacerations can bleed profusely. Initial care
should include firm direct pressure for several minutes. If bleed-
ing does not abate, secure scalp closure is necessary to assist in
local pressure and minimize the potential space for hematoma
formation. If the galea aponeurotica is lacerated and suture is
available, the tissue should be primarily repaired to further limit
the space available for hematoma expansion. For skin closure,
staplers are excellent in this circumstance because staples are
rapidly applied and effective and the scars are less noticeable on
the scalp. Sutures may be used but are not necessary. If a scalp
C
447

FIGURE 21-9  Abdominal laceration with omentum emanating from
the wound. This signifies the possibility of serious visceral injury and
mandates immediate surgical evaluation. (Courtesy Ramin Jamshidi,
MD.)
wound is bleeding and needs to be closed but no instruments
are available, a hair tie may be performed. Hair is parted along
the incision and twisted into cords on either side of the incision.
Cords opposing one another across the laceration are tied
together to approximate the wound edges6,32 (Figure 21-10).
The timing of skin suture and staple removal depends on the
individual wound. Healing and wound remodeling are gradual
processes; at 1 week after injury, a typical wound has just 5% to
10% of the original tensile strength. Most of the healing process
takes place over the first 6 weeks, at which point the tensile
TRAUMA
strength reaches 70% of baseline.21,55 Leaving skin closure mate-
rial in place longer keeps tension off the wound but increases
the likelihood of visible scarring from the suture or staple itself;
therefore, the timing of removal varies based on the durability
and visibility of the affected area. On the face or neck, sutures
are removed at 3 to 5 days; on the fingers or hand, at 5 to 7
PART 4
days; on the scalp, leg, chest, or abdomen, at 7 to 10 days; on
FIGURE 21-10  String and hair-tying method for closing a scalp wound.
448
the back, arms, or feet, at 10 to 14 days; and across any major
joint, at 14 days. For each site, sutures should be left in place
longer if scar integrity seems poor, malnutrition has been
involved, or the orientation of the wound subjects it to excessive
tension. Sutures are removed with scissors, and staples are
removed with a staple remover or by laterally spreading a hemo-
stat between the skin and the staple. Once the sutures or staples
are removed, the healing wound may be reinforced with adhe-
sive strips or skin glue (as described earlier) to minimize tension
while healing continues, especially in a wilderness environment
where vigorous activity may strain the wound. Visibility of the
resulting scar is minimized by keeping it out of direct sunlight,
particularly for the first 3 months following injury.
DRESSINGS AND AFTERCARE
Wounds should be kept as clean as possible. Any wounds
addressed in austere environments are at increased risk for
infection and should be carefully monitored for cellulitis or
abscess (see Complications). The incidence of infection obviously
depends on the specific wound characteristics, anatomic location,
and context of injury. Although up to 25% of acute wounds reveal
Streptococcus, Staphylococcus, or Escherichia when cultured,
most studies have revealed just a 5% rate of infection. Weighing
this against the risk for adverse reactions and the effect of select-
ing resistant species, antibiotics are not prescribed for all trau-
matic wounds.42 The decision to administer prophylactic or
empirical antibiotics must be individualized to each situation.
Patient factors that should encourage consideration of antibiotics
include poorly controlled diabetes mellitus, malnutrition, recent
chemotherapy, prosthetic valve or organ transplant recipient,
peripheral vascular disease, renal failure, chronic liver disease,
chronic corticosteroid use, or other types of immunocompromise.
Wound factors include delay to cleansing and repair, extensive
devitalized tissue, heavy contamination or retained debris, bites,
oral lacerations, foot wounds, open fractures, or injury to poorly
perfused tissue (bone, joint, tendon).4,34,42
Tetanus is caused by Clostridium tetani, an organism found
in soil and the excrement of humans and animals. The often fatal
disease can be prevented by immunization, but 40% of Americans
age 60 years or older lack seropositivity.38 Tetanus immunization
status must be evaluated for all patients with traumatic wounds,
and a booster dose of toxoid and/or immune globulin adminis-
tered if the patient is at risk for infection (Table 21-6). The for-
mulation of tetanus toxoid booster depends on the age of the
patient and the vaccination history (Table 21-7).1,10 Recent updates
to the recommendations from the Centers for Disease Control
and Prevention include expansion of Tdap administration begin-
ning at 7 years of age, and inclusion of pregnant women and
adults 65 years of age and older.2
TABLE 21-6  Postinjury Tetanus Prophylaxis
History of Immunization
(Doses of Adsorbed
Tetanus Toxoid Clean and
Previously Received) Minor Wound All Other Wounds*
Unknown or less than Toxoid†,‡,§ Toxoid and TIG‡,§,||
series of 3 doses
Three or more doses
  Last within 5 years No prophylaxis No prophylaxis
  Last within 10 years No prophylaxis Toxoid
Last over 10 years Toxoid Toxoid and TIG‡,§,||
earlier
*Such as contaminated with dirt, soil, saliva, or feces. Includes punctures,
avulsions, missile injuries, crushing injuries, burns, and frostbite.
†Tetanus toxoid formulation depends on the age of the patient (see Table 21-7).
‡No toxoid should be administered to infants younger than 6 weeks of age.
§Patients with acquired immunodeficiency syndrome should receive TIG
regardless of immunization history.
||TIG 250 units intramuscularly (for both adults and children). Toxoid should not
be administered at the same site.
TIG, Tetanus immune globulin.

TABLE 21-7  Recommended Tetanus Toxoid Types
Age Tetanus Toxoid Formulation
<6 weeks No toxoid
>6 weeks and <7 years DTaP
7 years or older Tdap if never received; Tdap
Td if previously received Tdap
DTaP, pediatric diphtheria and tetanus toxoids and acellular pertussis; Td,
tetanus and diphtheria toxoids; Tdap, tetanus toxoid, reduced diphtheria
toxoid, and acellular pertussis.
Dressings serve a few limited purposes; they protect the
wound from the elements and contamination, absorb fluid from
the wound and thereby protect the surrounding skin, and provide
an environment conducive to healing. Generally these goals can
be achieved by dry gauze secured with a bit of tape. Gauze
dressings should be changed once daily or more frequently as
needed when soiled.
For wounds left open to heal by secondary intention, episodic
dressing changes are required to provide gradual debridement
and prevent desiccation. The simplest and most traditional
approach is to apply gauze moistened with water, normal saline,
or lactated Ringer’s solution directly onto the wound and cover
it with a layer of dry gauze. These dressings should be changed
3 times daily as the outer dry gauze wicks fluid away from the
wound surface. In the absence of infection, this process can be
simplified by the use of hydrogels that do not evaporate as
quickly as do crystalloid solutions. Tegagel and Curafil are two
of the most widely used hydrogels available in an amorphous
form (gel in a squeezable tube). This is a more effective formula-
tion for a wilderness provider (as opposed to prepackaged
individual gauze and hydrogel dressings). If hydrogels are used,
moist-to-dry gauze dressings can be changed just once a day.
The last few years have witnessed a proliferation of wound
care products intended to accelerate healing and increase the
simplicity of care. One of the most notable and applicable to
wilderness care is Mepilex. This is a silicone foam dressing
designed to wick exudates away from wounds while keeping
them hydrated to allow healing. This versatile adjunct self-
adheres to the skin surrounding the wound and can be left in
place for up to 5 consecutive days to manage open or weeping
wounds. The foam should be trimmed to cover the wound and
overlap onto surrounding skin by about 2 cm (0.8 inch). It should
be stored in dry conditions at a temperature under 35° C (95° F);
sunlight will discolor the material but not alter its function.
Antiseptic ointment is produced in a variety of formulations
by many manufacturers. These greasy or gelatinous materials
contain povidone-iodine, bacitracin, polymyxin B, or a combina-
tion of topical antimicrobials; no substantive evidence exists for
the superiority of one formulation over another. However, one
must be sure that the patient is not allergic to any of the agents
in the ointment. Antiseptic ointments are useful topical agents
for injured areas that do not penetrate the skin but are predis-
posed to desiccation (e.g., superficial abrasions or burns). The
viscosity of these ointments makes them particularly effective in
areas that are difficult to dress and are in constant motion (such
as the face or hands).
COMPLICATIONS
Cellulitis is diagnosed by the presence of a blanching erythema
around and spreading away from the edges of a wound and may
demonstrate proximal streaking along lymphovascular channels.
It is important to distinguish this condition from the hyperemia
that commonly surrounds the edges of a healing wound. Ery-
thema associated with normal wound healing is not as bright red
as is cellulitis, has less dramatic blanching with pressure, is sym-
metric around the edges of the wound, and extends not more
than a centimeter from the wound edges. If erythema is not
limited by these characteristics or if it progresses in size, wound
infection is present. The treatment for cellulitis is a systemic
antibiotic. The chosen antibiotic (first-generation cephalosporin
CHAPTER 21  Wound Management
or antistaphylococcal penicillin) should cover typical skin flora
but also take into consideration any particular exposures (e.g.,
open water injury, animal bite, soil contamination) that may be
associated with the trauma and dictate coverage of different
microbes.7 Cellulitis without abscess does not require suture
removal. If cellulitis persists or progresses after 36 hours of the
above treatments, the antibiotic spectrum should be broadened
and the wound reevaluated to ensure that there is not an under-
lying abscess.
Abscess is a suppurative soft tissue infection. Pus is a mixture
of dead organisms, leukocytes, and debris contained within a
deep tissue space. An abscess will continue to expand, causing
progressive pain, surrounding cellulitis, and potential systemic
illness until drained (Figure 21-11). Antibiotics may stunt the
growth or spread of associated cellulitis, but abscesses require
drainage. This is accomplished by removing any sutures, staples,
or tape keeping the wound closed. The abscess cavity is copi-
ously irrigated, and a soft probe is used to ensure that any locu-
lated collections are properly drained. An excellent probe is a
cotton-tipped swab dipped in antiseptic ointment to prevent
deposition of cotton threads.
Necrotizing soft tissue infections are true emergencies and
require surgical intervention. These can take the form of super-
ficial infections or deep fasciitis. The superficial variety can be
easily recognized by the foul-smelling, gray (dirty dishwater)
drainage, but necrotizing fasciitis can develop surreptitiously
because skin findings are often subtle and mistaken for simple
cellulitis. The signs of deep infection include pain on passive
motion, woody induration, and rapid spread.24 Antibiotics may
stall the pace of progression, but these conditions are uniformly
fatal if not addressed by a general surgeon. The definitive treat-
ment is wide incision and drainage along with fluid resuscitation
and intensive supportive care. This typically results in large,
disfiguring wounds.
Compartment syndrome results from elevated pressures within
a contained compartment; as pressure rises, it exceeds venous
pressure and, eventually, arterial pressure, resulting in tissue
ischemia. In the wilderness setting, this is most likely to occur
from blunt trauma, particularly with crush injury or a closed
fracture. The classic evidence of increased compartment pres-
sures is pulselessness, pallor, pain on passive motion, poikilo-
thermia, and paresthesia.58 Pain on passive motion is the most
sensitive and earliest sign to develop, but all are relatively late
signs of compartment syndrome. Immediate surgical evaluation
is needed because the definitive intervention is incision and
release of the involved compartment. If signs of compartment
syndrome develop from a penetrating injury, it suggests that there
was an occult vascular injury and an expanding hematoma is
trapped beneath the closure. The closure should be opened, the
blood or hematoma evacuated, and a fresh attempt made to
control bleeding. If compartment syndrome is not addressed,
irreversible tissue necrosis begins by 6 hours.
Persistent bleeding is a common concern of wilderness
medical providers. Typically this indicates a missed injury or
FIGURE 21-11  Minor puncture wound that has developed a secondary
abscess and associated cellulitis. (Courtesy Ramin Jamshidi, MD.)
449
 TABLE 21-8  Wound Care First-Aid Kit

Function Core Items Optional Items

Personal protection Gloves (nonlatex) Sterile gloves (nonlatex, nonpowdered)

Eye shield Surgical cap
Mask
Headlamp
Instruments Needle driver (15.2 cm [6 inches]) Hemostats (curved)
Scissors (iris tip)
Toothed forceps (Adson type)
Nontoothed forceps (DeBakey type)
Wound preparation 60-mL syringe Splash shield
18-gauge needle or blunt cannula Chlorhexidine surgical scrub brush
21-gauge needle
Water filtration system
Povidone-iodine swab packets
Closure materials 2-0 nylon (cutting needle) 5-0 nylon (cutting needle)
4-0 nylon (cutting needle) 6-0 nylon (cutting needle)
3-0 Vicryl (tapered needle) 4-0 Vicryl (tapered needle)
Skin stapler Mastisol (15 mL)
Dermabond skin glue vials
Adhesive strips (1.3 cm [0.5 inch])
Dressings Gauze (10 × 10 cm [4 × 4 inches]) Elastic roll (7.6 cm × 4.6 m [3 inches × 5 yards])
Porous paper tape (1.3 cm [0.5 inch]) Mepilex (10 × 20.3 cm [4 × 8 inches])
Gauze roll (11.4 cm × 3.7 m [4.5 inches × 4 yards]) Surgicel Nu-Knit (2.5 × 8.9 cm [1 inch × 3.5 inches])
Flexible, reusable splint QuikClot (10 × 10 cm [4 × 4 inches])
Medications 0.25% bupivacaine (10-mL vials) Silver sulfadiazine 1% cream (50 g [1.8 oz])
Antiseptic ointment (30 g [1 oz]) 5% lidocaine jelly (35 g [1.2 oz])
Cephalexin (500 mg)
Ciprofloxacin (500 mg)

inadequate direct pressure. If a wound continues to bleed tent detriment in motor function or sensation, ongoing drainage
through a dressing, the bandage should be removed to allow from the wound, a persistent open wound, burns over the face
direct inspection. Consider that a discrete vascular injury may or genitals, and burns over joints.
have been missed and that an exposed vein or artery requires
direct pressure or ligation.29 If a prolonged period of direct pres-
sure does not stop the hemorrhage, one may need to use hemo-
WOUND CARE KIT
static adjuncts or tourniquet application as discussed earlier. Many adjuncts are available to facilitate wilderness wound care,
Many wounds can be managed in a backcountry environment but a kit with core supplies will suffice in most circumstances.
without interrupting the activities. However, some injuries Table 21-8 lists suggested components of such a kit.
mandate evacuation. These include open fractures, compartment
syndrome, persistent bleeding, tourniquet use, progressive loss
of sensation or motor function, progressive infection, and full- REFERENCES
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ation upon the return to civilization.44 These include any persis-
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guide’s case report and review of wilderness wound management
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54. Stevenson TR, Thacker JG, Rodeheaver GT, et al. Cleansing the trau-
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SW, Cance WG, Chen H, et al., editors. ACS surgery: Principles and
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450.e1
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TRAUMA
PART 4

450.e2
 CHAPTER 22 
Wilderness Orthopedics
JULIE A. SWITZER, RALPH S. BOVARD, AND ROBERT H. QUINN

Life is sweeter nearer to the bone.  Henry David Thoreau

The textbook discussion of orthopedic trauma in wilderness
medicine has traditionally focused on discrete musculoskeletal
injury to individuals or small groups in the mountain, sea, or
desert setting. The scope of wilderness medicine today has
widened significantly to include injuries caused by terrorism,
military engagement, and forces of nature. Recent disasters,
such as the Great Indian Ocean tsunami of 2004, Hurricane
Katrina in August 2005, and the Haiti and Chile earthquakes of
2010, serve as powerful examples of situations in which ortho-
pedic injuries were myriad and provision of care was limited in

450

FIGURE 22-1  Improvised traction following the 2010 earthquake in
Haiti. (Courtesy Sam Slishman.)
significant part by the remoteness of setting or inaccessibility of
resources.
The wilderness practitioner needs to approach trauma outside
the normal clinic or hospital setting with a sense of anticipation
and improvisation. One needs to be prepared for a scenario
of chaos, inadequate medical supplies or support, sepsis, and
limited or delayed evacuation of patients. The tidy fractures of
individual sport injury or accidental trauma in a civilized society
have little in common with massive crush injuries, limb mangling
with segmental loss, and severed limbs of natural or terroristic
disasters. Issues of triage and prioritization become paramount.
Successful organization of resources and mobilization of person-
nel often determine the outcome of the operation. Improvisation
in splinting to stabilize or immobilize shattered limbs can mini-
mize neurovascular compromise and reduce morbidity and mor-
tality (Figure 22-1).
SCOPE OF THE PROBLEM
Musculoskeletal injuries account for 70% to 80% of injuries that
occur in a wilderness setting.11,20 Presumably as a result of the
use of flak jackets and core protective gear that shield axial and
central anatomic structures, bone and soft tissue injuries have
become more common, accounting for 70% of injuries in the
Iraq and Afghanistan wars.17 In the initial management of a mus-
culoskeletal injury that occurs in a wilderness or austere setting,
the following must be considered: cause and time of injury,
direction of the causative force in relation to the individual or
limb, and environment where the accident occurred. These
factors may indicate the severity of the injury and help deter-
mine the examination and treatment priorities that can affect the
outcome.
Stabilization of a victim’s cardiovascular and pulmonary status
is critical. Cardiovascular stabilization includes control of massive
hemorrhage. Once this has been accomplished, examination of
the musculoskeletal system should be undertaken in a systematic
CHAPTER 22  Wilderness Orthopedics
manner. Careful initial attention should be devoted to the spine.
After the cervical, thoracic, and lumbar regions of the spine have
been evaluated and stabilized (or cleared), the focus is brought
to bear on the pelvis and extremities.
PHYSICAL EXAMINATION
The physical examination should address circulatory, nerve, skel-
etal, and joint function.
VASCULAR FUNCTION
Penetrating or blunt trauma can injure major vessels that supply
the limbs. Fractures can produce vessel injury by stretching,
which can produce intimal flap tears, or by direct laceration.
Intimal injuries can occlude distal flow or lead to platelet aggre-
gation and delayed occlusion. Therefore, examination of vascular
function should be performed and repeated at regular intervals
before the victim’s arrival at the definitive care center. The color
and warmth of the skin or distal extremity should be assessed;
pallor and asymmetric regional hypothermia may indicate vascu-
lar injury. In the upper extremity, the brachial, radial, and ulnar
arteries should be palpated. In the lower extremity, the femoral,
popliteal, posterior tibial, and anterior tibial arteries should be
palpated. If blood loss, hypothermia, or obesity makes these
pulses difficult to assess, the temperature, color, and capillary
refill must be relied upon to determine vascular integrity. Any
suspected major arterial injury mandates immediate evacuation,
after appropriate splinting.
NERVE FUNCTION
Nerve function may be impossible to assess in an unconscious
or uncooperative person. In the conscious person, the results of
light touch and pinprick tests should be carefully documented.
For spinal and pelvic injuries, the dermatomal distribution of
spinal nerves is assessed and muscle function is evaluated by
observing active function and grading the strength of each muscle
group against resistance (Figure 22-2). If possible, once the vic-
tim’s condition has been stabilized, nerve function to the distal
extremities is documented. Initial findings should be compared
periodically, with repeat examinations during transport. Any
change and, in particular, any deterioration in condition should
be noted.
SKELETAL FUNCTION
The skeletal anatomy should be carefully inspected and palpated.
Angular deformity suggests a fracture; palpable crepitus confirms
the diagnosis. The health care provider in the field should
perform appropriate splinting after placing the limb in anatomic
alignment using gentle axial traction. After noting the degree and
orientation of the limb’s position when the victim is found, there
should be no delay in aligning and splinting fractures. The
risk-benefit ratio of fracture reduction and realignment in the
wilderness of protecting the neurovascular status and reducing
pain substantially outweighs the common in-hospital routine of
imaging before manipulation. Distinguishing intraarticular or very
proximal or distal fractures must wait for the definitive care facil-
ity, where imaging studies can be done. Similarly, distinguishing
a wrist or ankle ligamentous injury from a fracture is not required
for initial treatment.
Diagnosis is usually made by palpation of the limb and frac-
ture location. If a tuning fork is available, it can be used in the
following manner: the tuning fork is struck and placed on one
end of a limb in question. If the vibration cannot be auscultated
at the other end of the bone, or if the vibration is significantly
diminished when compared with the other limb, a discontinuity
(fracture) may exist. Ultrasound can also be employed if doubt
remains regarding the existence and location of a fracture.
Palpation of long bones begins distally and proceeds across
all joints. A splint should be applied if there is palpable crepitus,
swelling, deformity, or resistance or block to motion.
451
 Schematic demarcation of dermatomes
(according to Keegan and Garrett) C2
shown as distinct segments. There is
actually considerable overlap between
any two adjacent dermatomes. An C3
C2 alternative dermatome map is that C4
provided by Foerster (see References). C5
C3 C6
C4
C5 C7
T1 C8 T1
T2 T2
T3 T3
C6 C6 T4
T4 T5
T5 T1 T6
T7
T6 T8
T7 T9
C5 T10
T8 T11
T9 C7 C8 T12
T10 L1
L2
L3
T11 L4
C6 L5
T12 S1
L1 C8 C7 C8 S2
C7
S2, 3 S3
L2 S4
S5 S1
L3
L5 S2

L4 L1
L2

L3
TRAUMA

L5 S1 S2
PART 4

L4

S1 S1
L5
L5
L4 L4

Levels of principal dermatomes

T10 Level of umbilicus
C5 Clavicles L1 Inguinal or groin regions
C5, 6, 7 Lateral parts of upper limbs L1, 2, 3, 4 Anterior and inner surfaces of lower limbs
C8, T1 Medial sides of upper limbs L4, 5, S1 Foot
C6 Thumb L4 Medial side of great toe
C6, 7, 8 Hand S1, 2, L5 Posterior and outer surfaces of lower limbs
C8 Ring and little fingers S1 Lateral margin of foot and little toe
T4 Level of nipples S2, 3, 4 Perineum
FIGURE 22-2  Sensory dermatomes. (Netter illustration. Copyright Elsevier Inc. All rights reserved.)

In general, one can trust that an alert and cooperative patient
will not consciously participate in maneuvers that will cause
further harm. Unless the patient is being stoic or purposefully
overriding pain, the patient will not attempt to stand or ambulate
with a potentially unstable spine, or bear weight on a fracture at
risk for displacement or instability. A patient who can comfort-
ably perform a range of motion or bear weight on an injured
extremity, either before or after immobilization, is generally
acting safely. The rescuer needs to be particularly cautious with
someone who is attempting to “play through the pain.”
JOINT FUNCTION
Each joint has a normal range of and limits to motion to ensure
stability. Making the diagnosis of a joint injury in the field allows
appropriate splinting and prevents further damage during trans-
port. If the victim can cooperate, each joint is taken through an
active range of motion to quickly locate any injury. When this is
not possible, passive motion of each joint is evaluated after pal-
pation in order to detect swelling and/or crepitus.
Any dislocation should be promptly reduced after complet-
ing the neurovascular examination. This generally considerably
relieves the victim’s discomfort. Once relocation has occurred,
stability is evaluated by careful controlled motion. Joints with
associated fractures or interposed soft tissues may still be unsta-
ble after reduction. Care should be taken during splint applica-
tion to prevent recurrent dislocation or further soft tissue injury.
A report of details of the reduction or relocation maneuver,
including orientation of the pull, amount of force involved,
amount of sedation, and residual instability of the joint, should
be provided to the definitive care physician (see Reduction and
Relocation Maneuvers, p. 458).

452
POTENTIALLY LIFE-THREATENING
MUSCULOSKELETAL INJURIES
SPINAL INJURIES
Cervical Spine Injuries
In the wilderness, cervical spine fractures or dislocations can be
the result of a fall from a height, high-velocity ski crash, combat
injury, or diving accident. Because head and cervical spine inju-
ries are highly correlated, a victim with a significant head injury
should be considered to have a cervical spine injury, especially
if the individual is unconscious. Ideally, a person with a sus-
pected cervical spine injury is placed on a backboard with neck
immobilization to prevent further injury and then promptly evac-
uated. Approximately 28% of persons with cervical spine frac-
tures also have other spinal fractures3; therefore, the person
providing care should protect the entire spine.
When a cervical spine injury is suspected, field examination
involves grading motor strength, documenting sensory response
to light touch and pinprick, and noting the presence or absence
of the Babinski reflex (see Figure 22-2). When appropriate sup-
plies are available, a rectal examination should be done. Com-
plete lack of tone and failure of the sphincter muscles to contract
when pulling on the penis or clitoris (bulbocavernosus reflex)
indicates spinal cord injury.
Neurologic deficit often results from a cervical spine fracture.
Catastrophic spinal cord injury caused by a cervical spine fracture
from the occiput to the C4 level is usually fatal because of paraly-
sis of the diaphragm and respiratory muscles. The corollary to
this is that surviving victims often have partial deficits or are
neurologically intact. Axial cervical spine fractures may result
from flexion forces (most common), extension forces, or rota-
tional forces, or a combination of these. Cervical spine fractures
most commonly occur at C5-C6.3 Fracture of the C1-C2 complex
results from axial loading (C1 ring fracture, or Jefferson’s fracture)
(Figure 22-3) or from an acute flexion injury (C2 posterior ele-
ment fracture, or hangman’s fracture) (Figure 22-4). A pure
flexion event may dislocate one or both posterior facets, produc-
ing neck pain and limitation of motion. Because the interspinous
ligament is ruptured and this fracture-dislocation is highly unsta-
ble, victim transport must be done with the neck rigidly immo-
bilized to reduce the risk for posterior motion.
Fractures and dislocations may result in neurologic insult
distal to the bony injury. Because flexion is the mechanism that
most commonly causes cervical spine injuries, the neurologic
deficit is generally an anterior spinal cord syndrome. In this
setting, the victim suffers complete motor loss and partial sensory
loss but retains proprioception.
FIGURE 22-3  C1 ring, Jefferson’s fracture.
CHAPTER 22  Wilderness Orthopedics
FIGURE 22-4  C2 hangman’s fracture.
Thoracolumbar Spine Injuries
Thoracolumbar spine fractures occur most frequently at the
T12-L1 junction. Because the thoracic spine is well splinted by
the thoracic cage, when an axial or flexion force is applied, the
ribs diminish forces on the thoracic vertebral bodies and transmit
the forces to the upper lumbar levels. In the wilderness, falls
from significant heights or a high-velocity sporting vehicle crash
may produce these fractures (Figure 22-5). Thoracolumbar spine
fracture may also be associated with other fractures that occur
with axial loading, such as femoral neck fracture (Figure 22-6)
and calcaneus fracture (Figure 22-7). These injuries commonly
occur when there is an axial force, such as a fall onto the lower
limbs from a height. Therefore, an individual who sustains a
presumed hip fracture or calcaneus fracture because of a fall from
a height should be carefully evaluated for possible associated
spine injury.
When a thoracolumbar spine fracture is suspected, careful
neurologic examination should be performed as part of the sec-
ondary survey, and close attention paid to motor function, the
presence or absence of cord level reflexes, and any dermatomal
pattern of diminished light touch and pinprick. Because signifi-
cant fluctuations in sympathetic tone may occur, the rescuer
should monitor the blood pressure and body temperature, taking
appropriate steps to cool or warm the victim. If evacuation
cannot be performed immediately, hemodynamic and neurologic
function should continue to be noted and documented. The
victim should be logrolled, maintaining perfect spinal alignment,
and carefully placed on a backboard. A scoop stretcher may be
used in this situation (see Chapter 23).
FIGURE 22-5  Wedge compression fracture from axial or flexion
loading at the thoracolumbar junction.
453
 Wilderness Medical Society Recommendations for
Spine Clearance/Immobilization in the Austere Environment

Severely injured patient

Blunt trauma with
mechanism suspicious
for spine trauma
Altered mental status (GCS <15,
evidence of intoxication)
Neurological deficit
Thoracic or other significant
distracting injury

Isolated
penetrating trauma Yes No

Significant
Yes
Immobilize spine pain or
tenderness ( 7/10)

No
No

Patient voluntarily able

No immobilization
(further evaluation/treatment
may be required at
sophisticated point of care)
to flex, extend, and
Yes rotate spine (cervical
or thoracolumbar)
30° in each plane,
regardless of pain

FIGURE 22-8  Wilderness Medical Society recommendations for spine

clearance and immobilization in the austere environment. (From Quinn
TRAUMA

R, Williams J, Bennett B, et al: Wilderness Medical Society Practice

Guidelines for Spine Immobilization in the Austere Environment: 2014
Update, Wilderness Environ Med 25:S118, 2014.)

subject a patient to immobilization may result in unnecessary use

PART 4

of scarce and expensive resources and may place the patient, as

FIGURE 22-6  High-energy basic cervical femoral neck fracture with
greater trochanter fracture after a 40-foot fall while rock climbing.
Spinal Assessment (Clearing the Spine)
Asymptomatic patients without a distracting injury or neurologic
deficit who are able to complete a functional range-of-motion
examination may safely avoid immobilization without radiologic
imaging. Furthermore, in an austere environment, a decision to
well as rescuers, at increased risk for further injury. In this setting,
a more aggressive algorithm may be appropriately used to clear
the spine (Figure 22-8).24
Spinal Immobilization
Sound evidence is lacking to support reliance upon effectiveness
of spinal immobilization in every situation.24 Many methods,
improvised and otherwise, provide reasonable immobilization of
the spine but should not be assumed to be protective, should
not unnecessarily delay or complicate urgent evacuation, and

A B
FIGURE 22-7  Calcaneus fracture.

454

FIGURE 22-9  Pelvic injury after being thrown from a horse. Pubic
symphysis widening of greater than 2.5 cm (1 inch) is generally con-
sidered to be unstable.
should not cause significant patient discomfort or respiratory
compromise or impede access to the airway or sites of hemor-
rhage. Cervical spine immobilization that involves attainment of
standard neutral alignment is contraindicated (and generally
unnecessary) in the presence of certain circumstances of pene-
trating trauma, as well as in ankylosing spondylitis. In these situ-
ations, if the intent is to prevent further motion of the head and
neck, it is reasonable to achieve immobilization of the victim in
the position in which she or he is found.
PELVIC INJURIES
Pelvic fractures generally occur with a fall from a significant
height, high-velocity ski accident, or vehicle crash. The Young
and Burgess classification of pelvic fractures is based on the
mechanism of injury. Pelvic fractures are categorized as antero-
posterior compression, lateral compression, or vertical shear inju-
ries.5 These fracture patterns have been shown to correlate with
blood loss, associated injuries, multisystem morbidities, and mor-
tality.5,7,35 Anteroposterior compression injuries can result in rota-
tional instability if there is more than 2.5 cm (1 inch) of pubic
symphysis separation (Figure 22-9). Furthermore, if the posterior
pelvic ring is disrupted, there can be both rotational and vertical
instability. These injuries, which may include acetabular frac-
tures, are often accompanied by hemorrhagic, neurologic, uro-
logic, gynecologic, and gastrointestinal injuries (Figures 22-10
and 22-11).
The posterior pelvic ring accounts for approximately 60% of
pelvic stability. With a suspected pelvic fracture, it is important
FIGURE 22-10  Highly unstable pelvic ring injury with pubic rami frac-
tures and displaced iliac wing fracture. This patient also had a severe
bladder injury.
CHAPTER 22  Wilderness Orthopedics
Acetabulum
Femoral head
FIGURE 22-11  Right hip dislocation with acetabular and femoral head
fractures.
to determine whether there is injury to the posterior pelvis. Pos-
terior pelvic fractures are identified by instability of the pelvis
associated with posterior pain, swelling, and ecchymosis. This
victim should be immediately evacuated on a backboard, taking
care to minimize leg and torso motion.
Hemodynamic instability may occur with pelvic fractures,
particularly if the injury is the result of translational or shear
forces or if posterior pelvic structures are primarily involved.
Bleeding associated with a pelvic injury is usually from fractured
cancellous bone, retroperitoneal lumbar venous plexus injury, or,
rarely, pelvic arterial disruption. Military antishock trousers
(MAST), a SAM Pelvic Sling II, or even a bed sheet wrapped and
tightened with a windlass around the pelvis of an individual with
a suspected unstable pelvic fracture may provide stability and
accomplish adequate tamponade of bleeding from the fracture25
(Figure 22-12). Other similarly intended devices (e.g., T-Pod
Responder Pelvic Stabilization Device, VBM Pelvic Sling) are
available or may be improvised. The applied sling belt (pelvic
binder) or improvised contrivance should be left in place until
definitive care is available (Figure 22-13). Degloving injuries can
also be seen in high-energy pelvic injuries (Figure 22-14).
In addition to these high-energy injuries, simple nondisplaced
inferior or superior ramus fractures and avulsion fractures can
occur. On clinical examination, these pelvic fractures are gener-
ally appreciated as areas of tenderness without instability. Lateral
compression injuries are usually stable, with impaction of the
posterior structures.
GENERAL CONSIDERATIONS IN EXTREMITY
INJURIES TECHNIQUES FOR MANAGING
EXTREMITY INJURIES
Splinting Techniques
Splinting is performed so that alignment is maintained, further
soft tissue injury is minimized, and pain is substantially reduced.
FIGURE 22-12  SAM Sling.
455

FIGURE 22-13  Appropriate application of a sheet for an unstable
pelvic fracture (centered at the greater trochanters, as opposed to the
iliac wings).
TRAUMA
A victim with suspected cervical or thoracolumbar spine trauma
should be transported on a firm surface. Backboards or scoop
stretchers (see Chapter 23) are most effective, but improvisation
with hard pieces of wood, fiberglass, or straight tree limbs lashed
together may be needed. If cervical spine injury is suspected, a
PART 4
roll of clothes or a water bottle can be placed as high as the
victim’s midface on both sides of the head and secured into
position to prevent rotational movement. Tape applied from the
supporting stretcher across the objects and the victim’s forehead
adds stability. A child with a suspected spine injury should be
transported on a backboard, with the child’s body slightly ele-
vated relative to the head (Figure 22-15). Any victim with a
suspected major pelvic injury is transported in a similar fashion,
stabilizing the pelvis with a circumferential sheet, piece of cloth-
ing, or special belt and holding the lower extremities as immobile
as possible, with knees slightly flexed (see Figure 22-12).
Many different extremity splints are available for the wilder-
ness setting. These splints are lightweight, compact, and easy
to use. They are more elaborate than a simple hiking pole or
FIGURE 22-14  Prone patient with an unstable pelvic fracture and a
large degloving (Morel-Lavallee) flank lesion.
456
Backboard
Blanket to
elevate body
FIGURE 22-15  Child with suspected spine injury should be trans-
ported on a backboard with the child’s body slightly elevated relative
to his or her head.
branch that is more readily available. Intricate devices may have
considerable advantages for larger-scale evacuations involving
multiple victims in the setting of a natural disaster. Some are
designed to provide traction applied to the injured extremity.
With proper splint application, the injured limb can be immobi-
lized securely in a functional position until definitive care is
reached (Figure 22-16).
Air splints are generally manufactured in one shape. In the
setting of injured tissues and environments that might include
wide temperature variability, these splints can cause compression-
induced damage to an extremity. Therefore, an air splint is used
only if it has an automatic adjustment valve to compensate for
atmospheric pressure variability. These splints should be stored
in a minimally inflated state when the temperature is below
freezing, to prevent ice from causing splint dysfunction. Bead-
filled vacuum splints can be used. However, temperature and
altitude variations can make adequate and consistent inflation
less reliable. When bead-filled vacuum or air splints are used,
one must be vigilant to ensure that no excessive pressure is
applied to the already injured soft tissues.
Upper extremity splints may be made from plaster or fiber-
glass, which can be applied over a soft cotton roll. Lightweight
prefabricated fiberglass splints are easy to use and effective for
initial management of injuries (Figure 22-17). These splints are
prepadded and can be applied with either cold or warm water,
or even directly out of the package if water is not readily avail-
able. The warmer the water, the faster the fiberglass sets and the
B
FIGURE 22-16  Lower extremity splints.
 CHAPTER 22  Wilderness Orthopedics
FIGURE 22-17  Water-activated FareTec splint for distal radial fracture,
with wrist and hand in position of function.

FIGURE 22-20  SAM Splint.

extremity should be splinted in the position of function and

comfort whenever possible.
For the lower leg, air splints provide adequate immobilization
of tibia or fibula fractures and of ankle fractures and dislocations.
Splints made from plaster or fiberglass may be applied over
cotton padding and held in position with elasticized bandages.
The SAM Splint, an excellent first-aid item that can be molded
FIGURE 22-18  Swimmer in Exos fracture brace. to immobilize a wide variety of injuries, provides stability and
strength through its aluminum and foam core (Figures 22-20 and
22-21). The aluminum structure can be bent into three funda-
greater the exothermic reaction. Hot water should be avoided mental configurations (C-curve, reverse C-curve, and T-curve;
because it may generate an excessively exothermic reaction that Figure 22-22) to provide different degrees of stability, flexibility,
might burn the skin. The fiberglass is immersed in water, excess
water is gently wrung out, and the splint is applied. An elasticized
bandage helps hold the splint in place until the fiberglass hardens.
Air splints can adequately splint an upper extremity in a stable
position. Wooden or metal splints, custom made or improvised,
can be used to stabilize an injured extremity. New thermoplastic
casts and braces may be used in a wet outdoor environment and
immersed in water without compromising function or stability
(Figure 22-18). FIGURE 22-21  Versatile splint for upper or lower extremity.
Hand splints are applied with the metacarpophalangeal (MCP)
joints flexed to 70 to 90 degrees and the interphalangeal (IP)
joints extended. This places the collateral ligaments at maximal
length and prevents joint contracture (Figure 22-19). Wrist or
forearm splints are applied with the wrist in neutral position;
excessive wrist flexion or extension might detrimentally affect
median or ulnar nerve function in an already compromised limb.
The elbow is positioned in a splint or sling at 90 degrees.
For shoulder fractures, a commercially available sling or
improvised triangular bandage should be used to take the weight
of the arm off the injured structures. For dislocations, a swathe A
should be added. Although it may be difficult to place an injured
elbow in 90 degrees of flexion and neutral rotation, the upper

C
FIGURE 22-22  Basic SAM Splint adaptations. A, C-curve. B, Reverse
C-curve. C, T-curve (maximum strength). (Courtesy SAM Medical
FIGURE 22-19  Hand and wrist in position of function. Products.)

457

FIGURE 22-23  Slishman splint applied for femoral fracture following
the 2010 earthquake in Haiti. (Courtesy Sam Slishman.)
TRAUMA
and immobilization. The ankle is held in neutral position and the
splint applied firmly. For transport, the lower extremity is posi-
tioned with the hip and knee extended and the ankle in neutral
position. Victims with unstable lower extremity fractures or dis-
PART 4
locations are transported in the recumbent position with the
afflicted limb elevated.
For hip or femoral fracture or dislocation, properly applied
traction can decrease blood loss from hemorrhage into the frac-
ture site and substantially decrease pain. If proper traction cannot
be applied, splinting (particularly with a vacuum mattress) can
provide reasonable stability and pain control. Multiple portable
traction devices are commercially available (Figures 22-23 and
22-24). The ischium and/or pubis are proximal structures against
which the splint is set. The ankle is usually the structure through
which traction is applied (Figure 22-25). Lightweight splints that
may be of use in the wilderness setting include those known
either by their manufacturer or developer, such as Donway,
Thomas, Kendrick, Slishman, Reel, FareTec, Sager, CT-6, and
Hare splints (see Chapter 23). It behooves a backcountry health
care provider to be thoroughly familiar with any splinting device
being carried. If commercial splints are unavailable and effective
improvised splinting is not possible, the injured leg can be
strapped to the noninjured leg, with a tree limb or walking stick
placed between the legs. If possible, the victim is transported on
a backboard or similar device that limits motion of the pelvis and
lower extremity.
Reduction and Relocation Maneuvers
Even in the wilderness, the four principles of fracture reduction
should be followed:
FIGURE 22-24  Lower extremity splint.
458
1 2
3 4
FIGURE 22-25  Improvisation of an ankle wrap to be used for
traction.
• Traction: in-line or longitudinal force application
• Fracture fragment disengagement; included in this step is
recreation of the forces that created the fracture
• Reapposition of fracture ends
• Counteraction of forces that led to deformity
Steady traction and patience are the mainstays of fracture and
dislocation reduction and relocation maneuvers.4
For distal radial fracture, the usual dorsiflexion deformity is
reproduced and a flexion force is applied through the fracture.
Steady traction can assist with reduction (Figures 22-26 to 22-28).
For ankle fracture, traction is applied. Most fractures are
caused by an eversion and external rotational force. Reduction
is undertaken and a splint applied so that the ankle can be
splinted in inversion and internal rotation, known as the Quigley
maneuver. Care must be taken so that excessive force is not
exerted on a limb that has already sustained significant vascular
or nerve injury (Figure 22-29).
Traction Pins
Skeletal traction is applied in the setting of a fractured pelvis
(including the acetabulum) or femur. This mode of stabiliza-
tion can be used for temporary or more definitive treatment.
This technique can be used in a natural disaster setting (see
Figure 22-1).
A distal femoral traction pin is inserted from medial to lateral.
The knee is flexed during insertion to facilitate access to the
medial aspect of the distal femur and to allow for flexion of the
knee once the pin has been placed; if the pin is placed with
the knee in extension, the iliotibial band might be tethered and
thereby prevent knee flexion. The pin is placed approximately
two fingerbreadths proximal to the adductor tubercle. If the pin
is placed too far distally, it can enter the intercondylar notch of
the knee. If the pin is placed too far proximally, it can injure the
superficial femoral artery near its exit from the adductor hiatus,
or one of the branches of the superficial femoral artery near
the knee.
A proximal tibial traction pin is inserted from lateral to medial.
The pin is placed approximately two fingerbreadths distal to the
tibial tubercle and two fingerbreadths posterior to the anterior
tibial crest. These pins should not be placed in children, because
 CHAPTER 22  Wilderness Orthopedics
Reduction of Colles’ fracture by
manipulation method under local
(infiltration) anesthesia:
1: Hyperextension and traction
to break up impaction combined
with direct thumb pressure;
countertraction and fixation
of forearm by assistant

2: With continued traction, counter-

traction, ulnar deviation of the hand,
and thumb pressure, the ends of the
fragments are brought into apposition;
the operator’s index fingers press
on the proximal fragment while the
thumbs press on the distal one

3. The hand is now quickly flexed

at the wrist, maintaining traction
and pressure on the fragments
to bring them into alignment
FIGURE 22-26  Reduction maneuver for the most common distal radial fracture (dorsally angulated). (Netter
illustration, copyright Elsevier Inc. All rights reserved.)

proximity of the tibial tubercle apophysis puts this important
structure at risk during insertion of the pin (Figure 22-30).
A calcaneal pin can also be used to apply lower extremity
traction. This type of traction pin may be of particular benefit in
the setting of ipsilateral femoral and tibial injuries. It is usually
placed medial to lateral, with care being taken to avoid the pos-
terior tibial neurovascular bundle. The pin is driven through the
calcaneus and exits laterally (Figure 22-31).
If possible, balanced traction should be maintained. This
helps to counteract deforming forces and allows relatively com-
fortable movement in bed. There are no hard-and-fast rules for
the amount of weight to apply. If balanced traction is employed,
the rule of thumb is for enough traction to be applied that the
ipsilateral buttock is elevated slightly off the bed. When radiog-
raphy is available, traction is applied until the fracture fragments
are well aligned and nearly out to length. For an average-sized
adult, this likely will be between 6.8 and 13.6 kg (15 and
30 pounds).
External Fixators
External fixator application for fracture may be of benefit in the
setting of a natural disaster. For example, in the aftermath of the
earthquakes in Haiti in 2010, external fixator application for
femoral or tibial fracture was one of the most commonly employed
fracture treatment procedures. External fixators applied in the
field or in the setting of limited resources are usually applied in
a manner consistent with the use of the fixator as a neutralization
device. The external fixator maintains the relative position of
bone fragments, resists external deforming forces, and prevents
significant soft tissue injury (by the bone ends).
Principles of external fixator application are use of sterile
technique for threaded pin insertion; avoidance of critical

459
 A B
FIGURE 22-29  Quigley’s maneuver for ankle fracture reduction. Ante-
rior and inversion forces on the foot and ankle created by hanging leg
by the great toe, held medial to midline of the body (or hung with
stockinette as depicted).

Distal femoral
traction pin

A B
FIGURE 22-27  Distal radial fracture with distal radioulnar joint disloca-
tion sustained after a fall on an outstretched hand.
TRAUMA

structures during threaded pin placement; and creation of a

fixator construct that is as rigid as possible.
Characteristics that contribute to increasing external fixator
stability include
• Threaded pins of greater diameter
• Shorter distance between side bars and bone
PART 4

• Double, as opposed to single, side bars

• Threaded pin placement closer to the fracture
• Greater number of threaded pins
• Stronger side bar material
Appropriate external fixator application is possible when the Proximal tibial
pertinent cross-sectional anatomy is known. Safe zones in the traction pin
tibia are primarily along the medial aspect of the tibia. Safe zones

FIGURE 22-30  Proper positioning of distal femoral and proximal tibial

traction pins.

A B
FIGURE 22-31  Calcaneal traction pin placement in the setting of sub-
FIGURE 22-28  Reduced fracture-dislocation. talar dislocation.

460

Deep
peroneal
nerve
Anterior
tibial artery
and vein
Superficial
peroneal
nerve
A B
FIGURE 22-32  A, Cross-sectional area of leg. Tibial safe zone for external fixator pin placement is medial.
B, Cross-sectional area of thigh. Femoral safe zone is anterior and lateral.
in the thigh are at the anterior and lateral aspects of the femur
(Figure 22-32).
A few simple techniques may contribute to the longevity of
the fixator. The position and length of stab wound incisions in
the skin should not result in tension between the threaded pin
and skin interface. To prevent osteonecrosis, holes in the bone
for the threaded pins should be predrilled. Threaded pins should
be bicortical; however, to reduce the risk of nerve or vessel
injury, care should be taken not to advance the pins more than
a few millimeters beyond the far cortex.
OPEN FRACTURES OF THE EXTREMITIES
Recognizing an open fracture is imperative; without prompt
surgical treatment, the incidence of osteomyelitis in this setting
is high.13 With an open fracture, the fractured bone communi-
cates with a break in the skin. With subcutaneous bones (e.g.,
tibia), open fractures are easily identified, but with other bones
that have more surrounding soft tissue (e.g., humerus, femur,
pelvis), recognition is more difficult because the fractured bone
end usually retracts after it punctures the skin and is then covered
by soft tissue. A laceration near a fracture may be an indication
of an open fracture. Most open fractures persistently ooze blood
or fat globules from the laceration (Figure 22-33). Clothes should
be removed to allow the skin to be examined.
FIGURE 22-33  Type IIIB open tibia-fibula fracture that occurred as a
result of a fall while the individual was holding a chainsaw.
CHAPTER 22  Wilderness Orthopedics
Rectus femoris
muscle
Vastus
lateralis
muscle
Sciatic nerve
Classification of Open Fractures of the Extremities
Familiarity with the Gustilo-Anderson open fracture classification
system is useful. This assigns musculoskeletal trauma to one of
three major categories (types I to III) depending on the mecha-
nism of injury, extent of soft tissue damage, and degree of skel-
etal involvement.
Type I Fracture
• Wound is less than 1 cm (0.4 inch), with minimal soft
tissue injury.
• Wound bed is clean.
• Fracture is usually a simple transverse, short oblique frac-
ture, with minimal comminution.
Type II Fracture
• Wound is greater than 1 cm (0.4 inch), with moderate soft
tissue injury.
• Wound bed may be moderately contaminated.
• Fracture is usually a simple transverse, short oblique frac-
ture, with minimal to moderate comminution.
Type III Fracture.  Type III fractures involve extensive
damage to soft tissues, including muscle, skin, and neurovascular
structures. They often result from a high-velocity injury or have
a severe crushing component. The following special patterns are
classified as type III fractures:
• Open segmental fracture, irrespective of the size of the
wound
• Gunshot wound (high-velocity or short-range shotgun
injury)
• Open fracture with neurovascular injury
• Farm injury or other highly contaminated wound, irrespec-
tive of size
• Traumatic amputation
• Open fracture more than 8 hours old
• Mass casualties (e.g., war and tornado victims)
Subtype IIIA Fracture.  The wound is less than 10 cm (3.9
inches) with crushed tissue and contamination, or is the result
of high-energy trauma, irrespective of the size of the wound. This
includes segmental fractures or severely comminuted fractures.
Adequate soft tissue coverage is usually possible despite soft
tissue laceration or flaps.
Subtype IIIB Fracture.  There is extensive soft tissue loss
(> 10 cm [3.9 inches]) with periosteal stripping and bony expo-
sure. This is usually associated with massive contamination and
typically requires regional or free-flap reconstruction.
Subtype IIIC Fracture.  Subtype IIIC is a fracture in which
there is a major arterial injury requiring repair for limb salvage.
The Mangled Extremity Severity Score can provide prognostic
considerations for limb salvage versus amputation.15
461
 BOX 22-1  Antibiotic Options
Intravenous Solutions
Cefazolin (Ancef) 1 g q 6 hr and gentamicin (5 mg/kg) q 24 hr or
piperacillin with tazobactam (Zosyn) 3.375 g q 6 hr
Intramuscular Injections
Ceftriaxone (Rocephin) 1 g q 24 hr
Oral
Ciprofloxacin 750 mg bid and cephalexin (Keflex) 500 mg qid
Water Exposure
Ciprofloxacin 400 mg IV or 750 mg PO bid; or a sulfonamide and
trimethoprim combination (Bactrim DS: 800 mg sulfamethoxazole
and 160 mg trimethoprim) with either cefazolin (Ancef) 1 g IV q
8 hr or cephalexin (Keflex) 500 mg PO q 6 hr
Dirt or Barnyard Exposure
Add penicillin 20 million units IV daily or 500 mg PO q 6 hr
If Penicillin Allergy
Use clindamycin 900 mg IV q 8 hr or 450 mg PO q 6 hr in place of
penicillins and cephalexin (Keflex)
Alternatives
Erythromycin 500 mg PO q 6 hr or amoxicillin with clavulanic acid
875 mg PO bid
Bid, twice a day; IV, intravenously; PO, orally; qid, 4 times a day.
Management of Open Fractures of the Extremities
General care of an open fracture outdoors depends on evacua-
tion time. An open fracture requires prompt operative irrigation,
debridement, and stabilization. If evacuation can be completed
TRAUMA
within 8 hours, realign the fracture, administer a broad-spectrum
antibiotic, and splint the extremity. If bone ends extrude through
the skin, try to reduce the exposed bone back into the wound
below soft tissue coverage and cover with a moist (preferably
normal saline) gauze sponge, splint the extremity, and arrange
for prompt evacuation. If the evacuation time exceeds 8 hours,
PART 4
in addition to antibiotic administration and splinting, irrigation
and debridement may be attempted in the field. Antibiotic options
are listed in Box 22-1. If tetanus vaccine is available and has not
been given in the past 5 years, this should also be provided.
The likelihood of infection developing in the presence of an
open fracture is directly related to the volume and virulence of
bacteria present in the wound at the time of definitive wound
coverage or closure.19 Interventions in the field can be performed
in an effort to lower the eventual bacterial load and, therefore,
risk of infection. Organic debris should be removed from the
wound. Irrigation can be performed. Ample data have shown
that potable water is equivalent to sterile saline in reducing
wound infection, and relatively low volumes (< 1 L) can be
effective if irrigation is promptly accomplished. High-pressure
irrigation (> 8 psi) is generally effective at removing bacteria and
can be accomplished in the field with a pin hole in a hydration
bladder or by using a 19-gauge needle coupled with a 35-mL
syringe. Additives (povidone-iodine, hydrogen peroxide, hexa-
chlorophene, sodium hypochlorite) to the irrigant solution,
including antibiotics, are generally ineffective or even harmful.
Surfactants, such as castile soap, can be helpful in removing
bacteria, provided the soap can be completely removed with
irrigation. After cleansing, the wound should be covered and the
dressing left in place until definitive management. Each exposure
of the wound increases the chance of infection. Dressings soaked
with blood should be reinforced with a pressure dressing rather
than repetitively changed.
SIGNIFICANT SOFT TISSUE INJURIES OF
THE EXTREMITIES
Degloving injuries (sometimes referred to as Morel-Lavallee
lesions when associated with pelvic injury) and/or crush injuries
can occur in the wilderness (see Figure 22-14). Although they
are seen more commonly in high-energy urban accidents, they
can also occur as the result of a significant fall or crushing force.
462
Natural disasters and warfare can also result in a mangled or
crushed limb. Splinting, monitoring for compartment syndrome,
and expeditious evacuation are imperative.
TOURNIQUETS FOR EXTREMITY INJURIES
Although use of tourniquets outside of a medical facility histori-
cally has been considered anathema, there has been a resurgence
in their use in the field by the military. In the Iraq and Afghan
theaters, soldiers are trained in application of tourniquets on
themselves and others; tourniquet use in the setting of a mangled
or badly injured extremity has saved many lives. Sacrificing a
limb to save a soldier is a difficult but clear decision.21 A tourni-
quet should only be applied in the presence of a life-threatening
injury and should be left inflated until definitive care can be
instituted. Ischemia lasting for more than 2 hours risks permanent
limb damage and for more than 6 hours will generally lead to
amputation. The time of inflation should be conspicuously
marked on the patient’s limb or forehead. An improvised tour-
niquet may be employed; it should be at least 4 cm (≈ 1.6 inches)
in width and be applied with sufficient pressure (generally using
a windlass technique) to completely obstruct arterial flow.
AMPUTATION OF INJURED EXTREMITIES
In the wilderness, the amputation victim requires immediate
evacuation. Control hemorrhage by direct pressure, clamping or
ligation of severed vessels, or application of a tourniquet. Using
pressure points is generally ineffective. Without cooling, an
amputated part remains viable for 4 to 6 hours. Cleanse the
amputated part with saline or water, wrap it in moistened sterile
gauze or a towel, place it in a plastic bag, and transport the bag
in an ice water mixture. Do not use dry ice. Keep the amputated
part with the victim throughout the evacuation (Figures 22-34
and 22-35).
COMPARTMENT SYNDROME
A compartment syndrome begins when locally increased tissue
pressure reduces capillary blood flow to a muscle compartment.
When local blood flow is unable to meet metabolic demands of
the tissue, ischemia ensues. In the wilderness, compartment
syndrome most frequently occurs in association with a fracture,
crush injury, or severe contusion. It can also occur when the
victim has been lying for a period of time across an extremity
so that the body weight occludes the arterial blood flow. Elevated
local tissue pressure (compartment pressure within 10 to
20 mm Hg of diastolic arterial blood pressure) can also occur
with acute hemorrhage or after revascularization of an ischemic
extremity. Because perfusion pressure is the most important vari-
able in development of compartment syndrome, hypotension can
increase the risk.
FIGURE 22-34  Thumb amputation/avulsion as a result of a rider’s
thumb getting caught in a horse’s reins before he fell off the horse.
 the compartmental fascia in each of the four lower leg

CHAPTER 22  Wilderness Orthopedics

compartments.
If fasciotomy for compartment syndrome cannot be done
within 12 hours of the syndrome’s development, it should
not be undertaken. A retrospective analysis of individuals who
underwent late (> 35 hours after the injury) release for compart-
ment syndrome demonstrated significant complication and
amputation rates. Therefore, even in an urban trauma hospital,
delayed compartment release for compartment syndrome is not
recommended.10

RICE PRINCIPLE
The general principle for acute management of extremity injuries
is rest, ice, compression, and elevation (RICE). For unstable
fractures, immobilization is also indicated. Avoid heat for the first
72 hours after injury. Chemical cold packs work well, as do cold
packs made from ice or snow. If cold packs are unavailable, the
extremity can be immersed intermittently in a cold mountain
stream. If ice is used, mix some water in a bag with the ice to
more evenly distribute the cold. The cold pack to the injured
area may be held in place with an elasticized bandage. A piece
of fabric is placed between the cold pack and the victim’s skin
to prevent frostbite. The ice is applied to the elevated extremity
(above the level of the heart) for 30 to 45 minutes every 2 hours.
A compressive dressing helps decrease swelling but should not
be used if development of a compartment syndrome is possible.
In this situation, keep the limb at the level of the heart and avoid
compressive dressings.

UPPER EXTREMITY INJURIES

In the wilderness, without benefit of radiographic images, deter-
mination of the exact anatomic structures affected by an injury
can be a challenge. The following sections have been divided
FIGURE 22-35  Traumatic near-amputation of a foot that occurred in a manner based on location of the suspected pathologic
in a boating accident. Patient was treated with below-the-knee condition.
amputation.
SHOULDER GIRDLE INJURIES
Compartment syndrome can occur in the thigh, hand, foot, Clavicular Fracture
and gluteal regions. It is more common, however, in the lower Clavicular fracture usually occurs in the middle or lateral one-third
leg and forearm, because of tight fascia in these regions. The of the bone and is associated with a direct blow or fall onto the
conscious victim complains of severe pain out of proportion to lateral shoulder (Figure 22-37). Clavicular fracture is common in
the injury. The muscle compartment feels extremely tight, and snow skiing and mountain biking accidents. The victim complains
applied pressure increases pain. There may be deceased sensa- of shoulder pain, which may be poorly localized. Arm or shoulder
tion to light touch and pinprick in the areas supplied by the motion exacerbates the pain. To localize the injury, gently palpate
nerves traversing the compartment. Stretching muscles within the the clavicle to identify the area of maximal tenderness. Crepitus
compartment produces severe pain. The most reliable signs of a confirms the diagnosis. A pneumothorax can be associated with
compartment syndrome are pain, tight compartments, hypesthe- a clavicular fracture if the cupola of the lung is punctured; there-
sia, and pain on passive stretch. Pulselessness, pallor, and slow fore, auscultate the chest. Shortness of breath and chest pain on
capillary refill may not be observed, even with a severe compart- inspiration increase suspicion for a pneumothorax.
ment syndrome (Figure 22-36).
Emergency evacuation is required when compartment syn-
drome is suspected. The victim must be definitively treated in
the first 6 to 8 hours after onset to optimize return of function.
Emergency fasciotomy, the treatment of choice, relieves the pres-
sure. If a compartment syndrome develops and evacuation
cannot occur within 8 hours, one must decide whether the treat-
ing individual possesses the skill to perform a fasciotomy and
whether it can be performed in an aseptic manner. Fasciotomies
can convert a closed fracture into an open fracture and can
provide a conduit for limb- or life-threatening infection. If a limb
has nonfunctioning nerves and muscles resulting from compart-
ment syndrome months after the syndrome has occurred, the
limb can be salvaged with tendon transfers, whereas a limb that
becomes infected after fasciotomy performed in the wilderness
often must be amputated.
If a fasciotomy is being contemplated, antibiotics should be
administered if available. In the forearm, the procedure usually
involves making volar and dorsal incisions and splitting the
underlying fascia. In the lower leg, the procedure usually involves
making two long incisions, one on the medial aspect and another FIGURE 22-36  Developing compartment syndrome in the setting of
on the lateral aspect of the leg, and splitting, in a vertical fashion, a tibia-fibula fracture, 6 hours following a crush injury.

463
 FIGURE 22-37  Midshaft clavicular fracture sustained by a 13-year-old
snowboarder riding in the backcountry with his friends. Proximal
humerus demonstrates physis normal growth plate, often mistaken for
a fracture. Comparison view of the opposite shoulder may be obtained
if proximal humerus fracture is suspected.
Clavicular fracture may also be accompanied by injury to the
brachial plexus, axillary artery, or subclavian vessels. Thorough
neurovascular examination of the affected extremity is performed,
and the skin is examined carefully. Up to 5% of clavicular frac-
tures may be open because of the bone’s subcutaneous location.
The victim should be evacuated if there is a significant open
wound, suspected pneumothorax, or nerve or vascular injury.
Field treatment for a clavicular fracture consists of a sling or
figure-of-eight bandage and analgesics.
TRAUMA
Scapular Fracture
Injury to the scapula is uncommon in the wilderness, but it may
result from a direct blow or fall onto the back. Confirmation of
the injury often requires x-ray or computed tomography evalua-
tion (Figure 22-38). Scapular fracture can be seen in isolation or,
PART 4
with high-energy injuries, in conjunction with thoracic injuries,
such as rib fracture or pneumothorax. Palpation and auscultation
for breath sounds assist in making the associated diagnoses.
FIGURE 22-38  Three-dimensional computed tomography view of
scapula fracture. Complete disassociation of the glenoid from the
scapular body is present.
464
FIGURE 22-39  Anterior sternoclavicular dislocation.
Symptomatic, nonoperative treatment for a scapular fracture is
usually the course.
Sternoclavicular Joint Dislocation
Traumatic dislocation of the sternoclavicular joint generally
requires tremendous force, either direct or indirect, applied to
the shoulder. Consequently, it is rare. Anterior dislocation is most
common, with the medial head of the clavicle going anterior to
the manubrium of the sternum (Figure 22-39). The victim com-
plains of pain around the sternum and frequently has difficulty
taking a deep breath. When the dislocation is posterior, signifi-
cant pressure may be placed on the esophagus and superior vena
cava. The victim may complain of difficulty swallowing and have
engorgement of the veins of the face and upper extremities,
representing superior vena cava obstruction syndrome. A step-off
between the sternum and the medial head of the clavicle (com-
pared with the uninjured side) confirms this diagnosis.
Unreduced anterior dislocation does not produce neurocircu-
latory compromise and is treated with a sling. Reduction of a
posterior sternoclavicular dislocation should be attempted as
soon as possible if neurocirculatory compromise is present. The
victim is placed supine with a large roll of clothing or other firm
object between the scapulae. Traction is applied to the arm
against countertraction in an abducted and slightly extended
position. The medial end of the clavicle may need to be manually
manipulated to dislodge it from behind the manubrium (Figure
22-40). If this fails, forceful pressure is applied posteriorly to both
shoulders. This may need to be abruptly applied, in a manner
that “bows” the patient backward. This maneuver is repeated
several times, with a larger object placed between the scapulae
if reduction attempts are initially unsuccessful. Alternatively, with
the victim seated and the caregiver’s knee against the back
between the shoulders, both shoulders are pulled back. Although
it might seem macabre, if the victim becomes in extremis, the
medial end of the clavicle is grasped with a towel clip or pliers
and forcefully pulled out of the thoracic cavity. Once reduced,
the injury is usually stable. Posterior sternoclavicular dislocation
requires evacuation.
Acromioclavicular Joint Dislocation
Injuries to the acromioclavicular joint are commonly known as
shoulder “separations,” to be distinguished from a shoulder (gle-
nohumeral) “dislocation.” Acromioclavicular separations are clas-
sified as grade I, II, or III (Figure 22-41). These injuries are acutely
painful, but surgery rarely improves the clinical outcome. The
 CHAPTER 22  Wilderness Orthopedics
Sand bag
between
A shoulders

B
B C
FIGURE 22-41  Acromioclavicular joint injury. A, Normal anatomy.
B, Grade 2 injury. C, Grade 3 injury.

C
FIGURE 22-40  Technique for closed reduction of the sternoclavicular FIGURE 22-42  Grade 3 acromioclavicular separation of the left shoul-
joint. A, The patient is positioned supine with a sandbag placed der after a fall from a mountain bike.
between the shoulders. Traction is applied to the arm against coun-
tertraction in an abducted and slightly extended position. For anterior
dislocation, direct pressure over the medial end of the clavicle may
reduce the joint. B, For posterior dislocation, in addition to the trac-
tion, it may be necessary to manipulate the medial end of the clavicle
with the fingers to dislodge the clavicle from behind the manubrium.
C, For a stubborn posterior dislocation, it may be necessary to prepare
the medial end of the clavicle in a sterile fashion and use a towel clip
to grasp around the medial clavicle and lift it back into position. (From
Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and
Green’s fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
Coracoid

acromioclavicular joint is usually injured by a blow or fall onto

the shoulder (Figure 22-42). Because using the hand increases Clavicle
pain, the arm on the affected side is placed in a sling. As long
as the individual can tolerate the discomfort associated with such
an injury, evacuation is not necessary. AC joint
Glenohumeral Joint Dislocation
Dislocation of the glenohumeral joint is the most common bony Hill-Sachs
dislocation. Ninety-five percent of glenohumeral dislocations lesion Glenoid
occur in an anteroinferior direction (Figure 22-43). The usual
mechanism of injury is a blow to the arm in the abducted Acromion
and externally rotated position. This frequently occurs during
downhill skiing when a person crosses the ski tips or falls FIGURE 22-43  Axillary lateral radiograph demonstrating anterior gle-
forward over a mogul and lands face down with the arm(s) nohumeral dislocation that resulted following a fall while the patient
akimbo. It is also a common injury in kayaking. When a posterior was skiing in the backcountry.

465
 FIGURE 22-44  Traction and countertraction for dislocated shoulder
reduction.
glenohumeral dislocation occurs in the wilderness, it is often in
the setting of seizure or lightning strike. Usually, external rotation
is completely lost. Palpation of the shoulder reveals posterior
fullness that is not found on the uninjured side.
Recurrent dislocations and those in younger patients may be
easier to reduce than first-time dislocations in older patients.
Thorough motor, sensory, and circulatory examination of the
involved extremity is performed. The axillary and musculocuta-
neous nerves are the nerves most commonly injured with anterior
dislocation and therefore must be assessed carefully. Serial exam-
inations of distal pulses, capillary refill, and forearm compart-
ments are performed.
Treatment of shoulder dislocation requires manual reduction.
Common techniques include the Kocher, Milch, Stimson, Spaso,
and Legg maneuvers, scapular manipulation, and snowbird
TRAUMA
maneuver2,8,9,22,33 (Figures 22-44 to 22-50). Self-reduction has
been proposed but is arguably a challenging procedure. The
technique favored by the authors uses sustained, gentle traction-
countertraction to overcome muscle spasm, minimize rotational
maneuvers, and avoid leveraging (Figure 22-51).
Of interest to the wilderness caregiver might be the “Eskimo
PART 4
technique” used by natives of Greenland, in which the patient is
lifted from the ground by the affected arm (while lying on the
unaffected side) so that the patient’s body weight serves as
a countertraction.26 Mel Gibson, in his Lethal Weapon films,
demonstrates a body-slam technique that may be performed,
in the absence of an assistant or physician, against any solid
FIGURE 22-45  Repositioning a dislocated shoulder. Attached to the
victim’s forearm with a strap, rope, or sheet, the rescuer uses his body
weight to apply traction, leaving his hands free to manipulate the
victim’s arm. A second rescuer applies countertraction, or the victim
can be held motionless by fixing the chest sheet to a tree or ground
stake. (From Auerbach PS. Medicine for the outdoors: the essential
guide to first aid and medical emergencies, ed 6, Philadelphia, 2016,
Elsevier.)
466
FIGURE 22-46  Milch technique of closed reduction of anterior gleno-
humeral dislocation with the patient prone. The arm can be manipu-
lated in the same manner with the patient supine. (Redrawn from Lacey
T II, Crawford HB: Reduction of anterior dislocations of the shoulder
by means of the Milch abduction technique, J Bone Joint Surg Am
34:108, 1952. In Browner BD, Jupiter JB, Levine AM, et al: Skeletal
trauma, vol 2, ed 2, Philadelphia, 1998, Saunders.)
stationary object. The recurrence rate is evidently high with this
maneuver.
Regardless of the method employed, patient relaxation is criti-
cally important. The greatest barrier to successful reduction is
generally muscular forces.
Greater tuberosity or glenoid fracture may accompany acute
glenohumeral dislocation. Transient musculocutaneous and/or
axillary nerve neurapraxia occurs in approximately 20% of shoul-
der dislocations.31
Dislocation of the glenohumeral joint remains an injury of
potential long-term consequence for the patient. It is especially
important for the younger individual, whose risk for recurrent
dislocation may exceed 50%, to visit an orthopedic surgeon.31
Arthroscopic or open repairs of the damaged anterior capsule
and labrum may be appropriate in some cases after the first
injury, and recurrent dislocations of the glenohumeral joint
warrant surgical intervention to lessen the risk for further shoul-
der instability and progressive arthritic change. Individuals over
40 years of age have a significant risk for associated rotator cuff
FIGURE 22-47  Scapular manipulation technique for closed reduction
of anterior glenohumeral dislocation. (Redrawn from Anderson D,
Zvirbulis R, Ciullo J: Scapular manipulation for reduction of anterior
shoulder dislocation, Clin Orthop Relat Res 164:181, 1982. In Browner
BD, Jupiter JB, Levine AM, et al: Skeletal trauma, vol 2, ed 2, Phila-
delphia, 1998, Saunders.)
 CHAPTER 22  Wilderness Orthopedics
A B
FIGURE 22-50  A, Pushing the lower edge of the scapula toward the
spine while an assistant pulls downward on the affected arm to assist
in relocation of a dislocated humerus. B, The downward pull on the
arm may be slightly forward to help reposition the humerus back 
in the glenoid. (From Auerbach PS. Medicine for the outdoors: the
essential guide to first aid and medical emergencies, ed 6, Philadel-
phia, 2016, Elsevier.)

FIGURE 22-48  Pulling on the hanging arm to relocate a dislocated

humerus. (From Auerbach PS. Medicine for the outdoors: the essential ARM AND ELBOW FRACTURES
guide to first aid and medical emergencies, ed 6, Philadelphia, 2016,
Elsevier.) Proximal Humeral Fracture
Proximal humeral fracture can be difficult to differentiate from
shoulder dislocation. The mechanism often is a high-velocity fall
injury in the setting of glenohumeral dislocation and should be onto an abducted, externally rotated arm or a direct blow to the
evaluated for this injury if, after a week or two, active forward anterior shoulder. The victim complains of severe pain around
elevation or abduction is impaired.
If the reduction maneuver is successful, the arm is placed in
a sling until definitive care is reached. If possible, a posterior
dislocation is held in neutral or slight external rotation. Because
of the significant incidence of fractures with these injuries, radio-
logic examination is required to make the diagnosis and evacu-
ation is mandated. If the reduction maneuver is not successful,
the injured extremity is placed in a sling and evacuation is
arranged as soon as possible.

FIGURE 22-49  Stimson technique for closed reduction of anterior

glenohumeral dislocation. (Redrawn from Rockwood CA, Green CP, FIGURE 22-51  Reducing an anterior shoulder dislocation with steady
editors: Fractures in adults, vol 1, Philadelphia, JB Lippincott, 1984. In traction. Dr. Steve Paul demonstrates a proper controlled traction-
Browner BD, Jupiter JB, Levine AM, et al: Skeletal trauma, vol 2, ed countertraction technique for reduction of a glenohumeral shoulder
2, Philadelphia, 1998, Saunders.) dislocation.

467
 R
69
G
HH

FIGURE 22-52  Proximal humeral fracture sustained in a 75-year-old

hiker following a fall.

G
HH
the shoulder with palpation or any arm motion. Palpable crepitus
confirms the diagnosis. Although the inclination to attempt reduc-
tion may be compelling (this injury may be mistaken for a S
shoulder dislocation), acute reduction is not routinely required;
application of an arm sling is appropriate field management
TRAUMA

(Figure 22-52).
Fracture-dislocation of the proximal humerus can occur.
Although most dislocations with fracture are anterior, some can B
be posterior (Figure 22-53). Anterior or posterior fullness with
crepitus on the injured side, compared with the uninjured side, FIGURE 22-53  Bilateral proximal humeral fractures and posterior dis-
locations that occurred when an ultramarathoner suffered a seizure
suggests the diagnosis. This is a more severe injury than a sim-
during a race. Computed tomography scan of right and left shoulders
PART 4

ple shoulder dislocation, so very careful neurovascular exami­ demonstrating posteriorly dislocated humeral heads, perched on
nation should be performed. Any significant nerve or vascular respective glenoids. G, Glenoid; HH, humeral head; S, scapula.
injury should prompt evacuation to a definitive care center.
Humeral Fracture
Fracture of the shaft of the humerus may result from a direct
blow or torsional force on the arm. This fracture frequently
occurs with a fall, rope accident, or skiing accident. Fracture of
the midshaft or junction of the middle and distal thirds of the
humeral shaft can violate the spiral groove, the path of the radial
nerve (Figure 22-54). If there is arm pain with deformity and
crepitus, the arm is stabilized and the sensory and motor func-
tions of the radial nerve are carefully checked as part of the
overall neurovascular examination (Figure 22-55). Radial nerve
function is evaluated by checking sensation in the dorsal thumb
web space and documenting active wrist extension. When frac-
ture of the humeral shaft is suspected, a coaptation splint made
of plaster, fiberglass, a SAM Splint, or wood is firmly applied
with an elastic bandage on the medial and lateral sides of the
humerus. A sling is useful for comfort. Acute reduction of the
fracture is not required in the field.
Fracture Around the Elbow (Distal Humerus, Olecranon,
Radial Neck or Head)
Elbow pain, crepitus, deformity, and swelling after a fall could
represent a distal humerus, olecranon, or radial head or neck
fracture. A neurovascular examination is performed, and then a
splint is applied with the elbow at 45 or 90 degrees of flexion,
depending on the victim’s comfort. Reduction should not be
attempted without radiographic confirmation, unless deformity is
gross, because crepitus is more often associated with a fracture
than with a dislocation. Evacuation should be performed promptly
if there is an open fracture or a neurocirculatory deficit.
Fracture of the distal humerus is frequently extraarticular in
children and intraarticular in adults (Figure 22-56). Children gen-
erally sustain supracondylar fractures after falls from heights. The
FIGURE 22-54  Path of the radial nerve in the arm.
468

FIGURE 22-55  Midshaft humeral fracture in a 45-year-old man who
fell while ice climbing. He presented with radial nerve palsy.
extension type of injury is much more common than the flexion
type, and it usually occurs in children age 4 to 8 years. Deformity,
swelling, pain, and crepitus are present, and the diagnosis of
fracture is fairly obvious. A careful neurovascular examination
should be performed, focusing on motor examination of flexion
of the thumb and distal IP joint of the index finger, because
injury to the anterior interosseous nerve, which supplies innerva-
tion to these muscles, is frequently associated with these frac-
tures. If the radial pulse is absent, an attempt should be made
to flex or extend the elbow while palpating the radial pulse. If
the pulse improves, the limb is splinted in that position for
A B
FIGURE 22-56  Anteroposterior (A) and lateral (B) views of intraarticu-
lar distal humeral fracture-dislocation sustained in a fall from an all-
terrain vehicle.
CHAPTER 22  Wilderness Orthopedics
FIGURE 22-57  Closed, displaced olecranon fracture-dislocation. A
sling or posterior splinting is appropriate for this injury until definitive
care can be provided.
transport. If the pulse does not improve and definitive care is
more than an hour away, reduction is performed. After available
sedation is given, the supinated forearm is extended with gentle
longitudinal traction. The fracture is reduced by flexing the elbow
while maintaining longitudinal traction, and the elbow is splinted
in 90 degrees of flexion. Evacuation should be prompt.
Fracture of the proximal ulna (olecranon) results from a fall
onto the posterior elbow, or from violent asymmetric contraction
of the triceps muscle. The victim may be unable to extend the
elbow actively against gravity if the triceps is dissociated from
the forearm with a complete olecranon fracture. On initial exami-
nation, the victim has pain, significant swelling, and a palpable
gap in the olecranon. With severe trauma, olecranon fracture may
be associated with elbow dislocation or intraarticular fracture
of the distal humerus, which can only be diagnosed radiographi-
cally (Figure 22-57). A complete distal neurovascular examination
should be performed. The shoulder and wrist should be exam-
ined, and a splint applied in the position of function and comfort.
Open fracture, absent pulse, severe swelling, or neurologic deficit
should prompt immediate evacuation.
Fracture of the radial head and/or neck generally occurs in
young to middle-aged adults who fall onto an outstretched hand.
The victim complains of pain around the elbow with loss of full
extension, and pain at the radial head on the lateral side of the
elbow with direct gentle pressure and rotation of the forearm.
Fracture of the radial head or neck frequently produces elbow
hemarthrosis, which is characterized by fullness posterior to the
radial head and anterior to the tip of the olecranon (Figure 22-58).
The elbow is gently moved through a range of motion and placed
FIGURE 22-58  Fracture of the neck of the radius, sustained in a fall.
Pain on palpation at the lateral aspect of the elbow, in the region of
the radial neck and head, would be anticipated.
469
 in a posterior splint in 90 degrees of flexion with the forearm
supinated. On a prolonged expedition when definitive care
cannot be reached, the splint is removed after 3 to 5 days so that
the victim can perform intermittent range-of-motion exercises
(both flexion-extension and pronation-supination). With more
comminuted radial head fractures, attempts at motion produce
pain and crepitus, and motion remains restricted. These injuries
require operative treatment. Although most individuals lose some
extension and pronation-supination, early motion may prevent
permanent loss of motion when the radial head fracture is non-
displaced or minimally displaced. The arm is splinted in supina-
tion to prevent contracture of the intraosseous ligament and loss
of supination.
Elbow Dislocation
Dislocation of the elbow occurs with hyperextension or axial
loading from a fall onto an outstretched hand. The direction of
dislocation is generally posterior and lateral. The diagnosis is
clear, with posterior deformity at the elbow and foreshortening
of the forearm. After carefully assessing distal sensory, motor,
and vascular status, reduction is performed. With countertraction FIGURE 22-60  In Meyn and Quigley’s method of reduction, only the
on the upper arm, linear traction is applied with the elbow forearm hangs from the side of the stretcher. As gentle downward
slightly flexed and the forearm in the original degree of prona- traction is applied on the wrist, the physician guides reduction of the
olecranon with the opposite hand. (Redrawn from Meyn MA, Quigley
tion and supination. Downward pressure on the proximal forearm
TB: Reduction of posterior dislocation of the elbow by traction on the
to disengage the coronoid from the olecranon fossa may be dangling arm, Clin Orthop Relat Res 103:106, 1974. In Rockwood CA
helpful. Hyperextension should be avoided. Adequate analgesia Jr, Green DP, Bucholz RW, editors: Rockwood and Green’s fractures
can be extremely helpful. An alternative method (Parvin’s in adults, ed 3, Philadelphia, 1991, JB Lippincott.)
method) is to place the patient prone over a log or makeshift
platform and apply gentle downward traction on the wrist for a
few minutes. As the olecranon begins to slip distally, the arm is cartilage fragments are often a consequence of elbow dislocation.
lifted up gently. No assistant is needed, and if the maneuver is Follow-up evaluation and monitored therapy for range of motion
done gently, no anesthesia is required (Figure 22-59). A modifica- are essential to avoid chronic instability or possible arthrofibrosis.
TRAUMA

tion of this maneuver (Meyn and Quigley’s method) is to hang
only the forearm over the platform while applying gentle down-
ward traction via the wrist and guiding reduction of the olecra-
non with the opposite hand (Figure 22-60). Reduction provides
nearly complete relief of pain and restoration of the normal
surface anatomy. A posterior splint is applied with the elbow in
PART 4
A sling is provided for comfort. If reduction is not successful after
three attempts or if a nerve injury is suspected, a splint is applied
to the arm as it lies and evacuation performed.
Subluxation of the radial head in children (nursemaid’s elbow)
occurs when a longitudinal pull is applied to the upper extremity
(Figure 22-61). The orbicular ligament partially tears, allowing a

90 degrees of flexion and the forearm in neutral position. Col-
lateral elbow ligament injuries and possible interposed bone or
portion of it to slip over the radial head. An audible snap may
be heard at the moment of injury. The initial pain from the injury
subsides rapidly, and the child does not seem distressed but
refuses to use the extremity. Any attempt to supinate the forearm
brings a cry of pain and distress. If a definitive care center is
nearby, the injury is splinted and evacuation is arranged. Other-
wise, if the history and examination are consistent with the
diagnosis, reduction can be attempted. First, the slightly flexed
forearm is supinated; if this fails to produce the characteristic
snapping sensation of reduction, the elbow is gently, maximally
flexed in supination until the snapping sensation occurs (Figure
22-62). If the reduction is successful, the child is usually content

FIGURE 22-59  Parvin’s method of closed reduction of an elbow dis-

location. The patient lies prone on a stretcher, and the physician
applies gentle downward traction on the wrist for a few minutes. As
the olecranon begins to slip distally, the physician lifts up gently on
the arm. No assistant is required, and if the maneuver is done gently,
no anesthesia is required. (Redrawn from Parvin RW: Closed reduction
of common shoulder and elbow dislocations without anesthesia,
Arch Surg 75:972, 1957. In Rockwood CA Jr, Green DP, Bucholz RW,
editors: Rockwood and Green’s fractures in adults, ed 3, Philadelphia,
1991, JB Lippincott.)
FIGURE 22-61  Nursemaid’s elbow most commonly occurs when a
longitudinal pull is applied to the upper extremity. Usually the forearm
is pronated on presentation. There is a partial tear in the orbicular liga-
ment, allowing it to subluxate into the radiocapitellar joint. (From
Rockwood CA Jr, Wilkins KE, King RE, editors: Fractures in children,
ed 3, Philadelphia, 1991, JB Lippincott.)

470
 CHAPTER 22  Wilderness Orthopedics
FIGURE 22-62  Reduction of nursemaid’s elbow injury. Left, The
forearm is supinated. Right, The elbow is then hyperflexed. The res-
cuer’s thumb is placed laterally over the radial head to feel the char-
acteristic “snap” as the ligament is reduced. (From Rockwood CA Jr,
Wilkins KE, King RE, editors: Fractures in children, ed 3, Philadelphia,
1991, JB Lippincott.) FIGURE 22-63  Both forearm bones are fractured following a fall while
snowboarding.

and playing within 5 to 10 minutes, and no immobilization of

the joint is indicated. If the reduction is unsuccessful, the child are not usually comminuted but can be difficult to reduce (Figure
continues to avoid using the involved arm and should be evacu- 22-66). In cases involving an open fracture, significant distal
ated for definitive care. neurologic deficit, or abnormal circulatory examination, splinting
and evacuation should be prompt. The limb should be kept
FOREARM, WRIST, AND HAND FRACTURES elevated above the level of the heart during transport.
Radial Fracture Ulnar Fracture
Radial shaft fracture occurs with a fall involving angular or axial Ulnar shaft fracture is most often associated with fracture of the
loading of the forearm. A radial shaft fracture may be associated radial shaft at the same level. When isolated, it usually occurs as
with dislocation of the distal radioulnar joint (Galeazzi fracture) a result of a direct blow, the so-called nightstick fracture (Figure
(see Figure 22-27). Therefore, in the setting of known or sus- 22-67). Fracture of the ulnar shaft can be associated with disloca-
pected radial shaft fracture, the wrist should be examined for tion of the radial head (Monteggia lesion); therefore, elbow
tenderness, swelling, and deformity. The victim generally com- function should be carefully assessed. In the wilderness, the most
plains of pain. Deformity and crepitus are noted over the radial
shaft after a fall or direct blow. Any arm motion exacerbates the
pain. When both the radius and ulna are fractured, forearm
instability is marked (Figure 22-63). The joint above (elbow) and
joint below (wrist) should always be examined for tenderness,
crepitus, and deformity. Once a fracture of the radius or both
bones of the forearm is identified, the wrist, forearm, and elbow
are splinted in the position of function.
Fracture of the distal metaphyseal radius is generally associ-
ated with a fall onto the outstretched hand (FOOSH injury)
(Figure 22-64). Ulnar styloid fracture may accompany intraarticu-
lar fracture of the distal radius. Pain and crepitus are present,
and often deformity associated with displacement. When this
injury is suspected, distal neurovascular examination is per-
formed, focusing on sensory function of the median nerve.
Median nerve injury or compression at this level of injury mani-
fests primarily as decreased sensation in the volar palm and
fingers (thumb, index finger, middle finger, and radial half of the
ring finger). Weakness in the opponens and abductor pollicis
muscles might also be noted. If there is neurovascular compro-
mise and definitive care is more than 2 hours away, reduction
should be attempted. One hand is placed on the forearm to
provide countertraction and the other around the wrist of the
involved extremity. The wrist is dorsiflexed, and longitudinal
traction is applied as the wrist is returned to a neutral position.
A splint is applied to immobilize the wrist and elbow.
Distal radial and ulnar fractures occur commonly in children.
They are seen most frequently in girls age 11 to 13 years and
boys age 13 to 15 years. Familiarity with the Salter-Harris fracture
classification system is important (Figure 22-65). These fractures FIGURE 22-64  Distal radial fracture after fall.

471
 Diaphysis
(shaft of bone)

Epiphyseal Metaphysis
disk
(growth plate)
Epiphysis A

Normal Type I

A complete physeal fracture

with or without displacement

B
Type II Type III

A physeal fracture that A physeal fracture that

extends through the extends through the
metaphysis, producing a chip epiphysis
fracture of the metaphysis,
which may be very small

C
FIGURE 22-66  Technique for reduction of a distal radial fracture.
A, Initial fracture position. B, Hyperextend fracture to 100 degrees to
disengage the fracture ends. C, Push with the thumb on the distal
TRAUMA

fragment to achieve reduction. (From Green N, Swiontkowski MF:

Skeletal trauma in children, vol 3, ed 2, Philadelphia, 1998, Saunders.)

Type IV Type V tenderness, crepitus, and occasionally deformity (sunken knuckle

sign) are present (Figure 22-71). This fracture should be managed
A physeal fracture plus A compression fracture of with a short-arm or ulnar gutter splint.
PART 4

epiphyseal and metaphyseal the growth plate Fractures of the metacarpal necks occur by the same mecha-
fractures nism and usually involve the fourth and fifth metacarpals. These
FIGURE 22-65  Salter-Harris pediatric fracture classification.

frequent mechanism of injury is bracing against a fall or collision

with the forearm. Pain, localized swelling, and crepitus are
present. A long-arm splint is applied in the position of function.
Open fracture is an indication for prompt evacuation.
Wrist and Carpal Fractures
Wrist fractures occur with significant rotational forces or high
axial loading forces, as occur in falls onto the hand. The victim
first complains of pain and later of wrist swelling. Hand use or
forearm rotation produces significant pain. Many carpal bone
fractures are associated with wrist dislocation.
Carpal bone fractures cannot be accurately diagnosed without
radiographs. Scaphoid (navicular) fracture is the most common
fracture and is suspected when maximal tenderness is in the
“anatomic snuffbox” (Figures 22-68 and 22-69). If appropriate
splinting materials are available, a thumb spica splint is applied,
immobilizing both the radius and entire thumb. With fracture of
the hook of the hamate bone, the victim complains of pain at
the base of the hypothenar eminence (Figure 22-70). This injury
occurs when the hand is used to apply significant force to an
object with a handle on it, such as an ax or hammer, and great
resistance is met. A short-arm splint suffices for this injury, and
for other suspected carpal injuries, until definitive treatment is
obtained. With open fracture or one accompanied by median
nerve dysfunction, the victim should be promptly evacuated.
Metacarpal Fracture
Fracture of the metacarpal base or shaft occurs with crush injuries
or axial load, as when a rock or other immovable object is struck.
Fracture at the bases of the metacarpal is suspected when FIGURE 22-67  “Nightstick” ulnar fracture.

472
 CHAPTER 22  Wilderness Orthopedics
Extensor pollicis
longus
Scaphoid

Extensor pollicis
brevis Abductor pollicis
longus
FIGURE 22-68  The scaphoid (navicular) bone sits in the anatomic
snuffbox of the radial aspect of the wrist.
FIGURE 22-69  Scaphoid fracture with scapholunate widening.
H Irreducible or complex dislocations occur when the volar
FIGURE 22-70  Hook of hamate (H) fracture.
FIGURE 22-71  Sunken knuckle sign, fourth metacarpal.
fractures can be associated with significant flexion deformity. Up
to 40 degrees of flexion in the fourth and fifth digits can be
accepted without compromising hand function, so these fractures
seldom require surgical reduction and fixation. Rotational defor-
mity of the metacarpal is poorly tolerated, however, and should
be anticipated with suspected metacarpal fractures. With the MCP
and the IP joints flexed 90 degrees, the fingernails should be
parallel to one another and perpendicular to the orientation of
the palm. The terminal portions of the digit should point to the
scaphoid tubercle in an anatomic “cascade.” If this is not noted,
rotational deformity should be strongly suspected.
When malalignment or significant shortening with a suspected
shaft fracture is noted, the fracture is reduced with longitudinal
traction on the involved digit. A fractured metacarpal shaft or
neck is immobilized by applying an aluminum splint (or stick)
to the volar surface of the finger and palm and taping the
involved digit to the adjacent digit, with the MCP joint at 70 to
90 degrees. This position provides optimal length of the collateral
ligaments. Immobilizing the joint in this position prevents con-
tractures that can lead to subsequent loss of motion.
Fracture of the base of the thumb metacarpal often occurs
with an axial force directed against a partially flexed thumb
metacarpal (Figure 22-72). If the fracture extends into the joint,
it often requires operative fixation. If this fracture is suspected,
the thumb and wrist are immobilized in a thumb spica splint. An
open metacarpal fracture needs cleansing, debridement, and
antibiotic therapy for 48 hours or until definitive care is obtained.
Metacarpophalangeal Joint Dislocation
MCP joint dislocation is rare and may be produced by a crush
injury or when the hand is caught in a rope. This dislocation
may be dorsal or volar, with dorsal dislocation more common.
Clinically, the joint is hyperextended and the phalanx shortened.
Most dorsal dislocations are easily reduced. First, the proximal
phalanx is hyperextended 90 degrees on the metacarpal, and
then the base of the proximal phalanx is pushed into flexion,
maintaining contact at all times with the metacarpal head to
prevent entrapment of the volar plate in the joint (Figures 22-73
and 22-74). Straight longitudinal traction is avoided because it
may turn a simple dislocation into a complex dislocation. The
wrist and IP joints are flexed to relax the flexor tendons. The
joint usually reduces easily with a palpable and audible “clunk.”
A dorsal-volar splint is applied with the joint held at 90 degrees
of flexion.
plate is interposed in the joint. The joint is only slightly hyper-
extended, and the volar skin is puckered over the joint. These
dislocations are most common in the index finger, thumb, and
small finger. A single attempt at reduction using the technique
just described is indicated, but these dislocations usually require
open reduction. If reduction of an MCP joint dislocation is unsuc-
cessful, the joint should be splinted in the position of comfort
and definitive treatment obtained as soon as possible.

473
 Fracture

FIGURE 22-72  Fracture of base of the first metacarpal.

FIGURE 22-74  Dislocation of the right thumb; first metacarpophalan-
TRAUMA

geal joint.
The thumb MCP joint is most commonly injured. Dislocations
are reduced as already described. Injury to the ulnar collateral
ligament of this joint (skier’s or gamekeeper’s thumb) results from ture with subluxation or dislocation is difficult to differentiate
a valgus stress, as may occur when an individual falls holding from IP joint dislocation (Figure 22-77). Angular deformities in
an object in the first web space. The victim complains of tender- these fractures can be reduced using a pencil or thin stick placed
PART 4

ness over the ulnar aspect of the MCP joint. There may be insta- in the web space as a fulcrum to assist with reduction. Fracture
bility to radial stress with the joint held in 30 degrees of flexion, of the shaft of a phalanx is reduced by applying traction and
an indication for surgical repair. Often the adductor aponeurosis
becomes interposed between the ligament and its bony attach-
ment, resulting in a Stener lesion (Figure 22-75). In the field, a
thumb spica splint is applied and definitive care sought within
10 days. If splinting material is not available, the thumb is taped
until definitive care can be obtained (Figure 22-76).
Fractures of the Phalanges
Fractures of the digital phalanges occur with crush injuries or
when the digits are caught in ropes or equipment being used to
haul objects. Angular or rotational deformity and crepitus make
these fractures obvious. Without radiographs, intraarticular frac-

FIGURE 22-73  The single most important element preventing
reduction in a complex metacarpophalangeal dislocation is interposi-
tion of the volar plate within the joint space. It must be extricated
surgically. (From Rockwood CA Jr, Green DP, Bucholz RW, editors:
Rockwood and Green’s fractures in adults, ed 3, Philadelphia, 1991,
JB Lippincott.)
A B C D
FIGURE 22-75  Diagram of the displacement of the ulnar collateral
ligament of the thumb metacarpophalangeal joint. A, Normal relation-
ship, with the ulnar ligament covered by the adductor aponeurosis. 
B, With slight radial angulation, the proximal margin of the aponeuro-
sis slides distally and leaves a portion of the ligament uncovered. 
C, With major radial angulation, the ulnar ligament ruptures at its distal
insertion. In this degree of angulation, the aponeurosis has displaced
distal to the rupture and permitted the ligament to escape from
beneath it. D, As the joint is realigned, the proximal edge of the adduc-
tor aponeurosis sweeps the free end of the ligament proximally and
farther away from its insertion. This is the Stener lesion. Unless surgi-
cally restored, the ulnar ligament will not heal properly and will be
unstable to lateral stress. (Redrawn from Stener B: Skeletal injuries
associated with rupture of the ulnar collateral ligament of the meta-
carpophalangeal joint of the thumb: a clinical and anatomical study,
Acta Chir Scand 125:583, 1963.)

474
 CHAPTER 22  Wilderness Orthopedics
A B
FIGURE 22-76  Taping the thumb for immobilization. A, The buddy-
taping method. B, A thumb lock. If possible, padding should be placed
between the thumb and forefinger. (From Auerbach PS. Medicine for
the outdoors: the essential guide to first aid and medical emergencies,
ed 6, Philadelphia, 2016, Elsevier.)

correcting the deformity. The fractures are immobilized by taping FIGURE 22-78  Middle finger proximal interphalangeal joint
the injured digit to the neighboring uninjured digit or to a volar dislocation.
splint. Nailbed fractures or crushes are cleansed with soap and
water, covered with a clean dressing, and protected with a volar
splint. IP joint dislocations are relatively common and can usually
be reduced with gentle axial traction on the digit (Figures 22-78
and 22-79). Reduction is often accompanied by an audible “pop”
and improved ability to flex and extend through the IP joint.
After reduction, the finger should be buddy taped to the adjacent
digit. Prolonged (> 3 days) immobilization of the digit in a rigid
splint should be avoided to prevent finger stiffness.
Dorsal IP dislocations can cause a tear in the skin volar to the
joint. Although this tear may appear benign, the wound should
be cleaned as well as possible, because contamination of the
adjacent flexor tendon sheath can result in severe infection.
FIGURE 22-79  Radiograph demonstrating dorsal displacement of
Soft Tissue Injuries of the Wrist, Hand, and Digits base of the middle phalanx.
Injuries to the volar or dorsal aspect of the hand or wrist can
result in nerve and tendon injuries. A deep laceration over the
volar palm or digits often extends to the digital flexor tendons splinted in flexion to prevent further retraction of the lacerated
and nerves (Figure 22-80). Loss of sensation or inability to flex tendons and nerves. Lacerations on the dorsum of the hand may
the digit should prompt medical evaluation, because these struc- disrupt digital extensor tendons, although the functional loss may
tures will not recover without surgical intervention. Any wounds be less apparent due to interconnections with adjacent intact
should be carefully cleaned and bandaged and the fingers tendons.

HIP AND LEG INJURIES

FEMORAL FRACTURE
In general, healthy, active individuals sustain fractures of the
proximal femur only in falls from significant heights or from

FIGURE 22-77  Ring finger proximal interphalangeal joint dislocation FIGURE 22-80  Extended posture of ring and small fingers that strongly
that occurred while diving. suggests traumatic flexor tendon lacerations.

475

FIGURE 22-81  Comminuted femoral shaft fracture in a 30-year-old
TRAUMA
who rolled his all-terrain vehicle and hit a tree. Subcutaneous pieces
of bone laterally suggest how close this injury was to being an open
fracture.
high-velocity injuries sustained, for example, in motorized vehicle
PART 4
accidents or snow skiing or snowboarding. These fractures occur
in the femoral neck or intertrochanteric or subtrochanteric regions
(Figure 22-81; see also Figure 22-6). The victim complains of
severe pain within the proximal thigh. There may be generalized
swelling or deformity around the hip region. Movement of the
affected limb, which is noticeably shortened and externally
rotated, produces significant pain. After a careful sensory, motor,
and circulatory examination, the limb is realigned, and a splint
is applied if available. An improvised traction splint may need
to be fabricated. If none is available, the victim is transported on
a backboard, with the limbs strapped together or tied to a board
with a tree limb placed between them.
Femoral neck fracture is associated with significant risk for
posttraumatic femoral head necrosis (see Figure 22-6). Without
a radiograph, this fracture is impossible to distinguish from a
subtrochanteric or intertrochanteric hip fracture. Because there is
evidence that emergency treatment of a fracture of the femoral
neck in a young person decreases the risk for posttraumatic
avascular necrosis,28,30 rapid evacuation should be arranged for
any victim in whom this injury is suspected.18
Femoral shaft fracture occurs by similar mechanisms (see
Figure 22-81). Crepitus and maximal deformity are noted in the
midportion of the thigh. After neurovascular examination, the
limb is placed in traction or protected as noted previously. Gross
deformity of the shaft is corrected with gentle traction, and the
neurovascular examination is repeated. This fracture may be an
open injury, so the victim’s pants should be opened or cut to
complete the examination. Discovery of an open wound should
prompt rapid evacuation.
HIP DISLOCATION
Posterior hip dislocation is produced by axial loading of the
femur with the hip flexed and adducted13 (Figure 22-82). It gener-
ally occurs in a motor vehicle crash but can follow a fall or a
sledding or skiing accident. With posterior dislocation, the victim
476
complains of severe pain around the hip, and the affected limb
appears shortened, flexed, internally rotated, and adducted. Any
hip motion increases the pain. It is not clinically possible to
determine if there is an associated acetabular or femoral neck
fracture. With the rare anterior dislocation, the limb is externally
rotated, slightly flexed, and abducted. This type of dislocation is
generally produced by wide abduction of the hip caused by
significant force.
The victim is placed in the supine position for complete
survey of all organ systems. The distal limb is carefully examined
for associated fractures, and a thorough sensory and motor
examination is performed. The peroneal division of the sciatic
nerve is most susceptible to injury with a posterior hip disloca-
tion. Hip dislocation is an orthopedic emergency, because time
to reduction is directly linked to incidence of avascular necrosis
of the femoral head.6 Immediate transfer to a definitive care
center is desirable because hip radiographs may reveal an associ-
ated femoral neck fracture that could become displaced if closed
reduction is attempted. However, if it will be more than 6 hours
before the victim can be evacuated to a definitive care center,
closed reduction should be attempted. To perform the Allis tech-
nique (Figure 22-83), the victim is positioned supine on the
ground or a stretcher. If available, analgesic medication is admin-
istered. The caregiver stands above the victim and applies in-line
traction on the extremity while an assistant applies countertrac-
tion to the iliac wings. Posterior dislocations are reduced by
flexing the hip 60 to 90 degrees. Internal rotation and adduction
of the hip facilitate relocation. With anterior dislocation, traction
is applied with the leg slightly abducted and externally rotated
and the hip gently extended. Successful reduction is usually
indicated by an audible “clunk” and restoration of limb align-
ment. As with any reduction or relocation maneuver, adequate
analgesia and a slow, progressive increase in traction force are
helpful. This is not a technique that involves a sudden jerking
movement; gradual fatiguing of the muscles that, in spasm, may
be maintaining the hip in a dislocated position remains the most
likely means of achieving relocation.
Another technique for relocating a posteriorly dislocated hip
has been described.14 The Captain Morgan technique is named
for the similarity of the pose of the person executing this maneu-
ver and the posture that “Captain Morgan” assumes on the
eponymous bottle of rum. The caregiver maintains the patient in
the supine position. The caregiver flexes the patient’s hip and
knee to 90 degrees. The caregiver places his or her thigh under
the calf of the flexed, dislocated hip. With one hand pressing
downward on the ipsilateral ankle of the dislocated hip and the
other hand lifting upward behind the ipsilateral knee of the
dislocated hip, the caregiver plantarflexes her or his own ankle
of the leg that is under the patient’s thigh. This slow plantarflex-
ion, along with the concomitant downward pressure distally and
upward pressure proximally, allows the caregiver’s thigh to be
used as a fulcrum to facilitate the hip relocation (Figure 22-84).
FIGURE 22-82  Right hip dislocation with femoral head fracture.
 CHAPTER 22  Wilderness Orthopedics
A

FIGURE 22-85  Patellar fracture as a result of a direct blow to the

anterior knee.

and the femoral condyles suffer a direct impact, producing either

patellar fracture or fracture of the femoral condyles or distal
femoral metaphysis (Figures 22-85 and 22-86). Occasionally, with
high-energy trauma, a distal femoral fracture and ipsilateral proxi-
B C mal tibial fracture can occur concurrently.
FIGURE 22-83  A combination of Allis’s and reverse Bigelow’s maneu-
vers for reduction of a hip dislocation. A, The health care provider’s
position must provide a mechanical advantage for the application of
traction. In-line traction with hip flexed. B, Internal and external rota-
tions are gently alternated, perhaps with lateral traction by an assistant
on the proximal thigh. C, Adduction is often a helpful adjunct to in-line
traction. (Redrawn from Rockwood and Green: Fractures in adults,
vol 2, ed 3, Philadelphia, 1991, JB Lippincott.)

KNEE AND LOWER LEG INJURIES

Distal Femoral or Patellar Fracture
Fracture of the distal femur is frequently intraarticular and occurs
with high-velocity loading when the knee is flexed. With axial
loading on the femur, the patella becomes the driving wedge

Hand B
Hand A

FIGURE 22-84  Captain Morgan technique for reducing a dislocated

hip. (From Auerbach PS. Medicine for the outdoors: the essential guide FIGURE 22-86  A 70-year-old woman with a total knee arthroplasty
to first aid and medical emergencies, ed 6, Philadelphia, 2016, sustained a periprosthetic distal femoral fracture when she fell while
Elsevier.) hiking.

477

FIGURE 22-87  Open patellar fracture wound with typical stellate
appearance.
With a patellar fracture, the injury may be obvious on deep
palpation. This is often an open injury because there is very little
soft tissue overlying this sesamoid bone (Figure 22-87). After an
initial neurovascular examination, the limb is realigned. A pos-
terior splint is applied to the realigned limb for transportation.
As with all fractures, open wounds in the region of the fracture
or an abnormal nerve or vascular examination should prompt
immediate evacuation.
Knee Dislocation
TRAUMA
Knee (tibial-femoral) dislocation is a high-energy injury. It is
usually obvious because of the amount of deformity (Figure
22-88). The most common dislocation directions are anterior and
posterior. Knee dislocation represents a true emergency because
5% to 40% of these injuries have associated vascular injuries.1,29,34
A large series reported an above-knee amputation rate of 86%
PART 4
for vascular injuries associated with knee dislocations that were
not repaired within 8 hours of injury.12 The vascular injury occurs
because of tethering of the popliteal vessels by the soleus fascia
along the posterior border of the tibia. When this injury is sus-
pected, a careful screening neurovascular examination must be
FIGURE 22-88  Anterior knee dislocation. Significant attention should
be devoted to relocation, if possible, and to assessment of the neuro-
vascular structures that run posterior to the knee joint, such as the
popliteal artery and the tibial and common peroneal nerves.
478
performed. Intact distal pulses do not definitively rule out arterial
injury. Intimal flap tears can produce delayed popliteal artery
thrombosis. Injury to the peroneal nerve can also occur.
Many knee dislocations spontaneously reduce and may lead
the examiner to underestimate the seriousness of the injury.
Instability in extension to either varus or valgus stress indicates
disruption of at least one of the cruciate ligaments and signifies
the potential for a knee dislocation.
After initial examination, the persistent dislocation should be
reduced. Anterior dislocation is reduced with traction on the leg
and gentle elevation of the distal femur. Posterior dislocation is
reduced with traction in extension and anterior elevation of the
tibia. Posterolateral rotatory dislocation (which occurs when the
medial femoral condyle buttonholes through the medial capsule)
can be very difficult to reduce and usually requires open reduc-
tion. A transverse furrow on the medial aspect of the knee is
pathognomonic for this injury. For transport, a posterior splint is
applied to the limb, and the victim is moved on a backboard.
The possibility of an arterial lesion or emerging compartment
syndrome requires vigilance. Emergency evacuation is advised
because of the risk for amputation related to vascular injury.
The patellofemoral joint is more commonly dislocated than is
the tibial-femoral joint. Generalized ligamentous laxity may pre-
dispose to this problem. Patellofemoral dislocation, especially
recurrent, is more common in females than males and may be
associated with an accentuated Q angle, the angle created
between a line drawn from the anterior superior iliac spine to
the center of the patella and a line drawn from the tibial tubercle
to the center of the patella. Dislocation of the patella may result
from a twisting injury or asymmetric quadriceps contraction
during a fall. These mechanisms can occur with hiking, climbing,
and skiing accidents. The patella usually dislocates to a position
lateral to the articular surface of the distal femur. Although neu-
rovascular injuries rarely occur in association with a dislocated
patella, a screening examination should be conducted.
The patella can often be reduced by simply straightening the
knee. If this is not successful, gentle pressure is applied to the
patella to push it back up into the distal femoral articular groove.
A knee splint is applied with the joint in extension; weight
bearing is allowed. The knee is kept in extension until definitive
care can be obtained. A radiograph is ultimately required to rule
out osteochondral fractures, which can be associated with this
injury.
Tibial and Fibular Fractures
The tibial plateau is the broad articular surface and metaphysis
of the upper tibia that articulates with the distal femur. This area
can be fractured in a fall or leap from a height. A valgus moment
of force produces fracture of the lateral tibial plateau, whereas a
varus moment of force produces medial plateau fracture (Figure
22-89). Pain, swelling, and deformity are obvious on initial exami-
nation. With a tibial plateau fracture, significant hemarthrosis
develops quickly. Because of anatomic tethering of the popliteal
artery by fascia of the soleus complex, arterial injury may result
from this fracture, especially when it is associated with a knee
dislocation. Distal pulses and capillary refill should be assessed
at 1-hour intervals for a minimum of 8 hours or until evacuation
occurs. After an initial examination, the limb is carefully realigned
and a posterior splint applied for transportation.
Tibial shaft fractures may or may not be associated with fibular
fractures. These fractures result from high-impact trauma. They
were the most common ski injuries before the advent of modern,
higher, anatomically conforming ski boots; improved binding-
release systems; and shorter parabolic skis that reduced the lever
arm of skis. The injury was sustained when the body rotated
around a fixed foot (a ski caught against a rock, a tree stump,
or the slope), which produced a torsional spiral fracture of the
tibia and fibula.
Tibial shaft fracture is a common type of open fracture in the
wilderness setting (Figure 22-90). When this injury is suspected,
the entire limb should be inspected for distal sensory, motor, and
vascular function before realignment. A posterior splint is applied
for transport. The limb should be serially examined for the onset
of compartment syndrome.

FIGURE 22-89  Tibial plateau fracture sustained in fall from a height.
ANKLE AND FOOT INJURIES
Ankle and Foot Fractures
The articular distal tibia (pilon), medial malleolus, and distal
fibula, or any combination of these, may be involved in an ankle
fracture, which is generally produced by torsional moments of
force around a fixed foot (Figure 22-91). With the pilon tibial
fracture, axial loading from a fall or jump may also be involved.
Any significant pain and swelling should be noted as the footgear
is removed. Palpation along the medial and lateral malleoli
confirms the clinical suspicion. After footgear is removed to
inspect the skin for open wounds, neurovascular examination is
performed.
If there is a rotational deformity in the ankle, it should be
realigned with gentle traction before applying a posterior splint
FIGURE 22-90  Tibia fracture sustained in a snowmobile accident.
CHAPTER 22  Wilderness Orthopedics
FIGURE 22-91  Distal tibia-fibula fracture in a young Enduro rider:
Salter-Harris II fracture.
with the foot and ankle in neutral position. During transport, the
limb is elevated above the level of the heart.
Ankle Dislocation or Sprain
Ankle dislocation is almost always accompanied by fractures of
one or more malleoli. This dislocation generally occurs with falls
onto uneven surfaces or with twisting injuries of moderate veloc-
ity. The area about the ankle is carefully examined for open
injuries, and a neurovascular examination is conducted. The
ankle joint is aligned by grasping the posterior heel, applying
traction with the knee bent (to relax the gastrocnemius-soleus
complex), and bringing the foot into alignment with the distal
tibia. As with all reduction maneuvers, sustained gentle traction
to fatigue the muscles that are in spasm is most effective. After
this maneuver, the foot is reexamined, the wounds are dressed,
and a posterior splint is applied. During transport, the limb is
elevated above the level of the heart.
The most common musculoskeletal injury occurring in the
wilderness setting is ankle sprain. Inversion injuries usually
damage the lateral ligament structures, most commonly the ante-
rior talofibular ligament. The calcaneal fibular ligament and pos-
terior talofibular ligaments are less commonly injured. Eversion
injury to the medial ankle may strain the large medial deltoid
ligament (Figures 22-92 to 22-94).
An ankle sprain is often considered to be a minor injury, “just
an ankle sprain.” However, if a sprain is improperly rehabilitated
or if someone returns to activity too soon, it may result in a
chronically unstable joint. Ligament sprain, or tearing of the
fibers, is differentiated (or categorized) into three grades. Grade
1 injury is partial disruption of some of the ligament fibers. Grade
2 injury is significant disruption of a portion of the ligament
fibers. The main substance of the ligament remains intact, and
the injury is characterized by moderate hemorrhage. Grade 3
injury is complete disruption of the ligament fibers, which can
result in instability of the ankle joint.
The amount of discoloration and swelling of the ankle and
foot usually is consistent with the degree of injury. Even grade
3 injuries usually heal without surgery if treated appropriately.
An ankle stirrup for 3 to 6 weeks may be adequate for grade 1
injury. A walking boot or cast is often indicated for grade 2 to 3
479
 Interosseous membrane Tibialis anterior

Medial malleolus
Anterior inferior tibiofibular
ligament

Dorsal ligament
Anterior talofibular ligament

Interosseous talocalcaneal
ligament
Dorsal talonavicular ligament
Calcaneocuboid
ligament Navicular bone

Cuboid bone Dorsal calcaneonavicular

ligament
3rd cuneiform bone 1st cuneiform bone

Dorsal tarsometatarsal
Dorsal metatarsal ligament
ligaments 1st metatarsal bone
TRAUMA

FIGURE 22-92  Ligaments of the anterior ankle.

PART 4

injuries, with protected motion for 6 to 8 weeks. Ligament injury, slides forward within the ankle mortise (using the uninjured side
depending on degree, typically requires at least 6 and often 12 for comparison), the injury is likely grade 3. The foot and ankle
weeks for complete healing. are placed into a posterior splint or air splint. If possible, the
When ankle sprain is suspected, the footgear and sock are victim is kept from bearing weight on the limb. If the anterior
removed and a screening neurovascular examination is con- drawer test does not reveal instability and indicates a grade 1 or
ducted. Ankle ligaments and bone are palpated to help distin- 2 sprain, an elasticized bandage is applied or the ankle is taped.
guish between ankle fracture and sprain. The ankle is evaluated All injuries should be acutely treated using RICE principles. Com-
for instability with the anterior drawer test. This is performed by mercially available stirrup air splints aid ambulatory management
stabilizing the tibia with one hand and grasping the posterior of these injuries.
heel to pull the foot forward with the other hand. If the talus In the field, the ankle is taped to decrease pain and limit
swelling (Figure 22-95; see also Chapter 23). During taping, the
victim’s ankle is held perpendicular to the tibial shaft. This makes
Tibia
Anterior inferior
tibiofibular ligament
Talus Groove for
Anterior talofibular tibialis posterior
ligament Neck of talus Medial
Lateral Dorsal talonavicular malleolus
ligament Tibionavicular fibers Achilles
malleolus Dorsal talonavicular tendon
Calcaneofibular Navicular
ligament
ligament 1st cuneiform
bone
Navicular
bone

Calcaneus Dorsal Tibial posterior Posterior Medial

Lateral tendon Tibiocalcaneal tibiotalar tubercle
calcaneocuboid Plantar
talocalcaneal Interosseous ligament Cuboid calcaneonavicular
fibers fibers of talus
ligament talocalcaneal ligament and Sustentaculum
ligament associated fibers tali
FIGURE 22-93  Ligaments of the lateral ankle. FIGURE 22-94  Ligaments of the medial ankle.

480

A B C
FIGURE 22-95  Taping sprained ankle. Strips of adhesive tape are
placed perpendicular to each other (A) to lock the ankle with a tight
weave (B). The edges are covered to prevent peeling (C). (From Auer-
bach PS. Medicine for the outdoors: the essential guide to first aid and
medical emergencies, ed 6, Philadelphia, 2016, Elsevier.)
walking easier, because the ankle is not plantarflexed, and helps
prevent development of Achilles tendon contracture. If available,
an Aircast ankle brace provides additional ankle support and can
be used with a shoe or boot.
Fracture of the lateral process of the talus, which is a fairly
common lower extremity fracture in snowboarders, may be con-
fused with lateral ankle sprain, so radiographs are generally
needed to rule out this injury.9 Inversion injuries are also infre-
quently associated with fractures at the insertion of the peroneus
brevis tendon. This injury can be identified by point tenderness
at the base of the fifth metatarsal, but a radiograph is required
for definitive diagnosis. Early management is the same as for an
ankle sprain. The eponym Jones fracture is used to describe the
more worrisome transverse fracture to the metaphyseal portion
of the fifth metatarsal; nonunion is a concern with this injury
(Figure 22-96).
Hindfoot Dislocation
The subtalar joint may infrequently be dislocated in a significant
fall or jump when an individual lands off balance or on an
FIGURE 22-96  Base of fifth metatarsal fracture. This technically is not
a Jones fracture because it is in the metaphyseal region, not the meta-
diaphyseal region.
CHAPTER 22  Wilderness Orthopedics
FIGURE 22-97  Subtalar fracture dislocation.
uneven surface. The calcaneus may be dislocated medially or,
more commonly, laterally relative to the talus (Figure 22-97). The
position of the heel relative to the ankle is assessed. With either
dislocation, a reduction is attempted if it will be more than 3
hours until the victim will reach a definitive care center.
Medial dislocation is reduced more easily than is lateral dis-
location, in which the posterior tibial tendon frequently becomes
displaced onto the lateral neck of the talus, blocking the reduc-
tion. The maneuver is the same for both: The heel is grasped
with the knee flexed (relaxing the gastrocnemius-soleus complex),
the deformity is accentuated, linear traction is applied, and the
heel is brought over to the ankle joint. This maneuver is gener-
ally successful for medial dislocation, but lateral dislocation,
especially when associated with open wounds, often requires
open treatment. After reduction is attempted, a posterior splint
is applied and the limb is elevated above the level of the heart.
Even if reduction is successful, the victim must not be allowed
to bear weight until definitive care is obtained.
Midfoot Dislocation
Midfoot fracture-dislocation (Lisfranc injury) is described in the
metatarsal fracture section (Figure 22-98).
FIGURE 22-98  Lisfranc midfoot fracture-dislocation.
481
 midfoot by stabilizing the heel and placing force across the fore-
foot in the varus and valgus directions reveals instability. The
foot is placed in a well-padded posterior splint and elevated. The
patient is not allowed to ambulate. Swelling associated with
Lisfranc dislocation can produce a foot compartment syndrome.
Metatarsal shaft fracture occurs with crush injury or a fall or
jump from moderate height. Midshaft metatarsal fractures also
occur as “fatigue” (or “march”) fractures. These classic overload
injuries may result from prolonged hiking or running with poor
preconditioning. Pain and localized tenderness are hallmarks of
this diagnosis. The dull pain at the midshaft of a metatarsal (often
the second or fifth) may be converted to more severe pain with
associated crepitus by a jump from a log or a rock. These frac-
tures can be temporarily managed with a stiff-soled boot or
A orthotic insert. If there is fracture instability or extreme pain, a
short-leg splint is applied, and no further weight bearing is
allowed until more definitive evaluation and treatment can be
obtained.
Fracture of the Phalanges of the Toes
Toe phalanges are usually fractured by a crush mechanism that
can be prevented by use of steel-toed or hard-toed boots. A great
toe phalanx fracture can be a significant problem because force
is placed on this digit during the toe-off phase of gait (Figure
22-100). Phalanx fractures are managed by buddy taping the toe
to an adjacent uninjured digit with cotton placed between the
toes. Displaced intraarticular fracture of the proximal phalanx of
the great toe may need operative fixation. Stiff-soled boots mini-
mize discomfort during weight bearing.
B
Metatarsophalangeal and Interphalangeal
FIGURE 22-99  Fracture-dislocation of left ankle that occurred during Joint Dislocations
TRAUMA

a fall while bouldering. A, Anterior view with lateral displacement of
foot at subtalar joint. B, Medial aspect of lateral subtalar dislocation.
Tarsal Fracture
PART 4
MTP joint dislocation of the toe is relatively uncommon but can
occur when a moderate axial force is directed at the great toe.
Crush injuries and rock-climbing accidents while the victim is
wearing flexible-soled shoes can produce this injury; wearing
boots with reinforced toe boxes of adequate depth generally
prevents it. Injuries of this type at the great toe may be associated

The calcaneus and talus can be fractured when the victim lands with fractures of the metatarsal joint or phalanx. The dislocation
on the feet following a fall or jump from a significant height (see
Figure 22-7). With a calcaneus fracture, severe heel pain, defor-
mity, and crepitus are immediately evident after the boot is
removed. Talus fracture usually occurs when the foot is forced
into maximal dorsiflexion. Talus fracture may be impossible to
differentiate from ankle fracture on clinical grounds. One rule of
thumb is that an ankle fracture is tender at the malleolus level,
whereas a talus fracture is tender distal to the malleoli. Knowing
the point of the foot’s impact with the ground is also helpful in
differentiating a talus fracture from an ankle fracture. An ankle
fracture more commonly occurs as the result of a twisting injury,
wherein the ankle is inverted or, occasionally, everted. A talus
fracture most often occurs as the result of a high-energy mecha-
nism, such as a fall from a height. The load sustained by the
midfoot is axial and the ankle is dorsiflexed.
Talus fracture may be associated with subtalar or ankle joint
dislocation (Figure 22-99). Emergency evacuation should be
arranged when this injury is suspected because the injury is very
difficult to reduce closed, and pressure on the skin from the
displaced talar body can produce significant skin slough.
Fractures of the other tarsal bones are exceedingly rare but
can be defined by localizing tenderness to a specific site. A short-
leg splint with extra padding is applied, and the limb is elevated
during transportation.
Metatarsal Fracture
Fractures at the base of the metatarsals often accompany midfoot
dislocation, a so-called Lisfranc injury. The mechanism usually
occurs with axial loading of the foot in maximal dorsal flexion
as a result of a motor vehicle crash, most frequently with snow-
mobiling (see Figure 22-98). The victim complains of midfoot
pain and swelling. On removing footgear, crepitus and tender-
ness are noted at the bases of the metatarsals (especially the first,
second, and fifth metatarsals), and plantar ecchymosis may be
present. Overall foot alignment is maintained, but stressing the FIGURE 22-100  Great toe proximal phalanx fracture.

482
 CHAPTER 22  Wilderness Orthopedics
ACL

FIGURE 22-101  Gustilo type II open great toe dislocation occurred

during a fall while hiking in sandals.

is generally dorsal. Because these may be open injuries, the foot

must be inspected carefully. The joint is reduced in a manner FIGURE 22-102  Anterior cruciate ligament (ACL) tear.
similar to that used for dorsal proximal IP joint dislocation of the
hand. MTP dislocation of the great toe can occasionally require
open reduction if the head of the metatarsal buttonholes through inch); grade 2, 5 to 10 mm (0.2 to 0.4 inch); and grade 3 (com-
the sesamoid–short flexor complex. plete tear), greater than 10 mm (0.4 inch). If the mechanism of
The lesser MTP joints are generally dislocated laterally or a knee injury suggests that it is more likely to be ligamentous
medially. The most common mechanism for this injury is striking than bony, weight bearing as tolerated and range of motion as
unshod toes on immovable objects. The toes are relocated by tolerated are safe recommendations. Nonsteroidal antiinflamma-
applying linear traction with the victim supine and using the tory drugs (NSAIDs), compression dressing, and cold (e.g., ice)
weight of the foot as countertraction. Similar mechanisms produce application are palliative methods that may enhance the victim’s
dislocations of the IP joints, which are also reduced by applying ability to ambulate in the wilderness setting.
linear traction with gentle manipulation (Figure 22-101). Once The collateral ligaments stabilize the knee in the lateral and
reduced, the injured toe is taped to the adjacent toe for 1 to 3 medial directions (Figure 22-103). The medial collateral ligament
weeks, and the victim wears a protective boot with a stiff sole (MCL) is more commonly injured than is the lateral collateral
and deep toe box. ligament (LCL), because collisions to the knee usually occur on
the outer aspect or lateral side, which causes the medial joint to
“book” open. The opposite leg usually protects the knee from
OTHER SOFT TISSUE AND being struck medially so that the LCL of the contralateral knee
is often spared. Collateral ligament injuries are graded as 1, 2, or
MUSCULOSKELETAL INJURIES 3. A strain causing pain but having less than 5 mm (0.2 inch) of
discernable joint space opening compared with the uninjured
INTRAARTICULAR KNEE DISRUPTION knee is consistent with a grade 1 injury. A joint space opening
Sprains or tears of knee ligaments are common occurrences in of 5 to 10 mm (0.2 to 0.4 inch) is consistent with a grade 2 injury.
sporting events and other vigorous activities. They often involve
a sudden fall or a twisting mechanism.
The anterior cruciate ligament (ACL) restrains the tibia from
forward displacement relative to the end of the femur. The pos-
terior cruciate ligament (PCL) restrains the tibia from posterior
displacement relative to the femur. ACL injuries are most common
in pivot-twisting sports, such as basketball, soccer, and alpine
skiing, but can occur with simple falls or work injuries (Figure
22-102). PCL trauma is often seen in “dashboard” injuries, in
which the anterior knee is suddenly pushed backward. ACL MCL
injuries are more commonly seen than are PCL injuries, and the
incidence is higher in female than in male athletes. Biomechani-
cal issues in jumping and landing are thought to be largely LCC
involved and more relevant than is the hormonal or intrinsic knee
anatomy (“notch” size).
The individual who sustains this injury often sustains con-
comitant knee injuries, such as meniscus tear or injury to another
ligament in the knee. Tearing the ACL may be accompanied by
the sound of a “pop” in the knee. Usually, but not always, the
knee becomes swollen secondary to hemarthrosis. A sense of
instability is common. On examination, there may be marked
laxity to anterior stress on the tibia relative to the femur
(Lachman’s test).
Although it may be easy to produce anterior tibial transloca-
tion in extension, ACL injuries do not necessarily require immo-
bilization. Grading of sprains is based on laxity or translocation FIGURE 22-103  Medial collateral ligament (MCL) tear with lateral
anteriorly of the tibia on the femur: grade 1, less than 5 mm (0.2 condyle contusion (LCC).

483
 A joint space opening of more than 10 mm (0.4 inch) or the
absence of an end point with valgus stress applied to the knee
is consistent with a grade 3 injury. The MCL is attached to the
medial meniscus, so injury to the medial knee may also cause
injury to the medial compartment cartilage. If symptoms do not
improve in a timely fashion, further evaluation to rule out a
meniscal tear is appropriate.
MCL injury is typically treated with conservative management.
A hinged knee brace that stabilizes the knee from varus and
valgus stress is indicated.
Isolated injury to the LCL is less common than is that of the
MCL. It typically occurs when the outstretched leg is struck from
the medial or inner aspect, producing varus stress to the knee.
The LCL can be strained or torn. The LCL may be injured in
association with a cruciate ligament injury. Complex injuries to
the posterior lateral corner of the knee may also involve the
popliteus tendon and can be disabling in terms of knee stability.
The LCL connects from the lateral femoral condyle to the head
of the fibula but has no direct attachment to the lateral meniscus
(as does the MCL with the medial meniscus).
Most isolated LCL sprains, like MCL sprains, heal with conser-
vative management. The typical time frame of 6 to 12 weeks may
be anticipated for return to full unrestricted activity. A hinged
knee brace that protects the knee from valgus stress is indicated.
When associated with a multiligament injury, especially a cruciate
ligament disruption and posterior lateral instability, surgical repair
may be necessary to restore function.
Individuals and athletes who wish to return to competitive
sports typically have ACL injuries repaired; PCL tears are treated
on a case-by-case basis because many individuals can compen-
sate for this injury without surgery. An ACL-deficient knee often
results in ongoing instability (a “trick knee”), even in nonathletic
TRAUMA
individuals, and the risk for tearing the meniscus or causing other
damage to the knee is high. Rehabilitation from this injury usually
takes a minimum of 6 months.
Meniscal tears in the setting of a ligamentous injury are
common (Figure 22-104). Some tears (bucket handle tears) can
become caught in the joint, and may result in a “locked knee.”
PART 4
Manipulative procedures to slightly widen the joint space wherein
lies the lodged meniscal fragment might liberate an incarcerated
fragment. Sometimes, surgery is the sole solution for this problem.
ACHILLES TENDON RUPTURE
Achilles tendon rupture occurs most commonly in the 35- to
55-year-old age group. This injury usually happens as an indi-
vidual applies an eccentric (lengthening while contracting) load
to the calf and Achilles tendon. The affected individual often
Medial
meniscus
tear
FIGURE 22-104  Medial meniscus tear.
484
feels as though he or she has been struck by a baseball bat at
the posterior aspect of the ankle. Active plantarflexion is impos-
sible. In the Thompson squeeze test, the injured person kneels
on an elevated surface without sitting on the haunches and
allows the feet to hang over the edge of the surface. Squeezing
the calf does not result in involuntary plantarflexion on the
injured side.
Apply a short-leg splint as a temporizing measure. The affected
individual may bear weight as tolerated. This injury may be
treated with or without surgery.
HAMSTRING STRAIN OR TEAR
Hamstring strain or tear can occur when there is a hyperflexion
mechanism applied to the hip simultaneously with a hyperexten-
sion mechanism to the leg (eccentric load). Hamstring tear or
strain can also occur as an overuse injury. The best way to treat
this injury is to apply ice, stretch gently, and bear weight as toler-
ated. Most hamstring tears heal with conservative management.
If a complete tear or significant avulsion from the ischial tuberos-
ity occurs, surgical repair may be indicated. There are no
evidence-based recommendations for repair. However, in active
people with more than 2 cm (0.8 inch) of retraction from the
ischium, repair can result in decreased pain and improved func-
tion over time.
JOINT OR BURSAL EFFUSIONS
Joint or bursal effusions occur when there is excess synovial fluid
production. Effusions may result from trauma (e.g., hemarthrosis
with an ACL tear, or lipohemarthrosis with a tibial plateau frac-
ture). Because it is rarely possible to perform aspiration under
sterile conditions in the wilderness, the effusion should be treated
with NSAIDs, compression dressing, and application of cold. A
painful effusion without trauma in a person over the age of 40
years is more likely gout or pseudogout than infection. If there
is strong suspicion that the effusion may be infected (e.g., accom-
panied by fever, chills, and lack of trauma), antibiotics can be
administered, accompanied by prompt evacuation for aspiration.
OVERUSE SYNDROMES AND
SPECIAL CONSIDERATIONS
PLANTAR FASCIITIS
Plantar fasciitis is inflammation of the fascia (tough connective
tissue) on the sole of the foot. An individual with plantar fasciitis
complains of insidious onset of pain at the origin of the plantar
fascia, which is located at the most anterior medial aspect of the
heel pad. Any activities that stretch the plantar fascia elicit pain.
The pain is worst when first arising in the morning or after resting
and is accentuated when the ankle and great toe are dorsiflexed
(e.g., during push-off). Conservative treatment consists of (1) heel
cord stretching, (2) NSAIDs, (3) taping, and (4) wearing an
orthotic that cups the heel, has a soft spot under the tender area,
and supports the arch. It may take several weeks for symptoms
to improve, but conservative therapy is successful in 90% of
cases. An ankle-foot splint worn at night may help because it
holds the foot in a neutral position, keeping the plantar fascia
slightly stretched. The orthosis also provides significant pain
relief if used while walking.
CARPAL TUNNEL SYNDROME
Carpal tunnel syndrome (CTS) occurs when the median nerve is
compressed within the carpal tunnel (Figure 22-105). Located on
the palmar side of the wrist, the carpal tunnel is formed by the
transverse carpal ligament volarly and the carpal bones dorsally.
The flexor digitorum profundus and superficialis tendons to the
second through fifth digits, long thumb flexor, and median nerve
pass through this canal. Individuals with “compressive median
neuropathy” (CTS) complain of pain and paresthesias along
the palmar aspects of the radial digits. They also complain of
 CHAPTER 22  Wilderness Orthopedics
Thenar Hypothenar
muscles muscles

Median
nerve
Transverse
carpal ligament

A
Superficial branches of the
Median ulnar vein, artery, and nerve
nerve
Transverse carpal Palmar carpal ligament
Tubercle of the ligament
trapezium Tendons of the flexor
digitorum superficialis
Tendon of the
flexor carpi radialis Deep branches of the
ulnar vein, artery,
and nerve

Tendon of the flexor Hook of the hamate

pollicis longus
Tendons of the flexor
digitorum profundus

B
FIGURE 22-105  Anatomic basis of carpal tunnel syndrome. A, General view of the relationship between
the median nerve and the flexor retinaculum. B, Cross section of the distal carpal row, showing the struc-
tures in the carpal tunnel. (Redrawing based on an illustration by Li-Guo Liang, in Yu Hi, Chase RA, Strauch
B: Atlas of hand anatomy and clinical implications, Philadelphia, 2004, Mosby, p 513.)

frequently dropping objects. Symptoms are worse at night and
aggravated with prolonged wrist extension or flexion. The
Phalen’s sign, which is numbness and tingling in the median
nerve distribution after sustained wrist flexion, is suggestive of
CTS. Thenar muscle atrophy is seen only in severe cases. CTS
may occur during pregnancy, or it may be caused by endocrine
disorders (diabetes or hypothyroidism) or acute or chronic
trauma. Treatment consists of wrist splinting in slight extension,
activity modification, and NSAIDs.
STRESS FRACTURES
Stress fractures can occur in individuals who suddenly increase
their activity. Although tibial and metatarsal fractures are most
common, any bone can sustain a stress fracture (Figure 22-106).
Victims complain of pain with weight bearing, swelling, tender-
ness to palpation, and increased warmth at the fracture site.
Treatment consists of activity reduction, protective weight bear-
ing, and avoidance of activities that produce pain. As the pain
subsides, the activity level can be increased. Resolution of symp-
toms may require 2 to 3 months.
BURSITIS, INFLAMMATION, AND IRRITATION
The iliotibial band travels along the lateral thigh, from its origin
at the iliac crest to insertion at Gerdy’s tubercle on the proximal
lateral tibia. Irritation and inflammation occur along the path of
the iliotibial band at the bony prominences over which it runs,
proximally at the greater trochanter and distally at the lateral
femoral epicondyle. Treatment for these conditions in the wilder-
ness involves NSAIDs, ice, and, insofar as it is possible, decreased
activity. Stretching can also be of benefit for these conditions,
especially as a preventive measure or as treatment over the
long term.
Olecranon bursitis and prepatellar bursitis can occur in the
wilderness setting. If either condition arises and is painful, the
antiinflammatory interventions mentioned above can be of
benefit.
SPINAL DISORDERS
Back strain and pain episodes may dampen the enthusiasm of
even the most dedicated outdoor enthusiast. Most often, these
events represent low back strain with associated muscle spasm.
These conditions often occur in the setting of heavy lifting,
bending, or twisting activities. Treatment involves low-impact
exercise, such as walking on a level surface, ice, and NSAIDs.
Occasionally, symptomatic intervertebral disk herniation, pro-
trusion, or extrusion may occur. Typically this is painful and
manifests with or without focal radicular symptoms. In an indi-
vidual with severe, intractable pain, loss of motor strength, or
loss of bowel or bladder function, evacuation may be necessary.

485

FIGURE 22-106  A 53-year-old woman who sustained a fibular stress
fracture after a several-week hike along the Pacific Crest Trail.
TRAUMA
It is important to treat patients rather than diagnostic images.
Individuals with significant scoliosis, spinal angulation, spondy-
lolysis, spondylolisthesis, or arthritis on radiographs (or other
imaging studies) may still function normally. The 56-year-old
woman in Figure 22-107 has significant scoliosis yet remains
PART 4
vigorously active in yoga and carries a full backpack down into
the Grand Canyon on an annual pilgrimage (Figure 22-108).
CORTICOSTEROID INJECTIONS
Corticosteroid injections are commonly performed in the clinic
setting when degenerative joint disease is present or when the
FIGURE 22-107  Lumbar spine radiograph of active individual that
demonstrates significant scoliosis.
486
FIGURE 22-108  This 56-year-old woman does not let her scoliosis
slow her down. She is performing a yoga pose in the Grand Canyon.
pain of bursitis, tendinitis, or muscle inflammation limits activ-
ity.16,27 A corticosteroid injection combined with an anesthetic
drug can offer both diagnostic and therapeutic benefit. When
injected into a joint or area of inflammation, the anesthetic should
provide immediate relief of discomfort if that anatomic site is in
fact that of pain generation. The antiinflammatory benefits of the
corticosteroid component may not be evident for days or weeks.
If concern exists about a possible joint infection, a corticosteroid
should not be injected; treatment with appropriate antibiotics and
surgical referral may be indicated.
The experienced wilderness medicine practitioner can perform
these procedures in an emergency or disaster setting as long as
the sterile “no-touch” technique is used and the benefits of the
procedure are acknowledged to outweigh the risks.
For the sterile no-touch technique, adhere to the following:
1. Cleanse the injection site, wash the hands, use sterile dis-
posable needles and syringes, and use single-dose vials.
2. Change needles after drawing up the solution.
3. Do not touch the skin after marking and cleansing the
injection site.
4. Do not guide the needle with your finger.
5. Carefully inspect any aspirated fluid for turbidity or other
indication of infection.
An injectable anesthetic agent such as lidocaine may be used
to numb the skin initially. Alternately, a topical spray “skin refrig-
erant,” such as ethyl chloride, may be used. A combined solution
of the anesthetic (lidocaine 1% to 2% or bupivacaine 0.25% is
often used) and the corticosteroid preparation may then be
injected into the affected joint. Lidocaine and bupivacaine are
both amides and have a lower risk of adverse effects compared
with the cocaine-derivative ester anesthetics (e.g., benzocaine)
used in the past. The anesthetic solution serves as a diluent and
fluid vehicle to distribute the corticosteroid. Commonly injected
sites are the knee, shoulder, elbow, hip, wrist, ankle, and foot
(Tables 22-1 and 22-2).
Although many infiltrations are performed into the relatively
open joint space of the shoulder or knee, injecting tendon
anchors or ligaments often requires a “peppering” technique to
help disperse the solution throughout the structure. In this tech-
nique there is a single puncture of the skin with redirection of
the needle in the subcutaneous space to achieve multiple pen-
etrations of the tendon, ligament, or fascia. Tendon sheath injec-
tions require the caregiver to be able to insert the needle through
 approach beneath the patella may also be employed. A 10-mL

CHAPTER 22  Wilderness Orthopedics

TABLE 22-1  Joint Injections: Suggested Average Doses
syringe and 1.5-inch 22-gauge needle are used to inject 40 mg
and Total Volumes of triamcinolone acetonide (40 mg/mL) and 9 mL of 1% lidocaine
in a commonly used adult dose. The caregiver should attempt
Dosage Volume
to aspirate the joint prior to the injection. Inspection of the aspi-
Joint or Anatomic Site (mg)* (mL)†
rated fluid should determine the advisability of a corticosteroid
injection. Bloody aspirated fluid is consistent with a traumatic
Shoulder: subacromial or glenohumeral 40 5
ligament injury (often a cruciate tear) or possible tibial plateau
Shoulder: acromioclavicular 10 1
fracture, particularly if there is fat noted in the aspirant. Fluid
Elbow 20 2 with a cloudy appearance may be consistent with a rheumato-
Elbow: epicondyle (medial or lateral) 10 1 logic disorder or inflammatory process such as gout. If there is
Wrist 20 2 evidence of purulence, a corticosteroid injection should not be
Thumb 10 1 performed. Hyaluronic acid injections are sometimes used for
Finger 5 0.5 knee arthritis management but would not be an acute field
Hip 40 5 intervention.
Hip: trochanteric bursitis 20 2
Knee 40 5-10 SHOULDER INJECTIONS
Ankle 20 2
Foot 20 2 Subacromial Joint Injection
Plantar fasciitis 10-20 1-2 “Impingement” symptoms in the shoulder are often due to a
Toe 10 1 combination of subacromial bursitis and supraspinatus tendinitis.
Degenerative fraying of the long head of the biceps tendon and
From Saunders S, Longworth S: Injection techniques in musculoskeletal labrum often accompany these changes. The most commonly
medicine, 4th ed, Edinburgh, 2013, Churchill Livingstone. performed shoulder injection to address these symptoms is
*Dosage (mg): Kenalog-40 (Triamcinolone Acetonide Injectable Suspension,
USP), 40 mg per 1 mL (Bristol-Meyers Squibb Company, Princeton, New Jersey, directed into the subacromial space (Figure 22-109). Insertion of
08543). the needle beneath the posterior-lateral corner of the acromion
†Volume (mg): Combined volume of corticosteroid dose and 1% lidocaine usually allows direct placement into the subacromial space and
solution as anesthetic/dilutant. bursa while remaining above the supraspinatus tendon. The
injection should flow easily. If the needle is correctly placed and
the diagnosis is correct, immediate “diagnostic” improvement is
the sheath overlying the tendon while gently infiltrating the space often noted. A 5-mL syringe and 1.5-inch 22-gauge needle are
between the structures. used to inject 20 mg of triamcinolone acetonide (40 mg/mL) and
4.5 mL of 1% lidocaine; this is a commonly used adult dose.
CORTICOSTEROID MEDICATIONS Glenohumeral Joint Injection
Corticosteroid medications are categorized into three basic cat- This injection may be performed in a patient with degenerative
egories of potency and duration. The short-acting preparation is osteoarthritis of the glenohumeral joint, or “frozen shoulder.” A
hydrocortisone acetate; the intermediate-acting preparation is posterior approach frequently allows easy access to the joint with
methylprednisolone acetate (Depo-Medrol); and the long-acting less pain than would be caused by passing the injection through
preparations are triamcinolone acetonide (Kenalog) and triam-
cinolone hexacetonide (Aristospan).

RISKS AND SIDE EFFECTS OF

CORTICOSTEROID INJECTIONS
Possible risks and side effects associated with corticosteroid injec-
tions may include postinjection flare, prolonged numbness, neu-
rotoxicity, injury due to needle placement, elevation of blood
glucose, infection or sepsis, bleeding or hematoma, skin depig-
mentation, soft tissue calcification, subcutaneous atrophy, bony
osteonecrosis, or a vasovagal event causing loss of consciousness.

KNEE JOINT INJECTION

The knee may be injected with the patient either seated or in a
lying position. If seated, the tibial-femoral joint space can be
accessed either medially or laterally; if supine, a superior-lateral
approach to the retropatellar space is commonly used. A medial

TABLE 22-2  Tendon Injections: Suggested Average

Doses and Volumes
Small 10 mg of steroid plus local anesthetic in a total
tendons volume of 1 mL
(Example: 0.25 mL triamcinolone acetonide + FIGURE 22-109  Injection for shoulder impingement (subacromial
0.75 mL lidocaine) bursitis/supraspinatus tendinitis): The needle is advanced from the
Large 20 mg of steroid plus local anesthetic in a total lateral or posterior-lateral approach into the subacromial space for
tendons volume of 2 mL injection of the combined solution. Ideally, both a short-term diagnos-
(Example: 0.5 mL triamcinolone acetonide + 1.5 mL tic benefit (lidocaine) and prolonged therapeutic benefit (corticoste-
lidocaine) roid) will be used. The dosage is 40 mg of triamcinolone acetonide
and 5 mL of 1% lidocaine, for a total volume of 6 mL. (From Saunders
From Saunders S, Longworth S: Injection techniques in musculoskeletal S, Longworth S, editors: Injection techniques in musculoskeletal medi-
medicine, 4th ed, Edinburgh, 2013, Churchill Livingstone. cine, 4th ed, Edinburgh, 2013, Churchill Livingstone, p 113.)

487
 anterior structures. Palpation of the glenohumeral space and
gentle internal and external rotation of the relaxed upper arm by
an assistant help to guide needle placement. For a common adult
dosage, a 5-mL syringe and 1.5-inch 22-gauge needle are used
to inject 40 mg of triamcinolone acetonide (40 mg/mL) and 4 mL
of 1% lidocaine.
Acromioclavicular Joint Injection
A previous acromioclavicular joint “separation” (grade 1, 2, or 3)
often leads to arthritic changes and pain in the joint. The injec-
tion can be performed with the patient seated and the arm
hanging over the lap to help widen the joint space. Identify the
acromioclavicular joint space and insert the needle through the
capsule, injecting the solution as a bolus. For a common dosage,
a 1-mL syringe and 1.5-inch 25-gauge needle are used to inject
10 mg of triamcinolone acetonide (40 mg/mL) and 0.75 mL of
1% lidocaine.
Trochanteric Bursitis Injection
Trochanteric bursitis (now some­times called greater trochanteric
pain syndrome) is a relatively common problem. Patients who
do not improve with conservative measures may benefit from a
corticosteroid injection into the region of the trochanteric bursa
(Figure 22-110). The injection should be performed at the point
of maximal tenderness. With the patient lying on the unaffected
side, the skin over the greater trochanter is prepped using a
fenestrated drape and sterile procedure. Depending on the
patient’s body habitus, a spinal needle may be required to pen-
etrate the tough iliotibial band and reach the underlying bursa.
A 3-mL syringe and 1.5-inch to 3-inch 22-gauge spinal needle are
used to inject 20 mg of triamcinolone acetonide (40 mg/mL) and
1.5 mL of 1% lidocaine in a common adult dose.
TRAUMA
Olecranon Bursitis Injection
Olecranon bursitis may occur following a traumatic fall or injury
to the elbow with fluid accumulation of a hemorrhagic nature.
Spontaneous swelling may also occur without known antecedent
injury. Infection of the olecranon bursa is a frequent concern.
PART 4
FIGURE 22-110  Injection for trochanteric bursitis: The needle is
inserted over the area of maximal tenderness. It is important to pen-
etrate the tough fascial iliotibial band (ITB) to reach the underlying
trochanteric bursa; if the injection is placed external to the ITB, it is
unlikely to be effective. It may be necessary to use a 3-inch 22-gauge
spinal needle in large patients. The dosage is 20 mg of triamcinolone
acetonide and 3 mL of 1% lidocaine, for a total volume of 3.5 mL.
(From Saunders S, Longworth S, editors: Injection techniques in mus-
culoskeletal medicine, 4th ed, Edinburgh, 2013, Churchill Livingstone,
p 167.)
488
FIGURE 22-111  Injection for lateral epicondylitis (tennis elbow): The
needle is inserted over the lateral epicondyle of the humerus at the
origin of the extensor carpi radialis brevis (ECRB) muscle tendon. Inject
using a fan-wise, peppering technique. The dosage is 10 mg of triam-
cinolone acetonide and 0.75 mL of 1% lidocaine, for a total volume of
1 mL. (From Saunders S, Longworth S, editors: Injection techniques in
musculoskeletal medicine, 4th ed, Edinburgh, 2013, Churchill Living-
stone, p 131.)
Direct aspiration should be performed before injection to evalu-
ate the fluid aspirant. For a common adult dosage, a 2-mL syringe
and 22-gauge needle are used to inject 20 mg of triamcinolone
acetonide (40 mg/mL) and 1.5 mL of 1% lidocaine.
Medial and Lateral Epicondylitis Injection
Medial (golfer’s elbow) epicondylitis and lateral (tennis elbow)
epicondylitis are defined as tendinopathies rather than tendinitis
due to the chronic, granular histologic changes seen in the
tendon matrix. This frustrating condition is often of a slowly
resolving nature, and may benefit from corticosteroid injection
for symptom management if other conservative modalities have
failed. The injection can be performed with the arm resting on
the examination table while the patient is seated or with the
patient supine. The needle should be inserted at the tendinous
origin of the flexor or extensor group, respectively, rather than
at an area of tenderness in the flexor or extensor aponeurosis
(Figure 22-111). A 1-mL syringe and 0.5-inch 25-gauge needle
are used to inject 10 mg of triamcinolone acetonide (40 mg/mL)
and 0.75 mL of 1% lidocaine in a commonly used adult dose.
Iliotibial Band Injection
The iliotibial band syndrome, or iliotibial band friction syndrome,
can cause pain over the lateral aspect of the knee, most com-
monly in the region of the lateral femoral condyle or Gerdy’s
tubercle. The injection can be performed with the patient lying
supine and should be directed to the region of greatest tender-
ness. Care should be taken to avoid neurovascular structures in
the lateral knee, such as the peroneal nerve. A 2-mL syringe and
1-inch 23-gauge needle are used to inject 20 mg of triamcinolone
acetonide (40 mg/mL) and 1.5 mL of 1% lidocaine in a common
adult dose.
Pes Anserine Bursitis Injection
Overuse or trauma to the distal insertion of the medial hamstring
bundle at the medial aspect of the proximal tibia may result in
pes anserine bursitis or tendinitis. This common tendon is formed
by the sartorius, gracilis, and semitendinosus groups. The injec-
tion is best performed with the knee in flexed position and
should be directed at the area of greatest tenderness below the
medial joint line. For a common dosage for adults, a 2-mL syringe
and 1-inch 23-gauge needle are used to inject 20 mg of triam-
cinolone acetonide (40 mg/mL) and 1.5 mL of 1% lidocaine.
 CHAPTER 22  Wilderness Orthopedics
FIGURE 22-112  Injection for plantar fasciitis: The needle is inserted
from the medial plantar aspect of the heel and directed to the anterior
medial aspect of the calcaneus to reach the origin of the plantar fascia.
The dosage is 20 mg of triamcinolone acetonide and 2 mL of 1%
FIGURE 22-113  Right hip resurfacing for osteoarthritis in an active
lidocaine, for a total volume of 2.5 mL. (From Saunders S, Longworth
58-year-old man. Resurfacing arthroplasty provides a surgical option
S, editors: Injection Techniques in Musculoskeletal Medicine, 4th ed,
for osteoarthritis treatment that requires less bone resection than do
Edinburgh, 2013, Churchill Livingstone, p 213.)
more traditional total hip arthroplasty techniques.

Prepatellar Bursitis Injection

Trauma, contusion, or repeated sheer forces to the anterior knee 61-year-old patient who had previously suffered from advanced
may result in inflammation of the prepatellar bursae. This injury hip arthritis trekking in the Himalayas and climbing 6000-meter
may be acute or chronic. Aspiration of the bursa prior to injection peaks after staged cementless, bilateral hip arthoplasties.23 There
is advised. It is important to avoid injecting into the distal patellar were no signs of prosthesis loosening or abnormal wear of the
tendon. A 2- to 3-mL syringe and 1-inch 23-gauge needle are bearing materials in the mountaineer in Figure 22-115 at age 69,
used to inject 20 mg of triamcinolone acetonide (40 mg/mL) and 16 years after the first procedure and 8 years following the
1.5 mL of 1% lidocaine in a common adult dose. second.
Most individuals temper activities following total joint replace-
Plantar Fasciitis Injection ment. Current recommendations regarding a return to activity are
The pain associated with this relatively common problem is often variable. An experienced athlete can usually return to a sport in
focal at the common origin of the fascia from the inferior surface which he or she is skilled following total joint arthroplasty, given
of the anteromedial calcaneus. The injection is best accomplished reasonable limits (Table 22-3). Despite such recommendations,
with the patient lying prone with the foot relaxed on a pillow patients continue to “push the envelope” in returning to aggres-
or other support. Angle the injection from the medial aspect of sive sporting activities. Examples of highly successful returns to
the heel to avoid a direct weight-bearing area of the undersurface play after total hip or total knee replacement abound:
of the foot (Figure 22-112). A common adult dosage uses a 1-mL • Bo Jackson returned to professional baseball in 1993 after
syringe and 0.5-inch 25-gauge needle to inject 10 mg of triam- his total hip arthroplasty in 1992.
cinolone acetonide (40 mg/mL) and 0.75 mL of 1% lidocaine.
Field Block TABLE 22-3  Return to Activity After Total Knee and
The term field block is used to indicate injection or infiltration of Total Hip Replacement*
a local anesthetic into the anatomic area or region of injury for
pain management without attempting to anesthetize a specific Generally Safe Greater Risk Risky Activities
nerve.
Swimming Ice skating Downhill skiing
Hematoma Block Stationary bike/cycling Cross-country ski High-impact
A hematoma block involves diffusely infiltrating a reversible local Low-resistance rowing skating aerobics
anesthetic, such as lidocaine, into the region of a fracture hema- Walking Rollerblading Basketball
toma to achieve pain reduction sufficient to allow manipulation Hiking with poles on Horseback riding Football
in order to attain bony alignment. This can be a useful technique even terrain Softball Hockey
in a wilderness setting. Bier block, brachial plexus block, regional Low-resistance lifting Volleyball Soccer
nerve block, or other controlled methods of parenteral anesthesia Canoeing Hunting on uneven Gymnastics
are more applicable in a hospital setting. Bowling terrain Power lifting
Croquet Fencing Rock climbing
Golf Nordic track Parachuting
RETURNING TO THE WILDERNESS Tennis: doubles Hang gliding
AFTER TOTAL JOINT REPLACEMENT Table tennis Rodeo
Ballroom dancing Distance running
Increasing numbers of outdoor enthusiasts have had total joint Classic cross-country Hardball
replacement surgeries, primarily of the knee and hip, and have Lacrosse
skiing
returned to their previous activities. New technologies, such as
Tennis: singles
hip resurfacing, have been developed to possibly improve lon- Horseshoes Rubgy
gevity of arthroplasty for young active individuals (Figure 22-113). Shooting
Given appropriate physical therapy and rehabilitation, many indi- Shuffleboard
viduals can regain near-normal function. Although the possibility
of reinjury, prosthesis damage, accelerated prosthetic loosening, *There is no absolute consensus regarding return to activity after joint
or periprosthetic fractures remains a concern, many individuals replacement. These suggestions are a synthesis of survey results from The Hip
Society, The Knee Society, and The American Association of Hip and Knee
are willing to accept such risks to enjoy the pursuit of wilderness Surgeons. Virtually all agree that it is important to limit impact loading and
passions (Figure 22-114). rotational or levering forces on the artificial joint. Failure to control these forces
It was barely 50 years ago that Sir John Charnley implanted increases the possibility of prosthetic dislocation, biomechanical failure, or
the first total hip in England. He would be amazed to see a periprosthetic fracture.

489
 A B
FIGURE 22-114  A and B, A 70-year-old woman with a total knee arthroplasty sustained a periprosthetic
distal femoral fracture when she fell while hiking. C, One year after open reduction and internal fixation of
her fractures, she hiked the same trail.
TRAUMA
• Golfer George Archer had a right hip replacement in 1996
and won the Senior PGA Tour in 1998.
• Golfing great Jack Nicklaus had a total hip arthroplasty in
1999 and returned to high-level play.
PART 4
• Figure skater Rudy Galindo had bilateral ceramic-on-
ceramic total hip arthroplasties in 2003 and was landing
triple jumps with Champions on Ice in 2004.
• A 69-year-old mountaineer, after bilateral total hip arthro-
plasties in 1987 and 1995, climbed two peaks over 6000 m
in the Andes.
• Floyd Landis had a hip resurfacing in 2006, was riding a
stationary bike 5 days after surgery, and has since returned
to competitive cycling.
A cautionary and common sense approach is advised. Although
one may attempt to return to a “skill” sport in which one has
participated in the past, it is not recommended that one attempt
to learn a “new” sport that requires advanced proprioceptive
FIGURE 22-115  Bilateral total hip arthroplasties in a patient who, fol-
lowing her second surgery, climbed to the summit of Mt. Rainier.
490
C
skills and/or significant impact loading, as categorized in Table
22-3. Sports and fitness regimens vary significantly with the com-
petence, confidence, and risk tolerance of the individual. High-
risk and high-impact activities may cause accelerated wear and
loosening of implants that lead to the need for early revision.
The necessity for revision arthroplasty has a markedly increased
cost and rate of complications relative to primary joint replace-
ment, and the functional result tends to deteriorate with each
successive revision.
Although dislocation of a normal hip is a rare event caused
by high-energy trauma, hip replacements dislocate with relative
ease. If this occurs, the reduction maneuver is the same as
described above.
PROSTHETICS IN THE WILDERNESS
Orthotics and limb replacement devices have given individuals
who have sustained amputations, whether from trauma, congeni-
tal disorder, or cancer, the chance to participate in wilderness-
based adventures that in the past may have been unattainable.
Computer-assisted prosthetic design now enables much better
custom-fitted prostheses and therefore provides the opportunity
for recipients to participate in outdoor activities with other “able-
bodied” individuals, often on an equal basis. Some persons have
claimed that the new prostheses, in certain instances, offer an
enhanced level of performance, as in the case of the South
African runner Oscar Pistorius, with his bilateral graphite-carbon
“feet.” In the wilderness setting, there may be significant benefits
in not worrying about frostbite or getting one’s foot back into a
cold boot at dawn (Figure 22-116). However, additional concerns
remain. These include limb swelling, skin breakdown in a limb
stump, inability to change a sock liner on a regular basis, and
possibility of prosthesis damage.
Intrepid mountaineers, such as Tom Whittaker, who became
the first below-the-knee amputee to summit Mt. Everest in 1998,
testify to the capabilities of a motivated athlete despite limb loss32
(Figure 22-117). Whittaker founded and has worked for years
with the Cooperative Wilderness Handicapped Outdoor Group
(C.W. HOG). Many members of this organization suffer from
spinal cord injuries, cerebral palsy, amputations, or other
 CHAPTER 22  Wilderness Orthopedics
FIGURE 22-116  Tom Whittaker marked his tent at Mt. Everest base
camp with a spare prosthesis so that his 70-year-old father, who hiked
to 18,000 feet after a total hip replacement, could find the correct tent.
(Copyright Tom Whittaker Collection.)

neuromuscular problems. In spite of this, they have participated

in diverse activities and mountaineering (Figure 22-118).

NEW TECHNOLOGIES FOR CASTING

AND BRACING
The Flemish army surgeon Mathijsen first introduced muslin
rubbed with calcium that formed a hard shell and provided the
first plaster of Paris casts in 1852. Synthetic fiberglass became
popular in the 1980s and has become the dominant material used
in casting and splinting in the United States. Plaster remains
desirable in some situations because it molds easily and is inex-
pensive. Both plaster of Paris and fiberglass are removed using FIGURE 22-118  Tom Whittaker assists fellow Cooperative Wilderness
a cast saw. When wet, plaster of Paris becomes sodden and Handicapped Outdoor Group (C.W. HOG) member Carl Brinker with
heavy and loses stability. Waterproof linings, such as Gore-Tex, rappelling down an 80-foot basalt cliff. (Copyright Tom Whittaker
may allow fiberglass casts and splints to be used in wet environ- Collection.)
ments. Other materials, such as Aquaplast and Orthoplast, may
be softened in a hot water hydrocollator and have specific indica-
tions in appropriate patients.
New prefabricated casting and bracing materials have evolved
from ski boot technologies. These use dry heat–formable poly-
mers laminated with closed-cell foam and antiabrasive fabrics to
provide custom-fitted musculoskeletal support devices. These
materials are waterproof, lighter than fiberglass, durable, and
remoldable, and use adjustable closure systems. Such products
offer improved patient comfort and allow early return to hiking,
skiing, or water sports (Figure 22-119).

FIGURE 22-117  Tom Whittaker on Aconcagua’s Argentine Andes. FIGURE 22-119  New dry heat–formable thermoplastic technologies,
Note carbon flex prosthesis on right lower extremity. (Copyright Tom such as this Exos fracture brace, are durable, waterproof, and light-
Whittaker Collection.) weight, allowing earlier return to outdoor activities.

491

FIGURE 22-120  Prompt evacuation in certain scenarios is crucial.
DECISIONS ABOUT EVACUATION
The decision to evacuate an orthopedically injured individual
depends on the goals of the expedition or mission and available
support. Criteria for evacuation of an injured person in a family
of four spending a week hiking in the Rockies differ from those
of a military campaign or group of 25 climbers in the Himalayas
with physician support and a field hospital at base camp. In all
cases, party leaders should have a plan for contacting evacuation
support teams if a serious injury occurs (Figure 22-120).
Musculoskeletal injuries that warrant immediate evacuation to
a definitive care center are listed in Box 22-2. These include any
suspected cervical, thoracic, or lumbar spine injury. A victim who
has a suspected pelvic injury with posterior instability, possibly
significant blood loss, or injury to the sacral plexus should be
BOX 22-2  Indications for Emergency Evacuation
Suspected spine injury
Suspected pelvic injury
Open fracture
Suspected compartment syndrome
Hip or knee dislocation
Vascular compromise to an extremity
Laceration with tendon or nerve injury
Uncertainty of severity of injury
emergently evacuated on a backboard. Any open fracture requires
definitive debridement and care within 8 hours to prevent deep
infection. Victims with suspected compartment syndromes must
be evacuated on an emergency basis. Joint dislocations involving
the hip or knee warrant immediate evacuation because of the
associated risk for vascular injury or posttraumatic avascular
necrosis of the femoral head.
Lacerations involving a tendon or nerve warrant urgent evacu-
ation to a center where an extremity surgeon is available. In all
but the most serious wilderness expeditions, arrangements should
be made to evacuate the victim when the treating individuals are
not reasonably certain of the nature of the injury or its appropri-
ate management.
REFERENCES
Complete references used in this text are available
online at expertconsult.inkling.com.
REFERENCES
1. Almekinders LC, Logan TC. Results following treatment of traumatic
dislocations of the knee joint. Clin Orthop Relat Res 1992;284:203.
2. Baykal B, Sener S, Turkan H. Scapular manipulation technique for
reduction of traumatic anterior shoulder dislocations: Experiences of
an academic emergency department. Emerg Med J 2005;22:336.
3. Bohlman HH, Ducker TB, Lucas JT. Spine and spinal cord injuries in
the spine. In: Rothman RH, Simeone FA, editors. The Spine. 2nd ed.
Philadelphia: WB Saunders; 1982.
4. Browner BD, Jupiter JB, Levine AM, et al. Skeletal trauma, vol. 1. 2nd
ed. Philadelphia: WB Saunders; 1998.
5. Burgess AR, Eastridge BJ, Young JW, et al. Pelvic ring disruptions:
Effective classification system and treatment protocols. J Trauma 1990;
30:848.
6. Reference deleted in proofs.
7. Dalal SA, Burgess AR, Siegel JH, et al. Pelvic fracture in multiple
trauma: Classification by mechanism is key to pattern of organ injury,
resuscitative requirements, and outcome. J Trauma 1989;29:981.
8. Dyck DD Jr, Porter NW, Dunbar BD. Legg reduction maneuver for
patients with anterior shoulder dislocation. J Am Osteopath Assoc
2008;108:571.
9. Fernandez-Valencia JA, Cune J, Casulleres JM, et al. The Spaso tech-
nique: A prospective study of 34 dislocations. Am J Emerg Med 2009;
27:466.
10. Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syn-
drome: Course after delayed fasciotomy. J Trauma 1996;40:342.
11. Gentile DA, Morris JA, Schimelpfenig T, et al. Wilderness injuries and
illnesses. Ann Emerg Med 1992;21:853.
12. Green NE, Allen BL. Vascular injuries associated with dislocation of
the knee. J Bone Joint Surg Am 1977;59:236.
13. Gustilo RB, Anderson JT. Prevention of infection in the treatment of
one thousand and twenty-five open fractures of long bones: Retro-
spective and prospective analyses. J Bone Joint Surg Am 1976;58:453.
14. Hendey GW, Avila A. The Captain Morgan technique for the reduction
of the dislocated hip. Ann Emerg Med 2011;58:536.
15. Johansen K, Daines M, Howey T, et al. Objective criteria accurately
predict amputation following lower extremity trauma. J Trauma 1990;
30:568.
16. Kesson M, Atkins E, Davies I. Musculoskeletal Injection Skills.
Edinburgh: Elsevier Science: Butterworth-Heinemann; 2003.
17. Leland A, Oboroceanu MJ: American war and military operations
casualties: Lists and statistics. <http://www.fas.org/sgp/crs/natsec/
RL32492.pdf>.
18. Ly TV, Swiontkowski MF. Treatment of femoral neck fractures in
CHAPTER 22  Wilderness Orthopedics
young adults. J Bone Joint Surg Am 2008;90:2254.
19. Merritt K. Factors influencing the risk of infection in patients with
open fractures. J Trauma 1988;28:823.
20. Montalvo R, Wingard DL, Bracker M, et al. Morbidity and mortality
in the wilderness. West J Med 1998;168:248.
21. Nessen SC, Lounsbury DE, Hetz SP, editors. War surgery in Iraq and
Afghanistan: A series of cases, 2003-2007. Washington, DC: Borden
Institute; 2008.
22. O’Connor DR, Schwarze D, Fragomen AT, et al. Painless reduction of
acute anterior shoulder dislocations without anesthesia. Orthopedics
2006;29:528.
23. Peters P. Mountain sports and total hip arthroplasty: A case report
and review of mountaineering with total hip arthroplasty. Wilderness
Environ Med 2003;14:106.
24. Quinn R, Williams J, Bennett B, et al. Wilderness Medical Society
Practice Guidelines for Spine Immobilization in the Austere Environ-
ment: 2014 Update. Wilderness Environ Med 2014;25(4):S118–33.
25. Routt ML Jr, Falicov A, Woodhouse E, et al. Circumferential pelvic
antishock sheeting: A temporary resuscitation aid. J Orthop Trauma
2006;20:S3.
26. Sagarin MJ. Best of both (BOB) maneuver for rapid reduction of
anterior shoulder dislocation. J Emerg Med 2005;29:313.
27. Saunders S, Longworth S. Injection Techniques in Musculoskeletal
Medicine. 4th ed. Edinburgh: Churchill Livingstone; 2013.
28. Schatzker J, Barrington TW. Fractures of the femoral neck associated
with fractures of the same femoral shaft. Can J Surg 1968;11:297.
29. Shelbourne KD, Porter DA, Clingman JA, et al. Low-velocity knee
dislocation. Orthop Rev 1991;20:995.
30. Swiontkowski MF, Winquist RA, Hansen ST Jr. Fractures of the femoral
neck in patients between the ages of twelve and forty-nine years.
J Bone Joint Surg Am 1984;66:837.
31. te Slaa RL, Wijffels MP, Brand R, et al. The prognosis following acute
primary glenohumeral dislocation. J Bone Joint Surg Br 2004;86:58.
32. Tom Whittaker: <http://www.tomwhittaker.org>.
33. Ufberg JW, Vilke GM, Chan TC, et al. Anterior shoulder dislocations:
Beyond traction-countertraction. J Emerg Med 2004;27:301.
34. Varnell RM, Coldwell DM, Sangeorzan BJ, et al. Arterial injury com-
plicating knee disruption: Third place winner: Conrad Jobst award.
Am Surg 1989;55:699.
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1986;160:445.
492.e1
 CHAPTER 23 
Splints and Slings
MISHA R. KASSEL, TERRY O’CONNOR, AND ALAN GIANOTTI
Splints and slings1 have been staples of medical care for
thousands of years. For instance, orthopedic splinting was
well documented in ancient Egypt more than 5000 years ago49
(Figure 23-1).
First and foremost, splints and slings stabilize injuries by limit-
ing movement (Box 23-1). Limiting movement minimizes pain
and decreases potential further tissue damage. Splinting eases
transportation from the field, minimizes blood loss, and aids in
healing.19 In general, all fractures and dislocations should be
splinted before transport unless the patient’s life is at immediate
risk or the rescue scene is unsafe.20 Basic splint types include
rigid, soft, anatomic, and traction splints. Splint choice is based
on the fracture type and available materials. In improvisational
situations, splints can be made from just about any material.
Examples include newspapers, pillows, umbrellas, and other
supportive materials (Figure 23-2).8
SPINE IMMOBILIZATION
Spinal cord injuries are rare, affecting 40 to 50 individuals per
million annually in the United States. These injuries may result
492
in long-term disability.32 The 5 million people each year who are
placed in spine immobilization after traffic collisions account for
most spinal cord injuries. In one wilderness study, only 3.6% of
mountain trauma patients who were alive when rescued had
spine injuries.27
Spine stabilization has traditionally been first accomplished by
manual techniques and then by mechanical devices (e.g., back-
boards, collars, straps), which we review below. We will also
review newer immobilization devices. In light of recent evidence
and guidelines, the indications, risks, and benefits of spine immo-
bilization merit review.
INDICATIONS FOR SPINE IMMOBILIZATION
The most common scenario for prehospital spine immobilization
is an injury sustained during a motor vehicle collision. All-terrain
vehicles, automobiles, snowmobiles, motorcycles, and other
off-road vehicles are the most common causes of high-
force spine trauma in the wilderness setting. Falls and other
high-force mechanisms are other causes. Worrisome symptoms
include spine pain or palpable tenderness, altered mental status,

FIGURE 23-1  A fractured and splinted forearm showing signs of
healing. Egyptian mummy from Dynasty V. (From Arab S: Medicine in
ancient Egypt. http://www.arabworldbooks.com/articles8b.htm.)
FIGURE 23-2  Improvised cervical spine and ankle stabilization (pillow,
towels, cardboard, and tape) in Port au Prince, Haiti, 2010. (Courtesy
Anil Menon, MD.)
BOX 23-1  Principles of Splinting
Visualize the injured body part.
Continually recheck the patient’s neurovascular status.
Traction is indicated if the pulse is not palpable.
Gentle traction involves less than 10 pounds of force.
Cover open wounds with sterile dressings.
Immobilize the joints above and below the injury.
Padding prevents further tissue damage.
Do not reset open or protruding fractures.
Splint the extremity in the position in which it was found.
Splint the patient before transport (if he is stable).
Ice and elevate the injury after immobilization.
Modified from Bowman W, editor: Outdoor emergency care: comprehensive
prehospital care for nonurban settings, 4th ed, 2003, Sudbury, Massachusetts,
Jones and Bartlett; and Campbell J: Extremity trauma: international trauma life
support for prehospital care providers, 6th ed, Upper Saddle River, New Jersey,
2008, Brady.
neurologic complaints, or a head injury. Factors that may com-
CHAPTER 23  Splints and Slings
plicate a spine injury are extremes of patient age, patient alcohol
or drug use, and a communication barrier between patient and
caregivers. If the examination is unreliable because another injury
distracts the examiner, important information about the spine
injury may be missed9 (Box 23-2).
BENEFITS OF SPINE IMMOBILIZATION
In an attempt to improve outcomes, techniques for immobiliza-
tion of the patient with potential spine injury have been imple-
mented in the prehospital setting. Spine immobilization as
performed on urban trauma patients remains the standard of care.
Evidence-based reviews reveal that although spine immobiliza-
tion efforts are well intentioned, a definitive understanding of
their effects on neurologic injury and spine stability and their
adverse effects (including death) in trauma patients remains
uncertain.32
Spine immobilization is intended to prevent worsening of an
existing spinal cord injury or the creation of a spinal cord injury
in the case of a ligamentous disruption. Previous reviews of the
medical literature reference multiple reports of worsening neu-
rologic deficits after patients with spinal cord injuries are
moved.9,51,52 Recent expert reviews reveal that these episodes of
neurologic deterioration are more likely a result of the original
injury itself and not poor prehospital care or immobilization.45
The authors report that the most frequently referenced cases
of missed spine injuries resulting in neurologic deterioration
occurred after arrival in the emergency department.6,15,54 Some
data suggest that nonimmobilized patients had better neurologic
outcomes than patients with similar injuries who had been immo-
bilized.25 Such evidence suggests that not only is secondary injury
due to transport rare, but real risks to the patient due to spine
immobilization warrant consideration.
RISKS OF SPINE IMMOBILIZATION
Extreme settings mandate a different interpretation of “urban”
recommendations to fit the wilderness scenario. Wilderness data
are limited, so prehospital spine immobilization is still considered
prudent when practical. The routine use of spine immobilization
without consideration of risks, however, can greatly increase the
complexity of a wilderness care scenario, potentially leading to
increased complications and even death for the patient and,
perhaps, adverse effects for rescue personnel.
Placing a patient in spine immobilization can adversely affect
breathing and airway management. The American Heart Associa-
tion 2010 evidence-based guidelines state that “Routine C-spine
immobilization is Class III (potentially harmful) unless clear
trauma is evident in the history or exam, because it may unnec-
essarily delay or impede ventilations.”4 One study conducted on
healthy volunteers showed that placing a patient on a backboard
restricts respiration, with older patients having a greater degree
of restriction.55
Studies have shown that C-spine collars cause increased intra-
cranial pressure, which may be clinically significant for patients
BOX 23-2  Indications for Spine Immobilization
Spine pain or tenderness
Traumatic mechanism of injury
Altered mental status
Distracting injury
Unreliable examination (e.g., as a result of alcohol or drug use)
Neurologic complaints
Head injury
Extremes of age
Modified from Brabson T, Greenfield M: Prehospital immobilization. In Roberts
JR, Hedges JR, editors: Clinical procedures in emergency medicine, 5th ed,
Philadelphia, 2007, Saunders.
493
 with head injuries.18,29 Therefore, hard cervical collars should be Severely injured patient
removed immediately after exclusion of a C-spine injury, espe- Altered mental status (GCS <15,
cially from patients with head injuries. Blunt trauma with
mechanism suspicious evidence of intoxication)
C-spine collars are contraindicated in patients with penetrating
for spine trauma Neurological deficit
neck injuries, because they may interfere with management of
Thoracic or other significant
neck wounds or even conceal wounds. Penetrating wounds to
distracting injury
the spinal cord are rare. Cervical immobilization creates the real
possibility of causing greater morbidity.26
Isolated
Pressure ulcers are very painful complications that can result
penetrating trauma Yes No
from spinal immobilization. Pressure ulcers begin forming within
30 minutes of immobilization. This is particularly troubling when
one considers that the mean time a patient spends on a back-
board can exceed 2 hours in an urban setting. This time is likely Significant
Yes
protracted in wilderness settings.12 Immobilize spine pain or
Complications of full spine immobilization are listed in tenderness ( 7/10)
Box 23-3.

CONTRAINDICATIONS FOR No
No
SPINE IMMOBILIZATION
Strict contraindications for spine immobilization are few but Patient voluntarily able
include emergency evacuation from an unsafe environment. No immobilization to flex, extend, and
Examples of such environments, with the risk of impending (further evaluation/treatment Yes rotate spine (cervical
danger, include areas of toxic spills, fire hazards, congested
may be required at or thoracolumbar)
traffic, and other situations in which application of an immobili-
sophisticated point of care) 45° in each plane,
zation device would delay immediate evacuation to safety. In
regardless of pain
these dangerous situations, expedited removal with manual cervi-
cal stabilization is advised.31 When the patient is in a safe loca- FIGURE 23-3  Wilderness Medical Society recommendations for spine
tion, full spine immobilization can be applied as indicated. clearance and immobilization in the austere environment. (Reprinted
with permission from the Wilderness Medical Society. Copyright
GUIDELINES FOR SPINE IMMOBILIZATION 2014 Wilderness Medical Society).
TRAUMA

The emergency medical community has considered precaution-

ary immobilization to be uniformly safe, conservative, and in the
best interest of the patient. However, in some cases, spine immo-
bilization may not be in the patient’s best interest.
In light of this recent thinking, efforts to minimize unwar-
ranted or potentially hazardous immobilization have begun as
PART 4
or tenderness to the posterior neck and back, and the neurologic
examination must find normal motor and sensory function in the
extremities.28
For the wilderness setting, a similar guideline has been

evidenced by development of selective immobilization guide-
lines. Several states and emergency medical systems (EMSs)
across the nation are beginning to use protocols that decrease
the number of trauma patients subjected to prehospital spine
immobilization. Studies show that prehospital care providers can
safely apply these spine injury assessment protocols and not miss
clinically significant spine injuries.16,40,50
The guidelines that have been adopted by multiple prehospi-
tal systems are typically based on the Canadian C-spine rule and
the National Emergency X-Radiography Utilization Study (NEXUS)
low-risk criteria. Each has similar parameters, requiring that the
patient be awake, alert, and conversant, and without significant
distracting injury or intoxication. In addition, the guidelines
further state that the physical examination should reveal no pain
BOX 23-3  Complications of Spine Immobilization
Tight straps and a rigid board may cause discomfort or distress.
Tight straps may cause vascular compromise.
An immobilized position may interfere with normal respiratory
function.
Complications from emesis include aspiration.
Intracranial pressure may become elevated.
Pressure ulcers may develop.
Penetrating neck injuries may be associated with morbidity.
Loose straps may be inadequate for spine immobilization.
recently proposed. The treatment algorithm was specifically cali-
brated so as to minimize the risk of exacerbating a potentially
unstable spine injury weighed against the risks to rescuers and
victim in the austere setting.45 (Figure 23-3). Further research is
still warranted to better classify appropriate indications, validate
guidelines, and further assess the risk-benefit ratio for spine
immobilization in the wilderness.
CERVICAL SPINE IMMOBILIZATION TECHNIQUE
High cervical spine (C-spine) injuries have great potential for
morbidity and disability. The goals of C-spine immobilization are
to minimize movement and maintain “neutral” alignment. Stan-
dard C-spine immobilization is performed with a hard collar in
conjunction with a backboard, vacuum mattress, or similar
device. Typically, lateral support devices are also employed. The
modern standard cervical collar has five contact points and makes
use of the head, C-spine, and thorax. The thorax contact points
include the trapezius muscles (posterior), clavicle, and sternum
(anterior). Hard collars alone do not adequately limit cervical
motion. Backboards and lateral support devices are required in
conjunction with a hard collar (Figures 23-4 and 23-5). Newer
vacuum spine boards also serve this purpose (Figure 23-6). The

From Brabson T, Greenfield M, editors: Prehospital immobilization. In Clinical

procedures in emergency medicine, 5th ed, Philadelphia, 2007, Saunders;
Campbell J: Extremity trauma: international trauma life support for prehospital
care providers, 6th ed, Upper Saddle River, NJ, 2008, Brady; Hamilton RS, Pons
PT: The efficacy and comfort of full-body vacuum splints for cervical-spine
immobilization, J Emerg Med 14:553, 1996; and Kwan I, Bunn F, Roberts I:
Spinal immobilization for trauma patients, Cochrane Database Syst Rev (2): FIGURE 23-4  Standard hard cervical collars. (Courtesy Laerdal Medical
CD002803, 2001. Corporation.)

494

A
C D
FIGURE 23-5  A to C, Different lateral support devices. D, Complete
spine immobilization. (Courtesy Laerdal Medical Corporation.)
patient’s neck requires manual stabilization in a neutral, in-line
position until he or she is fully immobilized. Standard emergency
medical services equipment includes lateral support devices
(foam or plastic). In the wilderness setting, these devices can be
improvised by rolling clothes, sheets, or blankets and placing
them on both sides of the head while securing everything in
place with tape (see Figure 23-2).24
C-SPINE IMMOBILIZATION DEVICE
The application of a C-spine immobilization device depends on
the position in which the patient is found and the device that is
available. Universal application diagrams are generally helpful
with regard to in-line stabilization, neutral neck alignment, chin
positioning, and collar placement. Diagrams for application of
improvised C-spine collars or C-spine collars on patients who are
found in sitting positions are also helpful (Figures 23-7 to 23-10).
SPECIAL CONSIDERATIONS
Special populations require accurately sized equipment. This
includes people with a very long or short neck for whom a
FIGURE 23-6  Vacuum lateral support device. (Courtesy Rick Lipke,
Copyright 2014 by Conterra, Inc. All rights reserved. Used by
permission.)
CHAPTER 23  Splints and Slings
FIGURE 23-7  Improvisational “horse collar.” (Courtesy Ferno-
Washington, Inc.)
standard cervical hard collar is not effective. Children who are
younger than 8 years old are at risk for further injury when
immobilized on a standard backboard because of a proportion-
ately large head, which may cause increased flexion during a
collision.56 Modifications to counter this anatomic feature include
raising the shoulders to the level of the head by placing a pad
underneath the shoulders (Figure 23-11). This should be consid-
ered for all children who are on backboards.42,43
Cases of neurologic deterioration, and even death, have now
been reported with the use of a cervical collar in patients with
ankylosing spondylitis.53 In these patients, a cervical collar is
contraindicated.
IMPROVISATIONAL TECHNIQUES
The key ingredients to an improvisational C-spine device include
maximizing stability and fit while limiting airway compromise
and allowing access for mouth opening, thus limiting aspiration
FIGURE 23-8  Fashioning an improvised cervical spine collar from a
SAM Splint. (Courtesy Alan Gianotti, MD.)
495
 A B C

D E F
TRAUMA
PART 4

G H I
FIGURE 23-9  Improvised cervical spine collar from a SAM Splint. A, Fold 36-inch splint 5 inches from the
end. B, While bracing the thumbs on either side of the fold, pull the edges to create a V-shaped chin rest.
C, Place the chin rest below the patient’s chin, and place the rest of the splint loosely around the patient’s
neck. D, Bring the end forward and down in an oblique direction until it touches the chest. E, While sup-
porting the chin, bring the chest portion of the splint around the chin to create a chin post. Squeeze to
deepen the chin post. F, Insert the index fingers on either side of the splint and pull. G, Squeeze to create
lateral posts to ensure a snug fit. H, Squeeze the back of the splint to create more stability. I, Fold up any
excess splint and secure it with wrap or tape. (Courtesy SAM Medical Products.)

risk.21 A “horse collar” technique involves a towel, blanket, or
other available and malleable material rolled to the desired thick-
ness and placed underneath the patient’s neck. The ends are
crossed over the patient’s chest and secured. As with the cervical
hard collar, the patient’s C-spine is maintained in a neutral posi-
tion during application and for as long as possible afterward by
manual in-line stabilization2,9 (see Figure 23-7).
A structural aluminum malleable (SAM) splint can also be
molded into a C-spine collar. Studies have shown it to be as
effective as a Philadelphia collar, with the advantage of being
small, lightweight, versatile, and portable. These characteristics
are advantageous in the wilderness setting (see Figure 23-9).38 A
similar device can be fashioned by wrapping sleeping mattress
padding or closed-cell foam around the support of a rolled wire
splint (Figure 23-12).
THORACOLUMBAR IMMOBILIZATION
A full-length immobilization device best accomplishes immobili-
zation of the thoracolumbar spine. In addition, a cervical collar,
lateral neck stabilizers, and backboard straps are essential for full
spine immobilization. If the patient is already upright, standing,
or lying supine, application of full-body immobilization is
straightforward, as described later in this chapter. However, with
the suspected cervical injury of a seated patient, an intermediate
device is required. There are many forms of this short board,
such as a Kendrick Extrication Device (see Figure 23-10). Short
boards are applied only after manual in-line stabilization and
cervical collar placement have been performed. When the short
board is in place, the patient can be safely transferred to full
spine immobilization.9
FULL SPINE IMMOBILIZATION
From a supine (lying) position and after placement of a cervical
collar, the patient is logrolled, or the slide and transfer technique
is used to place the patient onto a board or vacuum splint. With
the logroll technique, three people are required to transfer a
patient onto a board. The first person is positioned at the head
and applies in-line stabilization, the second is at chest level, and
the third is at pelvis level. On the command of the person at the
head, the patient is rolled onto the least-injured side. The board
is slid underneath the patient while the back is evaluated for
injuries. With the lift and slide technique, multiple attendants are
also required. One individual maintains manual, in-line stabiliza-
tion of the head and neck while the other rescuers straddle the
victim in preparation for lifting the upper torso, hips, pelvis, and
lower extremities. A final assistant is responsible for placement

496
 CHAPTER 23  Splints and Slings
A B

C D
FIGURE 23-10  A, Kendrick Extrication Device (KED). B, Manual in-line stabilization of the cervical spine
with the KED slid behind the patient. C, Applied KED with cervical collar in place. D, Patient transferred
to long board. (Courtesy Ferno-Washington, Inc.)

of the spine board. When all participants are ready, the individual
stabilizing the head and neck directs the others to raise the
patient off the ground to enable the remaining rescuer to slide
the spine board under the patient from the foot end. Body
straps and lateral neck stabilizers are then placed (Figures 23-13
and 23-14).9
Choices for full-body splints include hard backboards, scoop
stretchers, and full-body vacuum splints (Figures 23-15 to 23-18).
Full-body hard backboards have been traditionally used. Unfor-
tunately, their size and weight make them undesirable for back-
country use. Secured straps minimize spine movement during
transport. These are especially important with vomiting patients,
when the airway is potentially compromised and a quick change
of position is required to allow for removal and drainage of
emesis.9 Hard backboards are uncomfortable. Spine pain that is
induced by a backboard may be misinterpreted, and this can
complicate and delay therapy.23 Because rigid backboards can
induce pain, patient agitation, pressure ulcers, and respiratory
compromise, a recent position statement from EMS physicians
and trauma surgeons has advocated limiting their use.41
Logrolling is not required with scoop stretchers, thereby mini-
mizing spine movement (see Figure 23-16). Scoop stretchers, like
other rigid devices, are otherwise compromised by the same
disadvantages listed above.
Vacuum splint devices offer certain advantages over rigid
hard backboards. They can be applied more quickly and are
significantly more comfortable (Figure 23-19 and see also Figure
23-18). They also offer a similar degree of spine immobiliza-
tion.30 Several studies have demonstrated that a vacuum mattress
provides significantly superior spine stability, increased speed
of application, and markedly improved patient comfort when
compared with a backboard. Vacuum mattress immobilization of
the potentially injured spine is the current recommendation of
the International Commission for Mountain Emergency Medi-
cine.19 During mountain rescue, vacuum splints are therefore
the preferred device for total spine immobilization (Figure 23-20
and see also Figures 23-18 and 23-19). In circumstances in
remote austere settings with limited resources where quick extri-
cation is necessary, semirigid spine boards can be improvised
(Figure 23-21).

497
 A

FIGURE 23-13  Logroll technique for spine immobilization. (Courtesy

Terry O’Connor, MD/Ketchum, Idaho, Fire Department.)

C
FIGURE 23-11  Backboard considerations and increased cervical
flexion for children who are younger than 8 years old. A, A young child
immobilized on a standard backboard. Note how the large head forces
the neck into flexion. Backboards can be modified by an occiput cutout
(B) or a double mattress pad (C) to raise the chest. The actual clinical
consequences of this observation are unknown. (Modified from
Herzenberg JE, Hensinger RN, Dedrick DK, et al: Emergency transport
and positioning of young children who have an injury of the cervical
spine, J Bone Joint Surg Am 71:15, 1989.)
TRAUMA

FIGURE 23-14  Lift and slide technique for spine immobilization.

PART 4

(Courtesy Terry O’Connor, MD/Ketchum, Idaho, Fire Department.)

FIGURE 23-12  Wire splint/closed-cell foam improvised cervical collar.

(Courtesy Terry O’Connor, MD.)

FIGURE 23-15  Standard rigid backboard. (Courtesy Laerdal Medical

Corporation.)

498
 CHAPTER 23  Splints and Slings
A

FIGURE 23-17  Example of a full-body vacuum splint used for wilder-

ness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff
Department, Utah.)

LOWER EXTREMITY SPLINTING

Although the principles of lower extremity splinting are similar
to those of upper extremity splinting, the ramifications are not
the same in terms of evacuation. Lower extremity fractures are
B more likely to involve weight-bearing bones and thus to require
rigid splinting. Specific recommendations, including positions of
function, are found in Tables 23-2 and 23-3.
One needs look no further than Joe Simpson’s 1985 epic
self-rescue from the Peruvian Andes, which was described in
Touching the Void, to appreciate the pain of an unsplinted
weight-bearing fracture48:
The moment I jumped I knew I would fall…. I had lain
face-down in the gravel, clenching my teeth, waiting for
the pain to subside. It remained with me, burning my
knee unbearably as it had never done before… I stood
and fell, writhed where I fell, cried and swore, and felt
sure in my heart that these were my last spastic efforts
before I lay still for good.

D
FIGURE 23-16  A, Scoop stretcher. B, Stretcher placed beside the
patient. C, Stretcher slid under the patient. D, Stretcher locked in place
with straps secured. (Courtesy Ferno-Washington, Inc.)

SPLINTING OF THE EXTREMITIES

UPPER EXTREMITY SPLINTING
The most common upper extremity injury scenario is bracing
from a ground-level fall. Rigid and soft splints are used to stabi-
lize upper extremity injuries. It is always important to leave
fingertips exposed to allow continuous assessment of neurovas-
cular status.9 Common examples of upper extremity splints
include malleable, cardboard, air, vacuum, pillow, and sling and
swathe splints. Specific splinting recommendations for upper
extremity injuries are given in Table 23-1. When feasible, FIGURE 23-18  Conterra Vacuum Spine Board. (Courtesy Rick Lipke,
upper extremity injuries are splinted in a position of function Copyright 2014 by Conterra, Inc. All rights reserved. Used by
(Table 23-2). permission.)

499
 TYPES OF EXTREMITY SPLINTS
Rigid Splints
Green Rigid splints can be improvised from materials such as cardboard,
wood, and wire. Proprietary vacuum splints and air splints are
commonly used in the field. Rigid splints are attached to the
extremity with a variety of fasteners, including tape, straps,
gauze, and Velcro. For all splints, ample padding is essential,
especially over bony surfaces and swollen tissue to minimize
pressure damage and pain.8
Yellow Cardboard splints have the advantage of being lightweight,
inexpensive, easy to apply, and radiolucent.9 They can be
premade or improvised (Figures 23-22 to 23-24 and see also

Red
1 2

1) The top of the patient’s head should be even with the top seam of
the device.
2) Connect the straps in “stoplight” color order; first red, then yellow,
then green. This is the proper sequence for nonrigid devices like
the VSB and VSI.
TRAUMA

3 4
PART 4

3) Connect the blue and black decell straps over the shoulders and
under the arms.
FIGURE 23-20  Example of vacuum spine board applied in high-angle
4) Make sure the pelvic binder is over the lower third of the pelvis rescue. (Courtesy Andy Rich, Remote Rescue Training.)
and tighten.

Mold the
VSB around
the patient’s
head and
shoulders
6

5) Close the valve and plug in the pump (not too tight!). Mold the VSB
around the patient’s head and shoulders while pulling the air out of
the device (you cannot overpump).
6) Retighten the straps.

• Stow the VSB with the buckles clipped together and the pump nested in
the center of the device.This will ensure that it is ready for the next use.
• We recommend that the VSB and pump be stored inside its protective
bag. This will ensure that the device is clean and ready for use. It will
also add years to the life of the product.
FIGURE 23-19  Application instructions for vacuum spine board.
(Courtesy Rick Lipke, Conterra EMS/Rescue.)
FIGURE 23-21  Example of improvised spine immobilization. (Cour-
tesy Terry O’Connor, MD.)

500
 CHAPTER 23  Splints and Slings
TABLE 23-1  Upper Extremity Splints TABLE 23-2  Splinting Guidelines: Positions of Function

Splint Indication Splint Position

Figure-of-eight splint Medial clavicular fractures Volar wrist splint Neutral forearm (thumb up) with the wrist in
Sling and swathe splint Shoulder and humerus injuries 20 degrees of flexion
Sugar-tong splint Ulnar and radial Neutral forearm with the wrist in 20 degrees
  Proximal Humeral fractures gutter splints of extension; metacarpophalangeal
  Distal Wrist and distal forearm fractures joint in 50 degrees of flexion; proximal
Posterior arm splint Stable elbow and forearm injuries interphalangeal joint in slight flexion (e.g.,
Volar splint Wrist fractures and fractures of the 10 degrees); distal interphalangeal joint in
second through fifth metacarpals extension
Gutter splint Phalangeal and metacarpal fractures Thumb spica splint Forearm neutral with the wrist in 20 degrees
Thumb spica splint Scaphoid fractures, thumb dislocations of extension and the thumb slightly flexed
and fractures, and ulnar collateral to allow for thumb–index finger opposition
ligament injuries and alignment of the thumb and the
Volar finger splint Fractures of the distal phalanges and forearm
interphalangeal joints Finger splint Finger in slight flexion
Sugar-tong and Elbow at 90 degrees of flexion with a neutral
Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint
use: recommendations for treatment protocols, Am J Emerg Med 19:137, 2001;
posterior arm position of the forearm and the wrist
Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, splints
Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos Posterior leg splint Ankle at 90 degrees
in clinical medicine: basic splinting techniques, N Engl J Med 359:e32, 2008;
Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel G, editors: An Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint
introduction to clinical emergency medicine, Cambridge, UK, 2005, Cambridge use: Recommendations for treatment protocols, Am J Emerg Med 19(2):137,
University Press; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts 2001; Boyd AS, Benjamin HJ, Asplund C: Splints and casts: indications and
J, Hedges J, editors: Clinical procedures in emergency medicine, 5th ed, methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M,
Philadelphia, 2009, Saunders. et al: Videos in clinical medicine: basic splinting techniques, N Engl J Med
359:e32, 2008; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J,
Hedges J, editors: Clinical procedures in emergency medicine, 5th ed,
Philadelphia, 2009, WB Saunders.

TABLE 23-3  Lower Extremity Splints

Splint Indication

Knee immobilizer splint Knee injuries

Posterior ankle splint Distal tibial and fibular injuries;
ankle, tarsal, and metatarsal Long backboard Short backboard
fractures
Stirrup splint Ankle fractures
Buddy taping Toe fractures
Traction splint Femoral fractures

Modified from Boyd AS, Benjamin HJ, Asplund C: Splints and casts: indications
and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath Board splint Ladder splint
M, et al: Videos in clinical medicine: basic splinting techniques, N Engl J Med
359:e32, 2008; Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel
G, editors: An introduction to clinical emergency medicine, Cambridge, UK,
2005, Cambridge University Press; and Chudnofsky CR, Byers SE: Splinting
techniques. In Roberts J, Hedges J, editors: Clinical procedures in emergency
medicine, 5th ed, Philadelphia, 2009, Saunders.
Padded board Cardboard splint

Aluminum splint Half ring

Air splint
FIGURE 23-22  Premade cardboard splint. (Courtesy Ferno- FIGURE 23-23  A variety of splints. (From Geiderman JM, Katz D:
Washington, Inc.) General principles of orthopedic injuries. In Marx J, Hockberger R,
Walls R, editors: Rosen’s emergency medicine: concepts and clinical
practice, 7th ed, Philadelphia, 2009, Saunders. Used with permission.)

501
 A B

FIGURE 23-24  Improvising a pelvic compression device. This card-
board splint is used to treat the lower extremity. (Courtesy Alan
Gianotti, MD.)
TRAUMA
C D
FIGURE 23-25  Vacuum splinting. A, A variety of vacuum splints.
B, Stabilizing the fracture while laying the splint flat under the injured
limb with the valve on the outside. C, Securing the splint. D, Remov-
ing air from splint to complete the application. (Courtesy Ferno-
Washington, Inc.)
Soft splints allow for more laxity than do rigid splints, but can

be combined with rigid splints for extra stability.

Figure 23-2). When improvising, it is important to cut the card-
board so that the corrugations run lengthwise to maintain the
PART 4
Pillow splints are soft splints adapted for wrist and hand
injuries. Their main advantages are ease of application and
comfort.9 As with other soft splints, they allow for more move-
ment at the fracture site but are bulkier than other splints.

material’s intrinsic strength. Splints can be individually fitted

using the unaffected extremity as a model and placed on the
affected extremity. They are usually secured with adhesive tape.
Disadvantages include loss of integrity when wet and greater
laxity as compared with other splinting options. The distorted
and grossly swollen extremity is difficult to splint using this
technique.19
Although they are initially malleable, vacuum splints are a
type of rigid splint (Figure 23-25). These splints are made of
many tiny plastic pellets in a closed, airtight bag. The bag is
placed around the injured extremity, and air is manually
extracted via a hand pump to form a rigid “mold” of the injured
extremity. The extremity is left in its position of injury to mini-
mize pain (Figure 23-26). No external force is applied, thereby
maximizing circulation.9 Unfortunately, vacuum splints are
expensive, moderately bulky, affected by changes in altitude,
and penetrable. In addition, any perforation renders the splint
nonfunctional.19
A lightweight, inexpensive, and popular rigid splint is the SAM
Splint. Constructed of an aluminum center that is sandwiched
between thin strips of foam, this splint is also malleable and
versatile.9 It is very strong and pliable, and it can be used for
nearly all extremity requirements.
Other malleable splints include ladder splints (i.e., pliable
metal splints) and rolled-wire splints, both of which are readily
available at most outdoor sporting goods stores8 (Figure 23-27).
Given their weight, size, reliability, versatility, and cost, malleable
splints have become a popular choice for the universal
wilderness medical kit.19 They may also be fashioned with impro-
vised padding, such as mattress padding or foam (see Figure
23-12).
Soft Splints
A soft splint earns its name from the soft, padded material that FIGURE 23-26  Upper and lower body vacuum splints used for wilder-
is used to secure the injury. Soft splints include sling and swathe ness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff
splints, pillow splints, and blanket-roll splints10 (see Figure 23-2). Department, Utah.)

502

FIGURE 23-27  Pliable metal ladder splints. (Courtesy Ferno-
Washington, Inc.)
Sling and swathe splinting can be used alone or in combina-
tion with other forms of splints. Shoulder, clavicle, upper arm,
elbow, forearm, wrist, and even hand injuries are commonly
stabilized with a sling and swathe. For a shoulder injury in which
it is not possible to adduct the arm, a pillow (or similar material)
can be used to bridge the empty space, with the sling supporting
the arm and the swathe stabilizing it.9 This technique takes
advantage of the chest wall to provide the splint foundation.
Distal humeral injuries necessitate a sling and swathe splint in
combination with rigid splints. Sling and swathe splinting is used
alone for many clavicle, shoulder, and proximal humeral injuries.
Its advantages are its light weight, portability, and improvisational
versatility.
Air splints are hybrid splints that are made from inflatable yet
durable plastic. These splints are most often used for the elbow,
knee, and ankle (Figure 23-28). They are placed around the
injured extremity and inflated to the desired pressure and rigid-
ity.8 They have the advantages of being lightweight and portable.
Variable external pressures can be used to control hemorrhage.
External pressure has the potential to limit distal perfusion. Air
splints should be temporarily deflated (e.g., for 5 minutes
every 90 minutes) to decrease the risk for ischemic damage.10 Air
splint pressure varies with altitude and temperature. For these
reasons, it is important to reevaluate neurovascular status during
transport.19
SAM Splints
Malleable splints, such as SAM Splints,58 no longer fall into the
category of improvised splinting. These splints are commonly
found in the standard wilderness medical kit. They are light-
weight, reusable, versatile, and padded, and not affected by
changes in pressure or temperature. They are radiolucent to
allow radiographs to be taken with the splint in place. The
malleable SAM Splint is pliable in its native form, yet easily
FIGURE 23-28  Lower extremity air splint used for a wilderness rescue.
(Courtesy Ed Gray.)
CHAPTER 23  Splints and Slings
A
B
C
FIGURE 23-29  Basic SAM Splint adaptations. A, C-curve. B, Reverse
C-curve. C, T-curve (maximum strength). (Courtesy SAM Medical
Products.)
strengthened with creasing. The basic SAM Splint adaptations
are depicted in Figure 23-29. In addition, the SAM Splint can
be molded to form an adequate C-spine collar (see Figures 23-8
and 23-9).
Improvised Extremity Splints
Improvised splints can be made from branches, boards, padded
pack straps, or rolled-up newspapers or magazines. Anatomic
splints involve an uninjured neighboring body part, primarily a
digit. Slings can also be made from unused clothes.8 In these
cases, one need not pack additional materials. Improvised splints
have a disadvantage in that they are less effective than commer-
cial splinting devices.19
TECHNIQUES OF SPLINTING
PELVIC SPLINTING
Pelvic fractures are potentially life-threatening injuries.34 Splinting
is essential for pain and hemorrhage control. Pelvic fractures are
often difficult to diagnose in the field but must be suspected
when a high-force mechanism of injury has led to pelvic pain or
an altered sensorium. A pelvic compression device should be
applied.19 Appropriate stabilization with such a splinting device
slows hemorrhaging and stabilizes fracture fragments.9 Open-
book fractures (i.e., diastasis of the pubic rami with posterior
pelvic disruption) create a large surface area for potential hemor-
rhage. Circumferential compression of the pelvis is recommended
for emergency stabilization.7 This can be accomplished by pelvic
circumferential compression devices, a pneumatic antishock
garment (PASG), compression devices incorporated into vacuum
spine boards, or improvised techniques such as pelvic sheeting10
(Figure 23-30; see also Figure 23-24).
Optimal pelvic stabilization is achieved by applying a sling
around both greater trochanters and the symphysis pubis.7 Pelvic
circumferential devices are similar in function (Figure 23-31).
A pelvic compression device can be improvised in the wilder-
ness. Sheets, jackets, and other long fabrics are readily available
on most expeditions. The sheet or fabric is wrapped around the
503
 FIGURE 23-30  Pelvic compression device incorporated into vacuum
spine board. (Courtesy Rick Lipke, Conterra EMS/Rescue.)
pelvis over the greater trochanters and the symphysis pubis and
pulled tight and secured to increase pressure at the wound and
to decrease the potential space for hemorrhage. The PASG
and the military antishock trousers, which were commonly used
in the past, have generally fallen out of favor (Figure 23-32).
TRAUMA
Proponents of PASG and military antishock trousers point to the
position paper of the National Association of EMS Physicians for
support. The paper states that the PASG is beneficial in the
setting of a ruptured abdominal aortic aneurysm and that it is
potentially beneficial in many other scenarios (e.g., hypotension
from pelvic fractures, gynecologic bleeding, ruptured ectopic
PART 4
pregnancy, severe traumatic hypotension, and uncontrolled
A PASG use include diaphragmatic rupture, penetrating thoracic
B Femoral fractures result from high-force trauma. These fractures
“Click”
C pected femoral fracture in the nonambulatory patient. The pro-
FIGURE 23-31  Application of the SAM Pelvic Sling. A, Remove all
objects from the pockets. Place the sling under the patient’s hips.  and other adverse sequelae while achieving realignment of bone
B, Place the black strap through the buckle, and pull it completely
through. C, Hold the orange strap with one hand and pull the black
strap in the opposite direction under tension until a click is heard.
Maintain tension, and place the black strap against the sling surface
to secure. (Courtesy SAM Medical Products.)
504
FIGURE 23-32  Military antishock trouser/pneumatic antishock gar-
ment. (Courtesy Common Cents EMS Supply.)
lower extremity hemorrhage).17 Postulated successful mecha-
nisms for correcting hypotension include increasing peripheral
vascular resistance, tamponade of local hemorrhage, and
increasing blood return from the lower extremities.33 PASG dis-
advantages include prolonged scene time, pressure changes with
altitude (e.g., potential compartment syndrome with air travel),
and interference with normal pulmonary function.39 In addition,
animal studies have demonstrated lactic acidosis after prolonged
use. Rapid deflation may cause hypotension as a result of volume
redistribution. Studies have not shown improvement in hospital
duration, and others have shown increased mortality rates.13
PASGs are bulky and expensive. Absolute contraindications for
injury, splinted lower extremity fracture, gravid uterus, or abdom-
inal evisceration.33 Thus, routine use of the PASG in the field is
not recommended. In the case of isolated femoral fracture, a
PASG can be used, but other viable options are more readily
available in the wilderness.
HIP AND FEMUR SPLINTING
can be diagnosed clinically in the appropriate wilderness setting.
Deformity, swelling, and tenderness along the thigh and in the
face of significant trauma are highly suggestive of a femoral
fracture.22 Femoral fractures produce significant hemorrhage; a
closed femoral fracture may bleed more than 1 L into the thigh.14
Femoral shaft fractures also have a mortality rate that ranges from
20% to 54%.37
A general indication for traction splint placement is any sus-
posed benefits of traction splints are to minimize blood loss, pain,
fragments.9
It is important to note that proposed benefits of traction
beyond typical splinting are purely anecdotal. There are no
definitive studies demonstrating morbidity or mortality benefits
from prehospital use of traction splints.44,59
 Contraindications to traction splint placement are fractures
that involve the knee, pelvis, or ankle, or that include damage
to the sciatic nerve.37 Unfortunately, such comorbidities are
common with severe wilderness injuries, which makes it impos-
sible or dangerous to anchor the traction splint.5 Controversy
exists regarding whether a traction splint should be placed with
an open femoral fracture, but this is not a strict contraindication.
In general, it is argued that splinting these patients in the field
increases on-scene time and endangers their well-being.5,36
In summary, in a patient with an isolated femoral fracture and
no other apparent injuries, traction splints may be appropriate,
but there is no medical evidence to show they would improve
the patient’s ultimate outcome. Although their use is well inten-
tioned, the proposed benefits are theoretical. Traction splints take
some time to apply properly, and in a patient with multiple
injuries, that time must be weighed against using other stabiliza-
tion maneuvers and moving the patient toward the place where
the injuries can be definitively treated.
There are many femur traction splint devices, and all are
based on the same principle: a rigid frame that anchors at the
proximal pelvis and extends traction beyond the distal heel.
The proximal aspect is padded against the ischial tuberosity.
Traction to the fractured femur is applied with a heel strap that
is anchored off of the distal frame. The thigh, knee, and leg are
also secured with soft straps.19 Traction devices that have a
half-ring design (e.g., Thomas or Hare splints) can cause hip
flexion of up to 30 degrees. This can cause incomplete fracture
realignment unless the leg is elevated to match the angle.9 Trac-
tion splints that do not have a posterior half-ring (e.g., Sager
splints) do not compress the sciatic nerve and can be used with
groin injuries. They can also be used for patients with pelvic
fractures or for bilateral femoral fractures by applying a splint
to each leg.47
Traction splint application is not always intuitive (Figures
23-33 to 23-36). Two rescuers are needed for proper placement.8
Manual traction should be applied to reduce the fracture until
the splint can be placed.1 As with any splint placement, it is
important to establish pain control, check neurovascular status
both before and after splint placement, and fully explain the
process to the conscious patient. After the proximal femur splint
is in place, the thigh strap is fastened. The ankle harness is placed
just above the malleoli and attached to the distal splint. Traction
(6.8 kg [15 pounds]) is applied, and the remaining straps are
applied. After the traction splint is in place, the patient should
be logrolled onto a backboard to minimize fracture fragment
movement.8 Improvised traction splints in small studies have
been shown to create similar pounds of traction at 30 minutes.57
Traction splint complications result from improper strap and
splint placement and include sciatic or peroneal nerve injury,
pressure wounds, hemorrhage, and pain.10,19,37,47
Different femur traction systems can be improvised out of very
little material. A double-runner system is a very straightforward
technique that can be used in a wilderness setting (Figure 23-37).
The patient’s own boot can be used to improvise a hitch and a
traction system (Figure 23-38). One more option is a Buck’s trac-
tion device, which uses a foam pad and duct tape and can be
better for longer transports because it distributes the force of
traction over a larger area (Figure 23-39). For the proximal
anchor, one can use a Cam lock/Fastex slider system and attach
it to a tent pole, ski pole, or other similar device (Figures 23-40
and 23-41).
ANKLE SPLINTING
Ankle sprains are common orthopedic injuries incurred during
expeditions and the most common of all sprains.2 There are liter-
ally hundreds of examples of available over-the-counter ankle
supports, braces, an
constraints of the patient’s hiking boot. The time-tested alterna-
CHAPTER 23  Splints and Slings
tive is athletic tape. The taped sprained ankle has talofibular liga-
ment support (for a limited duration), and tape does not add
significant weight to the medical kit. All wilderness health care
providers should be adept at taping ankles.
SHOULDER DISLOCATION
Anterior shoulder dislocation is a common injury. The arm is
most comfortable in an abducted position. This can be accom-
plished with a rolled blanket, pillow, jacket, or SAM Splint that
has been fashioned into a triangle (Figure 23-42).
A shoulder spica wrap can be used for support if a shoulder
dislocation has been reduced (Figure 23-43).
HUMERUS SHAFT INJURY
Humeral shaft fracture is often treated with a sling or with a sling
and swathe splint alone. For pain control, a splint is often desir-
able (Figure 23-44).
ELBOW DISLOCATION
A dislocated elbow can be reduced in the field with the appro-
priate analgesia and experience. The dislocated elbow can also
be splinted in place and the patient transported for definitive
care (Figure 23-45).
ELBOW FRACTURE
A sugar-tong splint is useful for most elbow injuries. These most
commonly include supracondylar, olecranon, and radial head
fractures (Figures 23-46 and 23-47).
WRIST FRACTURE
The volar wrist splint is used for most wrist fractures, dislocations,
sprains, lacerations, and other wrist injuries. A T-beam volar wrist
splint, fashioned by applying a T-curve to the folded SAM Splint,
can be used for greater support when traveling over rough terrain
or when more support is desired (Figure 23-48).
METATARSAL FRACTURES
Ulnar gutter splints are used for fourth and fifth metatarsal injuries
and for corresponding digit injuries (Figure 23-49).
THUMB INJURIES
A thumb spica splint is used for suspected scaphoid (navicular)
fractures, thumb dislocations and fractures, and ulnar collateral
ligament injuries (Figure 23-50). If splinting material is not avail-
able, the thumb should be taped until more definitive care is
available (Figure 23-51).
FINGER INJURIES
Finger splints are used for finger fractures, fingertip injuries, and
lacerations (Figure 23-52).
FEMORAL FRACTURE
A femoral traction splint can be improvised in a variety of ways
with a SAM Splint. One practical wilderness example involves
the use of ski poles and a SAM Splint. An improvised version of
a half-ring splint is made from two ski poles, a small piece of
metal, and a 91.4-cm (36-inch) SAM Splint (Figure 23-53).